Compendium

of Paediatric Dentistry
edited by
ak-Kowalczyk
Authors:

Grazyna Marczuk-Kolada MD, PhD

Prof. Dorota Olczak-Kowalczyk MD, PhD Compendium
Lidia Postek-Stefanska MD, PhD
Piotr Sobiech MD, PhD
of Paediatric Dentistry
Prof. Joanna Szczepanska, MD, PhD
Anna Turska-Szybka, MD, PhD
edited by
Prof. Dorota Olczak-Kowalczyk MD, PhD

Med Tour Press International

\'/YOAW�IC TWO MC:DYCZtl[
 Reviewers: Table of contents
Prof. Teresa Bachanek MD, PhD
Prof. Jolanta Pytko-Poloùczyk MD, PhD Foreword ....................................................................................................................... 9

Editing and proofreading:

Part I ............................................................................................................................. 11
Wieslaw Krajewski PhD Child at the dental office
Graphie design, typesetting:
SaroProjekt Olga Saracen Chapter 1 ....................................................................................................................... 11
Child at the dental office
Cover design and graphie design: Chapter 2 ....................................................................................................................... 22
Olga Saracen Dental staff's relationship with the child and their parent
Chapter 3 ....................................................................................................................... 30
Cover photo:
Pharmacological management ofthe child for dental treatment
https://www.freepik.com/ Chapter 4 ....................................................................................................................... 43
Dental examination ofpaediatric patient and initial treatment plan
© Copyright by Med Tour Press International Ltd. 2023
Part II ........................................................................................................................... 65
Ali rights reserved. The publication is subject to the protection provided Development and developmental abnormalities
by Polish and international law, including in particular the provisions of of the dentition and masticatory organ
on copyright and related rights and on combating unfair competition.
Chapter 5 ....................................................................................................................... 65
ISBN 978-83-87717-35-3 Tooth and periodontal development
Chapter 6 ....................................................................................................................... 7 5
Publisher: Anatomiccil and histological differences in the structure
.J ofdeciduous and permanent teeth
Med Tour Press International Sp. z o.o.
Chapter 7 ........................ __ ............................................................................................. 84
Otwock 05-400, ul. Sportowa 3 suite 5 Developmental abnormalities ofthe teeth
Chapter 8 ..................................................................................................................... 102
Developmental defect ofenamel and dentin
Chairman of the Board, Publishing Bouse Editor in Chief:
Chapter 9 ..................................................................................................................... 126
Juliusz Minakowski MD, PhD Teeth eruption. Developmental phases ofthe dentition
email: [email protected] Chapter 10 ................................................................................................................... 139
[email protected] Physiological signs and pathological symptoms ofteething.
www.medtourpress.pl Tooth eruption disorders
Edition I, Otwock, 2023
PART III .................................................................................................................... 150
Caries disease
Translation from Polish:
"dogadamycie.pl" Sp. z o.o. Chapter 11 ................................................................................................................... 150
Aetiology ofdental caries
Printing: Chapter 12 ................................................................................................................... 160
Epidemiology ofdental caries in developmental age
Totem.corn.pl
Chapter 13 ................................................................................................................... 167 Part VI ........................................................................................................................ 370
The carious process - clinical and radiological diagnosis Periodontal and oral mucosa diseases in children and adolescents
Chapter 14 ................................................................................................................... 182
General principles of caries management in children and adolescents Chapter 27 ................................................................................................................... 370
Chapter 15 ................................................................................................................... 198 Oral mucosa! diseases in children
Non-invasive methods for treating caries in children and adolescents Chapter 28 ................................................................................................................... 386
Chapter 16 ................................................................................................................... 204 Gingival and periodontal diseases in developmental age
Invasive methods of caries treatment in children and adolescents
Chapter 17 ................................................................................................................... 226 Part VII ...................................................................................................................... 400
Prevention of dental caries Odontogenic infections in the child
Chapter 18 ................................................................................................................... 247
Fluoride in prevention of dental caries Chapter 29 ................................................................................................................... 400
Periapical abscesses - pharmacological and surgical treatment
PART IV ..................................................................................................................... 261 Chapter 30 ................................................................................................................... 407
Dental pulp diseases Extractions of deciduous teeth - indications, contraindications,
technique, complications
Chapter 19 ................................................................................................................... 261
Dental pulp diseases and periapical tissue lesions in children Part VIII .................................................................................................................... 418
and adolescents - diagnosis, causes, course of the disease process Patient with a general medical problem at the dental office
Chapter 20 ................................................................................................................... 274
Treatment of dental pulp diseases and periapical lesions in deciduous teeth Chapter 31 ................................................................................................................... 418
Chapter 21 ................................................................................................................... 294 Specifics of the management of patients with intellectual
Specificity of pulp disease treatment of immature permanent teeth and/or physical disabilities
Chapter 32 ................................................................................................................... 423
Part V.......................................................................................................................... 315 Oral diseases and general health
Acquired damage to teeth of non-carious origin
Index ........................................................................................................................... 429
Chapter 22 ................................................................................................................... 315
Dental trauma - epidemiology, causes, classifications, complications
Chapter 23 ................................................................................................................... 325
Specifics of the dental examination of the dentally traumatised child
Chapter 24 ................................................................................................................... 330
Trauma to deciduous teeth - diagnosis, treatment, prognosis according
to the International Association of Dental Traumatology
Chapter 25 ................................................................................................................... 341
Trauma to permanent teeth - diagnosis, treatment, prognosis according
to the International Association of Dental Traumatology
Chapter 26 ................................................................................................................... 363
Abrasions, attrition, abfraction and erosion
Foreword

Changes in the modern world, especially in the fields of technology, information

technology, the emergence and implementation of new technologies also have an impact
on the development of medical science and modern clinical medicine. This also applies
to dentistry, which has undergone complex transformations in recent years in particular.
Related to this is the need to improve systems for training future medical staff and to
modernise and update educational programmes in medical schools. This justifies the
need and desirability of preparing modem academic textbooks, which will convey the
latest professional knowledge necessary in everyday medical practice in a synthetic and
at the same time activating way for readers.
Developmental dentistry is a difficult medical speciality. It requires not only exten­
sive dental and general medical knowledge, but also the ability to approach the young
patient in the right psychological way, taking into account their developmental stages
and the attitudes and behaviour of their parents or carers.
The authors of the "Compendium of Paediatric Dentistry" have attempted to write
an academic textbook that meets and fulfils the requirements and standards of contem­
porary practice in the development and preparation of this type of modern teaching aid.
The scope of the textbook covers the oral health problems of developmental age
patients, taking into account the variety of aspects and specificities of dental care for
the young patient. The authors' aim was to present all stages of a child's treatment, star­
ting with the first visit to the dental office, through diagnosis and clinical diagnosis and
treatment procedures. All the material in the handbook is divided into eight parts, each
divided into chapters - there are 32 in total. The individual sections of the handbook
cover the following topics:
• a child in the dental office,
• development and developmental abnormalities of the dentition
and the masticatory organ,
• dental caries,
• dental pulp diseases,
• acquired damage to teeth of non-carious origin,
 • periodontal and gingival tissue diseases in children and adolescents,
• periapical infections in a child,
• a patient with a general medical problem at a dental office.
The chapters conclude with items of scientific literature from recent years. This con­ Part I
ditions the validity of the presented content discussed on the basis of scientific evidence.
The textbook is the collective work of a team of authors - academics, university ac­
ademics, specialists involved in medical clinical practice. Their professional experience
Child at the dental office
and the fact that the content of the work is based on the latest scientific reports are deter­
minants that influence its content value, the modernity and topicality of the knowledge
provided.
Chapter 1
I would like to thank the authors and co-authors of the individual chapters for their
efforts and contributions in compiling and preparing this edition. We thank the reviewers Child at the dental office
for their insightful and positive evaluation of the manuscript and the scientific publisher
Med. Tour Press for the very good editorial and editorial cooperation and the high edito­ Dorota Olczak-Kowalczyk
rial level of this new publishing position.
I am convinced that the "Compendium of Pediatric Dentistry" textbook will be ap­
preciated and of particular interest to dental students of English-speaking faculties of
Polish medical universities. It fills a gap in the dental literature recommended in accor­
dance with medical and dental education programs at medical universities constituting An important element of dental care for the developmental-age patient is the forma­
a source of current knowledge in the field of pediatric dentistry. tion of attitudes and health-promoting behaviours in relation to the oral health of the pa­
I dedicate this book to all dental practitioners who undertake the burden of dental tient himself and his parents (carers), including the child's behaviour in the dental office
care for children and young people, and to my family, who understand the challenges ensuring his cooperation and friendly relations with the dental staff.
associated with it. In assessing a patient's potential cooperation, it is important to know the patient's pe­
riods of psychosocial development, to assess the patient's behaviour, i.e. attitude to treat­
Prof Dorota O/czak-Kowalczyk MD, PhD ment and anxiety level (Tab. 1.1), as well as the numerous determinants of the child's
Warsaw, December 2023 behaviour and the anxiety they experience.
The assessment of the child's behaviour in the office can be done using appropri­
ate methods, e.g. Frankl 's behaviour rating scale (FBRS), the child anxiety and be­
haviour assessment method according to Venham or the Haupt behaviour scale modified
by Carthers et al. Simple in practical application and also reliable is the Frankl scale. Its
drawback is the lack of sufficient information about the uncooperative child.
A child's behaviour in the practice is conditioned by a number of factors, including
those related to the child themselves, their parents (carers) and the dental environment
(Tab. 1.2).

11
Compendium of Paediatric Dentistry Child at the dental office

Tab. I. I. Frankl's behaviour rating scale. Child

Behavioural category Behavioural characteristics
refusal of treatment, crying forcefully and demonstratively, According to Piaget's developmental theory, psychosocial development begins at birth
Definitely negative
fearfulness or other features of extreme negativity and has a staged nature (Tab. 1.3). In order to reach maturity, a child has to go through each
reluctance to accept treatment, is uncooperative behaviour, stage in turn. The child's current developmental stage and the course of the previous stage
Negative some signs of negation but does not expressing them out loud,
i.e. is sullen, withdraws (avoidance reactions)
influence the child's behaviour and determine the behaviour of the dental staff.
acceptance of treatment with some reserve, sometimes cau-
Positive Tab. 1.3. Stages of child intellectual development according to Piaget's theory.
tiously, cooperates, follows dentist's instructions
good communication with the dentist, cooperative, interested
Age Intellectual
Definitely positive Characteristics of intellectual development
in the procedure and the dentist's activities, cheerful, satisfied development stage
- exploring the outside world through the senses of taste,
Tab. 1.2. Determinants of children's behaviour in the dental office. touch, hearing and manipulation,
- the need for proximity to the mother,
Determinants of child behaviour 0-24
months Sensorimotor stage - sense of ownership,
- period of psychosocial development, - singling out one's own self - the stubbornness of a two-
- personality and temperament, year-old,
- general health, - indivisible and short attention span,
- intellectual, sensory, physical fitness, - forming first habits
.
_ developmental disorders, behavioural and emotional dis- - intensive speech development,
Child-related orders, - egocentrism,
_ the way the child is brought up (parents, grandparents, - animism (attributing characteristics to inanimate objects
educators, contact with other children), of living organisms),
- dental anxiety, - rigidity of thinking- inability to adapt to change, i.e.
- previous "medical" and "dental" experiences, inclu?ing new information, changes in the external appearance of
experience of pain, inadequate preparation for a v1s1t, etc. objects,
- mother's age, father's age, - pre-logical (transductive) reasoning- sees a cause-and-
- parents' level of education, effect relationship between elements occurring simulta-
- the economic status of the family, neously, although no such relationship actually exists
- mother's and father's own level of dental anxiety and their (e.g. "if it is dark it is always night") and reverses the
Related to parents attitudes towards dental treatment, cause-and-effect sense,
(guardians) - parents' level of health awareness and lifestyle, 2-7 years Preoperational stage
- symbolism,
- parents' level of emotional intel Iigence, 2 years: development of self-control and sense of selfl1ood,
- the emotional state of the parents, behaviour dependent on adult attitudes, lack of ability to
- parenting style, take another person's perspective, _sensing emotions and
parental attitude towards the child adapting to them,
- the conditions in the waiting room and the surgery (equip- 3-4 years: attention intractable and indivisible, emotional
ment, appearance, work organisation), labile, causes of anxiety: noise, stranger, darkness,
- psycho-physical characteristics of the staff, such as appear- 4.5-7 years: curiosity - age of questions, egocentrism - un-
Associated with the dental derstanding the world only from one's own point of view,
ance, tone of voice, body language, empathy, composure,
community focusing attention on only one aspect of a situation, irre-
sense of humour or observational skills,
- staff competence - knowledge of dentistry and child psy- versibility of the thinking process (returning to the starting
chology, interpersonal communication skills point), fear caused by imagination and of being ridiculed,
4-5 years: shame emerges (the child begins to cover self-up,
to defend access to own body)

12
13
Compendium of Paediatric Dentistry
Child at the dental office

- egocentricity and rigidity of thinking disappear, peer contacts, school, learning, experiences). It can be defined as a set of diverse mental
- reversibility of thinking (the possibility of returning characteristics (ways of thinking, behaving and feeling) that distinguish people from one
to the starting point),
- durability of memorisation, another.
- logical thinking, a sense of responsibility and the conse- Certain temperamental traits may favour developmental disorders. The ICD- l O clas­
quences of one's own actions,
Concrete operatio- sification distinguishes between two categories of disorders - developmental and emo­
7-11 years - a sense of fairness and the need to comply with rules
nal stage
previously established, tion and behavioural. Developmental disorders are, for example, intellectual disabilities,
- the principle of constancy, speech and language disorders, dyspraxia, holistic developmental disorders (including
- the ability to rank according to a characteristic,
- classification capacity - grouping according to a specific autism spectrum disorders). Examples of emotional and behavioural disorders include
criterion, psychomotor hyperactivity, mixed behavioural and emotional disorders, social functio­
- numerical concepts
ning disorders (e.g. selective mutism), mood disorders, anxiety and eating disorders.
- ability to apply logic and abstract reasoning,
- advanced level of problem solving - a calm and method-
Attention deficit hyperactivity disorder (ADHD) is a genetically determined disorder.
ical approach to a problem rather than a trial-and-error Symptoms of attention deficit hyperactivity disorder are:
11-15 Formal operational method, - excessive impulsivity (difficulty in applying rules of behaviour, quick, ill-considered
years stage - difficult adolescence: crisis of authority, rebellion against
rules, sensitivity to criticism, excitability, emotional in- reactions, difficulty in predicting the consequences of behaviour),
stability, preoccupation with physical appearance, - hyperreflexia (excessive activity in relation to the stimulus and age),
- fear of not being accepted, especially by peers
- attention deficit disorder (poor ability to concentrate on a task and its completion,
Temperament is a set of innate traits that form the basis of a child's personality for­ listening, distraction by a minor stimulus).
mation, which are revealed early in life and are only slightly altered by the environment Emotional overexcitability is characterised by the ease of an emotional response dis­
and developmental processes. According to Thomas and Chess' theory, a child's tempe­ proportionate to the strength of the stimulus that triggered it. Its symptoms can be anger,
rament is a behavioural style characterised by activity, regularity, initial reaction, adap­ malice, increased timidity for no apparent reason.
tability, intensity, mood, distractibility, persistence-attention span, and sensory threshold. Autism spectrum disorders are characterised by speech and communication abnor­
Taking these characteristics into account, three types of temperament are distinguished: malities, stereotypical behaviours and interests. Children with autism spectrum disorders
easy (biological regularity, drive towards new stimulation, rapid adaptation to change, are characterised by: often difficult temperament, greater activity, impaired adaptive be­
dominance of positive mood and moderate intensity of response), haviour, greater withdrawal, less perseverance, lower sensitivity to stimuli and a prepon­
difficult (irregularity of biological functions, withdrawal in response to new stimuli, derance of negative emotions, reduced ability to focus attention, control behaviour and
slow adaptation to change, predominance of negative mood, high intensity of re- carry on a conversation. They have an uncharacteristic tone of voice and a tendency to
sponse), echolalia, a tendency to behave routinely, take words literally, avoid eye and physical
slow-to-warm-up (slow adaptation to change, withdrawal in response to new stimuli, contact, delve into their own interests and not share them with others. They may over­
moderate intensity of mood expression, more frequent irregularity of biological func­ react or underreact to sensory experiences, e.g. smell, touch, tastes, sounds.
tions compared to easy temperament). Anxiety disorders are among the most common emotional disorders in childhood.
Temperament differentiates people, e.g. by their ability to control their emotions, Children manifest many so-called normative fears and anxieties, i.e. those occurring
their resistance to fatigue or their ability to comply with demands. It is a component within the typical developmental trajectory (Tab. 1.4) Normative anxiety is particularly
of personality that shapes a person's behaviour at every stage of life. Personality is high at the age of 6-7 years. An anxiety disorder is referred to when it interferes with
the result of the interaction of temperamental traits and the wider environment (family, normal functioning.

14
15
Compendium of Paediatric Dentistry Child at the dental office

Factors causing a child's anxiety in the dental office can be: unfamiliar surroun­ The aetiology of DFA is complex. Among the factors contributing to its occurrence
dings and people, sounds coming from the surgery (another child crying, the sound in childhood are:
of a drill), the smell of dental medicines, the taste of medicines and materials, visible - age - severity of dental anxiety higher in younger children,
traces left after the procedure (e.g. b lood or instruments), the position on the chair, - female gender,
discomfort and pain. previous negative dental experiences, especially a child's first dental experience,
- too late a child's first visit (> 2 years),
Tab. 1.4. Normative anxiety stimuli, i.e. occurring in the course of child development.
complications of untreated caries,
Age Stimuli triggering developmental anxiety - low self-esteem,
0-6 - high vulnerability and insufficient psychological readiness of the child for treatment,
loud noises, separation anxiety
months - poor quality of life related to oral health,
6- 1 8 strangers, unfamiliar situations, separation from parent, loud noises (thunder,
- low overall satisfaction with life,
months bang), large objects, noisy people
animals, loud noises (hoover, thunder, flushing water), darkness, dark colours, low economic status of the family,
2-3 years large objects, rain and wind, unexpected movement, approaching large objects, - up to the age of 8 - parent's dental anxiety.
absence of parents, strange people
The age at which children go to the dentist for the first time, ensuring that the expe­
old, wrinkled people, masks, wizards, darkness, animals, loud noises and
3-4 years rience is pleasant for the child and the appropriate frequency of visits (every six months
sounds of machines, loss of loved ones, bodily harm
animals, bad people, sorcerers, ghosts, bodily harm, sight of blood, darkness, or every year) play an important role in preventing DFA. A child's first visit to the dental
5-6 years monotonous unpleasant voice, bell, toilet fl ushing, elements: fire, water, office should take place between 6 and 12 months of age. Early registration with the child
thunder, lightning
and regular visits enables the child's gradual adaptation to dental treatment, health-pro­
darkness, shadows interpreted as ghosts, "bad" people, lack of acceptance,
7-10 years failure, bodily harm and physical danger, loneliness, insects, repeated fear of moting education, shaping of the parents' health-promoting attitude and implementation
separation of preventive measures.
physical appearance, thunder and lightning, peer rejection, lack of group Various scales are used to assess anxiety in children. In older children and adoles­
I 0-1 2 years
acceptance, school achievement, darkness and bodily harm
cents, scales containing questions answered in a multi-item gradation are used, e.g. den­
1 3-18 y ears rejection by surroundings, physical appearance
tal fear survey short version (DFS), while in the youngest children picture scales where
the child indicates a face expressing their current feeling, e.g. modified child dental an­
xiety scale faces (MCDAS(f)).
Dental anxiety is defined as a state of negative emotion arising in response to an
unknown threat. Dental fear is a natural emotional response to a known threat. Dental Parents
phobia is a severe dental anxiety. Fear is believed to be the result of external threats,
while anxiety is believed to be a subjective sense of a threatening state. A clear distinc­
The child's behaviour at the dental officeis also influenced by the child's upbringing
tion between anxiety and fear is difficult, as situations of immediate threat and subjective
style, parental attitude, the parents' level of emotional intelligence (the ability to under­
feelings of threat often overlap. In dental practice, the terms "dental anxiety" and "dental
stand their own and other people's emotions and how they use them), the parents' level
fear" are often used interchangeably. The term dental fear and anxiety (DFA) is also
of awareness and attitude towards oral health, as well as their own "dental" experience,
increasingly used. Recognising a child's dental anxiety is key to achieving cooperation.
socioeconomic factors (family economic status, age and education level of parents) and
If unrecognised and not eliminated, it builds up and is a common reason for avoiding
trust in the dentist. The child's behaviour is positively influenced by a parent who does
treatment.

16 17
Compendium of Paediatric Dentistry Child at the dental office

not feel anxious, who is motivated to take action and who is convinced ofthe necessity the authenticity of the response and the possibility of learning how to cope with a new
ofdoing so. situation.
Parenting style is the ways and methods in which ail family members interact with
the child. The most commonly cited parenting styles in the family are: Dental environment
autocratie - imposing a course of action without justification, absolute obedience
required, The dental environment can be defined as the conditions in the dental practice
liberal - leaving the child completely free, leading to problems with obedience resulting from its equipment and appearance, the selection ofdental staff and the orga­
and compliance with the rules in place, nisation ofwork, which ensure the quality ofdental care and an atmosphere conducive
- democratic - respect for the rights ofall family members, fair distribution ofrespon­ to building positive relationships with the child and his/her parents (carers).
sibilities and privileges, freedom ofbehaviour within the limits ofreason, trust, The waiting room and dental office should be decorated in light, subdued colours,
inconsistent - indeterminate parental behaviour, lack of consistency, variability well lit (wann white lighting) and regularly aired. The child-friendly colours are yel­
ofresponses in similar situations, low, green and blue. The waiting room is intended to facilitate the child's adaptation to
occasional - periodic introductions ofrules that are not followed later. the dental environment and to provide parents and the child with knowledge about oral
Parents' attitudes towards their children can be categorised as positive - accepting health. Therefore, it should be equipped with a child's corner (e.g. small chairs, table,
the child and bis or ber needs, interacting with the child, reasoned freedom, recognising toys, colourful posters or pictures, crayons, drawing boards, aquarium, film staries,
the child's equal rights within the family, or negative - avoidant, spurning, overly de­ books) and educational material (posters, brochures, film). It is important to ensure
manding, overly protective. that sounds and smells from the dental office do not reach the waiting room.
Parents whose attitudes towards their child are positive, recognise and provide for The practice should be equipped with modern equipment and materials, inclu­
their child's needs, are objective, patient, willing to explain and cooperate with the ding those not used for adult patients, e.g. coloured filling materials, standard steel
dentist. Negative attitudes make it difficult to cooperate with the child. Parents may be crowns. The possibility of performing anaesthesia using computer-controlled sys­
overly permissive, impose their authority, display a careless or coercive attitude, make tems, a nitrous oxide inhalation sedation device with scented sedation masks ' the use
excessive demands on the chiId, show intolerance and excessive criticism of the child 's ofsmaller instruments (e.g. small-headed contra-angle handpieces, 018 mirrors and
.

behaviour, and lack interest in the child's real needs. Parents may also attempt to dictate forceps for deciduous teeth), safety instruments (such as a metal finger, blacks, holds
to the dentist how he or she should proceed or may obstruct the child's communication for root canal instruments, a tongue-piece or a cofferdam) is advantageous. Moving
with the dentist. Sometimes a parent requests treatment of a child under general anaes­ equipment should not be within reach of the child. The hygiene station should be
thesia because be or she considers it too traumatic, repeats questions asked to the child adapted to the user, i.e. the child (mounting height of the washbasin) and equipped
by the dentist or changes the dentist's orders. He or she may also use counterproductive with a display of hygiene products intended for children and adolescents and an
statements, such as "don't be afraid" or "it won't hurt", which intensifies the child's instructional poster.
feelings offear. Staff. Important characteristics ofdental staff are the so-called psycho-physical qua­
Factors that have a particularly negative impact on a child's behaviour in the dental lities, i.e. appearance, tone ofvoice, body language, empathy, composure, sense ofhu­
office are the negative dental experiences of the parents themselves and their excessive mour, observational skills and professional competence, i.e. lrnowledge and skills in
anxiety about the child's well-being. In these situations, parents may communicate their dentistry and child psychology. Contrary to popular opinion, children's preference for
anxiety or fear to the child. Overprotectiveness, over-involvement in "helping" or, con- the colour of the dentist's apron has not been proven. Sorne children prefer a dentist in
ve'5cly, foccing a child to be heroic, takes away the child's ability to contcol, ceduces a white apron, others in a coloured one.

18 19
Compendium of Paediatric Dentistry Child a t the dental office

Work organisation. The child's anxiety about visiting the dental office is reduced concomitant psychological factors. lnt J Paediatr Dent 2007; 1 7(6):391-406. - 13. Lee DW et al.
The influence of parenting style on child behaviour and dental anxiety. Pediatr Dent 2018;40(5):
by a friendly atmosphere both in the registration desk and in the waiting room and the
3 27-3 3 3 . - 14. Leko J et al. Reliability and Validity of Scales for Assessing Child Dental Fear
treatment room itself, by scheduling routine check-ups and preventive appointments at and Anxiety. Acta Stomatol Croat. 2020;54( I ):22-3 1 . - 15 . Olczak-Kowalczyk D, Szczepa11ska
the right time of day (before noon and early afternoon), by the short waiting time to enter J, Kaczmarek U. Contemporary dentistry of the developmental age. Med. Tour Press lnt. 2017. -
16. Oliveira LB et a l . Children's Perceptions of Dentist's Attire and Environment: A Systematic
the surgery and by the short duration of the visit. The position of the patient in the dental Review and Meta-analysis. lnt J Clin Pediatr Dent. 2020; 13(6): 700-716.
chair (reclining, sitting, semi-recumbent) depends on the child's preference, the type of
procedure, and how the treatment area is isolated. A way to distract the child may be to
watch cartoons during the dental procedure (glasses, monitor). I t is advisable to work
with 4 or 6 hands and to communicate with the assistant "without unnecessary words".
The assistant should be familiar with the order and execution of the various steps in the
procedure, as well as with the risks arising from their incorrect execution or a sudden
change in the child's behaviour.
I t is important that the visit follows the same pattern, which increases the sense of
security in the child. The dentist invites the child from the waiting room into the surgery
and then invites the child into the chair, explains what he or she will be doing and per­
forms the intended procedure or examination. At the end, he or she hands over the award
and talks to the child and carer about the procedure carried out and further preventive
and curative treatment. It is important that the pace of subsequent activities is not too fast
and that explanations are sufficient to alleviate the child's anxiety.

References
I . Antoszewska B. Going beyond the white coat - the child as a subject in the dentist-patient
relationship - theoretical aspect Disability. Discourses of Special Pedagogy.20 1 6:24:260-269. -
2. Arnrup K et al. Attitudes to dental care among parents of uncooperative vs. cooperative child
dental patients. Eur J Oral Sci 2002; 1 10(2):75-82. - 3 . Blomqvist M et al. Oral health, dental anx­
iety, and behavior management problems in children with attention deficit hyperactivity disorder.
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adolescents. A systematic review. Eur J Paediatr Dent. 201718(2): 12 1 - 1 30. -5. Frankl SN et al.
Should the parent remain in the operatory? .J Dent Child. 1962;29: 150-163. - 6. Gupta A et al.
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& Sons, Inc. 20 1 4. - 8. Howard K E, Freeman R. Reliability and validity of a faces version of the
Modified Child Dental Anxiety Scale. Int l Paediatr Dent. 2007; 1 7(4):281-8. - 9. Jayakaran TG et
al. Preferences and choices of a child concerning the environment in a paediatric dental operatory.
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I 0. Klingberg, G, Raadal M, Arnrup K. Dental fear and behaviour management problems. Pe­
diatr dentistry: A Clinical approach, 2009;2, 32. - 11. Klingberg G. Dental anxiety and behaviour
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20 21
 Dental staff's relationship with the child and their parent

Tab. 2 . 1 . Sample guidance for parents (carers) on how to behave during the visit.

Desirable parental (carers) behaviour Unwanted parents (carers) behaviour

Chapter 2 - maintained calmness, visible opti mism, - visible or perceptible stress, tension, ner­
smile, friendly attitude towards staff, vousness,
- showing trust in the dentist, - showing guilt for bringing the child to the
Dental staff's relationship with the child and their parent - telling the child about their own positive dentist (the child should understand that the
dental experiences, visit is for his/her own good),
- showing confidence that the chi l d will be - passing on bad dental memories or negative
Dorota Olczak-Kowalczyk happy with the visit to the dentist and that comments about visiting the dentist,
the parents will be proud of the child, - obstructing the child's communication with
- fostering communication between the chi ld staff, e.g. answering questions for the child,
and the dental staff (keeping quiet, not inter­ - Seemingly reassuring statements e.g. "it
rupting, not speaki ng for the child), won't hurt", "the dentist won't hurt you",
- preparing a reward for the child, showing criticism of the child e.g. "why can't you
Ensuring proper relations of the dental staff with the child and its parents requires
pride in the child's behaviour during the behave as politely as ... ?". or scaring the
parallel actions in three spheres: cognitive - by informing about the planned procedure visit, praising the child in front of people child "don't move or you might get hurt! ",
in a way adapted to the child's needs and capabilities, emotional - by reducing the child's important to the chi ld, e.g. grandmother and - suggesting a course of action or method of
grandfather, nursery teacher treatment to a dentist
fear of the planned procedure (parents, playing a key role here, should be prepared in
advance, i.e. made aware before the visit of how their attitude influences the child's be­
Communication with the child and their parent involves the entire dental team. Com­
haviour) (Tab. 2.1), behavioural - by shaping behaviour.
munication consists of two layers - verbal and non-verbal - which should be compatible
In each sphere, the determinants of the child's behaviour in the dental office must be
with each other. An example is to encourage the child to speak not only verbally (e.g.
taken into account, especially the child's stage of development, temperament, the imma­
by asking a question), but also non-verbally, i.e. by showing interest with an appropriate
turity of the personality that is just developing. The child is not aware of the health ben­
gesture or facial expression. When facial expressions and body language do not match
efits and necessity of dental care. It does not feel the need for treatment and is not inter­
the verbal content, communication is disrupted.
ested in it, except to avoid discomfort and pain. The basis for action in all three spheres
In addition to the environment and staff characteristics (described above), the follo­
is correct communication, the gradual adaptation of the child to the dental environment
wing are important in relation to non-verbal communication with the patient:
and the use of non-pharmacological and pharmacological methods to shape the child's
- facial expressions (smiling - changing the child's relation to the environment to
behaviour. It should be emphasised that pharmacological methods can be introduced as
a more cheerful one, looking into the child's eyes, keeping the gaze at the child's eye
an adjunct and when non-pharmacological methods are insufficiently effective.
level),
- kinesics (gestures, body position and movements: nodding head, open posture,
smooth and calm movements, first physical contact - gentle, repeated several times),
Communication
- proxemics (spatial behaviour: calmly crossing the boundaries of successive zones'
slowly entering the child's intimate zone (0-45 cm from the face); as the distance
A child is accompanied by a parent or legal guardian during a dental visit, so the
decreases, reduce the rate of speech and speak the words more clearly),
communication process involves the child, the parent (guardian) and the dental staff. The
- para-language (voice qualities and manner (pace) of speaking: appropriate volume -
parent's role in the communication process should decrease as the patient grows older, in
too quiet or loud statements arouse anger, low tone of voice, slow pace of speaking,
order to increase their participation in the educational, diagnostic and treatment process
fluency - avoiding pauses, slips of the tongue and so-called "yyyy" fillers).
and to develop a sense of responsibility for their oral health.

22 23
Compendium of Paediatric Dentistry Dental staff's relationship with the child and their parent

In verbal communication it is important to: Due to the child's short attention abilities, the visit of the youngest children
- addressing the child directly, using the child's name, treating the child as a paitner in the sho uld be as short as possible. The visit should begin with a calm conversation with
conversation whose opinions and feelings are important, showing interest and understan­ the parent. During the interview, the dentist and parent should sit opposite each other,
ding (the child must not feel unimportant and his/her statements must not be disregarded), knees touching, the child being on the parent's lap (sense of security), facing the
- truthfulness, dentist. It is important to introduce an atmosphere of trust and calm (slow pace of
language that is simple and understandable to the child, without medical terminology speech, tone of voice, gentle facial expressions of the dentist and smile, touching the
and jargon, child). A two-year-old child is shy of new people and new places, so it is important to
replacing dental nomenclature with terms he can imagine (e.g. gavage - a stick or an let him touch objects and learn their meaning. The oral examination of a child in the
abacus, slipper - a trunk of an elephant that wants to drink, cofferdam - a raincoat, first two years of life is best carried out in the knee-to-knee position (knee-to-knee
carious cavity - worms in the tooth, a slow speed handpiece - a hoover that pulls technique). Ask the parent to turn the child 180 degrees (so that the child is facing
them out, turbine high speed handpiece - a shower or whistle, blower - a windmill, the parent), then to lie on the parent's lap with the child's legs around the parent's
fluoride varnish - vitamins for the teeth, anaesthetic - a tooth sleeper, etc.), waist and head on the dentist's lap. This position allows the child to see and feel the
avoiding words that evoke negative emotions, e.g. "weepy", "fearful", parent, provides visibility of the mouth to the practitioner and parent, enables hy­
the use of supportive forms of communicating content, e.g. imagery (drawings, dia­ giene instruction and fluoride varnish application.
grams, models, intraoral camera) or animism. With older children, opportunities for communication and cooperation are ex­
H umour reduces the emotional distance between people and improves communi­ panding. The dentist's attention should be directed directly at the child. At 3 years
cation. However, it should be selected according to the child's developmental stage. old, the child likes to please adults, has an imagination and enj oys stories. At 4 years
Children aged 12- 15 months to 3 years will find it amusing to pretend, for example, that old, he is talkative, but listens with interest and responds well to verbal cues. It is
a finger is a toothbrush, or that a toothbrush is for washing legs. Children aged 2-4 years advisable to tell the child what the various dental procedures look like and to show
make fun of giving things or activities different names. They will laugh, for example, at them what the equipment is used for, preferably using animism. It is important to
the misidentification of colours or the search for teeth in the ear. Children aged 3-5 years remember that children's attention spans at this age are impermanent and indivisi­
like to play with the sound of words (not the meaning), make up words and rhyme, and ble. For a chi Id of 3 and 4 years of age, the presence of parents is still important. At
school-age children like riddles and jokes (e.g. "what has both a tooth and a tree?"). the age of 5, the child is no longer afraid of the absence of his or her parents during
a visit, is open to new experiences, curious (age of questions), but sees the world
The course of a child's visit to the dental office one of the conditions for adaptation only from his or her point of view and focuses attention on only one aspect of the
to the dental environment
situation. I t is proud of the items it owns. It is not until around the age of 7 that ego­
Building a relationship with your child and gradually adapting them to the dental en­ centrism disappears; logical thinking and a sense of responsibility develop. Children
vironment require a first visit as early as possible and several regular visits. Particularly want to understand what the dentist is doing, to actively participate in the visit. By
important, however, is the child's first visit to the dental office, which should take place treating the child subjectively, the dentist makes the child feel important and able
between 6 and 12 months of age. Regardless of the age of the child, the first visit should to control the visit. Children in the period of concrete operations feel the need for
be preceded by education of the parents on how to prepare the child for the visit, the justice and compliance. They want to feel appreciated if, in their perception, they
conduct of the visit, the possible reactions of the child during the visit and the attitude of deserve it. In the case of pre-school and early school-age children, it is beneficial to
the parent, as well as the non-pharmacological and pharmacological methods possible reward behaviour at the various stages of the procedure and at the end of the visit
during the developmental period the child is in. (e.g. praise, orders, diplomas and brave patient stickers).

24 25
Compendium of Paediatric Dentistry Dental staff's relationship with the child and their parent

Example of an older child's first visit: establishing relationships, and often hygiene neglect, impaired perception of pain asso­
1 . Approaching a child sitting in a chair: ciated with oral diseases, and lack of interest in prevention and dental treatment.
keep your distance and do not touch the child or light the lamp,
- start the conversation with something of interest to the child (a toy, clothes, hair­ Non-pharmacological methods of shaping the child's behaviour
style, event), which will make it easier to establish contact,
- inform about the purpose of the visit, e.g. "today we are going to look at your Non-pharmacological methods of shaping the child's behaviour in the dental office
teeth, check how many there are", tell the child how this will be done, show the include communicative and aversive methods: presence vs. absence of parents, protective
mirror and probe, calling it, for example, "a tooth feeler". stabilisation and immobilisation. The American Academy of Paediatric Dentistry (AAPD)
2. Examination of the child: distinguishes between basic (verbal and non-verbal communication, "say-do", voice con­
ask for the child's permission to look at his/her upper teeth ("let's count the teeth trol, positive reinforcement, presence or absence of a parent in the office, inhalation with
on top") and light the lamp (must not shine into the eyes), touch the lip, a mixture of nitrous oxide and oxygen) and advanced (protective stabilisation, sedation and
r
initially work f om the front, at the child's eye level, general anaesthesia) behavioural methods. The "tell-show-do" method is the most com­
- gently enter the "intimate area" (up to about 45 cm from the child's face), i.e. monly used, parent-accepted and safest non-pharmacological method (Tab. 2.2).
move away frequently, Dental treatment is not a life-saving treatment and can therefore be deferred in certain
tilt the seat backrest gradually, situations. If the child's behaviour makes it impossible to carry out routine treatment
introduce the mirror, then the probe (place the probe in front of the teeth, touch the despite communication-based methods, the dentist will consider with the parents ano­
tooth, ask: "do you feel me scratching the tooth?", "does it tickle?", then interpret ther treatment modality, such as sedation. When there is a need for immediate treatment,
the answer, reward with praise; "we have seen the front teeth, now let's see the a risk-benefit analysis of the use of a method other than communication-based should be
back teeth... and open your mouth wider! Oh yes, you did it/you did it well! ", made. This requires the consent of the parents and possibly the child.
"you really have nice teeth! ".
Tab. 2.2. Non-pharmacological methods of shaping the child 's behaviour in the office dentistry.
Adolescents are a special group of patients who require insightful attention and com­
munication skills. A teenager must not be patronised. He or she should feel the dentist's Methods Description
positive attitude and willingness to listen and understand. He is convinced that he is Communication
constantly being assessed and has a strong sense of his own uniqueness. Any criticism Verbal and non-verbal
described above
communication
should be avoided, as a major problem in adolescence is the threat of non-acceptance.
verbal description of the action ("tell"), auditory and tactile demon-
An adolescent should be approached as an adult, while bearing in mind that, despite his stration of aspects of the intended treatment ("show"), execution
criticism and clear negativity, he needs adult support and the setting of clear boundaries. in the manner previously presented to the child ("do"); the child
should know what is going to happen, how to behave, what he or
Talking about things that interest the teenager (e.g. music, film, computer games, sports)
she may feel; at during the treatment, visual control using a mirror
is helpful in creating a relationship with him or her. I t is worth expressing admiration or intraoral camera is advisable; for children of all ages (most effec-
and appreciation for his achievements or interests, so that he feels valued, superior. If "Tell-show-do" tive > 4 years of age), especially those having their first visit or who
are afraid due to a previous negative experience in another dental
the teenager is not accompanied by his or her parents during the visit (they remain in the office or inadequate information received from parents or peers. For
waiting room), all information should nevertheless be passed on to them. children of any age (most effective > 4 years of age), especially
those making their first visit, and also those who are frightened be-
Problems can arise with teenagers who use drugs. Symptoms of addiction can include
cause of a previous negative experience at another dentist's surgery
depressive states, mood changes, frustration, helplessness, self-alienation, difficulties in or incorrect information received from parents or peers.

26 27
Compendium of Paediatric Dentistry Dental staff's relationship with the child and their parent

the child signals discomfort, e.g. by raising his or her hand; the Aversive
Signalling duration of the activity causing discomfort is I imited, e.g. counting - controversial, requires explanation to parents of their actions
(enhancing control) by the dentist; the child's participation in the treatment process and their consent to their use
increases the feeling of safety; only for children who communicate use of changes in volu111e of voice, strength, tone and rate of speech
to attract the child's attention, reinforce the dentist's authority and
rewarding appropriate behaviour in the practice:
establish the child-adult relationship (sudden, loud and strong
- social reinforcement -- verbal praise, reinforced with appropriate Voice control commands used to stop undesirable behaviour); used conditional-
facial expressions and demonstrative information about the ly when the child does not allow the procedure to be carried out;
appropriate behavior of parents and other members of the staff should be ended with positive reinforce111ent; for children of all
of the office - describe the child's efforts, help, emphasize his ages (except hearing i111paired patients); parents should understand
Positive the purpose of its use
efforts;
reinforcement reinforcing appropriate behaviour by removing the unpleasant
- unsocial reinforcement - material rewards, e.g. a toy, sticker, sti111ulus when the child starts to behave in a desirable way (not to
diploma; for children of all ages; do not promise a reward before Negative be confused with punishment! ) ; an example is selective exclusion
the procedure, we reward after the behavior; positive behaviours reinforcement of the parent - the parent leaves the practice (or removes themselves
are rewarded immediately and consistently, while ignoring from the child's sight) during the child's misbehaviour - once the
undesirable behavior behaviour has improved the parent returns to the practice
learning the expected behaviour by observing the consequences it partial or total immobilisation of the child, e.g. holding the child's
has caused; it also allows for tbe elimination of unknown factors head or limbs by a dentist, assistant or parent; use to be considered
Physical restraints
("the unknown is scary") in the context of another person: on a case-by-case basis as it can cause physical and psychological
trauma
Modelling (imitation) - direct imitation - observing a procedure performed on a child of a
similar age and preferably of the same sex; References
I . American Academy of Pediatric Dentistry. Behavioral guidance for the pediat­
- indirect i mitation - watching a video of the procedure being
ric dental patient. The Reference M anual of P ediatric Dentistry. Chicago, Ill.: A merican
performed
Academy of Pediatric Dentistry; 2021 :306-24. - 2. Carrillo-Diaz M et al. How Can We Re­
ignoring the patient's undesirable behaviour and directing bis or her duce Dental Fear in Children? The !111portance of the First Dental Visit. Children (Basel).
attention to something else, using various techniques, e.g. telling 2021 ; 8( 1 2) : 1167. - 3. Cianetti S et al. Evidence of pharmacological and non-pharmacological
Distraction a fairy tale or watching a cartoon during the treat111ent reduces the interventions for the manage111ent of dental fear in paediatric dentistry: a systematic review pro­
child's perception of unpleasant sensations; for children of all ages, tocol. B M J open 2017;7(8), e0 16043 . - 4. Gerald Z, Wright GZ, Kupietzky A. Behavior M anage­
especially useful < 3-4 years old ment in Dentistry for Children. Second Edition. John Wiley & Sons, Inc. 2014. - 5. Klaassen M A
et al. Dental fear, communication, and behavioural 111anagement problems in children referred fo r
Systematic introducing stimuli in the relaxed patient, taking into account the dental problems. Int J Paediatr Dent 2007;17(6): 469-477. - 6. Law CS, Blain B . Approaching
desensitisation hierarchy fro111 weakest to strongest; the next sti111ulus is introduced the pediatric dental patient: A review of nonpharmacologic behavior management strategies CDA
only after the previous one has been accepted; it is necessary to J 2003 ;3 l : 703-713. - 7. Olczak-Kowalczyk D, Szczepanska J, Kacz111arek U. Contemporary
inhibition ofanxiety
relax the child before introducing the stimulus, as it cannot occur dentistry of the developmental age. Med Tour Press Int. 2017. - 8. Oliver K, M anton DJ. Con­
reactions by means
simultaneously with the anxiety; the child should be taught to te111porary behavior management techniques in clinical pediatric dentistry: out with the old and in
of a causal stimulus
recognise the sy111pto111s of anxiety, to assess its intensity and the with the new? J Dent Child 2015; 82(1):22-28. - 9. Porritt J et al. Understanding children's dental
for the anxiety by
relaxation technique (e.g. breathing control - breathing with a hand anxiety and psychological approaches to its reduction. Int J P aediatr Dent 2012;22(6):397-405 .
simultaneously inducing
on the stomach, relaxing successive 111uscles); for children who l 0. Roberts JF et al. Behaviour M anagement Techniques in Paediatric Dentistry. Eur Arch
the patient into a state of
communicate Paediatr Dent 20 I 0; 11: 166-174.
relaxation

28 29
 Pharmacological management of the paediatric dental patient

The most commonly used local anaesthetics are lidocaine, articaine and mepivacaine.
Chapter 3 The addition of a vasoconstrictor, e.g. adrenaline or norepinephrine, allows the drug
to accumulate at the site of administration, which consequently prolongs the duration
of action, allows a reduction in dose and the risk of symptoms resulting from toxicity
Pharmacological management of the paediatric dental patient of the administered drug. I t also ensures less bleeding in the area of anaesthesia. It is
contraindicated in patients following radiotherapy to the craniofacial region, cerebral
Dorota Olczak-Kowalczyk, Piotr Sobiech
haemorrhage, in allergy to bisulphate and for pulp regeneration procedures requiring
provocation of bleeding, in patients with hyperthyroidism, in those using antidepressants
(phenothiazine, MAO inhibitors). The characteristics of the anaesthetics used in children
and the maximum doses are shown in Table 3. l . When selecting the dose of anaesthetic,
the patient's general condition, the site of anaesthesia administration, vascularisation of
Pharmacological methods include analgesia prior to therapeutic procedures, local
the tissue, the method of application, and in children, age and body weight are addition­
anaesthesia, sedation and general anaesthesia.
ally taken into account.
As a rule of thumb, the lowest dose needed to provide effective anaesthesia should
Pain therapy
be given. Anaesthetics shall not be used in the case of hypersensitivity to the active sub­
stance, amide local anaesthetics or to any of the excipients.
Pain therapy is administered before any painful procedure (advance analgesia) and
continues during the procedure and in the post-operative period if post-operative pain is
Tab. 3 .1. Characteristics and dosages of the most commonly used anaesthetics in paediatric
expected. It relies on the use of methods with different points of entry, i.e. combining the dentistry.
action of local anaesthetics with drugs that have a general effect. The use of drugs with
Maximum
different mechanisms of action and different groups makes it possible to achieve an anal­
Maxi- doses for chil-
gesic effect while reducing their doses and the risk of side effects. The type of medication mum dos- dren according
used, and the dose given should be recorded in the patient's records. es recom- to the AAPD
Anaesthetic Characteristics Restrictions Comments
mended and according
Systemic painkillers (most commonly paracetamol and non-steroidal anti-inflamma­ by manu- to the manufac-
tory drugs (NSAIDs), e.g. ibuprofen, less commonly opioid analgesics, e.g. codeine, facturers turer's safety
tramadol) are usually administered orally in doses and in a form adapted to age and body data sheets
2% lido- Amide agent Newborns 3 mg/kg AAPD: 4.4 mg/ I ml: 20 mg
weight (suspension, tablets), and less commonly rectally (suppositories) in children.
caine(Lig- with a benzene b.w. with- kg b.w. with lidocaine
Topical anaesthetics can be applied to the mucosa! surface (lozenges, sprays, mouth­ nocainum ring metaboli- out adre- adrenaline ( J ampoule 2
washes, gels) or by submucosal injection. hydrochlori- sed in the liver, naline (max. 300 mg) ml - 40 mg
cum) with- recognised as 7 mg/kg data sheet: I carpoule
Sur face-applied agents are usually benzydamine (an NSAID drug that can be used out or with the safest b.w. with usually a single 1.8 ml - 3 6
in cases of oral or pharyngeal mucositis and after procedures in this area), lidocaine and adrenaline adrenal ine dose of 20-30 mg)
benzocaine. Surface lidocaine is not recommended for infants and young children, es­ I : 100000 (max. 500 mg
I : 200000 mg)
pecially to relieve teething disorders, as overdose can lead to convulsions, severe brain
damage and even circulatory failure. Due to the risk of methemoglobinemia, topical gels
and lotions containing benzocaine are contraindicated in children under 2 years of age.

30 31
Compendium of Paediatric Dentistry Pharmacological management of the paediatric dental patient

4% Articaine Amide agent < 4 years, 7 mg/kg AAPD: 7 mg/kg I ml: 40 mg sleep", "sleeper", "sleep juice", "jel ly", "sleeper doesn't taste very good so we wash it
hydrochlo- with thiophene myocardial b.w. (max. b.w. (max. 500 of articaine down with water", "sleeper could spill out so we keep it in a tiny bottle", "you' l l feel
ride with ring, highest conduction 500 mg) mg); ( I carpoule
adrenaline toxicity, 4 ti mes safety data 1.7 ml
a little pinch". The preferred position of the patient for anaesthesia is lying down. His
disorders,
I : I 00 000 more potent plasma cho- sheet: do not - 68 mg) eyes should be covered with transparent glasses. The carpoule with the exposed needle
I : 200 000 than lidocai ne, l i nesterase exceed a close should be out of the child's sight. ft should be brought close to the child's face, moving
metabolised in deficiency, of 5 mg/kg b. w.
blood with plas- severe hy- behind the head or over the chest.
ma esterase potension When perfonning anaesthesia: stabilisation of the patient's head, withdrawal of the
acute heart
lips, cheek and tongue and tension of the tissues at the injection site (with the exception of
failure
the palate) is achieved by inserting the fingers of the non-working hand (usually the left)
3% mepiva- Amide-type < 4 years 6.6 mg/kg AA PD: 4.4 mg/ I ml of 3%
caine (Mepi- agent with a old, in- b.w. (max. kg b.w. mepivacaine into the child's mouth in the appropriate position and resting them on the bones of the jaw.
vacaine) benzene ring, completely 400 mg) (max. 300 mg) - 30 mg During the injection, it is advisable to speak to the child, e.g. " I ' l l count to five and
2% mepiva- comparable controlled safety data mepivacaine,
the tooth will already be poured with sleeper", to distract him or her, and to watch the
caine with in effect to epilepsy, sheet: do not and I car-
adrenaline lidocaine, me- myocardial exceed 3 mg/kg poule ( 1 . 8 eyes and face.
tabolised in the conduction b.w. ml) - 54 mg After the anaesthesia is administered, we inform the child that "while the tooth
liver, vasocon- disorders, mepi vaca i ne
strictor (more pregnancy I ml of 2% is falling asleep" he or she will feel that "the lip is getting thick" but is not actual ly
often without mepivacaine changing ( can be shown in a mi1TOr), and that "the anaesthetic does not taste very good,
the addition of - 20 mg
so we will wash it off with water".
vasoconstric- mepivacaine,
tors) and I car- At the end of treatment, we provide information to parents and child about the duration
poule ( 1 . 8 of soft tissue anaesthesia and the risk of biting the lip, cheek, the need not to eat or drink
ml) - 3 6 mg
hot drinks until the anaesthesia has subsided and to observe whether the child is biting
the anaesthetised tissue, and the possibility of swelling or bruising in the anaesthetised
Calculation of the maximum patient dose:
area (cold compress recommended) and minor pain (analgesic recommended). In case
maximum dose / kg body weight x body weight in kg of biting or persistent postoperative pain, bleeding, swelling or redness, parents should
take their child to a doctor.
Example:
D ata: The most commonly used methods of local anaesthesia in paediatric dentistry are
2% lidocaine - maximum close 3 mg/kg without adrenaline topical anaesthesia, local anaesthesia and inferior alveolar nerve block (IANB).
Child weight - 20 kg Topical anaesthesia of the mucosa is achieved by direct contact of the anaesthetic
l carpoule 1.8 ml - 3 6 mg lidocaine (prilocaine, benzocaine, lidocaine) with the area to be anaesthetised (e.g. at the intended
Maximum dose = 20 x 3 = 60 mg lidocaine needle insertion site). The anaesthetic can be applied on a cotton wool swab, lignin roll
Maximum dose per number of carpulae = 60 / 36 = I .6 carpulae
or gauze pad for 1 -2 minutes, after drying the application site with a gauze pad and iso­
lating the lip or cheek. The anaesthetic effect is achieved after 2-5 minutes at a depth of
Prior to the administration of anaesthesia, parents and the child should be informed in 2-3 mm. Before anaesthesia is administered by injection, residuals of the superficially
an understandable way about what they will feel during and after the local anaesthetic. applied agent must be removed. The results of studies assessing the effectiveness of
She or he must not be deceived or surprised. Good terms include "put your tooth to using surface anaesthesia prior to needle insertion are inconsistent. Its usefulness prior

32 33
Compendium of Paediatric Dentistry Pharmacological management of the paediatric dental patient

to inferior alveolar nerve anaesthesia has not been proven. The disadvantages are the During inferior alveolar nerve anaesthesia, the child should have his or her mouth
unpleasant taste and the long application time. This type of anaesthesia is often expected open to its maximum width. The opening of the mandibular canal in children is lower
by parents believing that it provides a painless injection. than in adults, usually below the occlusal surface of the deciduous molars and, in older
Superficial anaesthesia is used prior to the administration of local anaesthesia, for children, at the level of the occlusal surface of the last molar.
extraction of deciduous teeth during physiological replacement, prior to the placement When performing anaesthesia of the inferior alveolar nerve on the right side, an ap­
of cofferdam clamps, curettage and scaling, placement of orthodontic brackets, wound proach "from the front" is advisable. The thumb of the dentist's left hand should be
care, taking impressions in patients with a strong vomiting reflex. placed in the coronoid notch of the mandible and push the soft tissues of the cheek aside
Local anaesthesia is usually sufficient for minor dental procedures performed on chil­ so that the pterygomandibular fold is located medially. The middle finger of the left
dren aged ::; 5 years. In the maxilla, in order to effectively anaesthetise a second deci­ hand should be on the back edge of the mandible. The syringe should be placed near
duous molar (roots covered by a thick layer of maxillary zygomatic process bone), it is the opposite corner of the mouth (on deciduous molars or permanent premolars). The
important to insert the needle distally in the region of the maxillary tuberosity. When needle insertion site is located in the recess created, internal from the thumb and external
anaesthetising the first permanent molar, anaesthesia should be administered at two from the pterygoid fold (Fig. 3 . 1 ) . The needle is inserted into the soft tissues until bony
points - also in the mesial buccal root area. To anaesthetise mandibular molars in younger resistance is felt (in the absence of resistance, withdraw the needle slightly and change
children, it is usually sufficient to inject the anaesthetic into the mucobuccal fold between the track), then retracted by about 1 -2 mm and aspiration is performed. On negative
the roots of these teeth. In children 6 years and older, regional anaesthesia is indicated. aspiration, the anaesthetic should be injected slowly, leaving a small amount necessary
It is impo1tant to perform aspiration and slow injection of the anaesthetic (maximum rate to anaesthetise the lingual nerve. The lingual nerve is anaesthetised by injection when
of administration: 1 ml/1 5-20 seconds). the needle is withdrawn. For positive aspiration, withdraw the needle by approximately
When performing local anaesthesia from the oral vestibule, it is important to stretch 1 cm, change the insertion path and repeat the aspiration. The anaesthetic effect should
the tissue at the site of administration (pulling back the lip, cheek) and dry it before occur after approx. 5- 1 0 minutes. When anaesthetising the inferior alveolar nerve on
administering the anaesthetic. The needle is inserted into the mobile pmt of the mucosa the left side, the dentist's left arm can be placed over the patient's head with the thumb
just at the border with the attached gingiva at a depth of 1 -2 mm with the bevel point­ positioned as described above.
ing towards the bone and a few drops of anaesthetic are administered so that the tissue
is anaesthetised before the needle is inserted deeper. It is beneficial to administer the
agent slowly as the needle is moved. When administering, move the lip, cheek. Once the
aspiration is performed and a negative result is obtained, the anaesthetic is slowly ad­
ministered. Palatal anaesthesia is usually accompanied by discomfort, so it is beneficial
to use surface anaesthesia or pressure with a finger or cotton-tipped chopstick around Fig. 3 . 1 . Place of needle inser­
the needle insertion site. In children, anaesthesia from the vestibular side, which can be tion during anaesthesi a of
called intrapapillary local anaesthesia, is usually sufficient. inferior alveolar nerve.

Complementary to the local anaesthesia performed in the oral vestibule (anaesthe­

sia of the upper, middle, anterior alveolar nerves in the maxilla and anaesthesia of the In children, intrapapillary local anaesthesia (both papillae: mesial and distal, or, if
inferior alveolar nerve in the anterior part of the mandible), anaesthesia of the anterior this is not possible, the distal papilla) is recommended, especially as an adjunct to local
palatine or naso-palatine nerve in the maxilla and the lingual nerve. A small amount of anaesthesia of mandibular molars in patients aged :S: 5 years, and as the only anaesthetic
anaesthetic is administered slowly until the mucosa shows signs of anaemia. prior to the placement of a cofferdam or standard steel crown, and for extraction of inci­
sors and deciduous canines.

34 35
Compendium of Paediatric Dentistry Pharmacological management of the paediatric dental patient

Recommended technique for intrapapillary infiltration: overdose of an anaesthetic (very rare) or so-called relative overdose, i.e. administration
- performing topical anaesthesia on the labial/buccal side, of the correct dose to an overactive patient, as well as administration of the anaesthetic
after approximately 2 minutes, insert the needle into the base of the distal interdental directly into the vessel. The factors modifying the patient's reaction to the anaesthetic
papilla on the labial/ buccal side to a depth of 1 -2 mm; the syringe should be posi­ are: young age, systemic diseases (e.g. kidney, liver, circulatory failure), metabolic aci­
tioned parallel to the plane of the occlusion and perpendicular to the line of the dental dosis, hypovolaemia, malnutrition and some drugs ( e.g. �-blockers). Lower doses should
arch, be used in patients with the above factors. Children are more prone to toxic reactions due
slow deposition of several millilitres of anaesthetic (to achieve a change in colour to their lower weight. Reactions usually occur within 1 0 minutes after administration
also on the palatal/lingual side of the papil la), of the anaesthetic, manifesting as central nervous system and cardiovascular disorders.
repeat the procedure on the mesial side of the tooth. Local complications of local anaesthesia are:
A modification of the intrapapillary local anaesthesia is the "transpapillary" anaes­ fracture of the needle (too thin and short),
thesia, the so-called indirect palatal injection, in which the needle is directed at a slight - pain of anaesthesia (type and technique of anaesthesia),
angle towards the root apex. In the first stage, an anaesthetic is introduced to a depth of pain after the anaesthesia has subsided (tearing, excessive stretching of tissues),
1 -2 mm and a small amount of anaesthetic is administered, then the needle is introduced - insufficient anaesthesia (poor technique, too little anaesthetic, anatomical anomalies,
deeper, reaching the wart on the inner side of the dental arch and administering another inflammation of tissues, stress or resistance of the patient),
dose of the anaesthetic. - tissue hematoma (damage to a blood vessel),
In children, intraseptal anaesthesia (an alternative to intraosseous anaesthesia) may - abscess,
also be used, while classic intraosseous anaesthesia - only in patients with erupted teeth trismus (intramuscular appl ication in the pterygomandibular space),
( contraindicated in the area of the tooth germ). In the case of teeth with completed root inferior alveolar nerve block,
development and erupted adjacent teeth, intraligamentary anaesthesia can be performed. paraesthesia, transient facial nerve palsy,
They should be considered in people with bleeding diathesis. However, it is fraught with excessive exsanguination and tissue necrosis,
a high risk of bacteraemia and the possibility of local complications ( e.g. damage to particularly common in children - biting of the anaesthetised tissues, most commonly
the root cement, necrosis of the gingival papilla, submucosal and subperiosteal abscess, the lower lip, followed by the tongue and upper lip.
difficult wound healing, postoperative tooth pain, "tooth elongation"). In the case of
endodontic treatment with insufficient anaesthesia of the tooth pulp, the anaesthetic can Sedation and general anaesthesia
be administered intrapulpally. However, this route of administration is painful, and the
effect is short-lived. The use of pharmacological methods, such as sedation and general anaesthesia, is
Anaesthetics can be administered using a computer-control led local anaesthetic mainly considered when behavioural methods are ineffective, in intellectually disabled
delivery system (CCLAD).They have applicators that look like a pen, which reduces patients and in patients with co-morbidities where stress may worsen the patient's condi­
the child's fears. They provide automatic aspiration and gradual, slow dosing of the tion (e.g. epilepsy, hypertension). The conditions for their use are:
anaesthetic under computer control, which reduces the patient's discomfort. Examples of personnel possessing appropriate qualifications, including in the field of patient ven­
devices: The Wand and The Wand STA, The Sleeper One, QuickSleeper, Calaject. tilation and cardiopulmonary resuscitation,
General complications of local anaesthesia of the nature of toxic or allergic reac­ - equipment of the office with specialized equipment (apparatus for monitoring ba­
tions rarely occur. More often, fainting occurs, which is the result of dental anxiety, and sic vital parameters, cardiopulmonary resuscitation, inhalation sedation/anaesthesia,
not an undesirable effect of an anaesthetic. A toxic reaction may occur as a result of an source of medical gases),

36 37
Compendium of Paediatric Dentistry Pharmacological management of the paediatric dental patient

equipping with the necessary drugs: for resuscitation (adrenaline, amiodarone), re­ sedation by intravenous route, drugs can be administered only in the presence of an
versing the action of benzodiazepines (flumazenil), reversing the action of narcotic anaesthesiologist.
drugs (naloxone), infusion fluids, Possible complications of sedation are: airway obstruction, central breathing disor­
- the correct qualification of the patient and obtaining the written consent of the patient, ders (hypoventilation or even apnoea), circulatory arrest, vomiting, allergic reactions.
parent or legal guardian, Mild sedation of the child can be achieved by oral administration 2 hours before
proper preparation of the patient and parents (caregivers) - familiarization with the hydroxyzine treatment at a dose of0.5- 1 mg/kg (maximum dose of25 mg). Hydroxyzine
procedure, rules of cooperation with staff and possible feelings during the procedure, exhibits sedative, anti-anxiety, antihistamine, hypnotic, anti-emetic, muscle tension re­
possible nutritional break, ducing, weak anticonvulsant and analgesic effects. It intensifies the effect of depressive
- providing post-operative care until the return of consciousness and normal basic para­ agents on the CNS.
meters of vital functions: blood pressure, heart rate, body temperature, respiratory rate. Minimal sedation (so-called pharmacological sedation) does not require the pres­
The qualification of a child for sedation requires an assessment of, for example: body ence of an anaesthesiologist and is most often achieved by oral, intranasal or rectal ad­
weight and development, general condition, including the presence of general diseases, ministration of a single dose of midazolam (0.3 mg/kg) or inhaled nitrous oxide/oxygen
drugs used, allergies, local condition of the oral cavity and the scope of dental treatment mixture. On an outpatient basis, it is contraindicated in children under 1 2 months of age,
and the condition of the upper respiratory tract in terms of the potential threat of their with systemic diseases that impair the patient's functioning (ASA 2: 3) and in pregnancy.
patency (e.g. snoring, obstructive nocturnal apnoea), the course of previous treatments It requires constant monitoring of the patient's clinical condition.
under sedation or general anaesthesia and possible unexpected reactions. Nitrous oxide (Np) inhalation sedation (NP) is possible in cooperating patients,
The use of pharmacological agents allows to obtain a state of sedation: e.g. in the case of severe dental anxiety or with a strong vomiting reflex, with asthma and
- minimal (anti-anxiety) - preserved state of consciousness and verbal contact, full epilepsy in the asymptomatic period. Contraindications to its use are: cold, tonsil hyper­
patency of the airways, trophy and impaired permeability of the upper respiratmy tract, the first trimester of preg­
- moderate (conscious) - impaired consciousness, reaction to stronger acoustic or tac­ nancy, some mental diseases, pneumothorax, emphysema, bronchial distension, chronic
tile stimuli, full patency of the airways, bronchopulmona1y disease, vitamin B l 2 and folic acid defic iency, lack of verbal contact.
deep - unconscious patient, reaction only to strong stimuli, often requires opening the Nitrous oxide exhibits anxiolytic (fear-relieving), euphoric and weak analgesic ef­
airway, less often to support breathing, fects (requires additional analgesic treatment or local anaesthesia). The effect appears
- anaesthesia, i.e. general anaesthesia - consciousness suppressed (pharmacological very quickly after its administration (even after 30 seconds) and quickly disappears after
sleep), analgesia (no reaction to strong pain stimuli) and often muscle sagging, re­ discontinuation of administration. In dentistry, it is recommended to use 50% of the Np
quired airway c leansing and respiratory support. concentration in the N2O/O2 mixture (in accordance with European and American guide­
According to the Announcement of the Minister of Health of April 30, 2020 "On the lines, the maximum permissible concentration is 70%). The Np/O2 mixture is adminis­
publ ication of a uniform text of the regulation of the M inister of Health on the organiza­ tered to the patient through a nasal mask tightly adjacent to the nasal region. During the
tional standard of health care in the field of anaesthesiology and intensive care", sedation procedure, it is advisable to titrate, i.e. modify the concentration of oxide in the mixture,
is an action aimed at eliminating anxiety, fear and calming the patient, while anaesthesia enabling an appropriate level of sedation to be achieved and at the same time reducing
- performing general or regional anaesthesia for surgical procedures and for diagnostic the risk of side effects such as nausea and vomiting. The use of nitrous oxide in a con­
or therapeutic purposes. centration of up to 50% requires an assessment of the patient's state of consciousness,
Pharmacological agents can be administered by inhalation, intramuscular, oral, in­ his reaction to commands and physical stimuli, skin colour, breathing - air flow, its fre­
travenous, rectal. Due to the risk of side effects and the risk of deepening the state of quency and chest movements.

38 39
Compendium of Paediatric Dentistry Pharmacological management of the paediatric dental patient

Midazolam is a benzodiazepine that has a sho1tanxiolytic, sedative, retroactive, and fast-acting General anaesthesia in outpatient conditions - contraindications in the case of:
effect (20-30 minutes after oral administration). Intravenous midazolam may be administered - children under 1 year of age,
by an anaesthetist. Possible side effects of midazolam are agitation instead of sedation, apnoea, - high risk of anaesthesia assessed on the basis of physical condition according to the
pressure drops, hiccups, nystagmus. This medicine exacerbates respiratory depression caused American Association of Anaesthesiologists (2: III on the ASA scale),
by other medicines (e.g. opioids, barbiturates, other sedatives and anaesthetics). The action of - the risk of difficult intubation, e.g. in patients with craniofacial malformations, muco­
midazolam reverses flurnazenil administered intravenously at a dose of 5-10 µg/kg (maximum polysaccharidosis, the need for prolonged monitoring (e.g. in children with tonsillar
dose of 1 mg). Monitoring of the clinjcal status of the patient when midazolam is used should be hypertrophy, history of sleep apnoea),
extended to include the use of a pulse oxin1eter and blood pressure measurement. - respiratory tract infections for up to 2-6 weeks after symptoms have resolved.
Moderate or deep sedation and general anaesthesia are performed by an anaes­ Local contraindications for general anaesthesia are: acute inflammation of the oral
thesiologist. Indications for general anaesthesia can be divided as related to the general mucosa and acute gingivitis, symptoms of viral diseases in the oral cavity (e.g. herpes
condition of the patient and resulting from the need for dental treatment. These include: simplex virus, measles, smallpox), oral candidiasis.
- lack of possibility of cooperation due to age (mental and emotional immaturity, in­ The formal aspects of preparing for a dental procedure under general anaesthesia are:
ability to communicate) and lack of cooperation in the absence of effectiveness of - dental examination (clinical and radiological), determination of the treatment plan
other methods shaping dental posture, and documentation of the examination results,
autism, informing parents about planned treatments and their extent and written consent of
- moderate and severe intellectual disability, the child's carers for planned therapeutic activities (dental conservative treatment and
psychiatric problems, e.g. anxiety disorders, phobias, tooth extractions),
- progressive neurodegenerative diseases, e.g. congenital metabolic diseases, - written parental consent for general anaesthesia (so-called anaesthetic consent),
- serious comorbidities, such as a complex heait defect, where treatment without anaes- up-to-date laboratory results (morphology, basic coagulation indices, ionogram,
thesia or sedation could be riskier than under general anaesthesia with full monitoring, blood group),
- documented allergy to local anaesthetics or other contraindications to their use, optionally: antibiotic shield, haematological preparation,
- congenital angioedema, oral anaphylaxis syndrome, movement disorders (e.g. cere- - prophylactic vaccination against hepatitis B.
bral palsy, ataxia), An important element of safe anaesthesia is adequate fasting time.
previous treatment failure under sedation and local anaesthesia, For dental treatment, intubation through the nose and accurate protection of the respi­
a complex or extensive dental procedure, which can only be performed under general ratory tract is more beneficial than intubation through the mouth. Dental treatment under
anaesthesia, including: general anaesthesia should be comprehensive and ensure a long-term therapeutic effect.
• the presence of numerous teeth with decay or requiring extraction in young children, Important are:
• impacted teeth or extractions of broken fragments of permanent teeth, - selection of materials and methods for restoring lost tooth tissues ensuring longe­
• urgent need for oral health care in a child with numerous teeth affected by caries vity (for the restoration of molar deciduous teeth, it is advisable to use prefabricated
(e.g. before cardiac surgery, immunosuppressive or oncological treatment), stainless-steel crowns),
• treatment of extensive injuries, - atraumatic surgical treatment and protection of post-extraction wounds (e.g. spon­
• the presence of inflammatory conditions (abscesses, inflammatory infiltrates) re­ giosa, stitching),
quiring immediate treatment due to the risk of general complications, e.g. brea­ prophylaxis - fluoride varnish, iodine povidone (after excluding iodine allergy) or
thing disorders or dysfunction of other organs. chlorhexidine varnish,

40 41
Compendium of Paediatric Dentistry

- thorough cleaning of the oral cavity from post-treatment residues (filling residues,
lignin, etc.) before removing the respiratory protection.
After the treatment has been completed: Chapter 4
- communicate post-operative recommendations to the child's caregivers,
- inform them of possible complications and the need to see a dentist with the child if
Dental examination of the paediatric patient and initial
necessary (e.g. late post-extraction bleeding, fever, pain),
treatment plan
- emphasise the need for regular dental check-ups and caries prevention.
At home, the child can be discharged under the care of adults, with stability and full Joanna Szczepanska
normalization of basic vital parameters, conscious, contacting and able to move to an
age-appropriate range, in the absence of nausea and vomiting.
Possible local complications after surgery performed under sedation or general
anaesthesia are: postoperative swelling due to tissue traumatisation, injuries to the tem­
poromandibular joints (e.g. joint contusion, joint capsule damage, hyperluxation, luxa­ Dental examination of the child
tion), postoperative dentin hypersensitivity, dental pulp diseases.
The process of providing health care to a child should always take place in the pre­
References
sence of a parent or legal guardian. The participation of the carer during dental treatment
1. American Academy of Pediatric Dentistry. Use of local anaesthesia for paediatric dental patients.
The Reference Manual of Pediatric Dentistry. Chicago, lll: AAPD; 202 1 :332-7. - 2. American Acad­ facilitates the child's wellbeing, provides legal security for the dentist and allows consent
emy of Pediatric Dentist1y. P ain management in infants, children, adolescents, and individuals with to be obtained on an ongoing basis, not only at the start of treatment, but also if the diag­
special health care Needs. The Reference Manual of Pediatric Dentistry. Chicago, Ill.: American Acad­
emy of Pediatric Dentistty; 202 1 :377-85. - 3 . Ashley PF et al. Sedation of children undergoing dental nosis or treatment method changes.
treatment. Cochrane Database Syst Rev. 2018 1 7( 1 2);doi: 1 0 . 1 002/1 465 l 858.CD003877. - 4. Ashley The dental examination of a child consists of a subjective examination (family, ge­
P et al. Best clinical practice guidance for conscious sedation of children undergoing dental treatment:
neral medical and dental history), a physical examination carried out by sight and touch,
an EAPD policy document. European Archives of Paediatric Dentistry 202 1 ; 1 0 . 1 007/s40368-02 1 -
00660-z. - 5. Faytrouny M et al. Comparison of two different dosages of hydroxyzine for sedation in and possible additional examinations and consultations with other specialists. It allows
the paediatric dental patient. lnt J P aediatt· Dent 2007; 1 7(5):378-382. - 6. Gerald Z, Wright GZ, K upi­ a preliminary or definitive diagnosis, the development of a preventive and therapeutic
etzky A. Behavior Management in Dentistry for Children. Second Edition. 20 1 4 John Wiley & Sons,
Inc. - 7. Girdler N M et al. Clinical sedation in dentist1y. John Wiley & Sons, 2009. - 8. Klingberg G et management plan and its presentation to the patient's parents (carers). The initial diagno­
al. Local analgesia in paediatric dentistty: a systematic review of techniques and pharmacologic agents. sis may be revised during the treatment process or after further follow-up tests.
Eur Arch Paediatr Dent 20 1 7;18 :323-329. https://doi.org/1 0.1007/s40368-0l 7-0302-z. - 9. Kolakows­ The examination already begins by observing the child's behaviour while waiting
ka A, Pigan A. Local anaesthesia in developmental patients. New Stomat 2019;4: 1 38- 1 43 .
10. K ilhnisch J et al. Best clinical practice guidance for local analgesia i n paediatric dentistry: an to be admitted and while collecting a history from the caregivers - what is the child's
EAPD policy document. Eur Arch P aediatr Dent. 201 7;18(5):3 1 3-32 1 . - 1 1 . Kupietzky A, Houpt M I . manner of speaking and does he or she respond to our questions. ·11 is important to note
Midazolam: a review of its use fo r conscious sedation i n children. Pediatr Dent 1 993; 1 5 :237-237. - 1 2 .
Meechan J G . Pain contt·ol i n local analgesia. Eur Arch Paediatr Dent. 2009; I 0:71-76. - 1 3 . Nelson T,
in the medical record at each visit the child's response to the examination and treatment
Nelson G. The role of sedation in contemporary pediatric dentistry. Dental Clinics, 20 l 3;57( I ): I 45- and the possibility of cooperation. Attention should also be paid to the child's physical
16 1 . - 14. Olczak-Kowalczyk D, Szczepat'tska J, K aczmarek U. Contemporary dentistry of the de­ appearance, including clothing appropriate to the season and general hygiene status.
velopmental age. Med Tour Press lnt. 20 1 7. - 15. Salma AN, Ramakrishnan M. Use of anaesthesia
in paediatric dentistry: a cross-sectional survey. lnt J Pedod Rehabii. 2016; I :5-9. - 16. Swi<1tkows­ When asking for personal information, particular attention should be paid to the age
ka A, Swi<1tkowska-Bury M. Sedation in dentistry - current anaesthetic guidelines. New Stomatol of the child and the information obtained during the general medical and dental history
2020;3 : 82-92. - 17. Wilson S. Pharmacological management of the paediatric dental patient.Pediatr taken should be analysed in relation to it.
Dent 2004;26(2): 131-136.

42 43
Compendium of Paediatric Dentistry Dental examination of the paediatric patient and in itial treatment plan

Family and general medical history The dental history should include the following:
in children with deciduous teeth:
The socio-demographic data obtained should include information on place of resi­ - the beginning and course of deciduous teeth eruption, eating habits of the newborn
dence and number of children in the family, parents' education, as well as the presence and infant (feeding method - breast milk feeding, formula feeding, and supplemen­
of developmental or genetic defects in the family. Questions should relate to the child's tary feeding, falling asleep during breastfeeding or bottle feeding and the duration of
attendance at a nursery or pre-school or the type of school and class, e.g. music, sports, these activities),
special needs. in all patients:
This should be followed by information on the course of the pregnancy (uncompli­ - habits and parafunctional habits (soothing with a pacifier or sucking on a finger
cated, complicated and medications used), the type of birth (natural, caesarean section, (thumb), biting nails, grinding of the teeth (referred to as bruxism)),
complicated), the timing of the birth (premature - less than 37 weeks, on time - 37.-4 1 st - eating habits (eating between meals, eating sweets, drinking sugary or soda drinks
week, delayed - over 4 1 st week), baby's birth weight (very low - below 1 500 g, low - be­ and their frequency, reluctant chewing),
low 2500 g, normal - 2500-4000 g, high - above 4000 g) and the health of the newborn. - hygiene procedures (the age of the child at which tooth brushing was started and flu­
The general medical history should include acute and chronic illnesses as well as oride toothpaste was introduced, the frequency and time of the day of brushing teeth,
current illnesses and medications used. supervising the chil d when brushing teeth, the use of additional hygiene measures in
In a child with general illness, dental treatment and post-operative care sometimes the mouth),
need to be modified or assisted by pharmacological therapy. Patients with neurological - fluoride and non-fluoride prophylaxis methods used.
disorders may require treatment under general anaesthesia. In some cases, a preventive If a patient presents with a tooth injury, the dental history should be expanded to in­
antibiotic prophylaxis may be recommended for dental treatment including surgery with clude information focused on: the time, place and circumstances of the accident, previous
tissue disruption or haematological preparation. injuries and their treatment, possible complications. A child's visit to the dentist may also
Systemic diseases or their treatment may influence the occurrence of pathological relate to peTiodontal or oral mucosa! complaints or be related to developmental defects of
changes in the oral cavity. mineralised tissues, bite disorders. These states require, in addition to gathering a basic
interview, obtaining information focused in detail on the causes and symptoms associated
Dental history with them. Each subsequent visit of the child to the dental office requires an ongoing inter­
view regarding events that may have occurred between visits, in order to update medical
At the beginning of the visit, it is important to establish the reason for visiting the information. When a patient reports for a follow-up visit related to previously initiated
dentist with the child: a preventive visit, a periodic check-up or related to the continua­ treatment, a reinterview, clinical examination, and additional examinations are required to
tion of the treatment process, teething disorders - both premature and delayed. Common check the healing progress and possibly verify the diagnosis or method of therapy.
causes are pain related to caries and its complications, as well as trauma to the tooth.
If this is your child's first visit to a particular dental practice, it is important to first Clinical examination
gain an understanding of their previous treatment. Written information from the previous
dentist is sometimes necessary, especially when continuation of treatment is required. In the general examination, attention should be paid to the physical development of
Difficulties may arise especially if there have been complications following interrupted the child - body height and weight, hair, face and neck skin, hands, including the appea­
or completed treatment at another practice. A history of pulp inflammation or post-trau­ rance of nails (e.g. bluish may indicate a cyanotic heart defect), differences in size, shape,
matic conditions, for example, is described in Chapters 1 9 and 23 . symmetry within the head and neck (may indicate, among others, a genetic syndrome).

44 45
Compendium of Paediatric Dentistry Dental examination of the paediatric patient and initial treatment plan

By looking at the visually accessible skin, we assess its colour, pigmented changes, le­ In the vestibule of the oral cavity, the following are assessed:
sions, scars, inflammatory infi l trates, we also pay attention to those that may be the result - attachments of the frenulums of the lips (location and structure in relation to the age
of, for example, violence, i.e. bruising at different stages of healing. of the child, exsanguination and pull syndrome),
The extraoral examination should begin with a visual assessment of cranial size parotid glands (appearance and patency of the duct orifices),
and facial symmetry. Then assess the lymph nodes of the head and neck by palpation - occlusion (depending on milk, mixed and permanent teeth),
(size, hardness, displacement relative to the skin and ground, soreness). Significant - diastema (physiological and pathological),
lymph node enlargement is an indication for ultrasound examination. W hen examining - tooth wear (physiological and pathological),
the submandibular lymph nodes of each group A, B or C, the dentist tilts the patient's periodontal status (inflammatory changes, including the presence of swelling or fistu­
head to the side to be examined and gently compresses them in contact with the mandi­ lae, hypertrophic changes, gingival recessions, depth of pockets),
bular shaft; when examining the submandibular nodes, he tilts the patient's head down­ the condition of the buccal mucosa (lesions - their size and location).
wards. In addition, any flexures present, which may be indicative of inflammation or will In the oral cavity proper, we assess:
require further diagnosis, should be checked by touch. During the examination of the - attachments and the size of the tongue frenulum,
temporomandibular joints, the symmetry of movement of the joint heads, the degree of - tongue (size, covering or coating, presence of lesions on every surface, tooth impres-
oral dilation and mandibular movement, soreness and the presence of acoustic symptoms sions, condition of papillae),
such as crackles, clicks or squeaks are assessed. - the bottom of the mouth (by sight - the presence of exertion or lesions, duct orifice
The visual assessment of the lips takes into account their moisture content, the pre­ of the sublingual and submandibular glands, and palpation),
sence of lesions, tooth impressions, post-cleft scar, changes at the corners of the lips, hard palate (arching, presence of lesions - their size and location, presence of cleft
and the palpation takes into account the presence of thickening and soreness. We assess palate),
the child's breathing pattern - through the nose or through the mouth and on the type of - soft palate (the presence of lesions - their size and location, and the presence of cleft
swallowing (adult - somatic, infant - visceral, visceral, infantile). palate);
Attention should be paid to the symptoms of possible violence against the child, - palatine tonsils and palatoglossal and palatopharyngeal arches,
including malnutrition, growth deficiency and delay in psychomotor development, poor - the amount and consistency of saliva.
hygiene, dirty clothing and hair, lice, improper clothing in relation to growth and sea­ In order to objectify and compare the clinical status at subsequent visits, appropriate
son, asymmetry of limb and chest shapes, changes in the skin (discoloration, bruising, indicators are used in the assessment of the dentition, gums and oral hygiene status.
petechiae, scars, wounds, hair loss), which may result, for example, from bumps, burns, The hygiene test is carried out, among others, on the basis of the oral hygiene in­
pinching, burning, suffocation, bites, sucking. dex according to Green and Vermillion OHi (Oral Hygiene Index), dental plaque index
It is important to visually examine the area of the so-called "safety triangle" (ears, according to Silness and Loe PI.I Plaque Index), an approximate index of dental plaque
side of the face and neck, neck, top of the shoulders) and the inner side of the shoulders according to the Lange API Approximal Plaque Index.
and forearms. If the above symptoms are found, their exact characteristics in the patient's The oral hygiene index is most often used in children in a simplified version Simpli­
documentation, including photographic ones, are necessary. fied Oral Hygiene Index (OHJ-S), where the test is carried out on 6 index teeth on vestib­
Intraoral dental examination is carried out by sight, palpation and with the use of a ular of deciduous and permanent surfaces: 55/16, 51/ 1 1, 65/26 and 71/3 1 , respectively,
diagnostic kit and specialized devices. Before starting the examination, especially younger and on language surfaces: 75/36 and 85/46. This indicator has two components: debris
children, should be familiarized with the instruments not to frighten them, but gradually i ndex (DI-S) and calculus index (CI-S). The following criteria are adopted for the degree
prepare them for subsequent clinical activities, using the "te l l-show-do" technique. of plaque or calculus coverage of the tooth surface:

46 47
Compendium of Paediatric Dentistry Dental examination of the paediatric patient and initial treatment plan

0 - no plaque or calculus, Ways of staining dental deposits

I - plaque or supragingival calculus covering up to ½ of the tooth surface,
2 - plaque or supragingi val calculus covering more than ½ and less than ½ of the tooth There are now many plaque visualisation preparations available, both for profession­
surface or individual strands of the subgingival calculus, al use in the office and by the patient at home. They contain, for example, iodine with
3 - plaque or supragingival calculus covering more than 3/3 of the tooth surface or a thick glycerine, crystal violet solution, alkaline fuchsin or erythrosine. One of the most com­
band of subgingival calculus around the tooth neck. mon agents used to stain and visualise plaque is erythrosine, which is used in the form
The examination is carried out using a probe, moving it from the incisal edge or of a ready-made solution or a concentrated preparation requiring dilution, as well as in
occlusal surface towards the gingiva. The summed values separately for the presence of tablet form. Initially, the patient should rinse the mouth thoroughly with water to remove
plaque and calculus divided by the number of tooth surfaces examined are in the range food debris and dilute saliva. The teeth are then isolated with lignin rolls from saliva
0-3. W hen both components of CI and DI are added, the total OHI is 0-6. Calculus is rare access and air-dried. The ready-made erythrosine solution is spread on the crowns of the
in children and, therefore, when assessing the presence of plaque only, DI-S = 0.0-0.6 is teeth with a cotton swab or micro brush. Continue by asking the patient to spread the
assumed to indicate good, DI-S = 0.7-1.8 sufficient, DI-S = 1 .9-3.0 poor oral hygiene. preparation with the tongue over all tooth surfaces. The distribution of plaque staining on
The plaque index according to Silness and Loe (PI I) is used to assess the presence the tooth surfaces is then assessed. The dilution of the concentrated preparation produces
of plaque in the cervical region on 4 surfaces (vestibular, lingual, proximal and distal) a solution with which the patient should rinse the mouth thoroughly. If erythrosine is in
on 6 index teeth, for deciduous and permanent teeth respectively: 55/ 1 6, 5 1 /12, 63/24, tablet form, it is advisable for the patient to chew the tablet for 30-60 seconds.
75/36, 7 1 /32, 83/44. The evaluation criteria are as follows: Fluorescein, which is excited with ultraviolet light in the 500 nm range, can also be
used to stain the plaque. Fluorescein turns teeth blue and gums dark blue when exposed
0 - no bacterial plaque,
to ultraviolet. In contrast, plaque on the teeth is visible as a yellow colour and on the
1 - a thin layer of plaque invisible to the naked eye, but discernible when collected by
gums as a green colour. This allows the tile to be clearly distinguished from the substrate
gavage or after staining,
on which it is placed. A fluorescent lamp can also be used for this purpose, which stains
2 - plaque visible to the naked eye moderately accumulated in the gingival area,
the deposits orange.
3 - abundant plaque deposits in the gingival pocket or on the free gingiva margin.
There are also agents of colouring the plaque in three colours. A plaque put down
The sum of the values obtained at each tooth divided by the number of surfaces
over a 48-hour period stains reddish pink, an older one turns dark blue, and the acid-pro­
examined gives the PI.I value.
ducing plaque turns light blue.
Approximal Plaque Index - API is used to assess the quality of the hygiene proce­
dures carried out. The examination is carried out with a gavage after staining the deposits
in the 1 st and 3rd quadrants on the proximal surfaces from the oral cavity proper, in the
2nd and 4th quadrants on the proximal surfaces from the vestibular side. The API index
is obtained by adding up the areas with plaque in relation to the number of all areas
examined and multiplying the result by 100 to obtain a percentage value. The indicator
is interpreted as follows:
Fig. 4. 1 . Plaque staining
100-70% - poor hygiene, in three colours.
70-40% - average hygiene; improvement needed,
39-25% - hygiene quite good,
< 25% - optimal hygiene.

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Compendium of Paediatric Dentistry Dental examination of the paediatric patient and initial treatment plan

Assessment of the gingiva The GI value is the quotient of the sum of the values obtained for the gingiva at each
point tested and the number of points tested. The value of the indicator in the range of
Clinical examination of the periodontal condition in children's dentistry is carried out 0. 1 - 1 .0 indicates mild gingivitis, 1 . 1 -2.0 - moderate, 2. 1 -3.0 - severe.
using the WHO periodontal probe 62 1 with a maximum pressure of 20-25 g. To assess In the case of gingival enlargement, the Gingival Overgrowth [ndex according to
the severity of gingivitis in patients of all ages, the Gingival I ndex (GI) according to McGaw isused on a scale of:
Silness and Loe and the index evaluating only gum bleeding after 20 seconds from the O - no overgrowth, feather-edged gingival margin,
gingival tube (marginal bleeding free score; MBFS), which is expressed as the percen­ 1 - blunting of gingival margin,
tage of places tested without bleeding, are most often used. 2 - moderate gingival overgrowth (< ½ of crown length) and
The Gingival Index requires the assessment of the condition of the gum on 4 surfaces 3 - marked gingival overgrowth (> ½ of crown length).
(mesial-buccal, buccal, distal-buccal and palatine/lingual) around all teeth or indicator For the initial assessment of periodontal status and treatment needs in patients of de­
teeth in accordance with the PI.I index. velopmental age, a modified basic periodontal examination index (BPE) index is used,
Evaluation criteria in G l : which is discussed in Chapter 28.
The assessment of the dentition should take into account the condition of the teeth
and the presence of possible complications of dental disease, e.g. signs of peridental
infection (abscesses, fistulas).
The clinical examination of the dentition is carried out clockwise: starting with the
last tooth in the maxilla of the right side, continuing through the left side in the maxilla
0 - no inflammation, healthy gingiva,
and then the left side in the mandible and finally examining the right side in the mandi­
ble. Therefore, teeth are usually designated by the two-digit numbering adopted by the
FDI, like the movement of a clock, where the first digit indicates the quadrant number
- mild inflammation - a slight change in the and the second digit the tooth number. When examining the condition of the teeth, it is
colour of the gingiva and mild changes in
the structure of the tissue (slight oedema), no first necessary to recognise the type of teeth - deciduous or permanent - and the num­
bleeding on probing, ber of erupted teeth in each group in relation to the child's age, in order to assess any
disturbances in tooth eruption as to time and place. Using FDI two-digit numbering, in
the case of a supernumerary tooth in the permanent dentition, the number 5 0 is added to
the nmnber of the tooth closest to the supernumerary (e.g. if the supernumerary tooth is
adjacent to tooth 22 it is designated as 72 (22+5 0). In deciduous dentition, the letter "S"
2 - moderate inflammation - glazing, redness, oe­ is added to the number of the tooth closest to the supernumerary tooth.
dema, bleeding upon probing, The dental diagram should take into account lesions of caries, developmental defects
of the teeth and mineralised tissues, discolouration, acquired lesions of non-carious ori­
gin (trauma, attrition, erosion, etc.). The indicators used in the assessment of tooth abra­
sion, erosion is presented in Chapter 26, the classification of dental trauma in Chapter 22.
3 - severe inflammation - marked redness and When assessing the condition of teeth for the presence of caries, we note in the
oedema, tendency to spontaneous bleeding,
diagram - healthy tooth, caries (carious spot active/inactive, location of carious cavity,
ulceration.

50 51
Compendium of Paediatric Dentistry Dental examination of the paediatric patient and initial treatment plan

type of filling, extracted tooth). For the analysis of caries severity, both in the individual Additional tests:
patient and in the population, e.g. during epidemiological studies, the dmft/DMFT index
is used decay, missing, filling), the consequences of caries - the pulp-ulcer-fistula­ Many times, additional investigations, in addition to a properly performed history
abscess index (pufa/PUFA) and the caries assessment spectrum and treatment index and clinical examination, are necessary to make a diagnosis and select an appropriate
(CAST) (described in Chapter 1 2). treatment method. Depending on the reason for the patient's visit to the practice, these
The International Caries Detection and Assessment System II (ICDAS II) is used to examinations may concern: the presence of carious cavities, the condition of the pulp
detect and assess caries. It consists of images of a given clinical state of primary crown and periapical tissues, the assessment of the properties of saliva or the performance of
caries with a breakdown of the different tooth surfaces together with a description and bacteriological tests. It may be necessary to refer the patient for radiology, consultation
only descriptive criteria for the detection of caries at fissure sealers and fil lings. Each or laboratory tests.
of these cases is assigned a score ranging from O - a healthy tooth, through 1 and 2 - Additional methods for assessing carious lesions are divided into qualitative (subjec­
a lesion located in the enamel, to 3-6 - a cavity in the dentin (see Chapter 1 3) . tive) methods, including: radiological assessment ( conventional and digital radiography),
The primary method o fassessing the dentition is the visual-tactile examination ( qualitative optical methods (transillumination using optical fibres - FOTI, DI-FOTI, DIAGNOcam)
assessment). The dentition is assessed before drying (to note changes in enamel code 2) and quantitative methods: measurement of excited fluorescence (DIAGNOdent, QLF),
and after drying and plaque removal. When examining the condition of the teeth, it is also electrical methods (measurement of ECM IV resistance or electrical impedance -
important to ensure adequate visibility through proper lighting. Sometimes it is helpful to CarieScan, CarieScan Plus) and digital subtractive radiography.
illuminate the tooth with a dental mirror while the unit lamp is on, to use magnification To assess the condition of fissures and cavities as well as caries lesions on proxi­
by using a magnifying loupes. The diagnosis of carious lesions, in particular carious spots mal surfaces, both early stages of caries and secondary caries, an intraoral camera and
or very small cavities, especially in posterior teeth, can pose great difficulties. Elastomeric optical transillumination methods can be used, in which a polymerization or digital lamp
orthodontic separators that pull the teeth apart can be used to make the apical surfaces visible. (Fiber-Optic Transillumination (FOTI) or D igital Imaging Fiber-Optic Transillumination
They are inserted between the proximal surfaces on one visit, but the assessment of these (DI-FOTI) is used. In addition, the latter two methods can be used to look for cracks or
areas takes place on the next visit, hence they can sometimes cause discomfort. The tactile small fractures in the enamel and dentin following trauma, when these are not visible on
examination is then carried out using a ball-tipped probes or small burnisher. routine viewing. After cleaning the tooth, the fibre optic tip is placed on the vestibular
Intraoral signs visible on physical examination that may indicate child abuse are: side and the dental mirror is placed on the oral cavity proper. It is sometimes necessary
- cuts, burns, abrasions, bruises, petechiae on the oral mucosa (erythema, abrasions to use simultaneous magnification to visualise smaller cracks through the use of a magni­
and petechiae on the border between the hard and soft palate may be indicative of fying loupes. T he phenomenon of transillumination ( diaphanoscopy) involves shining
sexual violence), a cold light through a fibre optic, e.g. from polymerisation lamp. Passing a strong beam
- upper lip frenulum or frenulum of tongue injuries (in a child under 2 years of age, of light through the tissues of a healthy tooth produces an image of uniform brightness.
without a reliable explanation), The presence of a demineralising lesion or crack in the tooth causes the light to strike the
bites on the lips ( elliptical or oval shape), lesion and disrupt transmission, the light becomes scattered and therefore does not pass
- dental injuries and discoloration of teeth caused by pulp necrosis, through the lesion and i lluminates the tooth beyond the crack. Tissue damage manifests
untreated caries, itself in the form of a shadow of varying sizes, which can be seen in a mirror. With the
malocclusion as a consequence of trauma, FOTI device, the result is read out during the examination, but it is not possible to record
- symptoms of gonorrhoea, syphilis, herpes simplex virus type 2 infection, condyloma it. In contrast, in digital dental imaging with laser light in the DI-FOTI method, which
due to human papilloma virus infection. uses a wavelength in the infrared range, the images are transmitted with a beam of visible

52 53
Compendium of Paediatric Dentistry Dental examination of the paediatric patient and initial treatment plan

light to a computer so that the images can be archived and compared in fol low-up exa­ Optical techniques are also used for quantitative laser-induced fluorescence (QLF)
minations. However, the analysis of these images is based on a qualitative assessment. methods (Quantitative Laser Induced Fluorescence) and the more accurate QLF-D.
A device that uses laser transillumination is the DIAGNOcam. It can be used to (Quantitative Light induced Fuorescence-Digital). They are used to assess early carious
detect primary and secondary caries, enamel fractures or the tightness of fillings on lesions or the degree of de- and remineralisation of enamel, as well as to quantify plaque
all tooth surfaces. The laser beam, penetrating the tooth tissue, transmits the black or calculus by exposing teeth to light in the visible violet-blue wavelength range (380-
and white images directly to the camera and from there to the computer, where they 500 nm). The biofilm of a carious lesion shows an orange or red fluorescence genera­
are stored as digital images. The DIAGNOcam is a type of intraoral camera that emits ted by endogenous porphyrins, which are produced by certain Gram-negative anaerobic
infrared radiation using two laser diodes placed on both sides of the arms of the pincer­ bacteria. The intensity of the fluorescence is related to the activity of the bacteria. The
shaped examination tip - covering the tooth from the vestibular and lingual sides. advantage of the devices is the ability to determine the quantitative progress of caries as
Demineralised areas are visible as darker spots. The criteria described by Hintze et a numerical loss of fluorescence.
al. can be used to classify the location of the shadow in the tooth tissues: 0 - light
transmission unchanged, 1 - shadow visible in enamel, 2 - shadow visible in dentin. Examination of the condition of the pulp and periapical tissues
A method using the phenomenon of fluorescence involves the tissue under The examination should always start with a healthy single-name tooth lying on the
examination absorbing electromagnetic radiation and then emitting its own light. other side of the arch. The reason for this order of examination is, firstly, the subjectivity
The examination is carried out by placing the tip of the fibre optic from the buccal of the patient's assessment, who must compare the sensations experienced and, on this
surface of the tooth. The areas affected by demineralisation are characterised by basis, determine for the examiner the strength of the provoked reactions. Secondly, if
the presence of air-filled pores, resulting in a different refractive index compared to increased discomfort occurs during the additional examination, it may also affect the
healthy tissue. A tooth with decay or cracks will interrupt the light beam, resulting response of the control, healthy tooth.
in a change in the colour or appearance of the tooth surface. In addition to visual Tests to assess the condition of the pulp are a valuable, but additional instrument to
and radiological methods, the measurement of tissue fluorescence using the laser aid diagnosis. Only after a detailed history and clinical examination can a suitable test
beam of the DIAGNOdent device can be used to assess the condition of fissures and be selected to provide valuable diagnostic information. Pulp tests can be used to assess
cavities. It is not only used to detect carious lesions on smooth tooth surfaces, in the response of both nerve fibres (pulp sensitivity tests) and blood vessels (pulp viability
deep and narrow fissures, but also to evaluate the effects of preventive measures. In tests). The response of the pulp's neural structures to stimulation by thermal and elec­
DIAGN Odent, a 655 nm laser illuminates the tooth surface via an optical fibre and trical stimuli is assessed. The myelin fibres A8 found in the pulp are responsible for the
reabsorbs the infrared fluorescence reflected from a given spot in the tooth, displaying conduction of acute pain and are stimulated as a result of mechanical development and
its intensity from O to 99. The DIAGNOdent Pen wireless device, on the other hand, air drying of the defect. Pulp C-fibres conduct blunt pain and are activated by thermal
allows digital imaging of laser-scanned teeth. Different probes can be used to accu­ stimuli, trauma, inflammation and changes in pulp blood flow, volume and pressure.
rately assess individual tooth surfaces: Fissure (F) - for fissures and smooth surfac­ A cold, warm and electrical stimulus is used to study the response of nerve fibres
es, Approx (A) - for proximal surfaces, Paro - for subgingival deposits and calculus. (Electric Pulp Testing, EPT). Cold stimulus is the most commonly used test, including
Healthy tooth structure shows little or no fluorescence, carious lesions are visible in the developmental age group. This is due to the fact that in immature deciduous and
as dark spots with fluorescence proportional to the severity of the caries. A 4-point permanent teeth, nerve conduction in the pulp is weaker as a result of nerve connections
Hibst scale can be used for interpretation: 0-8 - no caries; 9-15 - l esions limited to not yet fully developed than in mature permanent teeth. For the cold pulp reaction test,
the outer half of the enamel thickness; 1 6-30 - lesions extending to the enamel-den­ ethyl chloride is mainly used, but other preparations such as carbon dioxide in the form
tin boundary; above 30 - dentin caries. of snow or dry ice, difluoro dichloromethane, the so-called "cold pulp", ( Endo-Frost

54 55
Compendium of Paediatric Dentistry Dental examination of the paediatric patient and initial treatment plan

(DOM) or tetrafluoroethene (TFE), are also used. The stimulation should last at least compression or severance of the nerve fibres or pulp ischaemia. A lowered excitability
15 seconds. When exposed to a cold stimulus, the healthy pulp usually reacts with mild, threshold in relation to a symmetrical tooth may be indicative of acute inflammation of
short-lasting pain. An increased or prolonged response is indicative of pulpitis. If the the tooth pulp, in chronic pulpitis the excitability threshold is elevated.
pain is severe but subsides when the stimulus is removed, a likely diagnosis is reversible A false-positive pulp reaction after trauma can occur when dead pulp responds po­
pulpitis. On the other hand, when the pain is severe and persists despite the removal of siti vely to vitality tests. The reasons may be general, such as the child's fear and giving
the stimulus, this indicates irreversible pulpitis. untruthful answers. On the other hand, the local causes of a false-positive reaction are
Warm gutta-percha sticks (65-200°C), warm water, rubbing with an eraser on the an incorrectly performed examination, e.g. contact of the electrode with a metal filling
contra-angle hand-piece, sometimes electric or battery-powered devices are used to or located too close to the gingiva, lack of good drying of the tooth. When the living
stimulate the pulp with a warm stimulus. The latter have a tip in the form of a ball pulp does not respond positively to the test, it is a false negative. General causes may
which, when heated, is placed near the tooth, but without touching it. Warm stimulation be difficulties in communicating with the patient, e.g. with psychiatric disorders or after
should last no longer than 5 seconds. The difficulty and risk of using these methods, the patient has swallowed a sedative or painkiller before the visit. Local risk factors for
especially in the lateral section of the mouth, is the possibility of thermal damage to the false results include: root resorption of deciduous teeth, pulp immaturity, post-traumatic
pulp or burning of the mucosa. Therefore, these examinations should be carried out after effects - pulp shock due to rupture or compression of the neurovascular bundle, hypoxia
the application of the cofferdam. of nerve fibres, pulp undergoing revascularisation and reinnervation, canal obliteration,
Testing the pulp response with an electrical stimulus in children is less commonly orthodontically treated teeth.
used, as the full maturity of the pulp nerve fibres is required for a reliable response, Laser Doppler flowmetry (LDF) is used to objectively and non-invasively assess
which is reached several years after tooth eruption and therefore takes much longer than pulp blood flow, especially after tooth trauma. The tip of the LDF probe touching the
root formation. The tooth should be isolated from saliva access and dried before exa­ tooth contains both transmitting and receiving optical fibres. The laser beam partially
mination. To prevent conductivity from neighbouring teeth or periodontium, celluloid reflects off the blood cells' flow, changing frequency according to the Doppler effect. The
strips should be placed between the test teeth. To close the electrical circuit, a passive flux of red ·blood cells is expressed as the product of their number and rate. The test result
electrode in the form of a metal holder is held by the patient or a metal clip is placed on is recorded as a sinusoid of varying amplitude and frequency. As the probe is sensitive
the patient's lower lip. The active electrode should adhere tightly to the tooth surface so to movement, different types of custom-made handpieces are used to keep it as stable
that the smallest possible stimulus causes the pulp to react. In addition, it is necessary to as possible during the examination. For better comparability of results, the test should
apply an active electrode such as toothpaste to the electrode tip to ensure adequate cur­ always be carried out at the same time of day and the patient should rest before the test.
rent flow. The most appropriate place to carry out the examination in incisor teeth is to The blood flow measurement continues until the most uniform recording fragment ap­
place the electrode at the incisal edge near the pulp horns, in premolar teeth at the top of pears for about 30 seconds.
the buccal cusp, in molars at the vestibular surface ½ from the occlusal surface or at the To assess the condition of periradicular tissues, dental examination for horizontal
top of the cusp. During the test, the intensity of the current is gradually increased until and vertical percussion, assessment of tooth mobility and imaging diagnostics are used.
the patient feels a warm or tingling sensation. During the percussion test, the sensitivity of the tooth to percussion and the tapping
The threshold of excitability of a tooth is the weakest stimulus at which a tooth reacts sound is assessed. It is carried out using the handle of a metal instrument. Tapping pain
with pain and varies depending on the patient, age, pain sensation, type of tooth. For a in the horizontal direction indicates damage in the cervical region, while in the vertical
healthy pulp, this threshold does not exceed 40 µA. Various pathological conditions - direction it indicates a pathological condition in the periapical region of the tooth. Ano­
pulpitis or trauma - alter the response of the tooth pulp. Post-traumatic disruption of ther test is the Smreker symptom - root tremor test, where during the horizontal per­
the pulp response can be caused by an increase in pressure exerted on the nerve fibres, cussion test, a tremor can be palpated in the area of the root apex, indicating that the

56 57
Compendium of Paediatric Dentistry Dental examination o f the paediatric patient a n d i nitial treatment plan

bony structure of this area has been largely destroyed. Gentler than tapping is the bite such a way as to ensure that the required clinical outcome is achieved with the lowest
test, which involves biting a roll of lignin or a cube of pink wax through the causative possible radiation dose. This principle also emphasises the need to optimise radiolo­
tooth. Also during the interview, information can be obtained from the patient about the gical examinations, which aims to use the lowest radiation dose while achieving ade­
occurrence of pain on biting while eating. quate image quality. The choice of exposure parameters is particularly important for
Examination of peri-radicular tissue response should be routine in assessing the ef­ smaller children and adolescents. Therefore, the recently introduced new rule with the
fects of trauma, untreated or chronic complications of pulpitis. However, it should not be acronym ALADAIP. As Low As Diagnostically Acceptable being Indication-oriented
carried out in most cases in freshly traumatised teeth, where inflammatory complications and Patient-specific) emphasises that the type of X-ray chosen should be diagnostically
in the periapical tissues are not yet expected, and further pain is induced. There are, how­ oriented and patient-specific, thus also taking into account the image resolution adapted
ever, injuries such as lateral luxation, intrusion or the subsequent effect of the injury in to the object under examination. Assessing root canals or the course of fracture lines
the form of replacement resorption, where such a complementary diagnosis is required in teeth requires a higher image quality than the dose needed to detect the presence or
after radiography. In such cases, the tapping sound is usually metallic. position of a tooth.
The examination of tooth mobility is aimed at assessing the condition of perira­ W hen choosing the right image, the question to ask is - what diagnostic information
dicular tissues that may have been damaged as a result of inflammation or injury. The do we need that cannot be obtained from a clinical examination or other tests. Intraoral
degree and extent of mobility of the tooth is examined: 1° - horizontal mobility < 1 mm, imaging should be a standard diagnostic instrument. The use of CBCT shoul d be consi­
II0 - vertical mobility within 1-2 mm, IIl0 - vertical and horizontal mobility > 2 mm. dered when the technique is essential to solve a clinical problem and the benefits
Code "O" indicates physiological mobility or pathological immobility - lateral luxation outweigh the additional radiation dose. In some cases, other diagnostic pulpectomy such
or ankylosis as a consequence of major trauma, e.g. avulsion and tooth replantation. as laser fluorescence (DIAGNOdent) or fibre optic transillumination (FOT I , DI-FOTI)
Increased tooth mobility is observed after luxation or root fracture, tooth group mobility can be used instead of X-ray. If, for various reasons, e.g. lack of cooperation from the
occurs after alveolar fracture. patient, an X-ray is not possible, the initiation of treatment will depend on the diagnosis
An important additional examination is diagnostic radiology. Radiographs can only and the urgency of the treatment. An X-ray may be postponed at a given time when the
f
be recommended after a thorough dental history with the identi ication of complaints, lrnowledge gained from the history and clinical examination is sufficient and the initi­
information on systemic diseases, a clinical examination of the patient and an analysis ation of treatment in view of possible complications is so important that postponement
of previous radiographs (they can provide the necessary information so that further ra­ should not be risked.
diographs can be dispensed with). Radiological diagnosis is abandoned or postponed
Tab. 4.1. Recommendations for diagnostic imaging in paediatric dentistry.
until the patient is under general anaesthesia in a non-cooperative situation caused, for
example, by a systemic disease, also by a disability that prevents comprehensive oral Primary Permanent dentition
Type of visit Mixed dentition
dentition immature
treatment, including the taking of an image of good quality. There are no age restrictions
for radiological diagnosis. The prerequisite is good patient cooperation. Information that x�ray bitewing com-
dental or bitewing bined with OPG or
a radiograph has been taken in a person under 16 years of age shoul d be recorded in the First-time exami-
X-rays, but if dias- dental or bitewing dental; OPG is indicated
nation related to
child's medical records and health booklet. The parent or legal guardian of the child temata are present X-ray combined with in patients with general
pathological pro-
they are sometimes O PG or dental X-ray disease or a history of
assisting with the shooting must be equipped with a protective apron and lead-rubber cess
not necessary extensive dental treat-
gloves, informed about the procedure and the radiation risk. She cannot be pregnant. ment
The As Low As Diagnostically Acceptable principle (ALADA) should be applied
in radiological diagnosis, i.e. an examination using ionising radiation should be used in

58 59
Compendium of Paediatric Dentistry Dental examination of the paediatric patient and initial treatment plan

Cone beam computed tomography (CBCT) is a three-dimensional image of den­

Follow-up of pa- X-ray bitewing radiographs every 6 to 1 2 months, i f prox imal surfaces
tients at risk of cannot be examined visually or with a probe or if carious lesions are not tal structures and bone in the craniofacial region. This technology can provide multi­
developing caries visible ple viewing angles that help provide a more comprehensive assessment compared to
X-ray bitewing X-rays every 1 2 lo 24 conventional dental imaging modalities. CBCT should be limited to only a very small
Patient check-up
months, if proximal surfaces cannot be X-ray bitewing X-rays number of clinical situations where two-dimensional imaging methods are insufficient.
without risk of
examined visually or with a probe or if every 1 8-36 months
caries development It can be an auxiliary diagnostic pulpectomy in the assessment of periapical pathologies
carious lesions are not visible
Assessment of the
and dental trauma, especially when the history and clinical signs are contradictory to
development of X-rays are usually the radiological picture. More often, volumetric tomography is used in multiple tooth
dental, bitewing or OPG X-ray
teeth or facial bone not recommended. trauma or extensive trauma to the jawbone, tumours, cleft lip and palate; less often in
structures
the diagnosis of developmental anomalies of the dentition (e.g. impacted teeth, ectopy,
Follow-up, examina- supernumerary teeth). When assessing cysts or cancerous tumours, this examination can
tion for endodontic the choice of image depends on the need to assess the particular clinical
treatment, dental situation be used to analyse the extent and position of the lesion in relation to neighbouring struc­
pathology etc. tures. CBCT is not a routine examination and is not used in the diagnosis of caries.

Depending on the clinical situation, it is advisable to take intraoral radiographs - dental or Microbiological tests and saliva evaluation
bitewing - and extraoral radiographs - pantomographic or cone beam computed tomography Caries risk assessment is based, among other things, on detecting the abundance of
(CBCT). A dental radiograph is used to analyse one or more teeth. It is an accurate radio­ cariogenic bacteria and testing the buffering capacity of saliva. A number of commercial
graph used in the evaluation ofroot development, morphology oftooth cavities, configuration tests are available with which such tests can be performed in a clinical setting, e.g. CRT
of the apex, retained and persistent teeth, diagnosis and monitoring of oral diseases - carious Bacteria, Caries Risk Test) or Dentocult SM Strip mutans and Dentocult LB.
lesions invisible during clinical examination and their extent, condition of periapical tissues Conducting the CRT test SM and LB bacteria should be carried out in the morning
and furcation area, root trauma and consequences of traumatic tissue damage, developmental before the patient should not eat food for an hour. The validity of the results obtained
pathologies of individouble teethdouble teeth (e.g. double teeth, invaginations), resorption is conditional on not taking antibiotics for 2 weeks, professional fluoride prophy­
(inflammatory, replacement external and internal), effectiveness of endodontic treatment - laxis within 48 hours or an antibacterial rinse for 12 hours before saliva collection. The
treatment progress, healing process or complications. double teethdouble teeth test begins with the patient chewing a paraffin cube for 30 seconds to obtain stimulated
The bitewing radiograph is useful for detecting caries at the proximal surfaces in mixed saliva. After this time, the saliva is spit out into a disposable cup. The saliva is
enamel and dentin, secondary caries, for assessing the tightness of tooth restorations and then transferred with a pipette to agar plates for MS and LB bacterial culture. The media
the condition of the alveolar margin. should be thoroughly covered with saliva and the excess should drain off. The plates are
Orthopantomograms (OPG) are used for a comprehensive assessment of the entire incubated in the incubator for 48 hours at 37 ° C. The density of th·e growing colonies of
dentition, bone structures and mutual relations. The development of the entire dentition, the respective SM and LB bacteria, which are compared with the attached standards is
'
the number and position of teeth (hyperdontia, hypodontia, oligodontia), impacted teeth, assessed and on this basis the number of colony forming units (CFUs) per millilitre of
developmental pathologies of the teeth, maxillary sinuses, pathological changes in the saliva is determined. The assessment criteria for MS and LB are as follows: bacterial
visible bones of the maxilla and mandible, i.e. gingival or periapical cysts, tumours, can count O - < 104 CFU/ml; 1 - 104 CFU/ml; 2 - 105 -106 CFU/ml and 3 - 2: 106 CFU/ml.
be analysed. Sometimes with extensive periapical inflammation, when intraoral imaging The Dentocult S M Strip mutans and Dentocult LB tests allow you to assess the
is painful, an OPG picture can be helpful. adhesion and growth of these microorganisms on the test strip. Two-thirds of the test

60 61
Compendium of Paediatric Dentistry Dental examination of the paediatric patient and initial treatment plan

strip is placed in the patient's mouth and rotated on the surface of the tongue about 10 A comprehensive plan of preventive and therapeutic management in
times. The strip is then put into a broth medium that contains bacitracin only for the developmental age should always take into account the age of the child and refer to
selection of SM or LB bacteria. After an appropriate incubation period, interpretation both the interview and the clinical examination and consist of the following elements:
of the results is made by a different researcher to the one who carried out the tests. It is nutritional and hygienic recommendations - adjustments to dietary pattern, frequency
assessed by plotting the density of the outgrown colonies, which are visible as light to and quality, and recommendations on the proper conduct of hygiene procedures as to
dark blue, convex colonies on the surface of the test strip. The assessment criteria for MS time, methods and preparations,
are as follows: 0-1 - < 105 CFU/ml, 2 - 105 - I0 6 CFU/rnl and 3 - 2': 106 CFU/ml saliva. For - prevention- contact fluoridation, sealing of fissures and anatomical cavities, removal
LB: 0-1 - undetectable level or < 104 CFU/ml and 2-3 - 104- 105 and 2': 105 CFU/ml saliva. of calculus,
Saliva bacteriological tests can be important in planning preventive and therapeutic man­ - conservative treatment directed towards minimally invasive management,
agements - professional and home hygiene procedures, fluoridation recommendations - endodontic treatment taking into account the degree of root development and the
and redue::ing the consumption of simple sugars. child's general condition,
For example, the Saliva Check Buffer set, used to analyse the possibility of neu­ - surgical treatment, including correction of the frenulum of the tongue or upper lip,
tralizing acids, which are soaked in test strips, by the patient's saliva, is used to test the - orthodontic or prosthetic treatment - depending on the malocclusion, teeth lost
buffering capacity of saliva. At the same time, the amount of saliva secreted in a unit through decay, trauma or congenital missing teeth,
of time can be examined. First, when chewing a piece of paraffin cube for 5 minutes - consultation with dentists from other specialities, including psychologists.
to stimulate the secretion of mixed saliva, the patient spits it out into a calibrated cup. Tooth treatment should give priority to teeth with complaints, including traumatised
Then, with the help of a pipette, saliva is sprayed onto the test strip. After 2 minutes, you teeth and teeth at risk of pulp and periapical tissue complications or loss. Due to the
can read the test value based on the appropriate colours: green blue - 3 points, blue - 2 highly dynamic progression of the carious process in developmental age, the principle
points, red-blue - 1 point, red - 0 points. The final interpretation is carried out using the of dental treatment planning in the youngest children is to protect as many cavities as
scheme included in the set: from very low, low to normal saliva buffer capacity. possible in· a short period of time.

References
Laboratory tests, additional tests and consultation
I . American Academy of Pediatric Dentistry. Prescribing dental radiographs for i n fants, chil­
Pathological changes in the oral cavity may be the first noticeable symptom of dren, adolescents, and individuals with special health care needs. The Reference Manual of Pedi­
system ic disease, cancer or nutritional deficiencies. Oral diseases, in turn, may be atric Dentistry. Chicago, I l l. American Academy of Pediatric Dentistry; 202 1 :258-6 1 . - 2. Dikrnen
B. lcdas 1 1 criteria (International Caries Detection and Assessment System). J I stanbul Univ Fae
risk factors for general comp! ications or require specialist preparation of the patient
Dent 20 1 5;49(3):63-72. http://dx.doi.org/ 1 0.1 7096/jiufd.3869 l . - 3. Gugnani N et al. I nternation­
for dental treatment and postoperative care. Depending on the clinical situation, it is al Caries Detection and Assessment System (JCDAS): A New Concept. Tnt J Clin Pediatr Dent.
often necessary to perform diagnostic tests, such as blood tests (iron levels, vitamins 20 1 I May-Aug; 4(2): 93- 1 00. - 4. Pudentiana Rr RE et al. Knowledge of Oral and Dental Health
Impacts the Oral Hygiene Tndex Simplified (OH I-S) of Primary School -Children.Tndian Journal
of group B , D, morphology with smear, acute phase proteins CRP (C-reactive pro­ of Forensic Medicine & Toxicology, 202 I , 1 5, 4: 2 1 79-2 1 83. - 5. Bhayat A et al. Correlating
tein), coagulation system, biochemical tests, i ncluding protein levels, electrolytes), dental caries with oral bacteria and the buffering capacity of saliva in children in Madinah, Saudi
Arabia. Journal of International Society of Preventive and Community Dentistry 20 1 3 , 3, 1 : 38-
sometimes general urine tests, histopathological or microbiological tests. It is ne­
43. - 6. Keerthana R et al. Recent developments in dental plaque. Drug Invention Today 20 1 8, I O,
cessary to cooperate with the paediatrician both in the diagnostic process and in the Special Issue I : 2769-2772 - 7. KUhnisch J et al. Best clinical practice guidance for prescribing
provision of dental care. dental radiographs in chi ldren and adolescents: an EAPD policy document.Eur Arch Paediatr
Dent https://doi.org/ I 0. 1 007/ s40368-0 1 9-00493-x. - 8. Mirska-Mii;:tek M. Diagnosis of carious
In order to provide the child with comprehensive dental care, it is necessary to coo­ lesions on the proximal surfaces of permanent teeth. Annales Academiae Medicae Stetinensis.
perate with specialists in other dental fields, speech therapist or psychologist. Annals of the Pomeranian Academy of Medicine in Szczecin. 20 1 0, 56, 2, 70-79. - 9. Nanda J et

62 63
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al. Correlation between dental caries experience and mutans streptococci counts using saliva and Part II
plaque as microbial risk indicators in 3-8-year-old children. A cross sectional study. J Clin Exp
Dent. 20 1 5 ;7( I ): 1 14-8.
I O. Vidya Babu et al. Evaluation of Efficacy of Three Different Commercially Available Kits
for Chairside Cariogenic Bacteria Test - Caries Risk Test, Saliva-check M utans and Cari Screen. D evelopment and developmental abnormalities
Report DOI: I 0. 7759/cureus.6504. - 1 1. Yoon 1-1 I et al. Detection of proximal caries using
quantitative light-induced fluorescence-digital and laser fl uorescence: a comparative study. J Adv of the dentition and masticatory organ
Prosthodont 2017 Dec;9(6):432-438 - 12. Yun Liu et al. A Two-Year Longitudinal Study of the
Effectiveness of the CRT@ Bacteria Test in Evaluating Caries Risk in Three-Year-Old Children.
Evidence-Based Complementary and Alternative M edicine 2021, Article ID 7488855, 11 pages
ttps://doi.org/ I 0. 1 1 55/2021I 7488855.
Chapter 5

Tooth and periodontal development

Anna Turska-Szybka

Tooth development proceeds through various chronological stages, which can be

summarised as follows: growth and differentiation, epithelial proliferation, histological
differentiation, organogenesis, mineralisation, eruption, attrition and atrophy.

Chronology and stages of tooth formation and. development

Tooth development begins in the human embryo around 6-7 weeks of age, along with
the appearance of thickening of the epithelium lining the mouth, which runs along the
edges of the bones of the maxilla and mandible, penetrating into the depths of mesenchy­
mal tissues and forming the dental lamina.
The dental lamina continues to grow after the formation of all deciduous teeth germs
(20 germs) between 6 and 8 weeks:
- posterior (secondary dental lamina), giving rise to the permanent first molars' genns
(at 16.-17 th week of embryonic life), second permanent molars (at 6 months of the
child's life) and third permanent molars at 5 years of age,
- lingually, initiating the development of the permanent incisors, canines and pre-mo­
lar teeth (between 20 weeks of foetal life and 10 months after birth).
At week 8, odontogenesis begins and doughnuts appear (bud stage), and at week
1 1, the histological differentiation process begins. This stage is called the cap stage.
The cap-shaped epithelium surrounding the mesenchyme is called the enamel organ the

64 65
Compendium of Paediatric Dentistry Tooth and periodontal development

(EO), while the mesenchyme forms the primary dental papilla of the tooth. As a result by any injury. Knowledge of the mineralisation process is important for understan­
of further growth of the enamel organ and the dental papilla, at the end of the 3,c1 month, ding diseases that affect the enamel, as they need to be countered immediately. The
the tooth crown develops and amelogenesis and dentinogenesis begins. integrity of the enamel is very important as its damage is permanent as there are no
In the late cap stage ( 1 2.- l 3th week), there are three distinct layers in the enamel or­ replacement cells.
gan: the outer enamel epithelium (OEE) that covers the convex side of the cap, the inner
enamel epithelium (IEE), that surrounds the primary papilla and the low-differentiated Maturation stage
epithelial cells filling the interior, named stellate reticulum, which will form the pulp of The maturation stage, also known as "apposition stage", is recognized by many to be
the enamel organ in the next developmental stage. the final stage of tooth formation. During this phase, both enamel and dentin increase in
The mesenchyme forming the dental papilla and dental fol licle (dental sac) contains thickness and cementum forms after eruption and follows the development of the root.
neural crest cells and is referred to as the ectomesenchyme. Any disturbance during this time will result in serious abnormalities, including enamel
In the bell stage (14.-17th week), the cells of the inner dental epithelium differen­ hypoplasia or hypocalcification. At birth, the calcification of the deciduous dentition is
tiate into enamel-forming cells - ameloblasts, responsible for the production of enamel. already very advanced and the development of the crowns of all teeth is complete by the
Apart from the ameloblasts stratum intermedium is formed. This structure lies over the age of one. The first signs of calcification of permanent teeth (first molars) are usually
ameloblasts and consists of two or three layers of cells. Mesenchymal cells of the pri­ visible at birth. The eruption of the deciduous dentition occurs during the first few years
mary dental papilla form odontoblasts (dentin-forming cells). The primary dental papilla of life, with root formation completed by the age of 4. From this age, the deciduous den­
develops into a dental papilla and then into a tooth pulp. tition is considered complete.
At the end of the 5 th month, hard, mineralised tissues form as a result of the
mineralisation process. The ectomesenchyme located around the developing teeth Histogenesis of enamel, dentin and pulp. Final differentiation and mineralisation
forms the dental follicle, which surrounds the entire tooth germ (enamel organ and The formation of tooth hard tissue is regulated by the reciprocal epithelial-mesenchy­
papilla). Cement and periodontium are formed from the dental follicle. The cap stage mal interactions (between the cells of the inner enamel epithelium and the mesenchymal
and the bell stage are very important centres of cell signalling that essentially guide cells of the tooth pulp). Osteoblasts of the alveolar bone originate from ectomesenchyme
the development process. Most of the signals exchanged between epithelial and me­ cells and enable the functional integration of the tooth into the jaw bones, together with
senchymal cells are growth factors, such as: bone morphogenetic proteins (BMP), osteoclasts derived from the bone marrow.
fibroblast growth factors (FGF), transforming growth factors (TGF-13) and factors Mineralisation of the tooth crown starts from the incisal ridge /peak of the cusp at
belonging to Hedgehog and W nt signalling pathways. Furthermore , during these the growth centres and progresses towards the neck. The formation of the hard tissues
processes at the interface between epithelium and mesenchyme, the final differen­ of the tooth-bone complex involves several key processes, in particular dentinogenesis,
tiation of the outer dentin surface takes place. In the developing crown of the tooth, amelogenesis, cementogenesis and osteogenesis.
the outer surface of the dentine becomes a dentin-enamel junction (DEJ). The border
of the neck of the anatomical crown is considered to be the point at which the inner Dentin formation - dentinogenesis
and outer epithelium of the enamel organ merge to form the Hertwig's epithelial Dentinogenesis is the formation of dentin by odontoblasts of ectomesenchymal ori­
root sheath (HERS). From this point onwards, the junction between the epithelium gin located at the periphery of the tooth pulp. The dentin is formed first (in the late bell
and mesenchyme becomes the outer surface of the dentin along the root, which is stage), both in the crown and root area. Dentinogenesis is initiated by the inductive in­
covered with cementum. In addition , the specific mineralisation process is also con­ fluence of an enamel - organ involving molecular signalling pathways such as Wnt and
trolled by biomolecules which, if stimulated, can inhibit the process if it is disrupted T GF-�.

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Compendium of Paediatric Dentistry Tooth and periodontal development

Odontoblasts at their secretary pole synthesize an organic matrix proteins, including pl eted . Therefore, amelogenesis stops when the tooth erupts, and no secondary or regene­
collagen, which in the form of a non-mineralized layer of predentin is deposited above the rative enamel is produced.
top part of the cells between their cytoplasmic processes. The first sign of the beginning of In the course of amelogenesis, there is a secretary phase, a resorption phase and a ma­
the formation of predentin is the formation of Korff fibres ( delicate reticular fibres) at the turation phase (post secretary). In the secretary phase, ameloblasts take the shape of very
border of the papilla of the tooth and the internal epithelium of the enamel organ. The pre­ tall epithelial cells with nuclei located at the base and a single, short, conical Tomes process
dentin is then mineralized by depositing calcium hydroxyapatite. Later, the crystallization at the apex, which releases matrix proteins into the extracellular space. The enamel ma­
centres of hydroxyapatite grow and enable the transformation of predentin into dentine. trix undergoes mineralization, which is initiated by hydroxyapatite crystals present in the
Calcium and phosphate ions cause the growth of hydroxyapatite crystals. adjacent dentin (primary enamel mineralization). The hydroxyapatite content in enamel
In the outer dentin (mantle dentine), mineralisation is globular, meaning that hy­ reaches 25-30%. Mineralization continues during the maturation phase.
droxyapatite crystals sunounded by a membrane-bound (matrix vesicles) grow and fuse Enamel hydroxyapatite crystals are arranged in many times larger structures - prisms.
together. Subsequently, in the further dentin layers, crystals form on collagen fibres with­ In the initial and final stages of the ameloblast secretary phase, the Tomes process is not
out matrix vesicles, and this mineralisation is linear. formed. The resulting glaze does not form prisms and is classified as aprismatic ena­
Incremental mineralisation of the dentin gives the appearance of growth lines. In mel. Ameloblasts on the surface facing the enamel produce the basement membrane -
a 5-day cycle, these are Ebner's growth lines. With the deposition of dentin, the odonto­ the primary enamel membrane. The remaining cells of the enamel-forming organ com­
blasts move towards the central part of the tooth pulp, leaving a Tomes fibre in the dentin bine with the internal epithelium, forming the enamel-forming epithelium covering the
matrix, the dentinal tubule. The diameter of the dentinal tubule is 2-3 �Lm at the base and enamel until eruption. The epithelium forms the enamel (Nasmyth's membrane).
1 µm at the enamel-dentin junction.
Dentinogenesis occurs both prenatally and postnatally, most intensively during tooth Formation of tooth pulp
development, and to a lesser extent can be observed throughout life when secondary and Tooth pulp originates from neural crest cells ( ectomesenchyme ). The proliferation
tertiary dentin is formed. The dentin formed after the formation of the tooth is called and condensation of these cells leads to the formation of the dental papilla, from which
secondary dentin. the mature pulp is derived '. The mature pulp shows a strong resemblance to embryonic
connective tissue, with a layer of highly specialised cells, known as odontoblasts.
Enamel formation - amelogenesis Pulp development takes place in three stages: bud, cap and bell. In the bud stage,
Amelogenesis is the formation of enamel by ameloblasts of epithelial origin, which epithelial cells of dental lamina, strands of epithelial cells protruding from the oral epi­
face the odontoblast layer. Ameloblast differentiation is initiated by more advanced odon­ thelium, proliferate into the adjacent ectomesenchyme. This rounded epithelial bud gradu­
toblasts and intermediate cells through molecular signals such as BMP and FGF. The ally expands and forms a concave surface, determining the stage of the cap. At this point,
main enamel matrix proteins are amelogenins, enamelins, ameloblastins and tuftelin, the cells of the oral epithelium and mesenchymal cells have transformed into an enamel
which are produced by ameloblasts into the extracellular space. Ameloblastin simul­ organ and a dental pap illa, respectively. Finally, there is the stage of the bell, in which
taneously stops the proliferation of ameloblasts, while enamelins and amelogenins are the morphological and histological differentiation of the pulp occurs. Cells differentiate
necessary for the deposition of hydroxyapatite crystals. into odontoblasts, secrete predentin, a collagen matrix that mineralizes into dentin and
Ameloblastins and amelogenins are removed during maturation when ameloblasts their shape becomes columnar. The dental papilla, which becomes a pulp, already at an
produce proteinases (e.g. MMP) that cleave these substances. The remains are absorbed early stage, the bud is characterized by an environment of densely packed cells consis­
by ameloblasts, and the enamel is transfom1ed into highly mineralized tissue. Half of ting mainly of fibroblasts. In the papilla, blood vessels and related nerve fibres are formed
ameloblasts undergo apoptosis during amelogenesis, the rest die after the process is corn- early, which nourish the growing organ. At the beginning of papilla development, blood

68 69
Compendium of Paediatric Dentistry Tooth and periodontal development

vessels are located in the central zone, but smaller capillaries eventually make their way rioles that supply individual pulp micro vessels. The vessels of the pulp are arranged in
f
to the periphery of the papilla and provide nutrients for the elongating odontoblasts. the following system: arterioles run centrally upwards and give of branches, fonning
The formation of dentin by odontoblasts in the central area marks the point at which the a capillary network around the periphery of the pulp, with blood draining into vessels in
dental papilla becomes the pulp. the centre of the pulp. The capillary network provides odontoblasts with a rich source
Depending on the location, the coronal pulp and the radicular pulp distinguished. of nutrients. The vessels of the pulp are comparable to those of the most vascularised
Histologically, the pulp forms layers: the middle (pulp proper), intermediate and peri­ parts of the brain and tongue, indicating that the pulp is a highly vascularised tissue. The
pheral layers formed by odontoblasts. T he middle layer consists of mesenchymal cells, tooth pulp is characterised by relatively high blood flow. It is estimated to be 40-50 ml/
fibroblasts, granulocytes, lymphocytes, plasma cells and mast cells, as well as blood min/l 00g of pulp tissue in a mature tooth, as determined by radioactive microsphere
vessels and nerve fibres. Fibroblasts produce the basic substance of the pulp and pre-col­ techniques. This flow is relatively high compared to the flow in other oral tissues and
lagen. Mesenchymal cells have the ability to transform into odontoblasts. T he interme­ skeletal muscles. Numerous anastomotic vessels have also been observed in the pulp
diate layer, called the Weil's layer, is a lean cell layer. I t contains single fibroblasts and of the tooth. These vessels may be arteriovenous anastomoses, venous anastomoses or
collagen fibres and elastic surrounding the walls of blood vessels, which together with U-loops. They provide direct communication between the arteries and veins, thereby
the nerves form the sub-ontoblastic plexus of Raschkov. Myelin-free nerve fibres move bypassing the capillary placenta.
away from the Raschkov weave, which penetrate between the odontoblasts and into the The pulp of permanent teeth with uncompleted root development has a higher capacity
tubules of the inner layer of dentin. Weil 's layer mesenchymal cells can transform into to regenerate and combat the effects of harmful irritants than the pulp offully formed teeth.
odontoblast-like cells. In the peripheral layer, the odontoblasts are arranged in a palisade The pulp is innervated sensitively and vegetatively. Sensory innervation is fanned
fashion. The nuclei of the odontoblasts are located at different levels, which mimics mul­ by spinal fibres originating from the second and third branches of the trigeminal nerve
tilayering. They are tall, cylindrical cells connected to each other by desmosomes. The (Gasser 's ganglion). They conduct pain stimuli when acted upon by the pulp. The vege­
protuberance of the odontoblast, called the Tomes fibre, contains numerous microtubules tative innervation is formed by both sympathetic and parasympathetic non-spinal fibres.
along which the vesicular transport of dentin matrix components takes place. The second The sympathetic originates from the superior cervical ganglion, while the parasympathetic
protuberance of the odontoblast passes through Weil 's layer into the middle layer of the originates from the pterygoid ganglion and the auricular ganglion. Vegetative innervation
pulp. Between the odontoblasts run numerous bundles of reticular (Korff's) fibres. constricts and dilates the lumen of blood vessels, thus regulating blood flow. Nerve fibres
The pulp is richly vascularized. The capillaries of the pulp pass into wide venous enter the pulp along with blood vessels through the apical foramen, forming a neurovascu­
vessels that come out of the pulp through the apex opening and connect with the peri­ lar bundle. In the pulp, at the bounda1y between the middle (proper) layer and Weil, they
odontal vessels. The pulp vessels have very thin walls. Even a slight inflammatory swel­ form a Rashkow plexus. The sensory fibres that depa1t here lose their myelin sheath and
ling, causing an increase in pressure, leads to the closure of the lumen of the pulp vessels, head towards the odontoblasts, forming the sub odontoblastic plexus. Some of them pene­
and consequently pulp necrosis. An extensive network of capillaries lying directly under trate the dentinal tubules and there remain in contact with the Tomes fibres.
the layer of odontoblasts provides them with an adequate supply of nutrients necessary The tooth pulp contains both sensory and autonomic nerves that perform vasomotor
for increased metabolism during dentin fonnation. The total blood volume in the pulp and defence functions. The sensory nerves that are involved in pulp pain perception and
may not be significantly increased. For this reason, accurate regulation of blood flow is transduction are branches of the maxillary and mandibular branches of the trigeminal
crucial and changes in pulp microcirculation can be the first sign of pulpitis. The pulp nerve. Small branches enter the apical foramen and develop coronally and circumferen­
microcirculation is supplied by the maxillary aitery, which is a branch of the external tially in line with the course of the blood vessels and then branch widely, adjacent to the
carotid artery. The maxillary artery leads to the alveolar arteries (anterior and poste­ cell-rich zone, forming the Rashkow plexus. The weave contains both large myelin A
rior superior alveolar arteries, inferior alveolar artery) and enters the tooth through arte- fibres (2-5 µm in diameter) and smaller myelin C fibres (0.3-1.2 µm). At about the level

70 71
Compendium of Paediatric Dentistry Tooth and periodontal development

of the cell-rich zone, the myelin fibres lose their myelin sheath. In the cell-free zone, they fibroblasts (extrinsic fibres) form a connection of primary and secondary cement with the
form a rich network of free nerve fibres, which are specific receptors for pain. From there, ligamentous apparatus of the tooth. Mineralization of the intercellular substance causes
free nerve endings can enter the odontoblastic layer and penetrate the pre-dentinous zone transformation into cementocytes. Mesenchymal cells of the dental follicle converted
or the inner dentin next to the outgrowth of odontoblastic cells, but not every dentinal into periodontal fibroblasts produce collagen fibres that form the ligaments of the tooth.
tubule will contain nerve endings. Myelin nerves reach their maximum development The introduction to the production of primary (cellular) cement is the separation by the
and penetration into the pulp only during the period of full tooth formation, which may epithelium of HERS of substances forming on the outer surface of den tin (on the bor­
explain why young teeth with unfinished root development are less sensitive than mature der with the dental follicle) of an unstructured layer with a thiclrness of approx. 10 µm,
teeth. Branching of nerve axons has been observed not only within the pulp, but also in called the hyaline pellicle. It contains proteins similar to the enamel proteins secreted by
the periapical region, where these axons can branch to supply pulp to adjacent teeth just ameloblasts (non-amelogenins).
before entering the pulp. A-fibres produce an initial, sudden, sharp pain in response to
external ,stimuli without the presence of tissue trauma, due to their peripheral location, References
I . Alqahtani, Sakher & Hector, Mark & Liversidge, Helen. (20 I 0) The London Atlas of 1-l u­
low excitability threshold and rapid conduction. In contrast, smaller C-fibres cause slow,
man Tooth Development and Eruption. Am J Phys Anthropol. 1 42 . 481-490. I 0.1002/ajpa.21258.
dull pain associated with pulp tissue damage and inflammation due to their much higher - 2. ALShami, A, ALHarthi, S, Binshabaib M , Wahi, M . Tooth M orphology Overview. J n :
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London: l ntechOpen; 20 1 9 [cited 2022 Feb 24]. Available from: https://www.intechopen.com/
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Apr;38(4):296-306. - 4. Caruso S, Bernardi S, Pasini M, Giuca M R, Docimo R, Continenza MA,
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E, Sierpinska T, Goh,biewska M. Enamel structure and its resistance to pathological factors - a
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is no sharp boarder between these forms. HERS cells are suggested to secrete acellular disturbances in number and shape of teeth and their treatment. I n: Koch G, Poulsen S, Espelid I ,
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M, Tyszler L, Buczkowska-Radlinska J. The vital pulp therapy in permanent teeth. Pomeranian
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medical and dental students. Edra Urban & Partner Wroclaw 2013, ed. I .
of deciduous and permanent teeth
An na Turska-Szybka, Dorota Olczak-Kowalczyk

The human dentition is divided into deciduous and permanent teeth and includes
incisors, canines and molars. Premolar teeth only occur in the permanent dentition. De­
ciduous and permanent teeth are similar both structurally and histologically, but there are
differences between them.

Morphological features

T he crown of each deciduous tooth is short in relation to its total length. The crowns
of deciduous teeth are smaller and lower than those of the corresponding permanent teeth
(Fig. 6. 1 ), and their incisal edges smooth, in contrast to permanent immature teeth (ma­
melons) (Fig. 6.2). The surface of deciduous incisal teeth is smooth, with no perikymata,
developmental grooves. The crowns are barrel shaped in the cervical region due to the
presence of of excess enamelon the buccal surfaces of the molars and on the labial and
lingual surfaces of the anterior teeth.
The buccal- lingual dimensions of the crowns of the occlusal surfaces of deciduous
teeth are smaller than in the vicinity of the cervical regions, while in permanent teeth
they are similar. The occlusal surfaces of molars are characterized by shallow fissures,
pits and grooves, unlike immature permanent teeth with deep fissures, pits and grooves.
Deciduous molars have flat, wide contact surfaces (contact surfaces) and permanent
teeth have contact points. The crown of an upper deciduous first molar has between two
and four cusps, depending on the degree of development of the distal cusps. The crown
of the second upper deciduous molar resembles the crown of the first permanent upper
molar and has four cusps, as does the first lower molar. Five cusps can be distinguished
on the occlusal surface of the second lower molar.

74 75
Compendium of Paediatric Dentistry Anatomical and histological differences in the structure of deciduous and permanent teeth

nent pulp horns are located near the enamel-dental border. The tooth cavity is wider at
the level of the tooth neck. On cross-section, the chambers are triangular, quadrilateral,
Fig. 6. 1 . Differences in the anatomy of a de­
round or near-round in shape (roots of incisal teeth). CBCT examinations show a more
ciduous molar (left) and a permanent molar complex structure of the pulp chambers and root canal systems.
(right); in the radiograph - shorter crown of the
deciduous tooth in relation to the length of the
roots, larger chamber and more prominent pulp
horns of the deciduous tooth located clo-ser to Roots
the enamel-dental junction, arched roots.
The roots of deciduous teeth are narrower and longer in relation to the height of
the crowns - in molars set divergently at the neck of the tooth, narrowing in the apex
direction (include the permanent tooth germ) - developmental variability (root forma­
Fig. 6.2. Smooth enamel surface and tion period, full formation, resorption - in permanent teeth, root resorption is always a
straight incisal margin course in a deci­ pathology). The roots of deciduous teeth are narrower and longer than the length of the
duous incisal tooth (left) and prominent
crown (Fig. 6. 1 ). The crown-to-root ratio of deciduous teeth is lower than that of their
mamelons (garland-like incisal margin)
and perikymata in a newly erupted per­ permanent dentition counterparts. The roots show partial resorption as the teeth erupt,
manent incisor (right). which can be confirmed radiographically.
Front teeth. In deciduous teeth, the roots are narrow mesio-distal, while in perma­
The deciduous central and lateral incisors of the maxilla are at the same height, which nent teeth they are wider. A specific feature of the roots of deciduous teeth is that they
changes when the permanent incisors erupt. The lateral and central incisors do not lie in curve labially to accommodate the permanent tooth germ.
the same plane, the lateral incisors are 1-2 mm above the central incisors and the occlu­ Lateral teeth. The roots of deciduous teeth are positioned more divergently com­
sal line. In the case of deciduous canines, the mesial inclination is longer than the distal pared to permanent teeth. They are long and slenderer compared to the size of the crown,
inclination. especially in molars the rnots bifurcate near the crown. the apical foramen is larger than
Permanent immature teeth are characterized by deep grooves on the occlusal surface, in permanent teeth, which helps with rapid healing due to good blood supply. Deciduous
pronounced dental cusps (numerous hills and fissures, pits and grooves on the surface of molars have the same number of roots as permanent molars: upper molars have three
the enamel), a large chamber with prominent corners of the pulp and a wide incompletely roots: palatal and two buccal roots - mesial and distal; lower molars have two roots:
developed root, apical foramen wide opened (root development takes about 3 years). mesial and distal. In the furcation area of molars, there are numerous ventriculo-osseous
Crowns of premolar teeth are narrower than molars. They have two nodules: buccal canals, which can provide a route for the spread of infection leading to inflammation of
and palatine/lingual (except for the second lower premolar tooth, which often has two the periradicular tissues in the furcation area. In the radiographic i mage, the focus of
lingual and one buccal nodules). Osteolitic lesion may then be visible.
In the development of the root of the permanent immature tooth, we distinguish
three periods of spatial arrangement of the canal walls: divergent, parallel, coinciding
Dental pulp chamber with the full formation of the root apex and the apex opening.
The shape of the tooth cavity mimics the overall outline of the crown and root. The
chambers and pulp horns of deciduous teeth are relatively larger compared to those of
permanent teeth, and the mesial pulp horns of molars are higher (Fig. 6.5). The promi-

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Compendium of Paediatric Dentistry Anatomical and histological differences in the structure of deciduous and permanent teeth

Histological features and the formation of fluor hydroxyapatite (Ca5 (PO4\OH 1 -xFx) and the presence of cal­
cium fluoride. Fluoride ions increase enamel hardness and acid resistance.
Enamel The process of mineralization of enamel takes place in stages, before the eruption - the
Tooth enamel consists of 96-98% inorganic compounds, 0.6% organic compounds formation of crystals and their growth (I and II calcification), and after its eruption - secon­
(glycoproteins - 0.22% in deciduous teeth and 0.15% in pennanent teeth; phospholipids) dary maturation of enamel. The first calcification statis from the prism perimeter central­
and 3.5-2% water. Calcium, phosphate and hydroxyl ions fonn a crystalline network of ly and is controlled by ameloblasts, the second occurs without their participation through
hydroxyapatite (HA) of formula CawCPO4)(OH\. The HA of the enamel of immature blood vessels. Calcification takes place in a layered manner, as evidenced by striating prisms
teeth contains a large amount of carbonate, chloride or citrate ions, as well as magnesium and Retzius lines. Amelogenins affect the length, structure and spatial orientation of crystals,
and sodium, zinc, strontium, lead. The number of carbonates increases in deeper layers while enamelins regulate the volume growth of crystals. Amorphous calcium phosphate is
and is greater in deciduous teeth than in permanent ones and is easily exchanged for flu­ transformed under their influence into crystalline hydroxyapatite. The degree of mineralisa­
oride ions. The enamel of deciduous teeth contains less fluoride in each layer compared tion of the enamel then does not exceed 30% and, once mineralisation is complete, it con­
to that of permanent teeth. The covariance between calcium and hydroxyapatite phos­ tains no living cells capable of tissue repair or reconstruction. Once the enamel and the cor­
phorus is similar for deciduous and permanent teeth at 1 .8-2.3, while Ca and P levels are rect shape of the tooth crown have been fonned, there is a resorption and maturation phase,
lower in deciduous teeth. where there is an almost complete removal of water and proteins from the enamel and its full
The enamel has a uniform thickness on all surfaces of the crown of deciduous teeth mineralisation. However, the enamel is permeable, allowing ion exchange with the external
and varies on individual surfaces of the crown of permanent teeth. The surface layer of environment and post-eruptive maturation of the enamel. Magnesium and carbonate ions
enamel contains densely arranged, parallel adherent hydroxyapatite crystals that form are replaced by fluoride, calcium and phosphate ions in place of the hydroxyl group. As the
enamel prisms. The enamel prism diameter of a deciduous tooth ranges from 2.9 ± 1 .2 enamel matures, its porosity and permeability decrease and its resistance to acids increases.
µm to 3.47 ± 0.48 µm, while that of a permanent tooth ranges from 3.84 ± 0.73 µm to 1eeth are most susceptible to decay during the first 2-4 years after eruption.
4.34 ± 0.95 µm. In deciduous teeth, a higher density of enamel prisms is observed, which The enamel of deciduous teeth shows a lower level of mineralisation (80.6%) than
increases in depth up to the enamel-dental junction. There are less mineralised interpris­ that of permanent teeth (89.7%). In deciduous teeth, the Retzius lines are regularly
matic spaces between the prisms, called micropores, which contain water and organic spaced every 30-50 µm. This is called the neonatal line (NNL). Diurnal cycles of mine­
components. In the less mineralised enamel, the spaces between the prisms are larger and ralisation are visible on individual prisms as fine transverse striations. The location and
the diameter of the prisms is smaller. The outer surface of the enamel of deciduous teeth width of the neonatal line is directly related to the length of gestation ( 1 2 µm for babies
is often formed by an aprismatic layer, which is also present in half of the permanent born on time and 24 µm for those born after the due date), and its width is related to the
teeth. However, its thickness does not exceed 5 µm. In the cervical area, the prisms are length of gestation and birth weight. The shorter duration of gestation is indicated by the
°
directed towards the occlusal surface at an angle of < 90 relative to the tooth axis in de­ placement of the NNL towards the incisal edge and closer to the enamel-dental junction.
ciduous teeth, while in permanent teeth they are directed apex-wise at an angle of > 90° , The width of the NNL also correlates with the type of delivery. fo natural-born babies,
which is important when preparing cavities on the proximal surfaces. it is approximately 12 µm. The line is thinner in the case of a caesarean section, wider
The differences between the enamel of deciduous and permanent teeth concern not when the birth was attended with complications.
only the thickness of the enamel and its mineral content, but also its layers - inner and In immature permanent teeth, the enamel is poorly mineralized, hydroxyapatite
outer. The outer layer of enamel contains more fluoride and less carbonate than the dee­ crystals are few, it contains more interprismatic substance. Permanent mature teeth
per layers (1 80.17 mmol F/kg enamel of deciduous teeth, 318.26 mmol F/kg enamel of show a greater degree of mineralization, hydroxyapatite contains a lot of calcium and
permanent teeth), which results from the exchange of hydroxyl groups for fluoride ions little carbonate, the interprismatic substance is more calcified.

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Compendium of Paediatric Dentistry Anatomical and histological differences in the structure of deciduous and permanent teeth

Oentin-enamel junction (OEJ) 111a nt1e dentine, the outermost part of dentin located at the enamel-dentin junction. In
DEJ is a complex and critical structure combining two mineralized tissues and pre­ subsequent layers, crystals are formed on collagen fibres, but already without the in­
venting the propagation of dentin enamel fractures. DEJ is Jess mineralized than enamel volvement of matrix vesicles (linear calcification pattern). During tooth development, it
or dentin, contains more organic matrix, and is probably associated with primary dentin. takes 24 hours for the newly deposited dentin layer to fully mineralise, so the dentin is
The DEJ has a three-tiered structure, 25-100 µm lamellae with their convexities facing fully mineralised from the start of development.
the dentin and their concavities facing the enamel; 2-5 µm micro Iamellae; and a srnal­
ler-scale structure. Chamber
The dentin in deciduous teeth is half as thin as in permanent teeth (thickness at the In the chamber, there is a thin layer of dentin between the charnber roof and the ena­
occlusal surface - 1.8 mm, at the proximal surface - 1.4 mm (permanent teeth 2.85 mm mel-dentin junction and forming the chamber floor, as well as a smaller distance between
and 2.3 mm, respectively), poorly mineralised, has more interglobular spaces (especially the DEJ and the root furcation.
in the cervical region) and a clearly marked Tomes granular layer, wide dentinal tubules The pulp of deciduous teeth differs from that of permanent teeth with incomplete
- cross-section near the pulp 4.08 µm, circumferentially 2.56 �Lm (permanent teeth 3.96 root development and mature teeth. The pulp of the deciduous tooth is characterised by
µm and 1.75 µm respectively), less regular course of dentinal tubules - 75% - straight, poor morphological organisation, large volume in relation to the thickness of the mine­
25% - wavy (permanent teeth - wavy). The secondary dentin is less regular than in per­ ralised tissues, lack of sub odontoblastic Raschkow nerve plexus and sensory fibres in
manent teeth. The presence of a neonatal line is characteristic. the dentinal tubules, morphological and functional variability of the pulp, depending
on the developmental phases of the root. Prior to the onset of root resorption, the pulp
lncremental growth lines in dentin is well vascularised, contains a lot of cellular elements and less fibrous elements, and
The formation of successive layers of pre-dentin takes place cyclically throughout therefore has a greater defensive capacity compared to mature permanent teeth. In the
life - 4 µm/24h in the pre-functional phase, 1 µm/24h in the functional phase. Daily resorption phase, the roots form in the immediate vicinity of the retrograde, atrophie and
increments vary slightly in the arrangement of collagen fibres. Microscopically, a 20 �un degenerative changes of the pulp, which gradually include subsequent parts, until the
layer of deposited dentin can be distinguished, separated by Ebner's incremental lines end of the entire pulp.
that reflect breaks in the 5-day secretory cycles of odontoblasts. The Ebner line formed The permanent tooth pulp with incomplete root development is rich in fibroblasts
during the perinatal period is called the birth (neonatal) line. It is found in deciduous and mesenchymal cells, vascularization (wide apex opening) and better hydration, nu­
teeth and first permanent molars. merous anastomoses, active cylindrical odontoblasts arranged in one layer (with age
ln permanent teeth with incomplete root development, the dentin layer is thin and poorly they change their shape and becorne crowded), a dense network of nerve fibres in the
mineralized, with wide dentine tubules (0 3.2 µm, in an adult - about 1.6 µm) and munerous corners of the pulp. It contains few fibrous elements, rarely the Weil layer, there is no
interglobular spaces. In mature permanent teeth, the dentin layer is thicker and more mineral­ Raschkov plexus (it develops after the root development is completed), which indicates
ized, with a sigmoid course of dental tubules with narrower Iight (0 about 1.6 µm). a lower reactivity of the pulp to stimuli.
Dentin mineralization is different from enamel mineralization. The delivery of cal­ The defence capabilities of the deciduous teeth pulp (except during the root re­
cium and phosphate ions leads to the growth of small hydroxyapatite crystals in protein sorption phase) and permanent teeth with incomplete root development is significantly
complexes (matrix vesicles) forming the nucleation nuclei of crystals. These vesicles greater compared to adult permanent teeth (formed apical opening, Jess vascularisation,
give rise to many foci of mineralization, the growth of which leads to their fusion into few cellular and many fibrous elements, low cell volume and crowding of odontoblasts).
uniformly mineralized tissue (globular calcification scheme). This scheme applies to The Jess mature the tooth, the greater its defensive capacity.

80 81
Compendium of Paediatric Dentistry Anatomical and histological differences in the structure of deciduous and permanent teeth

Cementum (rom micromorphological features. Eur J Oral Sei. 2006; 114: 343-348. - 13. Robinson C. Enamel
The permanent tooth cernent with incomplete root development is thin, with a pre­ maturation: a brief background with implications for some enamel dysplasias. Front Physiol. 2014
Oc t 8;5:388. doi: I0.3389/fphys.2014.00388. - 14. Sabel N, Dietz W, Lundgren T, Nietzsche S,
dominance ofacellular cementum and a small amount ofcellular cernent. The periodontal Odelius H, Rythén M, Rizell S, Robertson A, Norén JG, Klingberg G. Elemental composition
ligament is not well developed. Lamina durais relatively thick, trabeculae ofbone plaques of normal primary tooth enamel analysed with XRMA and SIMS. Swed Dent J. 2009; 33(2):
75-83. - 15. Sabel N, Johansson C, Kuhnisch J, Robertson A, Steiniger F, Norén JG, Klingberg
(trabeculae) are few in number and have a smaller thiclrness. In mature permanent teeth,
G, Nietzsche S. Neonatal lines in the enamel of primary teeth - a morphological and scanning
there is little cell-free cernent, with a predominance ofcellular cernent. electron microscopie investigation. Arch Oral Biol. 2008; 53(10): 954-963. - 16. Sabel N, Kling­
berg G, Nietzsche S, Robertson A, Odelius H, Norén JG. Analysis of some elements in primary
enamel during postnatal mineralisation. Swed Dent .1. 2009; 33: 85-95. - 17. Sabel N. Enamel of
Changes in the process of maturation of a young permanent tooth primary teeth - morphological and chemical aspects. Swed Dent J. Suppl. 2012; (222): 1-77. -
Immature permanent tooth - change in the arrangement of the enamel prisms, J 8. Schaffner, Markus and Adrian Lussi. Developmental and Histological Aspects of Deciduous
quantitative and qualitative changes in the enamel, graduai mineralisation of the ena­ and Young Permanent Teeth. Management of Dental Emergencies in Children and Adolescents
(2019): 10.1002/9781119372684.ch1.1. - 19. Sierpi11ska T, Stocka A, Gotybiewska M. Ename!
mel, thiokening and mineralisation of the dentin, narrowing of the lumen ofthe dentinal structure, saliva properties and bruxism as etiological factors responsible for pathological clash.
tubules, reduction in the volume of the charnber, reduction in the number of cellular Literature review. Protet Stomatol, 2008; LVlll, 2: 100-104.
20. Xiao M, Qian H, Lv J, Wang P. Advances in the Study of the Mechanisms of Physiolog­
elements in the pulp, progressive development and formation of the root, the shape of ical Root Resorption in Deciduous Teeth. Front Pediatr. 2022 Mar 30;10:850826. doi: 1 0.3389/
the occlusal surface flattens, the colour of the teeth darkens, transparency increases, in­ fped.2022.850826. - 21. White SN, Paine ML, Ngan AY, Miklus VG, Luo W, Wang H, Snead
creased resistance to acids, less susceptibility to caries. ML. Ectopie expression of dentin sialoprotein during amelogenesis hardens bulk enamel. J Biot
Chem. 2007; 282 (8): 5340-5345. - 22. Wang FS, Anderson P, Fan H, Davis GR. X-ray microto­
mographic study ofminerai concentration distribution in deciduous enamel. Arch Oral Bio!. 2004;
References 49(11): 937-944.
1. Aruede G, Pepper T. Anatomy, Permanent Dentition. [Updated 2021 Jul 9]. ln: StatPearls
[Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-. Available from: https://www.
ncbi.nlm.nih.gov/books/NBK570590/. - 2. De Menezes Oliveira MA, Torres CP, Gomes-Silva
JM, Chinelatti MA, De Menezes FC, Palma-Dibb RG, Borsatto MC. Microstructure and minerai
composition of dental enamel ofpermanent and deciduous teeth. Microsc Res Tech. 2010; 73(5):
572-577. - 3. Dzidziul 1, Gutowska 1, Noce11 1, Chlubek D. Comparison offluoride content in su­
perficial enamel layers of deciduous and permanent teeth - an in vitro study. Annales Academiae
Medicae Stetinensis. PAM Publishing House, Szczecin 2006; 17-21. - 4. Garnett J, Dieppe P. The
effects ofserum and human albumin on calcium hydroxyapatite crystal growth. Biochem J. 1990;
266: 863-868. - 5. Gutierrez P, Piîïa C, Lara VH, Bosch P. Characterization of enamel with vari­
able caries risk. Arch Oral Bio1. 2005; 50(10): 843-848. - 6. Kerebel B, Daculsi G, Kerebel LM.
Ultrastructural studies ofenamel crystallites. J Dent Res. 1979; 58(Spec Issue B): 844-851. - 7. Li
C, Risnes S. SEM observations ofRetzius lines and prism cross-striations in human dental enamel
after different acid etching regimes. Arch Oral Biol. 2004; 49(1): 45-52. - 8. Low IM, Duraman
N, Mahmood U. Mapping the structure, composition and mechanical properties of human teeth.
Mater Sei Eng C. 2008; 28: 243-247. - 9. Lynch R.J. The primary and mixed dentition, post-erup­
tive enamel maturation and dental caries: a review. !nt Dent J. 2013 Dec;63 Suppl 2:3-13. doi:
10.1111/idj.12076.
1 O. Maia AM, Fonsêca DD, Kyotoku BB, Gomes SL. Characterization of enamel in primary
teeth by optical coherence tomography for assessment ofdental caries. Int J Paediatric Dent. 201O;
20(2): 158-164. - 11. Majewska-Beska S, Szczepanska J. Genetie and Molecular Mechanisms of
Root Resorption - a Literature-Based Study. Genetyczne i molekularne mechanizmy resorpcji
korzeni Zyb6w - na podstawie pismiennictwa. Dent. Med. Probl. 2012, 49, 3, 329-335. - 12.
Radlanski RJ, Renz H. Developmental movements of the inner enamel epithelium as derived

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 Developmental abnormalities of the teeth

Tooth agenesis is diagnosed in the absence of a tooth germ on radiographs, after

Chapter 7 excluding a history of tooth loss (e.g. extraction, complete luxation) or the presence of
a retai ned tooth (Fig. 7 . 1 ). The absence of third molars is not considered agenesis. De­
pendi ng on the number of missing teeth, there are:
Developmental abnormalities of the teeth
- hypodontia - lack of 1 -5 teeth (the most common),
Dorota Olczak-Kowalczyk - oligodontia - lack of at least 6 teeth (frequency 0. 1 -0.9%),
anodontia - lack of all teeth (very rare).
The most common missing deciduous teeth are the lateral incisor teeth (usually of the
Developmental abnonnalities of the teeth may consist of a reduction or increase in m andible) or the medial incisor teeth, less commonly the maxillary second molars, the
the number of teeth (agenesis, hyperdontia), a reduction or increase in size, morphologi­ maxillary first molars and the mandibular second molars. In the permanent dentition, the
cal anomalies, disorders of the mineralised tissues (enamel, dentin, cementum), i.e. their mandibular second premolars, maxillary lateral incisors (often in people with cleft lip
degree of mineralisation and/or texture of protein structure. and palate) and maxillary second premolars are most commonly missing. An example of
The aetiopathogenesis of developmental abnormalities of teeth is still not completely a single tooth hypodontia is a solitary median maxillary central incisor (SMMCI) asso­
clear. Causes include genetic (chromosomal aberrations, single gene mutations), epige­ ciated with midline malformations, including skull, jaw, teeth, and nose bones. It occurs
netic and environmental factors (internal and external, local and general). They are usually in both deciduous and permanent dentition. It is the only one central incisor in the maxilla
not the result of the influence of a single factor, but of the interaction of various factors located exactly in the midline alveolar ridge and has a symmetrical crown shape.
(genetic, epigenetic and environmental). These factors may be present at the same or diffe­ Causal factors for agenesis include:
rent stages of tooth development (time) and interfere with odontogenesis at different levels - environmental, including local (e.g. inflammation or a neoplastic lesion in the sur­
(molecular, cellular, tissue), at one or more stages. The aetiopathogenesis oftooth develop­ rounding tissues, mechanical trauma, irradiation of tooth and bone attachments) and
mental abnormalities is therefore complex, multifactorial, multilevel and time-dependent general during pregnancy - abnormal nutrition, diseases ( e.g. rubella) and medication
(developmental stage of the tooth germ, time of exposure to the pathogenic agent). (e.g. anti-epileptic drugs, thalidomide) and in the child (e.g. systemic diseases, endo­
Dental malformations affecting all or most teeth are referred to as generalised, and crine disruption, chemotherapy),
one or a few teeth as localised. Local causal factors most often cause defects affecting - genetic - familial occurrence (autosomal recessive or dominant trait), one of the
a single tooth or a group of adjacent teeth. General factors usually result in defects of symptoms of 80 genetic syndromes, including ectodermal dysplasia, achondroplasia,
a group of teeth developing at the time of the factor and occur symmetrically ( chrono­ Down syndrome, Pierre Robin syndrome, van der Woude syndrome ( oligodontia is
logical defects). Defects affecting all teeth are not related to any specific period of odon­ usually found in genetic syndromes, anodontia much less frequently).
togenesis and are caused by genetic factors or long-term general environmental factors. Agenesis due to genetic factors is associated with mutations in the PAX9 gene on cln·omosome
14, MSXI on chromosome 4, AXIN2, more common in girls than boys; in pennanent than deci­
Tooth count abnormalities duous dentition, present in deciduous dentition is c01Telated with agenesis in pennanent dentition.
The treatment of tooth agenesis depends on the age of the child, the number of missing
Dental agenesis, or a decrease in their number, is the most common developmental teeth, the condition of the teeth presents in the mouth, the occlusal and occlusal conditions and
defect of dentition. Clinically, agenesis is indicated by delayed changing the sequence of the facial features. It can consist of enclosing a space or maintaining/restoring it to fill a gap
tooth eruption, significant spacing of teeth, lack of bulge of the alveolar ridge at the site in the future. In children with hypodontia accompanied by crowding in the second arch, auto
of tooth eruption, and persistent deciduous teeth over 1 2 years of age. transplantation of the tooth is considered.

84 85
Compendium of Paediatric Dentistry Developmental abnormalities of the teeth

maxill a, the incisive lateral teeth of the maxilla (found in the cleft palate line), the fourth
m olars of the mandible and the teeth in the premolar region of the mandible. Supernu­
m erary teeth in the lateral sections of the dental arches located atrium or buccally or lin­
guall y are referred to as paramolars and located behind the third molars as distomolars.
The aetiology of hyperdontia is not explained. The causes include genetic factors (fa­
mily history, symptom of genetic syndromes, including cleidocranial dysostosis (CCD),
Apert syndrome, Gardner syndrome, Marfan syndrome and cleft lip and palate. Hyperdon­
tia may be associated with hypodontia (concomitant hypodontia and hyperdontia).

Fig. 7. 1 . Agenesis of second molars, canines and lateral incisors of the maxilla and medial
incisors of the mandible in a 1 0-year-old girl with ectodermal dysplasia.

Increased number of teeth Fig. 7.2. Mesiodens in a girl aged 6 years - conical shape of the crown of the tooth located at the
site of the lost tooth 5 1 , radiograph shows distal displacement of the maxillary medial incisal teeth
True hyperdontia is an increase in the number of teeth above 20 in the deciduous - risk of diastema in the permanent dentition and retention of the permanent lateral incisors.
tooth and above 32 in the permanent tooth caused by the hyperfunction of the dental
lamina. Occurs more frequently:
in boys than in girls,
in permanent rather than deciduous dentition,
- in the maxilla than in the mandible,
in the anterior section of the maxilla than in the lateral sections.
In hyperdontia, teeth may be present:
atypical supernumerary teeth (dentes supernumerarii) of abnormal structure (dys­
morphic teeth): conical, rosaceous, drip-shaped, chisel-shaped, trunk-shaped, with
additional nodules,
typical supernumerary teeth of normal structure (eumorphic teeth), also referred
to as additional teeth (dentes supplementarii).
There are usually single supernumerary teeth (76-86%), then double ( 1 2-23%), more
often in the maxilla than in the mandible. Multiple supernumerary teeth are rare (< 1 %),
more common in the mandible. The most common supernumerary tooth is the mesiodens Fig. 7.3. Two mesiodens in a boy aged 8.5 years - conical shape of the crown of the left tooth and
truncal shape of the right tooth, pantomographic i mage shows distal displacement of the medial
(middle tooth) located in the middle line of the maxilla (rarely the mandible) between or maxillary incisor - risk of diastema in the permanent dentition and retention of the lateral incisors.
behind the medial incisive teeth (Fig. 7.2, 7.3). Rarely, these are the fourth molars of the

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Compendium of Paediatric Dentistry Developmental abnormalities of the teeth

Hyperdontia can cause retention, delayed, ectopic eruption and abnormal develop­ In microdontia of maxillary lateral incisors, the crown of the tooth is conical or peg­
ment of the root of the permanent tooth, displacement, rotation and resorption of the shaped, with a reduced mesio-distal dimension and proximal surfaces converging to­
roots of adjacent teeth, crowding, dentigerous cysts, diastema, neuralgic pain (Fig. 7.4). w ards the incisal edge.
It is found in many genetic syndromes ( e.g. Ellis-van Creveld syndrome, John­
son-Blizard syndrome, Kabuki syndrome, Silver-Russel syndrome), after radiotherapy
in the craniofacial region, in cleft lip and palate (Fig. 7.5). Generalised microdontia has
been observed in pituitary dwarfis m, Down syndrome, ectodermal dysplasia (Fig. 7.6).

Fig. 7.4. Rotation of the medial in­

cisal pulp of permanent teeth due to
the presence of two mesiodens.

Treatment depends on the type of hyperdontia, the position of the supernumerary

teeth, possible complications, identified both clinically and radiographically, the degree
of root formation of the adjacent teeth, and occlusal-occlusal conditions. When the su­ Fig. 7.5. Microdontic teeth 1 5, 25, 27, 35, 45 in a 1 5-year-old boy after early childhood
pernumerary tooth does not cause any complications and does not interfere with function radiotherapy in tbe craniofacial region.
or aesthetics, observation may be considered. More often than not, such teeth are extrac­
ted. Before extraction, it is advisable to perform a cone-beam computed tomography to
determine the precise position of the tooth. There is no consensus on the age at which Fig. 7.6. Generalised micro­
a patient's supernumerary tooth should be removed. dontia (conical and peg-shaped
teeth) in tbe deciduous dentition
in a girl with ectodermal dyspla­
Tooth size abnormalities sia.
True macrodontia
Size defects - a reduction or increase in the dimensions or shape of the whole tooth, - occurs more frequently in men,
or j ust part of it, are more common in permanent than deciduous dentition. Among them, - most often concerns incisive teeth of the maxilla, canines, rarely second premolars
microdontia, macrodontia, shortening of roots, long roots are distinguished. or third molars,
- isolated, which affects only one tooth, occurs less frequently than generalised,
Decrease (microdontia) or increase (macrodontia) - may be associated with other anatomical abnormalities,
True microdontia or macrodontia should be differentiated from relative microdontia, - the premolars and molars macrodense have a occlusal surface with numerous cusps
relative macrodontia, in which the dimensions of the teeth are nonnal or slightly altered and well-defined furrows and a single short root (Fig. 7.7).
and only appear smaller or larger as a result of excessive or insufficient development of The prevalence of rnacrodontia in the permanent dentition is estimated at 0.03-1 .9%.
the bone base. It is associated with general diseases and genetic syndromes such as insulin-resistant dia­
True microdontia occurs more often in women, often familially, most often involves betes mellitus, pituitaiy gigantism, auricular syndrome, hemifacial hypertrophy, KBG syn­
lateral incisive teeth and third molars of the jaw, may coexist with hypodontia, hyperdon­ drome, YYX syndrome, Ekman-Westborg-Julin syndrome, Rabson-Mendenhall syndrome,
tia or change in tooth shape. Kl inefelter syndrome. The pathogenetic mechanism ofmacrodontia is still unknown.

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Compendium of Paediatric Dentistry Developmental abnormalities of the teeth

Root elongation - rhizomegaly (radiculomegaly) may be a single defect or symp­

Fig. 7.7. Clinical picture of a giant man­ tom of ocular-facial-cardio-tooth syndrome and Klinefelter syndrome (Fig. 7.9). Elon­
dibular first molar in a 13-year-old boy
gation may involve the roots of one or more teeth. The canine roots are elongated in the
- numerous, irregularly located cusps,
well-defined furrows; in the X-ray image, eye-facial-dental syndrome.
giant single-rooted teeth: maxillary de­
ciduous first molar, maxillary and man­
dibular permanent first molars and man­
dibular second molar.
Reducing the length of the tooth root - rhizomicria, an anomaly of the short root
is a rare defect that:
is more common in women,
mani'fests itself with the same or smaller length of the root of the tooth as the height
of its crown, with rounded root apexes
rarely has a generalised form, Fig. 7 .9. Rhizomegaly of molars, premolars and canines, taurodontism of teeth 18, 37, 47,
most often occurs bilaterally and affects incisal teeth of the maxilla, less often other reduced root number of teeth 17 and 27.
teeth (mainly premolars),
often accompanies other developmental defects of teeth, e.g. hypodontia, hyperdon­ Abnormalities in tooth morphology
tia, microdontia, dens invaginatus, taurodontism, pulp chamber obliteration.
Aetiological factors include family history, environmental factors (trauma, pulpitis, The morphological anomalies include: double teeth, invaginated teeth, everted teeth,
anti-cancer therapy before root development, hypothyroidism) and genetic factors (den­ Hutchinson 's teeth, mulberry teeth, globodontia, conical, peg-shaped and bulbous teeth.
tin dysplasia and dentinogenesis imperfecta (DGI), Down syndrome, Turner syndrome, (Tab. 7.1). ·
Williams syndrome, Rothmund-Thompson syndrome). W hen the root of a tooth is short­
Tab. 7.1. Types of developmental abnormalities concerning tooth morphology.
ened due to direct trauma to the developing tooth, the root has a thin layer of dentin and
a wide-open apex. A shortened root after chemotherapy or radiotherapy in the orofacial Disorder Clinical picture
Double teeth: the result of a partial division of one tooth germ at the crown
region has a v- or u-shape and a closed apex (Fig. 7.8).
- gemination formation stage (a single, larger-than-normal tooth with a
bicuspid crown, one canal), more often in the maxilla ( Fig.
7.10)
the result of the fusion of two or more tooth germs at a time
when their crowns are not mineralised (they may have a
- fusion common chamber and a common or separate canals, sepa-
rate chambers and canals), more commonly in the mandible
( Fig. 7.11)
the effect of root fusion during or after their formation
Fig. 7.8. Shortening of the roots of the medial incisal teeth, maxillary first molars and mandibu­ when the crown is already formed, unlike twin and frac�
lar incisal teeth, microdontia of teeth 1 7 and 45, and absence of tooth set of tooth 1 5 - concrescence tured teeth, may be a developmental disorder or the result of
in a 13-year-old boy after anticancer treatment in early childhood local inflammation; i t applies more often to the maxilla and
(radiotherapy in the craniofacial region and chemotherapy). molars ( Fig. 7. 1 2)

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Compendium of Paediatric Dentistry Developmental abnormalities of the teeth

the presence of cusp-like projection of enamel (90% having

a pulp) on the tooth surfaces (mostly premolars, then in-
Dens evaginatus (DE)
cisal, mainly lateral jaws), which may be formed by enamel
or enamel and dentin
the presence of enamel and dentin invagination into the
Dens invaginatus, ID, dens in
tooth caused by the infold ing of the enamel-forming organ
dente, dens Saltersi)
into the dental papilla before the period of mineralisation
Globodontia
bulbous enlargement of the crowns of canines and molars
( Ear and Tooth Syndrome Symp-
without prominent cusps or furrows
tom)
are small in size, sharp-edged, smooth-surfaced and irregu-
Conical teeth
larly conical in shape
incisive teeth or canines with a crown with a convex mesial
Barrel-shaped teeth
and distal surface
crown of a tooth (usually a molar) with marked cervical nar-
Bulbous tooth
rowing
the mesial and distal surfaces of the crown of the lateral in-
Peg-shaped teeth cisor converges or tapers towards the incisal edge, resulting
in a significant reduction in mesio-distal diameter Fig. 7.1 1 . Fusion - formed from a supernumerary tooth and a medial incisor
on the right side of the maxilla.
Hutchinson incisor conical, peg-shaped incisal teeth (deciduous and perma-
nent) with a notched incisal edge
Pfluger's teeth and Furnier's first molars with numerous tiny protuberances (cusps) poor-
teeth, i.e. mulberry ly demarcated on the occlusal surface

Double teeth are classified as defects in tooth morphology or their size. In some
cases, they can be treated as a defect concerning both morphology and size.

Fig. 7. 1 2. Concrescence od deciduous tooth- connection through the cement

of the lateral incisor with the fang.

Double teeth are present:

more frequently in deciduous dentition (0.5-2.5%) than in permanent dentition
(approximately 0.3-0.5%),
Fig. 7. 1 0. Right medial gemination tooth and unerupted fusion left incisor with similar frequency in both sexes,
(combination of medial and lateral incisors). in the anterior segment of the dental arch (incisors and canines).

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 Developmental abnormalities of the teeth
Compendium of Paediatric Dentistry

The aetiology of double teeth is not clear. Causal factors include local environmental Dens evaginatus (DE) occurs more often in permanent dentition, more often in the
factors (trauma, lack of space in the dental arch) and general factors ( e.g. avitaminosis, female sex, often symmetrical ly on both sides of the dental arch.
hypervitaminosis A, systemic and infectious diseases, Rh factor incompatibility of pa­ The bulge in the DE in the anterior section of the dental arch, occurring on the pa­
rents, endocrine disorders, pituitary hyperfunction) and genetic factors (family history, latine/lingual surface, is referred to as the talon's cusp (Fig. 7 . 1 4). Premolar teeth with
symptom of genetic syndromes, e.g. a chondrodysplasia, Cornelia de Lange syndrome, additional cusps on the occlusal surfaces are referred to as nodular premolar teeth or
Gorlin-Goltz syndrome, Silver-Russell syndrome, Wolf-Hirschhorn syndrome). Leong's teeth.
The therapeutic management of double teeth depends on the type of dentition (de­
ciduous, permanent), the morphology of the double tooth, its position in the dental arch,
occlusal and aesthetic conditions. Caries prophylaxis, including fluoride and sealing of
cavities at risk of developing caries, is essential. Shape corrections are carried out (re­
duction 'by sanding, aesthetic fil ling of the furrow). Double teeth in the deciduous den­ Fig. 7.14. Talon's cusps on the l abial and pa­
tition can cause crowding, ectopic eruption and delayed eruption of permanent teeth, so latal surfaces of the medial incisal tooth and
observation of the eruption of permanent teeth and possible extraction of the dual tooth on the palatal surface of the maxi l l ary lateral
incisor.
is essential. In the permanent dentition, endodontic treatment and surgical separation of
fused teeth are attempted. The treatment decision should be preceded by a radiological
The aetiology of the disorder is unknown. The influence of environmental and ge­
diagnosis, preferably using CT. With separate tooth cavities, hemi section with or with­
netic factors has been suggested (it occurs fam i l ially and in genetic syndromes such as
out endodontic treatment is possible (Fig. 7. 1 3).
Sturge-Weber syndrome).
DE should be different from Carabel l i 's cusp, i .e. an additional cusp on the palatal
surface of the maxillary first molar, which is not considered a developmental disorder.
An erupted tooth can cause traumatic occlusion and abrasion leading to dental pulp
disorder, or fracture of the bulge, usually with pulp exposure. In the treatment of erupted
teeth, methods are primari ly used to prevent the above-mentioned complications.
Dens invaginatus (ID):
- affects the male sex more often,
- occurs mainly in the permanent dentition,
- most often applies to the lateral incisors of the maxi lla, then the medial incisors, pre-
molars, canines and molars,
- may occur simultaneously with other dental malformations, e.g. hypodontia, hyper­
dontia or macrodontia.

Fig. 7.13 . Separation of a fused tooth, removal of the medial part, restoration with composite
material (photo P. Sobiech).

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Compendium of Paediatric Dentistry Developmental abnormalities of the teeth

Oehlers et al. distinguished 3 types of insusceptible teeth:

type 1 - blindly completed intussusception of tissues

within the crown of the tooth,

type 2 - invagination of tissues exceeding the enam­

el-cement boundary, which ends blindly in the root, may
or may not communicate with the tooth pulp,

Fig. 7. 1 5 . Radiological image of an invaginated maxillary left lateral incisor - type TTIB accor­
ding to Oehlers (left); clinical image - barrel-shaped crown (upper right image), wider crown
compared to the unicuspidal tooth on the opposite side (lower images).
type 3 - invagination of tissues including crown and
root:
A - usually without connection to the tooth pulp,
forming a second apical or lateral pseudo hole,

B - connecting with the root canal and the periodon­

tal canal through pseudo-peak holes (Fig. 7 . 1 5).
The incidence of ID is estimated at 0.04-10%. The aetiology remains unclear. The
causes include genetic and environmental factors, including infection, trauma, changes
in tissue pressure, abnormal proliferation of the inner enamel epithelium deep into the
dental papilla, fusion of two tooth germs, focal increase or decrease in the growth rate
of the tooth germ.
Clinically invagination i suggests:
the presence of deep palatal pit or groove,
wider crown compared to a single-name tooth on the opposite side,
barrel-shaped or conical crown, Fig. 7. 1 6. Image of an invaginated permanent maxillary lateral incisor on the left side. Teeth on
pantomogra1� (upper left image) and on CT scan - barrel-shaped tooth crown (upper left
a deep hole on the lingual surface of the tooth in the area of the neck or an indentation . _
image), 111vag111at1on without connection to the tooth pulp, forming a second lateral pseudo
on the incisive edge with a furrow on the lip surface, tumour - type l llA according to Oehlers (lower images).
convex neck on the palatine surface or cervical nodule (Fig. 7.16).

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 Developmental abnormalities of the teeth
Compendium of Paediatric Dentistry

nt protection for can occur on one or both sides,

Thin and poorly minera lised hollow tissues do not provide sufficie
usually consist s of it can be an isolated defect or co-exist with other developmental abnormalities of the teeth.
the pulp, so dental pulp disease s often occur. Root canal treatment
less commonly, trea­
removing the invagintaion and treating the resulting wide canal, or
ation, root canal Tab . 7.2. Types of developmental disorders of the root.
ting the invagintaion and the canal proper separately. In a type 3 invagin
in the "invagina­ Disorder Clinical picture
treatment of only the invagination root canal treatment is possib le only
tooth. Extraction excessive vertical elongation of the tooth chamber with reduction
tion" while preserving the vitality of the pulp in main root canal of the of its bottom in the apical direction and root bifurcation in the case
of invaginated teeth is considered in the event of failure of endodontic
treatment and the Taurodontism
of multi-rooted teeth. The cause is the absence or delayed horizon-
nt due to the tal invagintaion of Hertwig's epithelial sheath
inabilit y to respect the root tip and before the start of orthodontic treatme
high risk of external root resorption. high positioned tooth root bifurcation, j ust at the transition to the
Cynodontia
me, Ellis-v an crown
Conical teeth are found in some genetic syndromes (e.g. Down syndro
may involve any tooth, most commonly mandibular molars and ea-
which the conica l
Crevel d'syndrome, ectode rmal dyspla sia) (Fig. 7 . 1 7). A dentitio n in Supernumerary root nines, followed by maxillary and mandibular premolars; the extra
conica l tooth is
shape has all the teeth in both dental arches is called a crocodile. The root may be normal or smaller in size and attached to another root
often mesiodens. most often the result of root fusion, more often in deciduous teeth
Single rooted molar than permanent teeth, more often in second than first molars, more
often maxillary than mandibular (not including third molars)
Root dilaceration dilaceration sharp deviation/bending in the crown-root axis
involves permanent first molars, sometimes deciduous second rno-
Jars and permanent medial incisors; characteristics: small crowns,
short, tapering roots and fissured tooth cavities with significantly
Molar-incisor malfor-
reduced height. At the level of the enamel-cement junction, there
mation, M IM
is a mineralized plaque formed by a partially mineralized collagen
matrix and a network of canals containing large blood vessels and
Fig. 7. 1 7. Peg-shaped tooth incisors of the mandible (left) and lateral conical periodontal ligament-like connective tissue
incisors of the mandible (right). focal enamel mass located apically from the enamel-cement j unc-
Enamel pearl
tion, most commonly on the roots of maxillary molars

Root abnormalities
In the aetiology of taurodontism, environmental factors (e.g. anti-cancer therapy)
Root developmental abnormalities are the most common developmental abnormali­ and genetic factors ( one of the symptoms of genetic syndromes, including amelogene­
ties of teeth. Definitions of individual root defects are presented in Table 7 .2. sis imperfecta, ectodermal dysplasia, Down syndrome, Klinefelter syndrome, Williams
syndrome) are listed.
Clinically, the crowns of taurodontic teeth have normal features. Radiological signs
Taurodontism:
are: elongation of the chamber body, short, low bifurcated roots, short canals, often
is more common in permanent than in deciduous dentition,
calcified pulp. Shaw distinguishes between hypotaurodonitism, mesotaurodonitism and
most often affects second and third molars, less often first molars,
can affect single or multiple teeth, hypertaurodontism.

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Compendium of Paediatric Dentistry Developmental abnormalities of the teeth

References
I . Agurto-SP et al. Proposal of Anatomical Terms for Alterations in Tooth Size: "Micro­
do ntia and Macrodontia". lnt J Morph, 2019,37( I ), 375-378 . https://dx.doi.org/ I 0.4067/S07 l 7-
950220 I 9000 I 00375 - 2 . Arandi NZ. Hyperdontia: Exploring the Developmental Abnormali­
ty J Pre Clin-Res. 2020; 1 4(4):178- 1 83 . - 3 . Ashish Shrestha A et al. Developmental anomalies
affecting the morphology of teeth - a review. RSBO. 2015; 1 2( I ):68-78. - 4. Ata-Ali F et al.
prevalence, etiology, diagnosis, treatment and complications of supernumerary teeth. J Clin Exp
Dent. 20 1 4;6(4):e414-e4 1 8 . 2014; doi: l0.4317/jced.51499. - 5. Canoglu E et al. Isolated bilateral
macrodontia of mandibular second premolars: A case report. Eur J Dent. 2012;6(3):330-334. -
6. Chetty M et al. Taurodontism in dental genetics. BDJ 202 1 ;7; doi.org/10. 1 03 8/s41405-021-
0008 l -6. - 7. Jeddy N et al. Single Rooted Permanent Premolars and Molars - A Rare Clinical
Presentation Confi med using Cone Beam Computed Tomography. J Clin Diagn Res. 2015;9(8):
r

] 5-17; doi: I 0.7860/JCDR/2015/13592.63 96. - 8. de La Dure-Molla M et al. Elements of mor­

phology: standard terminology for the teeth and classifying genetic dental disorders. Am J Med
Genet A . 2019; 1 79(10): 19 1 3-1981. - 9. Gomez F et al. Root canal morphology and variations
in mandibular second molars: an in viva cone-beam computed tomography analysis. BMC Oral
Hypothyroidism Mesotaurodontism - Hypertaurodontism - Health 2021 ;2 1 ,424; doi.org/10. 1 186/sl 2903-02 1 -01787-7.
moderate enlargement of the significant enlargement of the pulp chamber reaches 10. Hall RK. Solitary median maxillary central incisor (SM M CI) syndrome. Orphanet J Rare
pulp chamber at the expense the pulp chamber and shor­ almost the top of the root, Dis 2006; 1,12; https://doi.org/10. 1 1 86/1750-11 72 - l - I 2. - 11. Lagarde M et al. Simultaneous oc­
of the roots tening of the roots, but both very short canals in conical currence of triple teeth and double teeth in primary dentition: A rare case report and review of the
roots are still separated from very short roots literature. Clinical Case Report 2020;8(7): 1277-1286. - 1 2. Luder H U . M alformations of the tooth
each other root in humans Front Physiol 2015; 27; doi.org/ 1 0.33 89/fphys.2 0 1 5 .0307. - 1 3 . Munavalli A,
Kam bale S, Ramesh S, Ajgaonkar N . M andibular first molar with single root and single root canal.
J Conserv Dent. 2 015; 18(4):346-348. - 14. Roinioti TD, Stefanopoulos PK. Short root anomaly
Treatment of taurodontic teeth is difficult due to the diversity of the shape and size of associated with Rothmund-Thomson syndrome. Oral Surg Oral Med Oral Pathol Oral Radial
the pulp chambers, the calcification of the pulp and the complicated configuration of the Endod. 2007;103(1):19-22. doi: 10. 1 016/j .tripleo.2006.07.021. - 15 . Su J M et al.Three years of
root canal system. During root canal treatment, it is particularly difficult to stop bleeding, follow-up of otodental syndrome in 3-year-old Chinese boy: a rare case report. B M C Oral Health
2019;19(1):164; doi:10.l 186/s l2903-01 9-0860-z. - 1 6. Suda N, Moriyama K. Human Diseases
mechanical preparation (risk of perforation of the chamber floor). Root enlargement at Associated with Abnormal Tooth Roots. J Oral Biosciences 2009;51(4): 1 99-204. - 17. Tewari
the apex can be a complication during extraction. N, Pandey R K, Singh S. Concomitant hypodontia and hyperdontia: A report of two cases. Natl J
Maxillofac Surg 20 1 7;8(1 ):75-77; doi: 10.4103/0975-5950.208976. - 18. Yu M et al. M olecular
Root di laceration affects permanent teeth more often than deciduous teeth, posterior
mechanisms for short root anomaly. Oral Dis. 2021 ;27(2): 142-150. - 19. Zhang J et al. Treatment
teeth than anterior teeth. In anterior teeth, it is most commonly located in the ½ of the of type Ill dens invaginatus in bilateral immature mandibular central incisors: a case report. BMC
apical part of the root, and in first molars in the middle ½ of the root (Fig. 7. 18). Its Oral Health 2022;22,28 ; doi .org/ I 0 .1186/s12903-022-02059-8.

aetiology is not fully explained. It is associated with some genetic syndromes, such as
Ehlers-Danlos syndrome, Axenfeld-Rieger syndrome and congenital fish scales. Causal
local factors can be mechanical trauma (e.g. to the deciduous tooth), periapical infec­
tions, ankylosis of the deciduous tooth, cyst-like lesions and tumours.

Fig. 7.18. Dilaceration

of the tooth root 22.

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 Developmental defects of enamel and dentin

Chapter 8 Mineralised tissue defects are classified as defects:

enamel or dentine,
quantitative, qualitative and concerning both quantity and quality of tissue,
Developmental defects of enamel and dentin
consisting of incomplete mineralisation (hypo mineralisation, hypomaturation),
Dorota Olczak-Kowalczyk underdevelopment (hypoplasia) or overdevelopment (hyperplasia).

Developmental enamel defects

Abnormalities in the development of tooth mineralised tissues can be caused by envi­
ronmental (general or local) and genetic factors. Defects affecting a single tooth, or several Developmental defects of the enamel are classified as turbidity (opacity), hypopla­
adjacent teeth and teeth asymmetrically distributed in the dentition are usually caused by sia, discoloration. Discolouration and opacity are qualitative defects and hypoplasia is
a local factor. Tooth defects that occur symmetrically, known as chronological defects, are a quantitative defect of the enamel.
the result of a general environmental factor over a specific period of time. Defects unrela­ Opacity arises as a result of incomplete mineralization of the enamel. They can be in
ted to a specific stage of odontogenesis and affecting the entire dentition are the result of the nature of change:
a long-term general environmental factor or genetically determined (Fig. 8.1).

Developmental defects in mineralised tissues

- demarcated - white, yellow, brown clearly demarcated
from normal enamel,

a single tooth, of all teeth

several adjacent teeth, several teeth - located symmetrically
several teeth - located asymmetrically

chronological
l
non-chronological
- diffuse - white, irregularly or linearly distributed with­
out a clear border with the normal enamel.

Opaque enamel with high subsurface porosity is subject to mechanical damage after
genetic tooth eruption (abrasion, fracture).
general environmental
long-term, Enamel hypoplasia is a thinning of the enamel caused by the incomplete formation
local factors: factors of relatively environmental
- injury, short duration: of its protein matrix. It can take the form of:
insulated general factors:
- infection, - malnutrition,
defects - chronic diseases,
- ionising radiation, - infectious diseases,
- chronic
- idiopathic - metabolic disorders,
symptom of a poisonings
- poisonings
genetic syndrome

Fig. 8. 1 . Division of dental m ineralised tissue malformations according - pit-form (punctate hypoplasia),
to the location of the lesions.

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 Developmental defects of enamel and dentin
Compendium of Paediatric Dentistry

D evelopmental abnormalities of the enamel due to local factors

A malformation of the enamel of a permanent tooth (usually a single tooth) associa­
ted with the pathology of a deciduous tooth is referred to as Turner 's tooth. A lesion af­
fecting the enamel of a single incisor indicates a history of trauma to the deciduous tooth
before the age of three years, less commonly a periapical infection, while the enamel of
- grooves/lines (groove/liner hypoplasia), a premolar indicates a periapical infection (Fig. 8.2, 8.3).

- semi lunar incisal defect,

Fig. 8.2. Turner's teeth - enamel hypoplasia of a premolar due to periapical infection of a first
deciduous molar (left); hypoplasia of a permanent maxillary medial incisor due to penetration
of the deciduous incisor into the tissue.

- superficial lack of enamel

(partial enamel aplasia; plane hypoplasia).

Hypoplasia may be accompanied by opacity and dentin defects. Opacity and hypo­
plasia can be caused by the same aetiological agent, depending on the stage of amelo­
genesis in which it acts, the duration of action, its severity and individual susceptibility. Fig. 8 . 3 . Enamel hypoplasia and pulp necrosis of a prematurely erupted mandibular second
premolar caused by a periapical infection of a deciduous molar.
Among them, the most frequently mentioned are:
- local, e.g. mechanical trauma, infection, ionising radiation,
Developmental abnormalities of enamel caused by general
general, e.g. metabolic and endocrine disorders (hypoparathyroidism, hypothyro­ environmental factors
idism, hyperthyroidism, hyperpituitarism), systemic viral and bacterial infections
(syphilis, diphtheria, tuberculosis, measles, rubella, chicken pox and cytomegalo­ An example of a qualitative developmental defect of the enamel caused by systemic
virus infection), exposure to chemicals (e.g. :fluoride, tetracycline, amoxicillin, cy­ factors concerning the group of teeth is the molar incisor hypo mineralization (MIH)
tostatic, thalidomide, aromatic hydrocarbons such as polychlorinated biphenyls and involving at least one first permanent molar and often incisor (Fig. 8.4). Second decidu­
dioxins), malnutrition, nephrotic syndrome, neurological diseases (e.g. cerebral pal­ ous molars, premolars, second permanent molars and canines can also be affected. The
sy), heart defects, prematurity, low birth weight, neonatal hypocalcaemia, vitamin D prevalence of MIH is estimated at 13-14% of children worldwide.
deficiency, neonatal jaundice, maternal diabetes, neonatal asphyxia, Symptoms of MIH:
genetic: amelogenesis impe,fecta and defects constituting a symptom of a genetic - asymmetric occurrence of white, creamy-ye1low or yellow-brown opacities, of va­
syndrome, e.g. epidermolysis bullosa hereditaria. rious shapes, clearly demarcated from unaltered enamel,

1 04 1 05
Compendium of Paediatric Dentistry Developmental defects of enamel and dentin

lesions located near the incisal edge or on the occlusal surface, on other surfaces In the etiology of M IH, which is not thoroughly known, it is listed:
(usually in the ½ of the occl usal area), _ prenatal factors in the last trimester of pregnancy (e.g. maternal diseases, use of medi­
- predisposition to the development of caries and post-eruption mechanical breakdown cation, exposure to environmental pollutants, smoking),
to the enamel (fractures, wear), _ delivery by caesarean section, preterm birth and low birth weight,
possible hypersensitivity to cold, discomfort during tooth brushing, difficulties with _ factors acting in the first three years of life (e.g. childhood diseases, environmental
local anaesthesia (Fig. 8.4). pollutants, medication (e.g. glucocorticosteroids, amoxicil\in), renal failure, asthma.
High fever can impair the function of proteolytic enzymes involved in amelogenesis.
Respiratory diseases, by causing respiratory acidosis and hypoxia, can affect enamel
matrix pH and ameloblast function. The influence of genetic factors is also possible. It
should be emphasised that the formation of the enamel of the first permanent molars and
incisors occurs at the same time as that of deciduous molars. The presence of enamel
malformations in deciduous molars is therefore an indicator of their risk of occurrence
in the permanent dentition.
Long-term exposure to environmental factors disrupts the successive stages of amelo­
genesis, leading to enamel defects in more than one group of teeth, with a symmetrical
distribution. Causal factors may be chronic systemic diseases, especially those leading to
malnutrition, e.g. chronic liver failure, Crohn's disease, short bowel syndrome, as well as
chronic renal failure, endocrine disorders (Fig. 8.5, 8.6).

Fig. 8.4. Molar-incisor hypomineralisation - severe form.

MIH can also be indicated by the presence of extensive fillings in permanent first
molars with a shape that does not correspond to the typical location of carious lesions.
Depending on the severity of the lesions, the form is distinguished:

Fig. 8.5. Enamel opacities and generalised hypoplasia in a girl with short bowel syndrome,
partially fed parenterally (right) and a boy with Crohn's disease (left).
- moderate - limited opacity without mechanical posteruptive enamel
breakdown to the enamel, with hypersensitivity to strong stimuli,
e.g. cold air and water, but without reaction when brushing teeth,
changes in incisors slightly disturb the aesthetics,

- severe - limited opacity with mechanical poest-eruptive enamel

breakdown and caries, spontaneous, chronic hypersensitivity that Fig. 8.6. Enamel opacities and hypoplasia in a boy after renal transplantation for chronic renal
hinders chewing, tooth brushing, signi ficantly impaired aesthetics failure (left) and a girl with adrenal insufficiency.
that may have a negative psychological impact.

1 06 1 07
Compendium of Paediatric Dentistry Developmental defects of enamel and dentin

Fluorosis is a developmental abnormality of enamel caused by excessive exposure

of teeth to fluoride. The threshold dose of fluoride, exceeding which causes fluorosis, is
unknown. The most frequently suggested dose is 0.1 mg/kg per day. Fluorosis can occur
at lower doses. The risk depends on: the fluoride dose (exists with fl uoride content in
drinking water > 1 .5 mg/I or consumption of 3-4 mg of fluoride per day), the duration
of fluoride exposure, the age of the child, the individual sensitivity of the organism, the Fig. 8.7. Moderate form of
tooth fluorosis.
presence of factors influencing plasma fluoride levels and its absorption from the gastro­
intestinal tract (e.g. Ca and Mg levels, kidney function, metabolic activity). Fluorosis is
Ta b. 8. 1 . Classification offluorosis according to Dean.
diagnosed on the basis of the clinical picture and a history of overexposure to fluorine
Fluorosis assessment
compounds. Criteria
scale
Fluorosis:
Normal condition (0) smooth, glossy, pale enamel surface with a creamy-white
- occurs much more frequently in the permanent dentition, translucent surface
more often affects (and is more severe) teeth that mineralise later (e.g. premolars) Questionable (0.5) on the surface of the enamel a few white spots or white flecks
and the area around tooth cusps and incisal edges, Very mild ( I ) small opaque, paper white areas covering less than 25% of the tooth
surface
the first pennanent molars and permanent incisor of the mandible are rarely affected,
- the risk of fluorosis lasts for the first 6-8 years of life, including: Mild (2) opaque white areas covering less than 50% of the tooth surface
• up to age 4 - for incisors and first molars ( 15.-30 months of age - window of Moderate (3) all tooth surfaces affected; marked wear on biting surfaces; lesions
on all surfaces, brown stains and abrasions on occlusal surfaces
increased risk),
the entire surface of the enamel is damaged, the hypoplasia as-
• over 4 years of age - for premolars and second molars. sumes such proportions that the shape of the tooth may be altered.
Heavy (4)
The characteristic symptoms of fluorosis are: There are small or extensive depressions or brown discolouration;
the tooth often has a corroded appearance
- symmetrical distribution of lesions on the surfaces of the same-identified teeth,
the localisation of lesions on tooth surfaces depending on the stage of development
Developmental abnormalities due to genetic factors
of the enamel at the time of exposure to fluorine compounds,
smooth chalky-white opacities without a clear boundary with the unaltered ena­
Amelogenesis imperfecta
mel, usually arranged linearly according to the course of the perikymata, which may
Developmental disorders of enamel of the nature of amelogenesis imperfecta (AI)
merge to form image of spots,
affect both deciduous and permanent teeth enamel (Fig. 8.8). They occur alone or coexist
enamel hypoplasia (pitted, grooved or superficial exposing dentin),
with lesions located within other tissues of ectodermal origin. Mutations in genes en­
- yellow and brown spots caused by the retention of dyes,
coding proteins such as amelogenin (AMELX), enamelin (ENAM), kallikrein (KLK4),
porous, poorly mineralised enamel (fewer minerals, more proteins than healthy
enamelin (MMP20) and FAM83H are associated with the development of AI. AI can be
enamel) (Fig. 8.7).
inherited in an X-chromosome-coupled manner or as an autosomal dominant or reces­
Depending on the severity, Dean distinguishes between questionable, very mild,
sive trait. It occurs with a frequency of 1 :700 to 1 : 14 000 people.
mild, moderate and severe fluorosis (Tab. 8. 1).
The diagnosis of AI is based on a thorough family and medical history (exclusion of
long-term effects of general environmental factors) and assessment of dental characteristics.

108 109
Compendium of Paediatric Dentistry Developmental defects of enamel and dentin

Fig. 8.8. A melogenesis imperfecta i n a boy with mixed dentition. Fig. 8. 1 0 . Radiographic image of amelogenesis impe1fecta associated with hypo mineralisation -
normal thickness of enamel of unrooted teeth, contrast of enamel similar to dentin, correct struc­
ture of crowns of unerupted teeth (left) and A l associated with hypoplasia - visible hypoplastic
Witkop (1988) distinguishes 4 main types of amelogenesis imperfecta: defects of enamel changing the tooth contour (right).
1 - hypoplastic
• C{owns of teeth may be sm aller, no contact Discolouration of teeth
points, often discoloration (chalk, yellow,
brown), enamel thin and smooth or of the cor­ Tooth discolouration and staining is a change in the colom or translucency of a tooth caused
rect thickness with grooves or pits, open bite, by extrinsic or intrinsic factors. Depending on the location of the causal factor, in the structure
• on X-ray normal or slightly weaker enamel con­
of the tooth, the discoloration may be superficial - external (extrinsic discolouration) or internal
trast with enamel defects, irregular enamel outline,
(intrinsic discoloration) (Fig. 8.11). They are also classified as metallic and non-metallic.
11 - hypomaturation
hypersensitivity to stimuli, discoloured
(chalk, yellow, brown), enamel of normal
Discolouration of teeth
thickness, rough and soft susceptible to me­
chanical damage, often open bite,
slightly larger or dentin-like enamel contrast in
X-ray, normal crown strncture ofunerupted teeth,
I
external
I
internal
staining colllponent on the tooth surface coloring colllponent e!llbedded
I T T - hypocalcification or in the dental plaque in the tooth structure
image similar to the features of hypomata­
tion, predisposition to tartar deposition (Fig. l l
I
8.9),

•
pre eruption post eruption
slightly larger or dentin-like enamel contrast
on X-ray, normal crown structure of unerup­
ted teeth (Fig. 8 .10),
'
indirect
l l
lV - hypomaturation-hypoplastic with taurodontism. caused by a chelllical re- examples:
direct action on the tooth surface - DI, AI and other
discoloration in accor- (colour different fro!ll that of develop!llental examples:
dance with the colour the staining agent) abnorlllalities of - caries,
of the factor examples: enamel (e.g. fluorosis), - dental pulp
examples: - cationic and metal salt - diseases: hyperbil- diseases,
- food, !llouthrinses, irubinaemia, eryth- - measures used
- tannins in drinks, - llledications (e.g. ropoietic porphyria,
Fig. 8.9. The degree of enamel friction - chromogenic minocycl ine, iron
in endodontics,
alkaptonuria, - amalgam
varies depending on the time that has bacteria preparations),

-
- drugs: tetracyclines,
elapsed since the tooth erupted in a girl - impurities (mercury, ciprofloxacin
with a hypocalcified type lead, copper, nickel)

Fig. 8. 1 1 . Division of tooth discolouration.

110 111
Compendium of Paediatric Dentistry Developmental defects of enamel and dentin

Internal discoloration may be accompanied by developmental abnormalities of the Congenital erythropoietic porphyria, Gunther's disease is a very rare form of por­
teeth (amelogenesis impet:fecta, dentinogenesis impe,:fecta, developmental abnormalities ph yria inherited as an autosomal recessive feature. Its essence is a defect in the en­
of the enamel caused by local and systemic factors, including tooth fluorosis), as a result zyme uroporphyrinogen lil synthetase resulting in the accumulation of porphyrins in
of the incorporating of the staining component intotooth structure during development the bone marrow, erythrocytes, urine, faeces, skin, bones and teeth. Porphyrins have a
(pre-eruption) or after its completion (post-eruption). Their removal is not possible. hi gh affinity for calcium phosphate, so they are incorporated into tooth structures during
The risk of pre-eruptive discolouration occurs during the period of crown formation, their formation, causing a reddish, reddish-brown or even black discolouration known as
for deciduous teeth from the 4111 month of pregnancy to about 12111 months of age of the erythrodontia (UV-induced fluorescence). The lesions affect deciduous and permanent
child, for permanent teeth from the second half of pregnancy to about 8 years of age. The teeth, with the discolouration of deciduous teeth being more severe as porphyrins are
causes of pre-eruptive internal discolouration can be general diseases (erythropoietic deposited in the enamel and dentin, while in permanent teeth, only in the dentin.
porphyria, alkaptonuria, hyperbilirubinaemia) and the use of drugs, especially tetracy­ Alkaptonuria is a rare metabolic disease inherited autosomal recessively. Its essence
cline, ciprofloxacin. is a deficiency of the enzyme homogentisic acid oxidase, which catalyses the conversion
Hyperbilirubinaemia causes discolouration of the teeth (yellow green to green­ of homogentisic acid to maleylacetoacetic acid in tyrosine catabolism. Homogentisic
brown) due to the deposition of biliverdin (an oxidation product of bilirubin) in the acid accumulates both intracellularly and extracellularly and oxidises to benzoquinone
enamel and dentin layers during mineralisation. Hyperbilirubinaemia occurs in children acetate, which polymerises to form a melanin-like polymer. Deposition of the polymer
of different ages, so discolouration can affect both deciduous and permanent teeth (Fig. in the connective tissue, in bones, cartilage and teeth, results in their grey, bluish-black
8.12). The severity of the discolouration depends on serum bilirubin levels and is inde­ or bluish-brown discolouration.
pendent of the duration of jaundice. Causes of jaundice in a young child include sero­ Tetracycline stains are the result of combining a tetracycline molecule with calcium in the
logical incompatibility in the Rh system or major groups and biliary atresia, while in process of chelation and embedding into a hydroxyapatite c1ystal, mainly dentin, in a smaller
older children it includes hepatitis, damage from toxins, cancer, genetic and metabolic amount of enamel. It can also cause enamel hypoplasia. The tetracycline-calcium orthophos­
diseases. Congenital biliary atresia is considered the most common cause. Greenish in­ phate complex in hydroxyapatite is oxidised to red quinone by photooxidation. The severity
ternal discolouration may also result from the use of ciprofloxacin in the neonatal period. of discolouration depends on the stage of crown development and the activity of the mine­
ralisation process, the dose used, the duration of treatment and the type of drug (doxycycline
has a low affinity for binding to calcium). The 1isk of tetracycline discolouration is high with
daily doses ofthe drug above 3 g or when the duration of treatment is longer than 1 0 days. The
colour of the discolouration depends on the type of tetracycline. Chlortetracycline causes grey
discolouration, while tetracycline, oxytetracycline, tigecycline, glycylcycline cause yellowish
discolouration. The discolouration slowly darkens to brown or greyish brown when exposed to
sunlight (front teeth darken faster due to more frequent exposure to surilight).
Fully mineralised teeth are not susceptible to tetracycline-induced discolouration
(relative lack of free calcium); however, green-grey or blue-grey discolouration of ma­
ture teeth has been observed after prolonged minocycline or doxycycline therapy (over
one month). It is believed that minocycline:
- by binding to plasma proteins, it can penetrate the dental pulp, the subsequently formed
P ig. 8. 1 2. Discolouration of deciduous and permanent teeth of varying severity and location in
the dental arch and crowns i n chi ldren with congenital bil iary atresia (chronological changes). seconda1y dentin and oxidise when exposed to light (intrinsic staining theory),

1 12 113
Compendium of Paediatric Dentistry Developmental defects of enamel and dentin

- forms an insoluble complex by binding to membrane glycoproteins, which can then Exte rnal discolouration
transform into an insoluble black quinone by oxidation through contact with air, un­ Black external discolorations usually line up along the edge of the gum and rarely
der the influence of bacteria or by a chelation process with divalent metal ions, such
ex ceed the ½ cervical part of the crown (Fig. 8.14). The staining material is characterized
as iron, in saliva or gingival fluid (extrinsic staining theory).
b y the presence of ferric sulphide and a high content of calcium and phosphates. Ferric
Post-eruption internal discoloration is caused by the penetration of the staining
sulphide is probably formed by a reaction between hydrogen sulphide produced by bac­
agent into the dentin tubules (Fig. 8.1 3). Causal factors include:
teria (including Actinomyces strains) and iron in saliva or gingival fluid. Causal factors
- dental caries - discolouration ranging from white through yellow, yellow brown to
also include the intake of iron supplements by the mother during pregnancy and by the
black, child, an iron-rich diet, therapeutic agents such as silver nitrate and silver diamino flu­
dental caries - yellowish discolouration, oride, environmental exposure to iron, silver, magnesium. Purple-black discolouration
dental pulp diseases, including: can result from rinsing the mouth with potassium permanganate solution. The black spot
• necrosis and haemorrhage in the pulp - grey-brown discolouration (breakdown
(BS) is difficult to remove through daily tooth brushing and tends to recur after profes­
products of the pulp, formation of black iron sulphide due to the release of haem sional scaling.
from erythrocyte haemolysis),
• internal resorption - pink,
• pulp calcification - yellow, yellowish brown (reduction in crown translucency),
phenolic endodontic medicaments containing iodoform and antibiotics (e.g. Leder­
mix paste containing triamcinolone acetonide and demethylchlortetracycline, tri-an­
tibiotic paste consisting of ciproftoxacin, metronidazole and minocycline), MTA -
brown-grey discolouration,
filling materials, including amalgam - blue-grey discoloration, ' Fig. 8.14. Black external discolouration caused by iron supplementation.
- improper use of rinsing agents, e.g. alternating rinsing with a solution of sodium hy­
pochlorite (NaOCI) and chlorhexidine creates a dark brown deposit adhering to the
wall of the tooth cavity. Green and orange external discoloration are the result of chromogenic bacteria
(incl. Serratia marcescens and Flavobacterium lutescens). They most commonly affect
the gingival area of the maxillary incisors. Mouth breathing is a contributing factor. Mi­
nocycline, exposure to copper, nickel, mercury and lead dust can also be causes of green
discolouration. Causes of yellow and brown discolouration include tannins in foods,
chlorhexidine, quaternary ammonium compounds such as cetylpyridinium chloride,
other mouthwashes containing essential oils, delmopinol hydrochloride, stannous flu­
oride.Tooth discolouration associated with the use of cationic mouthwashes results
Fig. 8 . 1 3 . Post-eruptive internal tooth discolouration: brown - pulp necrosis due from the precipitation of anionic dietary chromogens (Fig. 8.15). It is therefore important
to caries (left) and due to chronic trauma - tongue piercing impaction (middle),
to limit the consumption of beverages containing polyphenols when using them.
grey discolouration after MTA application.

l 14 115
Compendium of Paediatric Dentistry Developmental defects o f enamel and dentin

Dentin defects are generally divided into congenital dentinogenesis impe;fecta,

( D GI) - types I-III, dentin dysplasia (DD) - types I and II. Mutations of the dentin sia­
loprotein gene occur in DGI II and III and DD type II, of the COLl A l or COL1A2 gene
in D GI l. The clinical and radiological manifestations of DGI types I and II are similar.
The incidence of developmental dentin abnormalities is estimated at 1:6000-1:8000 for
D GI and at 1: 100 000 for dentin dysplasia.
Fig. 8 . 1 5 . Orange discolouration of teeth, probably diet-related (left) and caused by the use of Dentin dysplasia (DD) is inherited in an autosomal dominant way. Its cause is prob­
chlorhexidine (right).
ably the migration of abnormal epithelial cells of the Hertwig's epithelial root sheath
into the dental papilla, disrupting the differentiation and function of the odontoblasts.
Yellowish, brown or grey discolouration can be caused by certain antibiotics (e.g. Type I DD is referred to as radicular dentin dysplasia (rootless teeth), type II as coronal.
minocycline, doxycycline, amoxicillin with and without clavulanic acid, linezolid), The symptoms of both types of DD are shown in Table 8.2. In DD type I, complete
glibenclamide (anti-diabetic drug), imatinib (anti-cancer drug) (Fig. 8.16). obliteration of the tooth cavity visible radiographically before eruption is characteristic.
The degree of pulp calcification of permanent teeth varies (Fig. 8. 1 7). DD type II has
m any symptoms similar to dentinogenesis imperfecta, including the bulbous shape of the
crowns of deciduous teeth with amber colour, but permanent teeth have a normal or only
slightly blue-grey colour (Fig. 8.1 8).

Fig. 8 .16. Dark discolouration of teeth in two girls with chronic myeloid leukaemia
during chemotherapy and after long-term antibiotic therapy.

Developmental abnormalities of dentin

T he developmental defects of dentin may be the result of disturbances in the for­

mation of its protein matrix and/or mineralization. They are rarely the result of environ­
mental factors, much more often mutations of genes encoding proteins involved in the
formation of type I collagen (over 85% of the organic phase of dentin) or non-collagen
proteins, including dentine sialoprotein (DSP), which control the course of mineraliza­
tion. W here the mutation involves a gene encoding a dentin-specific protein, e.g. DSP,
the defect only affects the dentin. Mutations in genes encoding proteins essential for the Fig. 8.17. Dentin dysplasia type I - clinically unchanged colour and shape of permanent
construction of type I collagen or non-collagenous proteins that perform the same role in teeth (top photos), obliteration of tooth cavities, tapered roots, dilution of tooth structure
on X-ray (bottom photo).
bone and dentin will also cause skeletal abnormalities.

116 117
Compendium of Paediatric Dentistry Developmental defects of enamel and dentin

Fig. 8. 1 8. Dentin dysplasia type IT - bulbous shape of canine crowns, amber-coloured clashes Fig. 8.19. Clinical and radiological picture of DGT type 11 in a girl with mixed dentition. Clinically,
of deciduous teeth - during eruption of permanent lower incisors (upper left photo), unchanged visible amber colour of the crowns of deciduous and permanent teeth, enamel chipping and abra­
shape of slightly discoloured permanent incisors (upper right photo). On X-ray complete obli­ sion of deciduous teeth ( upper radiographs); radiographically, bulbous shape of the tooth crowns,
teration of deciduous teeth cavities, well visible canines, normally developing permanent teeth marked cervical narrowing of deciduous and permanent teeth, short roots and complete obliteration
(bottom photo). of deciduous tooth cavities, calcifications in the chambers of permanent teeth.

Dentinogenesis imperfecta (DGI) (Capdepont's disease, iridescent dentin,) is inher­ Tab. 8.2. Clinical and radiological signs of dentinogenesis imperfecta and dentin dysplasia.
ited by the autosomal dominant pathway associated with chromosome 4q1 2-2 1 . Applies Type of dentition DGI 1/11 DGI III DD I DD II
to the dentin of deciduous and permanent teeth. Clinical and radiological symptoms of deciduous dentition yes yes yes yes
DGI types I and II in dentition are similar (Tab. 8.2). However, type II only affects the permanent dentition yes yes yes yes/no
dentition, while type I coexists with osteogenesis i mperfecta. DGI type I has also been Clinical Findings
observed in other genetic syndromes, such as Ehlers-Danlos syndrome and Goldblatt altered shape of tooth crowns yes yes no yes
syndrome. Common clinical signs of all types of DGI are a change in colour and a bell­ tooth crown colour: yellow/brownish amber/
greyish blue with iridescence
shaped, tubercular shape of the tooth crowns, frequent enamel breakage, and abrasion yes
of exposed dentin. In type I, the deciduous dentition is more affected; in type II, the (decidu-
yes yes no
lesions affect deciduous and permanent teeth equally (Fig. 8. 1 9). Type III DGI is popu­ ous teeth
only)
lation-specific (Maryland and Washington State). May be associated with osteogenesis
i mperfecta. Clinically, it may resemble DGI I or DGI II. A common symptom is shell
teeth in deciduous and permanent teeth, which are characterized by normal enamel,
yes
a thin layer of dentin, a large tooth cavity, a short root with a closed apex. (decidu­
yes yes/no no
ous teeth
only)

118 11 9
Compendium of Paediatric Dentistry Developmental defects of enamel and dentin

periapical bone yes yes/no yes no

pronounced cervical yes rarefaction in X-ray
yes/no no
constriction

Regional odontodysplasia is a non-hereditary, isolated developmental abnormality of

short, thin roots yes/no no no enamel and dentin with an unknown etiology, which most often affects one quadrant or
part of it, more often the jaw than the mandible, both deciduous teeth and pennanent teeth.
Its clinical manifestations include delayed development of tooth germs, delayed and
prolonged eruption of teeth (by up to 10 years), the presence of impacted teeth, gingivi­
conical'roots no yes no tis, mucosa! swelling and purulent fistulas in the area of the disorder, reduced tooth shape
with yellow or brown colouring, enamel hypo mineralisation and hypoplasia, hypomin­
eralisation and dentin abnormalities (fewer irregularly spaced tubules, wide intersphe­
rical spaces, amorphous areas). Radiographs show a lack of enamel/dentin boundary,
lack of roots no yes 110 thin layers of enamel and dentin, a large pulp chamber - "ghost teeth", pulp denticles,
shortened roots with wide canals and unclosed apices.
Developmental abnormalities of the teeth and mineralised tissues accompany many
yes/no genetic syndromes. Symptoms relating to the dentition in selected general conditions are
calcifications of the pulp (perma- shown in Table 8.3.
yes no yes/no
(denticles) nent teeth
only)

Tab. 8.3. Selected general conditions with developmental abnormalities of teeth

yes and mineralized tissues.
Rapid and complete (decidu- decidu-
obliteration of yes no General condition Symptoms concerning dentition
ous teeth ous teeth
the pulp chamber only) only) reduced number of teeth or lack of
deciduous and/or permanent teeth,
autosomal dominant Ill-
altered tooth shape (truncated, con-
heritance (hydrotic form)
ical, dowel-shaped), microdontia,
or recessive inheritance,
Ectodermal dysplasia taurodontism, impacted teeth, con-
crescent-shaped chambers no yes no recessive coupled to the X
genital teeth, enamel hypoplasia,
chromosome (hypohidrotic
delay in eruption or change in the
form)
order of eruption and placement of
teeth, persistent deciduous teeth
yes atypical structure of deciduous
(perma­ teeth, retained deciduous teeth, hy-
thistle/tube-shaped chambers no no Down syndrome trisomy of chromosome 21
nent teeth podontia, oligodontia of deciduous
only) and/or permanent teeth

120 121
Compendium of Paediatric Dent istry Developmental defects of enamel and dentin

abnormal chondrocyte a group of diseases caused by

di fferentiation and abnor­ mutations in the genes enco-
mal mi neralization of the congenital epidermolysis ding adhesion molecules or enamel hypoplasia, excess cellular
growth plate due to low enamel hypoplasia, caries, delayed bullosa acquisita other structural proteins that cementum
Vitamin D deficiency
serum 25-hydroxyvitam in eruption of deciduous teeth, vita­ determine the combination of
rickets
D [25(OH )D] levels due to min-D-related rickets type I epidermis and skin
inadequate vitamin D and/ delayed resorption of deciduous
or calcium supply during
teeth, arrested and delayed eruption
developmental period of permanent teeth, numerous su-
Cleidocranial syndrome disorders of the entire ske-
autosomal recessive in- delayed tooth eruption, enamel hy­ letal system; dominant au- pernumerary teeth, underdevelop-
heritance; mutations in the poplasia, discoloration f rom yel low (Marie-Sainton syndrome) ment of root cementum , enamel
Type I pseudo-deficiency tosomal inheritance
genes responsible for vita­ to brown, dentin defects, tendency hypoplasia, hypomineralization of
rickets / vitamin-D-depen­
min D hydroxylation in the to periodontal disease; in the X-ray enamel and dentin, often distorted
dent type I
l iver (type I B) or kidney i mage - large chambers of teeth, roots, deficiency of eellular cement
(type IA) short roots
dentin hypomineralization, mi­
cro-gaps within the dentin; in the
X-ray image - large pulp cham­ Dental treatment in the case of developmental abnormalities of enamel and
bers with pronounced horns (even dentin should take into account the individual needs of the patient. Treatment of teeth
Hypophosphatemia endopeptidase gene muta­
exceeding the enamel-den tin
rickets conjugated to X tions resulting 111 reduced that may become the cause of pain, mechanical damage and rapidly progressing caries
j unction), weakened pulp defence
chromosome; hypophos­ renal reabsorption of phos­ should begin as soon as possible after the tooth erupts. It is important to implement
mechanisms (more fibrous ele­
phatemia conjugated to X phate and abnormal bone
ments and a reduction in the num­ caries prophylaxis, prevent mechanical damage, eliminate hypersensitivity and restore
chromosome mineralisation
ber of odontoblasts), often tooth
abscesses not related to caries or
proper aesthetics and function. The choice of treatment method and restorative materials
tooth injury, less often enamel hy­ depends on the age of the patient, the type of tooth and its degree of maturity, the
poplasia type of developmental pathology and its severity. Daily use of the paste with casein
premature loss of deciduous teeth
phosphopeptide and amorphous calcium phosphate (CPP-ACP) hardens the tooth surface
(roots without resorption features),
periodontitis, enamel and dentin and reduces tooth sensitivity. The methods used to restore aesthetics are: whitening,
hypomineralization, lack of cellu­ enamel microabrasion, cosmetic reconstruction with resin-based composites, and in
mutation of the gene en­
lar cement or its thin layer preven­
coding non-tissue-specific adolescents - veneers and prosthetic crowns (Fig. 8.20, 8.21). In the developmental
ting anchori ng of collagen fibres
Hypophosphatasia alkaline phosphatase, dis­
and binding the tooth to the bone, period, standard steel crowns are also used to avoid tooth abrasion and maintain the
turbance of bone and tooth
in the X-ray image - large cham­ occlusal height (Fig. 8.21).
m ineralization
bers of teeth, a thin layer of mi­
neralized tissues (as a result of
abrasion), widening of the perio­
dontal ligament space
aplasia or thin acellular cement
Odontohypophosphatasia
layer

Fig. 8.20. Cosmetic reconstruction with composite materials and canines

in a patient with amelogenesis imperfecta.

1 22 1 23
 Developmental defects of enamel and dentin
Compendium of Paediatric Dentistry

es is im perfecta. Orphanet J Rare Dis. 2007;2:17; doi : I 0.1186/1750-1172-2-17. - 9. Costa-Silva

C M et al. Increase in severity of molar-incisor hypom ineralization and its relationship with the
colour of enamel opacity: a prospective cohort study. Int J Paediatr Dent 2011; 21 : 3 33-41.
I O. De Coster P J. Dent in disorders: anomal ies of dentin formation and structure. Endodontic
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pic
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rickets: enamel abnormalities and oral clinical findings. Scanning. 2014;36(4):456-461. - 13.
Garcia-Lopez M et al. Amoxycillin-Clavulanic Acid-Related Tooth Discoloration in Children.
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Fig. 8. 2 1 . Standard steel crowns on the second deciduous molars in a patient
with dentinogenesis impe,fecta during the eruption of the first permanent molars. cause discolouration of permanent teeth? J Cl in Diagn Res. 2013 ;7( 12):3081-3082. doi : 10. 7 860/
J CD R/20 1 3/6504.3 875. - 15. Hart PS, Hart TC. Disorders of human dentin. Cell s Tissues Organs.
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ch ildhood and fluorosis of later developing tooth zones. J Public Health Dent. 2011 ;71 (3):229-
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used as. resin-based composites in the initial treatment. The use ofresin-based composites dermolysis bul l osa. Arch Oral Biol 1993 ;38( 11 ):945-55 . doi : I 0.10 I 6/0003-9969(93)90107-w. -
J 8. Kumaraguru T et al. Tooth discoloration in patients with neonatal diabetes after transfer on
requires the removal of the enamel affected by the hypo mineralisation. Self-etching
to glibenclamide.Diabetes Care. 2009;3 2 : 1 428-30. - 1 9. Li Y et al. Analysis of the M icrobiota
systems are recommended. When leaving part of the enamel with hypomineralization, of Black Stain in the Primary Dentition. P LoS One. 2015; I 0(9):e0137030. doi : I 0.1371/journal.
as well as in severe fluorosis before etching, it is recommended to deproteinize it with a pone.0 I 3 7030.
20. Lygidakis NA et al. Best cl inical practice guidance for clinicians dealing with children pre­
5% solution of sodium hypochlorite for 60 seconds. In mild and moderate fluorosis, it is sent ing with molar incisor hypom ineralisation ( M l H ) : an updated European Academy of Paediat­
advisable to double the time of enamel etching. The extraction of molar tooth from MIH ric Dentistry policy document. European Arch Paediatr Dent https://doi.org/l 0. 1 007/s40368-02 l -
00668-5 - 21. M anton F e t al. Aetiology of M I H : a critical review. lnt J Paediatr Dent 2009; 19,
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when the formation of the bifurcation of its root begins. anomaly Pediatr Pol 2021 ;96(2): 153- 1 55. - 24. Olczak-Kowalczyk D et al. Oral health and liver
function in c.hildren and adolescents with cirrhosis of the liver. Prz Gastroenterol 2014;9(1):24-31.
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treatment, including surgical, orthodontic and prosthetic treatment and cooperation with sation. Bone 20 1 2; 50 (4): 989-97. - 26. Seow WK. Developmental defects of enamel and den­
a medical dentist providing medical care for the patient. tine: challenges for basic science research and clinical management. Aust Dent J . 2014;59(Suppl
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cisor Hypomineralization and Its Prevalence. Contemp Clin Dent. 2018;9(Suppl 2): S246-S250.
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1 24
 Teeth eruption. Developmental phases of the dentition

Chapter 9

Teeth eruption. Developmental phases of the dentition

Dorota Olczak-Kowalczyk, Anna Turska-Szybka
_ post-eruption (functional) phase - the tooth reaches the occlusive sur­
face, the root is fully formed, and the apex opening is closed, the peri­
odontium is shaped:
The process of eruption of a tooth involves the movement from the location occupied _ preocclusion stage - tooth movements before reaching the functional
bite position modified by environmental factors, such as pressure of
by the tooth germ in the jawbone into the oral cavity until the crown reaches an occlusal the cheek/lip and tongue muscles, forces exerted by adjacent erupting
position. The eruption is accompanied by the formation of the tooth root and periodon- ··. teeth,
_ post-occlusion stage - the tooth remains i n a functional position, adap­
tium. Depending on the position of the erupting tooth in the tissues and the advancement ting to the growth of the jaw/mandible and wear-related movements.
of its development, 3 basic phases of eruption are distinguished. These include:

The mechanism of the tooth eruption is not completely explained. It is thought to result
- pre-eruption phase - lasts from the end of the early phase of the bell to
the full formation of the crown and the initial part of the root, the germ from the interaction of the dental follicle, reduced enamel epithelium (REE), stellate reti­
of the tooth undergoes movements (active germ itself and passive due culum and alveolar bone. The coronal part of the dental follicle regulates osteoclast genesis
to the maxilla growth), which place it in the right position to start the (bone resorption), and the basal (root) part regulates osteogenesis (bone formation).
eruption,
The chemical mediators of osteoclasis secreted by the dental follicle are prostaglan­
Jins, epidermal growth factor (EGF), bone morphogenetic protein 4 (BMP-4) and trans­

rt. ·
forming growth factor B I (TGF-B I ), colony-stimulating factor- I (CSF- I ) and monocyte
. chemotactic protein- I (MCP- I ). REE secretes proteases that promote the formation of
the eruption pathway, breaking down collagen.
During the formation of the eruption pathway, there is degeneration of the fibres and

1�·
'
cells of the connective tissue directly covering the tooth, followed by degeneration of the
nerve fibres and reduction in the number of vessels. A triangular space is created above

· ,·
the erupting tooth where macrophages appear to help remove degraded elements, as well
- pre-functional-eruptive phase:
as osteoclasts responsible for bone resorption over the tooth. On the periphery of the
- intraosseous stage - slow movement of the tooth germ in the bone
(speed of about 1 - 1 0 µm per day) is accompanied by resorption pro­ permanent tooth eruption path there is a gubernacular cord, the fibi"es of which are likely
cesses (creation of the so-cal led eruption pathway) and bone apposi­ to direct the movement of the erupting tooth. The gubernacular cord, derived from the
tion in the root part,
dental lamina, connects the dental follicle to the gingival lamina propria.

•
.i.•�
.... --'i•.l
.
- supraosseous (mucosal) stage - the compound penetrates into soft
tissues and moves at a speed of about 75 �tm per day; by combining The phenomena occurring in the root portion of the tooth follicle are less well un­
the reduced enamel epithelium w ith the oral epithel i um, an eruption ·. .. ?'-_�
.
,f,-,i derstood. The ostogenetic significance of BMPs, Runx2, M MPs and the involvement of
channel is formed allowing the tooth to appear bloodless in the oral ' .,.
;

. tumour necrosis factor-a (TNF-a) was confirmed. Vascular endothelial growth factor
cavity, with the movement of the tooth in the occlusive direction, fur­ \·.·�
- ·.
.'·
. .·· ,

ther root and periodontal development takes place, (VEGF), by inducing angiogenesis, has also been shown to lead to increased pressure in

1 26 127
Compendium of Paediatric Dentistry Teeth eruption. Developmental phases of the dentition

the apical tissues (faster eruption after local injection of vasodilators and reduced erup­ I and 1.5 years in deciduous teeth and between 2 and 4 years in permanent teeth. At the
tion rates after injection of vasoconstrictors have been confirmed). It is also known that: sa m e time, the alveolar bone is being expanded, the alveoli and other periodontal struc­
the membrane of the root part of the dental follicle has the properties of gland cells, tures (gingiva, periodontium) are forming. After the appearance of a tooth in the mouth,
its stimulation by neurotransmitters of the nerve endings causes overpressure pushing the fibres of the periodontal ligament undergo better and better organization. Still, the
the tooth out (innervation-provoked pressure theory), fibres formed on the bone side are not connected to the fibres formed on the cement side.
soft tissues of the dental vesicle respond to muscle forces (mainly associated with This justifies the greater mobility of the tooth roots during eruption. At the time of the
chewing) that direct bone remodelling and tooth eruption (bite forces theory). first occlusal contact between the tooth and its antagonist, the fibres are arranged hori­
Tooth eruption is related to root and periodontal formation and the ability of the peri­ zontally around the coronal ½ of the root and are almost fully developed. The oblique
odontal ligament to adapt to the eruptive movement. With the development of the root fibres in the central ½ of the root are still formed. Only after the root apex is formed does
comes the development of the periodontium. From mesenchymal cells, cement-forming . the apical group of fibres develop. The stages of formation of the periodontal ligament
cementoblasts and fibroblasts differentiate. Fibroblasts secrete collagen fibres that be­ of deciduous and permanent teeth are the same, however, the time of its development in
come embedded in the cement. The first fibres run in coronally, hen they run along the permanent teeth is delayed compared to deciduous teeth. W hen the successor deciduous
developing root surface. I nitially, the fibres are aligned parallel to the root surface, but tooth appears, only the <lento-alveolar fibres, alveolar crest and horizontal fibres are or­
their orientation changes as the teeth erupt. In the second place, similar fibres appear on ganised. The remainder of the ligament is in the early stages of development.
the opposite side, on the surface of the bone. Fibres formed on the alveolar and cemen­ Jn the occlusal stage, when the tooth is in the occlusal position, the root is fully
tum side gradually elongate and eventually intertwine with each other. During the mu­ formed, the apex opening closes and active eruption of the tooth is completed. For de­
cosa! stage of tooth eruption, however, the fibre arrangement is loose and disorganised. ciduous teeth, the next phase of development is root resorption and tooth exfoliation. The
During the mucosa! stage of eruption, numerous inflammatory and mast cells are present approximate chronology of the development of deciduous and permanent teeth accord­
in the tissues surrounding the erupting tooth. The subepithelial connective tissue degenerates ing to Avery is presented in Tables 9.1. and 9.2.
and thins (cells undergo apoptosis, vascularisation decreases, nerve fibres degenerate). Matrix
Tab. 9. 1 . Approximate chronology of the development of deciduous teeth according to Avery.
metalloproteinases (MMPs) and phagocytic cells (macrophages, neutrophils, fibroblasts) are
involved in this process. There is an exposure of the enamel to the connective tissue. Enamel Onset of Com-
Complete Appear-
Deciduous minerali- Total mence-
proteins act as antigens, which is likely to cause local release of mediators such as histamine, teeth in the sation
crown ance in
root for- ment of
Exfolia-
formation the oral tion
leukotrienes, prostaglandins, proteases, cytokines and growth factors from mast cells. These order of (months in mation root re-
postnatally cavity (years)
reactions may be responsible for the appearance of symptoms associated with tooth eruption, eruption the foetal (years) sorption
(months) (months)
period) (years)
such as itching, inflammation, localised redness and increased saliva production. The cells of
Lower central
the reduced enamel and oral epithelium proliferate and migrate into the disorganised connec­ 3-4 2-3 7-10 1-2 4 7
incisal
tive tissue. A thick epithelial layer is formed covering the erupting tooth. In its central pait,
Upper central
epithelial cells are destroyed by macrophages, thus forming an eruptive channel lined with 3-4 2 8-1 1 1 -2 4 7
incisal
epithelium through which the tooth erupts bloodlessly. The periodontium develops from the
Upper lateral
root portion of the tooth follicle where collagen fibres undergo remodelling with degradative incisal 4 2-3 1 6-19 2 5 8
metalloproteinases and tissue inhibitors of metalloproteinases. Lower lateral
inci sal 4 3 12-15 1-2 5 8
When the crown of a tooth appears in the mouth, its root is formed in about 1/3 to ½ of
its length. The formation of the tooth root, depending on the tooth group, takes between

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Compendium of Paediatric Dentistry Teeth eruption. Developmental phases of the dentition

Upper first Deciduous dentition

4 6 25-28 2-3 6 10
molars
Jn the period preceding the appearance of the first deciduous tooth, the characteristic
Lower first 9
4 6 6-8 2-3 6
molars fe atures of toothless alveolar ridges are:
Upper
4.5 9 3 8 11 _ external position of the upper ridge in relation to the lower ridge,
9- 1 3
canines - sem icircular shape,
Lower - domed vaulting of the lateral parts,
4.5 9 1 7-20 3 7 9
canines
- in the anterior section, flattening of the upper shaft, flattened conical shape of the
Lower second
5 10 1 2- 1 6 3 7 10 lower ridge.
molars
Upper second Most often, the first tooth to appear in a child's mouth (around 6 months of age) is
5 II 20-26 3 7 10
molars the medial incisor of the mandible. Then, within 17.5-25 months, the next teeth erupt in
order: maxillary central incisors, maxillary lateral incisors, mandibular lateral incisors,
Tab. 9.2. Approximate chronology of the development of the permanent dentition according to Avery. maxillary and mandibular first molars, maxillary canine and mandibular canine, maxil­
Permanent lary and mandibular second molars. Teething is usually completed around the age of 3 1
Total crown Appearance in
teeth Beginning of Total root for- months.
formation the oral cavity
in the order mineralization mation (years)
(years) (years) According to the "6/4" rule, 4 deciduous teeth erupt every 6 months (at 12 months
of eruption
8 teeth are present in the child's mouth, at 18 months 12 teeth, etc.). The tim ing of the
Lower first
perinatal 3-4 7-8 9- 1 0 emergence of deciduous teeth in Polish children is shown in Table 9.3.
molars
Upper first After the incisal teeth have erupted, when the lateral parts of the alveolar ridges are
perinatal 4-5 8- 1 0 9- 1 0
molars edentulous, a spar and anterior physiological overbite are characteristic. After the erup­
Lower central
3-4 months 4 1 1-13 9 tion of subsequent groups of teeth and reaching the occlusive plane, deciduous dentition
incisal
Upper central is characterized by:
3-4 months 4-5 1 0- 1 2 9- 1 0 - sem icircular shape of the dental arches,
incisal
Lower lateral - flat occlusal plane,
3-4 months 4-5 1 0- 1 2 I 0-1 1
incisal
- in the anterior section: the overlapping midline between the incisors and the midline
Upper lateral
I 0- 1 2 months 4-5 6-7 1 2- 1 3 of the face, the contact of the edges of the incisors of the lower incisors with the pa­
incisal
Lower canines 4-5 months 5-6 1 1-13 1 2- 1 4 latine surfaces of the upper incisors below their cusps, vertical overjet from ½ to ½ of
Upper first the height of the crowns of the lower incisor,
1 -2 year 6-7 6-7 1 2- 1 4
premolars - in the lateral sections: the external position of buccal cusps of the upper molars in
Lower first relation to the lower ones and the contact of the palatal cusps with the intercuspidal
1 -2 year 6-7 7-8 1 2- 1 4
premolar
grooves of the lower teeth,
Upper second
2-3 year 7-8 8- 1 0 1 3- 1 4 - dental triads - except for the lower medial incisal teeth and the last upper molars
premolar
Lower second (Fig. 9. 1 ).
2-3 year 7 1 0-1 2 1 4- 1 5
premolar

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Compendium of Paediatric Dentistry Teeth eruption. Developmental phases of the dentition

_ is a long-term process (root resorption of incisor teeth take 1.5-2 years, of canines
and molars 2.5-5 years),
_ runs with interruptions and even recovery periods,
_ can be linear (layer upon layer) or sinusoidal,
_ usually starts in the area of the root adjacent to the permanent tooth root (lingual/
palatal surface of the apical part of the root in anterior teeth, furcal area and inner
surface of the roots in molars),
Fig. 9.1. Girl at 4 years of age - ful l deciduous dentition, maxil lary stomata, mandibular incisal
permanent teeth and first molars - intraosseous eruption stage. - can result in shortening of the root length (vertical) or its thinning (horizontal).
Root resorption begins as soon as the deciduous tooth is fully developed. The cells of
Tab. 9.3. Periods of eruption of deciduous teeth (in months), according to Szpringer-Nodzak et al. the deciduous tooth are genetically programmed to release or derepress the p53 gene, which
Teeth Boys Girls Total in combination with other genes controls the biochemical process of cell breakdown. It is
medial incisors 6-12 6-12 6-12 a process of asymptomatic, natural cell elimination called apoptosis (programmed cell death).
lateral incisors 8-14 6-16 6-16 In deciduous teeth, apoptosis causes the disappearance of pulp and periodontal cells, which
� canines 15-23 15-24 15-24 gradually reveals the internal and external surfaces of the mineralized tissues. Exposed sur­
first molars 12-19 10-17 10-19 faces of the mineralized tooth are colonized by elastic cells, forming areas of root resorption.
second molars 21-31 21-31 21-31 This process occurs through-out the root, is slow (can last months or even years), because
medial incisors 6-11 6-10 6-11 physiologically the level oflocal mediators stimulating elastic cells is ve1y low.
a;
lateral incisors 8-15 7- 1 8 7-18 The dental follicle of the permanent tooth bud secretes factors that induce and acce­
canines 15-22 16-24 15-24
lerate apoptosis and mediators that stimulate the activity of clasts. Odontoclasts, which,
::; first molars 12-19 10-18 10-19
like osteoclasts, arise and are activated in a mechanism regulated by the receptor acti­
second molars 21-31 21-31 21-31
vating nuclear factor NF-KB, its ligand, are responsible for the resorption of tooth mine­
ralised tissues. The presence of a permanent tooth germ is not a prerequisite for the
After the child is 3 years old, the period of preparation for permanent replacement of
resorption of the root of a deciduous tooth, as this process also affects deciduous teeth
deciduous dentition begins. Characteristic is:
without a permanent successor. The surface of the deciduous tooth root in the vicinity
abrasion of the crowns of deciduous teeth,
and facing the permanent tooth bud, however, is resorbed faster.
starting the resorption of the roots of the deciduous teeth,
The root cement is resorbed first, followed by the dentin and enamel. There are 4

w
the appearance or enlargement of spaces between deciduous teeth,
stages of r esorption: ¼ root, ½ root. ¾ root and exfoliation (Fig. 9.2, 9.3).
collapse forward of the line behind the second deciduous molars,

®� \fV
formation of wide planes behind the second deciduous molars,
(i0
ij
- a decrease in ovetjet in the incisal teeth and even the reduced ovetjet.
Root resorption of deciduous teeth begins 2-4 years before the teeth are replaced

RA R � � v=v
(Tab. 9. 1). It involves the incisors first, then the canines and finally the molars. Resorp­
tion of deciduous teeth roots:
starts earlier in the mandibular teeth than in the maxillary teeth and in girls than in boys, Ros O Ros I Ros 114 Ros 1/2 Ros 3/4 Ros c

- occurs symmetrically on both sides of the dental arches, Fig. 9.2. Stages of root resorption of deciduous teeth ( Fig. J . Komarnitki).

1 32 133
Compendium of Paediatric Dentistry Teeth eruption. Developmental phases of the dentition

duous tooth), and the eruption of the permanent tooth is inhibited. Incomplete resorption
of the root of a deciduous tooth is often the cause of the eruption of a permanent tooth
w ith the presence of deciduous teeth still in the alveoli, giving the image of "two teeth"
arra nged in two rows (Fig. 9.5). This phenomenon mostly affects the lower incisors,
Jess frequently the incisors and upper canines, with the permanent teeth in the mandible
a lw ays positioned lingually and in the maxilla either palatal or vestibular.
Fig. 9 . 3 . Successive stages of root resorption of mandibular deciduous molars.

In the pulp of a tooth whose root is resorbed, the number of inflammatory cells,
including macrophages, T and B lymphocytes, increases. With advanced resorption,
neuronal thickening, fragmentation and reduced innervation density are observed. The
gradual disappearance of nerve fibres allows painless exfoliation. Fig. 9.5. Lingual eruption of tooth
3 1 in the presence of tooth 7 1 .
Root resorption of deciduous teeth depends on general (genetic and environmen­
tal) and local factors. Local factors accelerating resorption include traumatic occlusion,
Mixed and permanent dentition
periodontitis, dental pulp diseases, endodontic treatment, crowding, cancerous changes.
Systemic factors are hormonal disorders (hypoparathyroidism, hyperparathyroidism, The appearance of the first permanent tooth at approx. 6 years (the first permanent
hypocalcaemia), dentinogenesis imperfecta, amelogenesis imperfecta, dentin dysplasia molar or medial incisor of the mandible) begins the period of mixed dentition, which
and odontodysplasia, Gaucher disease, Paget's disease, Perry-Romberg syndrome, Ste­ lasts until the exfoliation of the last deciduous tooth at the age of approx. 1 1 - 1 2 years.
vens-Johnson syndrome. It can also be idiopathic resorption (Fig. 9.4). During the period of mixed dentition, there are 3 stages : early l st transitional period,
inter-transitional period, and the 2 nd transitional period. During the first (early) stage of
mixed dentition (6-8 years), the eruption of the fi r st permanent molars and the replace­
ment of deciduous incisors with permanent teeth occur (Fig. 9.6).

Fig. 9.4. Girl 4 years old - accelerated, idiopathic resorption of the roots of deciduous teeth.

Resorption is delayed by, among other things, the absence or abnormal position of the Fig. 9.6. Boy aged 7 years - erupted first permanent molars
permanent tooth germ. Delay in the resorption of deciduous tooth roots is observed in hypo­ and medial incisors the maxilla and mandible.
thyroidism, pituitary dwarfism and in some genetic syndromes, e.g. in hyper IgE syndrome.
Jn the case of an abnormal position of the permanent tooth germ, the resorption pro­ In the inter-transitional period (8- 1 0 years), little change is observed concerning
cess may be disrupted and proceed asymmetrically. The deciduous tooth then stays lon­ the already erupted permanent teeth (the formation of their roots continues), and the re­
ger in the mouth than its counterpart on the opposite side (the so-called persistent deci- sorption of the roots of the deciduous canines and molars continues (Fig. 9.7).

1 34 135
Compendium of Paediatric Dentistry Teeth eruption. Developmental phases of the dentition

Ta b. 9.4 . Periods of eruption of permanent teeth (in years) in Warsaw children.

,..-
Teeth Boys Girls Total
,.--
medial incisors 6-8 6-8 6-8
lateral incisors 6-10 6- 1 0 6-10
canines 9- 1 3 9- 1 2 9-13
� first premolars 8-12 8- 1 2 8-12
second premolar 9-1 3 9- 1 3 9-13
Fig. 9.7. Girl aged 9.5 years - erupted permanent first molars and incisors
first molars 5-8 5-8 5-8
(fully formed roots), root resorption of deciduous molars and canines.
second molars 11-14 10- 1 4 1 0- 1 4
medial incisors 5-7 5-7 5-7
The second transitional period ( 11-13 years) is characterised by the replacement of lateral incisors 5-9 5-8 5-9
deciduous molars and canines with permanent premolars, canines, and eruption of se- � canines 9- 1 2 8-11 8-12
cond molars. In the maxilla, the eruption of the canine precedes the eruption of the first first premolars 8-12 8- 1 2 8- 1 2
premolar; in the mandible, the canine erupts before the first premolar (Fig. 9.8, 9.9). The second premolar 9-13 9- 1 3 9-13
timing of the eruption of permanent teeth in children in Poland is shown in Table 9.4. first molars 5-8 5-7 5-8
second molars 10- 1 3 I 0- 1 3 10- 1 3

The eruption of permanent teeth starts with the first molars (molar type of eruption)
or mandibular incisor teeth (incisor type of eruption). T hen appear the mandibular lateral
incisors, maxillary lateral incisors, maxillary first premolars, mandibular first premolars,
mandibular canine, maxillary second premolar, maxillary canines, mandibular second
premolars, mandibular second molars, and maxillary second molars. At around 1 6 years
of age, all erupted permanent teeth have fully formed roots (Fig. 9.9).
Fig. 9.8. Boy aged 1 1 years - erupted permanent teeth except for 25, 35
and 45, third molar budding.

Fig. 9.9. Boy aged 1 6 years - erupted permanent teeth except third molars, root development
Fig. 9.9. Boy aged 1 2 years - erupted permanent teeth except third molars, uncompleted root
of erupted teeth completed.
development of canines, premolars and second molars.

1 36 1 37
Compendium of Paediatric Dentistry

References
I . Avery JK. Oral Development and Histology. 3ed,Thieme, New York, 2011: 123-140. -
2. Boguszewska-Gutenbaum 1 -1 i wsp. The sequence of eruption of permanent teeth in Warsaw Chapter 10
children. New Stomatol 2013 4: 155. - 3 . Consolaro A. Shou ld deciduous teeth be preserved in
adult patients? How about stem cells? Is it reasonable to preserve them? Dental Press .I Orthod.
20 1 6;21 (2): 15-27. - 4. Gajdzik-Plutecka D et al. Timing of eruption of permanent teeth in War­
saw children. J Stoma 201 4; I , 67: 6-17. - 5 . Giovani PA, Salmon CR, Martins L, Paes Leme Physiological signs and pathological symptoms of teething.
AF, Rebou9as P et al. (2016) Secretome Profiling of Periodontal Ligament from Deciduous and
Permanent Teeth Reveals a Distinct Expression Pattern of Laminin Chains. PLOS ONE 11 (5):
Tooth eruption disorders
e0154957. https://doi.org/10.1371/journal.pone.0154957. - 6 . Haralabakis NB et al. Premature or
delayed exfoliation of deciduous teeth and root resorption and formation. Angle Orthod 1994; I : Dorota Olczak-Kowalczyk
151 -157. - 7. Harokopakis-Hajishengalis E. Physiologic root resorption in primary teeth: molecu­
lar and histological events. J Oral Science 2007; l : 1- 1 2 . - 8. Kim PH, SaLeslie B . l-1. M ultiple id­
iopathic resorption in the primary dentition: review of the literature and case report. Oral Surgery,
Oral M�dicine, Oral Pathology, Oral Radiology, and Endodontology 1999,88( 4): 501-505. - 9.
Jain P, Rathee M . Anatomy, Head and Neck, Tooth Eruption. [Updated 202 1 Jui 31]. I n: StatPearls
The process of tooth eruption is dependent on genetic and environmental factors, ac­
[Internet] . Treasure Island ( F L): StatPearls Publishing; 2022 Jan-. Available from: https://www.
ncbi.nlm.nih.gov/books/NB K549878/. ting locally or systemically (e.g. infectious, hormonal, metabolic). They can strengthen
l 0. Monteiro J et al. Pu Ipal status of human primary teeth with physiological root resorption. or weaken the functions of the various elements that condition the process. During the
l nt J PaediatrDent 2009; 9: 16-25. - 1 1 . Nasehi A, Mazhari F, Mohtasham N. Localized idio­
pathic root resorption in the primary dentition: review of the literature and a case report. Eur J teething period, there may be local and general symptoms that accompany the physio­
Dent 20 I 5;9 : 603-9. - 12. Net S et al. Recent perspectives vis-a-vis the biological basis of tooth logical process of eruption of teeth, as well as symptoms indicative of a disruption of
eruption. SADJ, 20 1 5,70(6):23 8-24 I . - 13. McNair A, Morris D. Managing the Developing Oc­ this process. Tooth eruption disorders can relate to the timing of tooth appearance in
cl usion A guide for dental practitioners. British Orthodontic Society 20 I 0. I S BN I 899297 08 I ;
https://www.bos.org.uk/Portals/O/Public/docs/Making%20a%20Referral/Managing-the-Devel­ the mouth (delayed or accelerated teething), the sequence of tooth appearance, the site
oping-Occulusion-Updated-Apr10.pdf. - 14. Popowics T, Boyd T, Hinderberger H . Eruptive and of tooth eruption (ectopic teeth) or manifest themselves as increased local or systemic
functional changes in periodontal ligament fibroblast orientation in CD44 wild type vs. knockout
mice. J Periodontal Res. 2014;49(3):3 5 5-362. doi: 1 0.1111/jre. 1 2113 . - 1 5 . Rabea AA. Recent
symptoms bccurring during teething.
advances in understanding theories of eruption (evidence-based review article). Future Dent J
2018;4(2): 189-196. - 1 6. Shimada A, Shibata T, Komatsu K . Relationship between the tooth Local and general symptoms accompanying teething
eruption and regional blood flow in angiotensin 11-induced hypertensive rats. Arch Oral Biol, 2004
( 49):427-433 . - 1 7. Wise GE, Zhao L, Grier RL. Localization and expression of CSF-1 receptor in
rat dental follicle cells. J Dent Res, 1997: 76(6): 1244-1249. - 18. Wise GE et al. Cellular, molec­ Symptoms occurring during tooth eruption may accompany physiological teething
ular and genetic determinants of tooth eruption. Crit Rev Oral Biol Med 2002;4:323-3 3 5 .
and may be indicative of local and general pathology. Local symptoms associated with
physiological eruption of deciduous teeth are inflammation of the gingiva around the
erupting tooth, bruising of the gingiva covering the tooth caused by extravasation of
blood from a vessel inj ured by the sharp edge of the erupting tooth (Fig. 10. 1), biting fin­
gers and objects, drooling (up to 18-24 months of age immaturity of the neuromuscular
control mechanisms of salivary swallowing), less commonly facial osculation.
General symptoms are: irritability, difficulty falling asleep, loss of appetite, runny
n ose (lasting less than 10 days), body temperature increased (< 38.5°C), diarrhoea and
vomiting less frequently (questionable relationship).

1 38
1 39
Compendium of Paediatric Dentistry Physiological signs and pathological symptoms of teething. Tooth eruption disorders

Various methods are used to eliminate teething symptoms. Massaging the gums can
be carried out with e.g. a clean finger, a microfibre thimble or a silicone finger pad, and
cleaning the gingival shafts can be carried out with e.g. a finger-wound swab moistened
w ith chamomile infusion, boiled water, a physiological salt solution or a tissue with
xylitol. Extruded teeth should be cleaned using a toothbrush (manual or sonic) and a
toothpaste containing 1000 ppm F, applied to the toothbrush in a minimum amount (not
Fig. I 0. 1 . Gingivitis around erupting tooth 52 ( left) and bruising mor e than a grain of rice).
of the gingiva over erupting tooth 54 (right).

Symptoms attributed to physiological teething are usually observed between four

Methods used to eliminate teething symptoms
days before and three days after the tooth appears in the mouth, in the so-called eight-
day eruption window. They more often accompany the eruption of incisor teeth in the Non-pharmacological: Pharmacological:

second six months of a child's life, i.e. at a time when the antibodies acquired from the - gum massage, - topical, e.g. gel,
mother disappear and are more intense when several teeth erupt at the same time. The oc­ - behavioural methods, - general (analgesics and
- chilled, solid chews (not fro- antipyretics: paracetamol
currence of general symptoms is related to the severity of gingivitis around the erupting
zen), I 0- 1 5 mg/kg b. w. or ibu­
tooth. An increase in inflammatory mediators in the mucosa around the erupting tooth - cleaning of gingiva and teeth, profen 5- 1 0 mg/ kg b.w.)
causes stimulation of nociceptors, which can cause discomfort and even pain. The oc­ - maintaining the dryness of the - consider overnight appli­
facial skin. cation.
currence of general symptoms during teething is associated with increased levels of in­
flammatory cytokines. Pathological symptoms at the time of tooth eruption are: eruption
cyst that may become suppurated, mechanical damage and infection of the gums caused
by inse1ting dirty fingers or objects into the mouth, increase in body temperature above It is not recommended to give the child hard or frozen objects due to the risk of me­
38.5 ° C. The eruption cyst is in the form of a soft, translucent exophytic lesion filled with chanical damage to the mucous membrane and choking, and liquid-filled chews, the use
blood or transparent fluid covering the crown of the erupting tooth (Fig. 1 0.2). It doesn't of topical agents containing belladonna (risk of seizures), benzocaine (risk of methemo­
occupy the bone. Its aetiology remains unknown. Most cysts disappear spontaneously, globinemia), lignocaine (overdose - risk of seizures, brain damage and cardiac arrest),
but if they become enlarged, surgical treatment involving decompression and exposure choline salicylate (risk of Reye's syndrome), sucrose, alcohol, parabens.
of the erupting tooth is indicated. The fever may be the result of local complications Physiological eruption of permanent teeth may be accompanied by local symptoms
related to the abnormal eruption, e.g. fusion of the erupting tooth cyst or general disease. similar to those occurring at the time of the first teething, as well as cough and runny
nose. Pathological local lesions are usually an erupting tooth cys_t and pericoronitis in­
flammation (Fig. 10.3, 1 0.4, 1 0.5). One cause of a cyst in an erupting permanent tooth
may be a lack ofresorption of the root of the deciduous tooth. Pericoronitis inflammation
is a bacterial inflammation of the soft tissues surrounding the crown ofa partially erupted
tooth, usually a mandibular third molar. It can be exacerbated by the accumulation of
food debris and tissue trauma caused by the opposing tooth.

Fig. I 0.2. Eruption cysts of the erupting deciduous tooth.

1 40 1 41
Compendium of Paediatric Dentistry Physiological signs and pathological symptoms of teething. Tooth eruption disorders

With regard to deciduous teeth, Szpringer-Nodzak distinguished the so-called teeth­

in g groups: premature - children with natal and neonatal teeth, early - children starting
te ething in 2-4 month of life, et term - in 5-8 months of age, delayed - at 9- 11 months
of age, late - 12 months of age and later.
Local factors of early eruption of individual teeth may be premature extractions of
Fig. I 0.3. Gingivitis around erupting permanent teeth. deciduous teeth (in the period up to one year before physiological exfoliation) if the
alveolar bone was destroyed as a result of the inflammatory process (Fig. 10.6). General
causes include genetic syndromes (e.g. Turner, adrenal-genital, fragile X chromosome
papillon-Lefevre, Sotos, Proteus), as well as many systemic diseases (e.g. congenital
hypertrophy of the adrenal cortex, hyperthyroidism, hypophosphatasia, histiocytosis X,
acute lymphocytic leukaemia, cyclic neutropenia).
Fig. I 0.4. Erupting cyst of an
erupting permanent premolar
associated with the presence
of a deciduous tooth root.

Fig. I 0.6 .. Early tooth eruption 44 and 45 associated with premature loss of deciduous teeth.
Fig. I 0.5. Periradicular soft tissue in­
flammation in the region of the erup­
ting mandibular second molar. Extreme examples of too early eruption are natal and neonatal teeth. A natal tooth
is a tooth that is present in the mouth at birth, while a neonatal tooth erupts in the first 30
days of a child's life. Prematurely erupted teeth are more common in girls than in boys
Disorders of the tooth eruption timing and are most often central incisors in the mandible (85%). Most of these are prematurely
erupted deciduous teeth (about 10% are supernumerary).
Tooth eruption timing disorder is the appearance of a tooth in the mouth at a time that Their crown may be fully formed or have smaller dimensions and an altered shape,
significantly deviates from the norm of tooth eruption times established for the population. such as conical. They are often discoloured, sometimes with underdevelopment of the
Disturbances concerning the timing of teeth can be caused by general or local factors. enamel. Due to the small degree of root formation, they can show great mobility. The
Early eruption is the appearance of the first deciduous tooth before the age of 5 aetiology of prematurely erupted teeth is not completely explained. Family history, shal­
months, and a permanent tooth before the age of 5 years. Delayed eruption is diagnosed low position of the tooth germ, hormonal disorders, infections with :fever, malnutrition,
when the first deciduous tooth appears at 12 months of age or later, and the first perma­ hypovitaminosis in the mother during pregnancy, prematurity, too low or too high birth
nent tooth appears after 8 years of age. The variability of eruption ± 6 months for deci­ weight of the child, cleft palate are mentioned as causes. They are one of the symptoms
duous teeth and ± 1 year for permanent teeth is within normal limits. Lack of eruption of of pachyonychia congenita, Ellis-van Creveld syndrome, Hal lermann-Streiff syndrome,
a single-image tooth for more than 6 months requires diagnosis. Pierre Robin syndrome and Sotos syndrome. Therapeutic management depends on their

142 143
Compendium of Paediatric Dentistry P hysiological signs and pathological symptoms of teething. Tooth eruption disorders

morphology, degree of root development and mobility and location. If there is little mo­
Examples of factors associated with delayed eruption of teeth
bility, it is preferable to leave the tooth. Extraction is considered for supernumerary
Local factors:
teeth, in cases of high mobility to prevent trauma (may cause Riga-Fede ulceration),
swallowing or aspiration, and teeth located on both sides of the cleft fissure in children mucosa I or bone barrier, gingival hyperplasia (e.g. fibromatosis), alveolar and
non-dental tumours, premature loss of deciduous tooth (> I year before phy­
with cleft l ip and palate (Fig. 1 0.7). After extraction, it is important to ensure that all root siological exfoliation), dental periradicular inflammation, delayed or lack of
remnants are removed, as leaving them behind is the reason for the later appearance of resorption of deciduous tooth root (Fig. I 0. 8), reinclusion, radiation damage,
supernumerary teeth, alveolar and palatal cleft, regional odontodysplasia, lack
abnormal tooth-like structures. The procedure is performed after the child is 2 weeks old,
of space in the arch, late development of the germ.
due to pre-existing jaundice and hypoprothrombinaemia.
Systemic factors:
systemic diseases: hypothyroidism, hypopituitarism, hypoparathyroidism,
rickets, osteosclerosis, anaemia, coeliac disease, cerebral palsy, kidney di­
\
sease, infectious diseases, e.g. mumps;
chronic pharmacotherapy: aspirin, paracetamol, ibuprofen, indomethacin, bis­
phosphonates (inhibit prostaglandin pathway and osteoclast activity), cytosta­
tic, drugs that cause gingival proliferation (cyclosporine A, calcium channel
blockers, antiepileptics);
chronic, long-term malnutrition (vitamin deficiencies, mainly D and C).
Fig. 1 0.7. N eonatal tooth Genetic factors:
with high mobility. Down syndrome, hyper lgE syndrome, Menkes disease (Fig. 10. 9), ectodermal
dysplasia, Ellis van Creveld syndrome, clavicle syndrome, mucopolysaccha­
ridosis, Gaucher disease, Gardner syndrome, congenital epidermolysis bullo­
Delayed tooth eruption can be caused by local, systemic or genetic factors. Delayed sa, amelogenesis imperfecta, osteogenesis-related dentinogenesis imperfecta,
eruption of teeth can also be an idiopathic disorder. Primary or idiopathic failure of erup­ dentin dysplasia, Gori in syndrome, H allermann-Streiff syndrome, Bloch-Sulz­
tion is referred to when teeth fail to erupt (completely or partially) despite the absence berger syndrome, Apert syndrome, Carpenter syndrome, cherubism and others.

of ankylosis and other causes, such as bone barriers. A primary defect in the eruptive
process associated with a mutation in the parathormone 1 receptor gene (PTH l R) is
thought to be the reason.

Fig. 10.9. A 3 .5-y ear-old boy with Men­

kes disease (curly hair disease) - de­
layed and eruption of maxillary teeth.

Depending on the aetiology of the delayed eruption of the tooth, therapeutic ma­
nagement may consist of surgical treatment (e.g. extraction, removal of obstructions,
exposure of the tooth), orthodontic treatment (traction, space creation and retention),
Fig. I 0.8. Girl aged 7 years - delayed eruption of tooth 1 1 due to delayed exfoliation of tooth 51.
treatment of systemic disease.

1 44 1 45
Compendium of Paediatric Dentistry Physiological signs and pathological symptoms of teething. Tooth eruption disorders

Tooth reinclusion consists in the gradual withdrawal of the tooth from the occlu­ orth odontic-surgical treatment or surgical extraction. Retention of the maxillary second
sive plane and sinking deep into the dental alveolus while maintaining the eruption of molar can cause tilting of the first molar and impede eruption of the premolar teeth and
adjacent teeth (Fig. l 0.10). Reinclusion is more common in the mandible, most often is therefore an indication for extraction.
affecting deciduous second molars, rarely permanent teeth.
The direct cause ofreinclusion is considered to be periodontal damage leading to the
fusion of the tooth with the bone - ankylosis, which results in inhibition of the replace­
ment of the deciduous tooth into a permanent one with further bone growth. Symptoms
of reinclusion are a lowering of the occlusal surface of the tooth in relation to neighbou­
ring teeth, lack of tooth mobility with root resorption visible on radiographs. Depending
on the degree of recessing of the tooth, reinclusion is distinguished:
A - partial:
A1 - lowering of the crown of a tooth to half the height of the crown of the adjacent
tooth,
A2 - reduction above half the crown height of the adjacent tooth,
B - complete - crown completely covered with mucous membrane, connected to the oral
cavity by a narrow canal.
Reincclusion can lead to:
Fig. I 0.10. Reinclusion of teeth 55, 64, 75 and 85.
disorders of the articulation of the permanent successor,
underdevelopment of the alveolar ridge,
inclination of adjacent teeth,
- extrusion of opposing teeth,
periodontal pathology in the area of the first permanent molars.
The method of treatment depends on the age and general condition of the child, the
speed of the cavity and the extent of the cavity and the presence of a permanent tooth
germ. In the presence of a permanent tooth germ, the most common treatment of choice
is removal of the deciduous tooth and orthodontic treatment (Fig. 10.11). I n the absence Fig. 1 0. 1 1 . Extraction of a re included tooth 64.

of a permanent successor, it is possible to perform the superstructure or extraction as part

of the orthodontic plan and in order to avoid later complications of the procedure. Disorders of the sequence of eruption of teeth
Tooth retention - partial or complete retention of the tooth in the bone -- affects more
often pe1manent teeth - most often the canines in the maxilla, third molars and second pre­ There are different patterns of tooth eruption sequences and a sequence different from
molars in the mandible, rarely deciduous teeth - usually the second molars of the maxilla. the most common in the population should not always be considered abnormal. A change
The cause may be lack of space due to crowding or premature loss of deciduous teeth, in the order of eruption combined with a disruption in the timing of eruption or an abnor­
abnormal position of the tooth germ. Retained teeth (impacted teeth) can give rise to mal position of the tooth in the arch may indicate the presence of a systemic abnormality.
tooth germ cysts. I n the absence of clinical symptoms, they are subjected to observation, Changes in the eruption sequence of permanent teeth are also a cause of malocclusion.

146 1 47
Compendium of Paediatric Dentistry Physiol ogical signs and pathological symptoms of teething. Tooth eruption disorders

Changing the location of tooth eruption i n fants. l tal J Dent Med 2017;2(2):45-5 4. - 1 5 . Shapira .f et al. Cytokine levels in gi ngival crevic­
ular flu id of erupting pri mary teeth correlated with systemic disturbances accompany ing teethi ng.
ped iatr Dent 2003;25 :44 1 -8 . - 1 6. Sobkowska -L et al. Symptoms of the Eruption of Permanent
The change in the location of tooth eruption may concern its position in the dental Teeth . lnt. J. Environ. Res. Public Health 2022, J 9, 330 I . https://doi.org/ I 0.3390/ijerph190633 01 .
arch (rotation of the tooth, tilting towards the vestibule, the proper oral cavity, mesially _ I 7 . Suri L, Gagari E , Vastardis H . Delayed tooth eruption: Pathogenesis, diagnosis, and treat­
ment. A l iterature reviews. Am J Orthodontics and Dentofacial Orthopedics, 2004: 126 (4):432-
or distally) or consist in the eruption of the tooth outside the arch (ectopia). It can be
445 . - 18. Szpringer-Nodzak M. Selected issues of the onset of first teething in chi ldren in the light
caused by a number of factors. These include shortening of the dental arch, parafunc­ of clini cal and experimental stud ies. Habilitation dissertation, Warsaw, 1979. - 19. Tsang AKL.
tions and dysfunctions, abnormal positioning of the germ, cleft alveolar ridge and palate, Teeth ing, teething pain and teething remedies. I nt Dent SA 2000; 12:48-6 1 .
20. US Food and Drug Administratio n. FDA drug safety communicatio n: Reports of a rare,
supernumerary teeth, missing or premature loss of a tooth, crowding of teeth, trauma. but serious and potentially fatal adverse effect with the use of over the counter (OTC) benzocaine
Ectopy is a tooth eruption outside the dental arch, e.g. in the maxillary sinus, on the gels and liquids applies to the gums or mouth. Available at: http:www.fda .gov/Drugs/DrugSafety/
hard palate, in the nasal cavity, in the eye socket. Permanent first molars are most com- ucm250024.htm. Accessed June I 0, 2011. - 21. U.S. Food and Drug Administratio n (2016). F DA
warn s against the use of horneopathic teething tablets and gels. https://www.fda.gov/NewsEv­
monly 'affected, more often in the maxilla than in the mandible, followed by maxillary ents/Newsroom/PressAnnouncements/ucm52346 8.htm. - 22. U.S. Food and Drug Administra­
canines, mandibular second premolar teeth and mandibular canines. Ectopy of first per­ tion. (2014). FDA recommends not using lidocaine to treat teething pain and requires new Boxed
Warning. Retrieved from http://www.fda.gov/Drugs/DrugSafety/ucm402240.htm. - 2 3 . Wake M
manent molars is usually accompanied by premature resorption of the distal root surface et al. Teeth ing and tooth eruption in infants: A cohort Study. Pediatrics 2000; 106: 1374-1379.
of the deciduous tooth, sometimes with pulp exposure. A distinction is made between - 24. William GD, Kirk EP, Wilson CJ et al. Salicylate intoxication from teething gel in infancy.
MJA . 2011; 1 94: 146-8. - 25 . Yaseen SM, Naik S, Uloopi KS. Ectopic eruption - A review and case
reversible ectopia, in which spontaneous correction of tooth eruption occurs, and irre­
report. Con temp Clin Dent. 2011 ;2( I ):3-7. doi: 10.4103/0976-237X.79289.
versible ectopia requiring treatment.

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I . AAPD, 2014 Guideline on I nfant Oral Health Care. http://www.aapd.org/media/policies_
guidelines/g_ infantoralhealthcare.pdf. - 2 . !spas RS et al. Teething signs and symptoms: persist­
ing m isconceptions among health professionals in New Zealand. N Z Dent J 20 1 3 ; 1: 2-5. - 3 .
Jaber L et al. Fever associated with teething. Arch D i s Child 1992;67: 23 3-234. - 4 . Mclntyre G ,
McIntyre G . Teething troubles? B r Dent J 2002; 192 :251-5. - 5 . Macknin M et al. Symptoms as­
sociated with infant teething: A prospective study. Pediatrics 2000;105:747-75 3 . - 6. M c Donald
R et al. Eruption of the teeth: Local, Systemic and congenital factors that i nfluence the process.
In Dentistry for the Child and Adolescent. Ed: Mc Donald R and Avery D. 9th, Mosby Elsevier
2011: 150-159 - 7. Macknin ML, P iedmonte M, Jacobs J et al. Symptoms associated with infant
teething: a prospective study. Pediatrics 2000;105:747-752. - 8. Massignan C, Cardoso M, Por­
poratti AL et al. Signs and Symptoms of Primary Tooth Eruption: A Meta-analysis. Pediatrics
2016; I 37(3):e2015350 I . - 9. M eixner l, Hag! B, Kroner C l . et al. Retained primary teeth in
STAT3 hyper-lgE syndrome: early intervention in childhood is essential. Orphanet J Rare Dis
2020;15, 244 https://doi.org/10.1186/s13023-020-01516-3 .
1 0. Olczak-Kowalczyk D et al. Selected issues related to the eruption of deciduous teeth.
N ew Stomata! 2011 ;2:73-76. - 11. Olczak-Kowalczyk D, Turska-Szybka A, Gozdowski D et al.
Longitudi nal study of symptoms associated with teething: Prevalence and mothers practices. Pe­
diatria Polska 2016; 91 (6):533-540. - 12. Olczak-Kowalczyk D et al. Clin ical manifestations in
the oral cavity in patients with hyper-lgE syndrome. Centr Eur J l mmunol 2013 ; 3 8 ( I ): 92-99.
- 13. Ramos Jorge J, Pordeus I, Ramos .forge M, Paiva S. Prospective longitudinal study of signs
and symptoms associated with pri mary tooth eruption. Pediatrics 201 1 ; 128:471-476. - 1 4. Rosu
S, Montanaro F, Rosu A et al. A randomised, open-label, parallel-group multicentre study on the
efficacy and tolerability of a non-medicated, patented gel for the relief of teething symptoms in

148 149
 Aetiology o f dental caries

PART III Aactcriul biofi l m Tooth c1rnmt!I

Caries disease sugar

difrusion aad dissociation II' • apalih'

.._ H,O - OU·

� I
'\.. c.2..
Chapter 11 ( .,__...nro.1·
........,.

Fig. 1 1 . 1 . Enamel demineralization caused by acids produced

Aetiology of dental caries by bacteria and remineralization associated with saliva function.

Dorota Olczak-Kowalczyk
According to Fejerskov and Manji 's theory, there are:
- factors directly involved in the development of caries (dental biofilm bacteria, tooth,
Dental caries is defined as a non-communicable, dynamic diet-modulated disease time, diet),
that develops with the involvement of a dental biof ilm, resulting in the loss of hard tooth - factors of the oral environment (e.g. amount, composition and buffering capacity of
tissue. The essence of the disease is the decalcification (demineralisation) of the hard saliva, presence of sugar, fluoride or antimicrobial agent),
tissues of the teeth due to a lowering of the pH by acids produced by bacteria on the - personal factors (e.g. educational level, health behaviour or economic level) (Fig. 11 .2).
tooth surface from the fermentation of carbohydrates (mainly lactic acid), followed by
the breakdown (disintegration) of the organic substances contained therein.
W hen the pH is reduced to critical values (for hydroxyapatite < 5.5, for fluorapatite
< 4.5), the liquid phase of the plaque and the saliva suffounding the enamel become
unsaturated in relation to the enamel minerals. This causes it to dissolve. The critical pH D outercircle
persists for a period of time but returns to physiological levels once the supply of sugars personal factors

is terminated. ■ centercircle
oral environment
Not every episode of pH reduction below 5.5 leads to a permanent loss of minerals.
factors directly
Saliva has the ability to buffer acids so that the pH returns to its output value. The plaque related to caries

phase and saliva surrounding the enamel go into a supersaturated state and lost minerals
are recovered by the enamel - enamel remineralisation (Fig. 1 l .1). As long as there is
a dynamic balance of the demineralisation-remineralisation system, mineral loss is com­
pensated for. These reactions occur at the ultrastructural level and are not clinically vi­ Fig. 11.2. Etiological model of caries according to Fejerskov and Manji.
sible. I f the equilibrium of the system is disrupted by a demineralisation enhancer, struc­
tural changes occur. The persistent advantage of demineralization over remineralization Dental biofilm, or plaque, is formed in several stages on the surface of the tooth, cre­
causes the progression of the lesion, which becomes clinically visible as the so-called a ting a structurally and functionally organized community of microorganisms. The next
spot lesion (white spot lesion), and then the loss of hard tissues of the tooth. stages of dental biofilm formation are:

150
151
Compendium of Paediatric Dentistry Aetiology of dental caries

dental pellicle formation - it is formed within seconds after mechanical cleaning of Dental caries is not an infectious disease, but a consequence of ecological changes
teeth; it consists mainly of proteins, glycoproteins, phosphoproteins and lipids de­ o f dental biofi lm. Oral environmental factors may promote or inhibit the formation of
rived from saliva and gum fluid and bacterial metabolites; it provides binding sites biofilm cariogenicity. The main items were:
for early bacterial colonizers, constitutes a barrier against acid diffusion, - sal iva - removal of food debris, bacteria and products of their metabolism, antimicro­
- microbial transport and reversible adhesion - bacteria are carried passively by saliva bial agents (immunological: antibodies of IgA, IgM, IgG class, and non-immunolo­
(only a few have the ability to move) and maintained by van der Waals forces be­ gical: enzymes, e.g. lysozyme, lactoferrin, salivary peroxidase and myeloperoxidase
tween membrane molecules and the bacterial cel l, system and other proteins), buffers: bicarbonate, phosphate, proteinate, ammonia and
- pioneer colonizers and irreversible attachment - specific bonds between bacteria l urea (bicarbonate buffer accounts for 80% of the capacity of stimulated saliva and
adhesins (initially S. sanguinis, S. oralis and S. mitis, then Actinomyces spp. and 50% - resting saliva, active at pH = 6. 1 -6.3, phosphate buffer at pH = 6.8-7.0, pro­
Neisseria spp.) and complementary receptors in the dental membrane; colony proli­ teinate buffer only at pH = 4.0-4.5); the amount of stimulated saliva secreted and the
feration and formation, calcium concentration in saliva in children is lower than in adults,
bacterial succession - colonizing species secondary to early colonizers (coaggrega­ - mechanical cleaning of teeth,
tion and coadhesion); metabolism of pioneering bacteria creates an environment for - probiotics, prebiotics and antimicrobial agents,
other bacteria, - nutrients, especially the presence and solubility of dietary sugar.
increase in biofilm - increasing microbiological diversity and greater thickness of The oral cavity of a person at bi1th is sterile, but after 8- 1 6 hours it is colonized by
the plaque, microorganisms passively transmitted from the mother and other people caring for the
maturation of the biofilm - slowing down growth, a matrix consisting of bacterial child, with milk and water. The first microorganisms colonizing the oral cavity (pio­
extracellular, soluble and insoluble glucans, fructans and heteropolymers is formed, neering) are aerobic and relatively anaerobic bacteria, mainly gram-positive cocci, in­
which is a biologically active structure (scaffolding maintaining the shape of the bio­ duding Streptococcus spp. (incl. S. salivarius, S. mitis, S. oralis). These bacteria form
film, water retention, nutrients and enzymes, inhibition of the penetration of unneces­ the environmental conditions necessary for the colonization of other microorganisms,
sary molecules, e.g. saliva antimicrobials), including gram-negative anaerobic bacteria such as Prevotella melaninogenica, Fuso­
bacterial detachment - some bacteria ( e.g. S. mutans) can actively detach and colo­ bacterium nucleatum and Veillonella spp. After tooth eruption or the appearance of an­
nize other places. other non-peeling surface ( e.g. acrylic obturator used in cleft palate), there is an increase
The composition of biofilms on different tooth surfaces varies, depending on local in S. mutans and S. sanguinis, fusiformis bacteria and black pigmented anaerobes. With
environmental conditions. Gram-positive microorganisms predominate in the fi ssures the age of the child, the diversity of oral microbes increases. At the same time, the baby's
and pits, mainly streptococci, Gram-positive bacilli rods predominate on the proximal microflora is becoming increasingly similar to that of its mothers. The greatest increase
surfaces, especially Actinomyces spp. M icroorganisms associated with caries in humans in diversity is seen between the ages of 6-24 months. The maturation of the oral micro­
are primarily acid-forming streptococci (especially S. mutans), lactobacillus spp. Acti­ flora is influenced by several factors, including the eruption of deciduous teeth (new
nomyces .spp., as well as the Bifidobacteria, Veil/one/la and Prevotella genus bacteria. niches for bacterial colonisation and adhesion) and a change in diet (increase in food
The mere presence of cariogenic bacteria in the biofilm is insufficient to cause the dis­ variety, introduction of solid foods). An important stage in the development of the oral
ease. Only the acidification of the biofilm caused by frequent consumption of sugars microflora is when the eight deciduous incisor teeth erupt. Once they have emerged,
promotes the dominance of S. mutans and acid-forming microbial species and the deve­ the composition and structure of the oral microflora remain relatively constant until the
lopment of a cariogenic biofilm. eruption of the remaining deciduous teeth is complete.

1 52 1 53
Compendium of Paediatric Dentistry Aetiology of dental caries

The age range in which a child's mouth is colonized by bacteria from the Streptoc oc­ The risk of developing caries associated with the tooth itself depends on the envi­
cus mutans group is referred to as the "infectious window". lt most commonly falls be­ ro nm ental conditions determining the cariogenicity and presence of dental biofilm, the
tween 19 and 31 months of age, with an average of 26 months. Colonisation may occur sensitivity of tooth tissues to bacterial acids, depending on the degree of mineralization
earlier. The presence of S. mutans .spp. and S. sobrinus was found even in 3-month-old of enamel and dentin.
infants in niches on the tongue. Most of the S. mu tans bacteria come from the mothe r The environmental conditions for individual teeth, individual tooth surfaces and even
of the child (71 % of the child-mother pairs were found to have genotypically identical different points on the same surface vary. They depend on many factors, including the
bacteria) less often than the father or other family members (vertical transmission) (Fig. shape of the dental arches, the position of the teeth in relation to the mouth of the salivary
11.3). Vertical transmission of cariogenic bacteria probably occurs at the level of the mi­ glands, the flow of saliva, the anatomy of the tooth and the presence of factors condu­
crobiome. An infant may inherit a microbial imbalance from a mother with dental caries, cive to the accumulation of dental biofilm, e.g. incorrect fillings, orthodontic appliances,
meaning that cariogenic bacteria will constitute the core microbiome in their mouth. tooth crowding or enamel hypoplasia. The places particularly at risk of developing caries
are grooves, pits and fissures as well as approximate surfaces.
Parents and other family members
The anatomical features of deciduous teeth conducive to the development of caries
Vertical transmission are: barrel-shaped crowns caused by the presence of thickening of the enamel, wide, flat
contact surfaces of molars (plaque retention).
The caries of immature permanent teeth is conducive to: deep grooves on the occlusal
surface, the presence of linear grooves (perikymata) on the surface of the enamel (plaque
Deciduous teeth �� Sibli ngs , cl ose colleague s accumulation).

Horiz
-,o-
n-ta
-1 transmission J The susceptibility of teeth to acids produced by bacteria depends on the degree of

-1'---_ _
mineralization of tooth tissues and their morphological maturity. A high susceptibility to
Permanent
teeth-�
1+4- --11 S. mu/ans l◄ sr o u ses_ e rs
rtn_
, p a_
____ _ _ _____,
acids and, at the same time, a rapid carious process in tooth tissue characterises decidu­
ous and permanent immature teeth.
'------

Fig. 1 1 . 3 . Routes of transmission of cariogenic bacteria to the child's oral cavity. In deciduous teeth, it is the result of high porosity and low degree of enamel mine­
ralization (the presence of incompletely mineralized prisms of enamel connected by an
Factors favouring the colonisation of the child's mouth by cariogenic bacteria are: interprismatic substance, the strips of Retzius, including the neonatal line).
habits that allow the transfer of the mother's saliva into the baby's mouth, In immature permanent teeth, the susceptibility to caries and the high dynamics of
- frequent consumption of sugars by the child, the pathological process in the tooth tissues are determined by: immaturity of the ena­
high levels of S. mutans bacteria in the mother's mouth, mel (low degree of mineralisation, few, small and contaminated hydroxyapatite crystals,
inadequate maternal oral hygiene, large amount of interprismatic substance, presence of a neonatal line in the enamel and
frequent consumption of carbohydrate snacks by the mother, dentin in the first molars), thin layer of dentin, mainly primary dentin (regularly distri­
low socio-economic status. buted, wide dentinal tubules, numerous interglobular spaces), presence of spiral Korff
The transmission of bacteria from child to child and between spouses is referred to as fibres running perpendicular to the enamel-dentin junction in the outer layer of the coro­
horizontal transmission. The first window closes after all the deciduous teeth have been nal dentin, the so-called "mantle dentin". The presence of spiral Korff fibres in the outer
erupted. For children whose oral cavity has not been colonised by cariogenic bacteria, layer of coronal dentin, the so-called mantle dentin (poorer mineralisation favouring the
this may occur during the second window of infectivity, beginning with the eruption of spread of demineralisation along the enamel-dentin interface).
permanent teeth between the ages of 6 and 12 years.

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Compendium of Paediatric Dentistry Aetiology of dental caries

The risk of developing caries is greatest during the first 2-4 years after a tooth erupts. meability of the biofilm to sugars, maintenance of a low pH deep within the biofilm,
After tooth eruption, both deciduous and per111anent, che111ical and physical changes protection of bacteria against antimicrobial agents and saliva buffers) and intracellular
occur in the outer layers o f the enamel, referred to as "post-eruptive 111aturation", as (energy reserve in the absence of sugars supplied with food). The more often sucrose is
a result of the exposure of the enamel to the oral environ111ent. The enamel becomes less co nsumed, the longer the pH remains below critical and is lower the higher the sucrose
porous (less permeable), harder and more resistant to acid de111ineralization. Freshly concentration. The neutralizing effect of saliva after ingestion of sucrose lasts about 40
erupted tooth's enamel contains carbonates (so-called "natural i111purities") responsible m in utes, and in the case of products containing starch (sticky, long-standing on the sur­
for its greater solubility. Carbon apatite dissolves at a pH of about 5. I n the process of face of the teeth) - up to 2 hours.
post-eruptive 111aturation, carbonate ions are converted into fluorine ions in the ena111el The main sources of sugars for children and adolescents are sweetened beverages and
apatites to form fluor hydroxyapatite, which may not dissolve even at a pH of about 4. sweets and confectionery. Cariogenic sugars contain many foods, e.g. pickles, ketchup,
As the fluoride content in the enamel increases and the carbonate content decreases, the . yoghurts and fruit cheeses, bread, breakfast cereals, etc.
enamel becomes less soluble for the acids. This is why the presence of fluoride in the oral Cariogenic biofilm formation is inhibited by proteins, especially milk proteins and
environment during development is so important. arginine, as well as polyphenols and fatty acids. Milk proteins inhibit the development
As time passes after a tooth erupts, the porosity of the enamel (responsible for per­ and adhesion of cariogenic streptococci to the acquired membrane, strengthen the acid
meability) also decreases and its hardness increases. A change in the hardness of the buffering capacity, reduce demineralization and enhance enamel remineralization. They
superficial layer of enamel is visible 2-3 years after the tooth appears in the mouth. It can cause the change of the cariogenic biofilm dominated by Streptococcus mutans and
take up to 10 years for the enamel to reach full hardness. S. sanguinis to less cariogenic, favouring the development of Actinomyces spp. The car­
Diet is essential in shaping the cariogenicity of dental biofilm by: cinogenicity of S. mutans biofilms inhibits egg albumin.
provision of nutrients, including non-milk external (free) sugars subject to bacterial Arginine is processed by the arginine deiminase pathway of some oral bacteria into
fermentation (glucose, fructose, sucrose, lactose) and processed starches and oligo­ citrulline, ornithine, CO2 , ATP, and ammonia. Ammonia causes an increase in cyto­
saccharides that are polymers of glucose (maltodextrins, glucose syrups), proteins, plasmic and environmental pH, which protects the bacteria from acid attack, provides
polyphenols, fatty acids, a source of energy (ATP) and enables the environment to maintain a relatively neutral
- cleaning of tooth surfaces, pH. Arginolytic activity is demonstrated by S. sanguinis, S. gordonii, S. parasanguis,
- stimulation of the salivary glands. S. mitis, S. oralis, S. rattus, some species of Lactobacillus and spirochetes. Arginine
The body's hydration, the type of food consumed, how and how often it is eaten, is contained in nuts, seeds (pumpkin, sunflower, sesame), dairy products, white meat,
the taste, smell, texture and retention of foods, and even the order in which each food is whole grains (oats, maize, buckwheat, brown rice). In addition to foods, supplements,
eaten are all important. also some toothpastes, are a source of arginine as a prebiotic.
The risk of the development of a cariogenic biofilm is increased by the frequent Polyphenols are a large group of chemical compounds with a diverse mechanism of
consumption of foods containing carbohydrates that undergo bacterial fermentation, the action. They can inhibit salivary amylase activity, growth of car,ogenic bacteria, acid
consumption of retentive and sticky foods, i.e. foods that remain on the tooth surface for production, bacterial glucosyltransferase activity and impair adherence of S. mutans bac­
a long time and foods that are eaten for a long time, such as sucking candies or lollipops. teria to tooth surfaces. They are present in fruits, vegetables, cereals, cocoa, tea, natural
Products containing starch (e.g. sponge cakes, crackers, crisps) are highly retentive. and cereal coffee, herbs and spices (coriander, oregano, dill, parsley, rosemary, licorice,
The most cariogenic sugar is sucrose which is not only a substrate for acid produc­ thy me, sage, cinnamon, cloves, nutmeg, ginger, turmeric and garlic).
tion by bacteria, but also a substrate for the synthesis of extracellular polysaccharides The mechanism involved in the antiproliferative effect of unsaturated fatty acids has
(adhesion of cariogenic bacteria, bacterial biofilm volume, structural integrity and per- n ot been thoroughly elucidated. They are believed to exhibit antimicrobial and bacte-

1 56 157
Compendium of Paediatric Dentistry Aetiology o f dental caries

riostatic activity ( confirmed action against S. mutans), inhibit the transport of nutrients 2 0 . Pitts, N et al. Dental caries. Nat Rev Dis Pri mers 3, 1 7030 (20 1 7). https://doi.org/ I 0.103 8/
through the bacterial cell membrane, reduce demineralization. Exposure of S. mutant nrd p.20 1 7 .30._ - 2 1 . Razmpoos h E et al. The Relationship of Nutrition Components and Lifestyle
biofilm to unsaturated free fatty acids, after treatment with sucrose, resulted in a decrease to Dental Canes: A Review Arti c le . .J N FS. 20 1 8 ; 3 (3) : 1 67- 1 74. - 22. Smullen J et al. The anti­
bacterial activity of plant extracts containing polyphenols against Streptococcus mutans. Caries
in its cariogenicity. Res: 2007;4 I :342-349. I 0. 1 1 59/000 I 0479 1 . - 23. Teng, F et al. Prediction of Early Chi l dhood
The hydration, taste, smell, texture of the food affects the function of the salivary Canes via Spatial-Temporal Variations of Oral M icrobiota. Cell Host Microbe 20 I 5 ; 18:296-306.
- 2 � - Xu l-1 et al. Maturation of the oral mi crobiota during primary tooth eruption: a longitudi nal,
glands. Saliva secretion is stimulated by elastic foods, rich in fibre, aromatic, e.g. raw prel1 111111ary study. J Oral Microbial. 2022; 1 4( I ):2051352. Published 2022 Mar 1 6. doi: I O. I 080/
fruits and vegetables, hard cheeses and food products rich in arginine. 2 0002297.2022.2051352. - 25 . Zero OT. Sugars - The Arch Criminal? Caries Res. 2004;38:277-
2 85 . - 26. Zheng X et al. Ecological Effect of Arginine on Oral Microbiota. Sci Rep 20 I 7;7:7206.
doi .org/ 1 0. 1 03 8/s4 I 598-017-07042-w.
References
1. Aimutis WR. Bioactive Properties of Milk Proteins with Particular Focus on Anticariogen­
esis, J Nutrition, Volume 1 34, Issue 4, April 2004, Pages 989S-995S. - 2. Amaechi BT, Tenuta ·
LMA; Ricomini F ilho AP, Cury JA. Protocols to Study Dental Caries In Vitro: M icrobial Caries
Models. Methods Mol B iol. 20 1 9;1922:357-368. doi: 1 0.1007/978-1-4939-90 1 2-2_32 . P M ID :
30838590. - 3. Berkowitz R.J. Mutans streptococci : acquisition and transm ission. Pediatr Dent.
2006; 28(2): 106-9. - 4. Caufield PW et al. Initial acquisition of mutans Streptococci by infants:
evidence for a discrete window of infectivity. J Dent Res 1 993; 1 : 3 7-45. - 5. Dzidic M et al. Oral
microbiome development during childhood: an ecological succession influenced by postnatal fac­
tors and associated with dental caries. I S M E J . 20 1 8; 1 2(9):2292-2306. - 6. Kennedy B et al. Oral
microbiota development in early childhood. Sci Rep. 20 1 9;9( I ): 19025. - 7. Lacruz RS et al. Den­
tal Enamel Formation and I mplications for Oral Health and Disease. Physiol Rev. 20 1 7 ;97(3):939-
993 . - 8. Li J et al. Anti-Caries Effect of Arginine-Containi ng Formulations in v ivo: A Systematic
Review and Meta-Analysis. Caries Res 2015;49:606-617. doi: 1 0.1 1 59/000435894. - 9. Lif H ol­
gerson P et al. A longitudinal study of the development of the saliva microbiome in infants 2 days
to 5 years compared to the m icrobiome in adolescents. Sci Rep. 2020 Jun 15 ; 10(1 ):9629. doi :
10.103 8/s4 I 598-020-66658-7.
I 0. Lynch RJ M. The primary and mixed dentition, post-eruptive enamel maturation and den­
tal caries: a review. I nternational Dental Journal. 20 1 3 ; 63(Suppl. 2):3-13. - 11. Machiulskiene
V et al. Terminology of Dental Caries and Dental Caries Management: Consensus Report of a
Workshop Organ ized by O RCA and Cariology Research Group of IADR. Caries Res 2020;54:7-
1 4. doi: 10. 1 1 59/000503309. - 12. Olczak-Kowalczyk D. (ed.) M onitoring the oral health status
of the Polish population 2016-2020. Assessment of oral health and its determinants in the Polish
population aged 5, 7 and 1 2 in 20 1 6. Editorial and Publishing Department of the Medical Univer­
sity of Warsaw, 20 1 7. ISBN: 978-83-763 7-4 1 6-1. - 1 3 . M itchell S.C. et al . Maternal transmission
of mutans Streptococci in severe-early childhood caries. Pediatr Dent.2009; 31 (3): 193-20 I . - 1 4.
Monse B et al. PUFA - an i ndex of clin ical consequences of untreated dental caries. Comm Dent
Oral Epidem iol 2010; 3 8 : 77-82. - 1 5 . Meyer F et al. Development, Properties, and B iomimet­
ic Preventive Agents. Dentistry Journal. 202 1 ; 9(8):88. https://doi .org/ I 0.3 390/dj9080088. - 1 6.
Nascimento M M . Potential Uses of Arginine in Dentistry. Adv Dent Res. 20 1 8 ;29( I ):98-103 .
doi : I O. I l 77/0022034517735294. - 1 7. Olczak-Kowalczyk D et al. Dental Caries Level and Sugar
Consumption in 1 2-Year-Old Chi ldren from Poland. Adv Clin Exp Med. 20 1 6, 25(3):545-550.
- 1 8. Olczak-Kowalczyk D et al. Food and dental caries. Part I . Milk and dairy products. New
Stomatol 20 1 7; 22( I ): 3 0-38. - 19. Olczak-Kowalczyk D et al. Food and dental caries. Part 2.
Foods containing polyphenols. New Stomatol 2017;2: 80-88 .

158 1 59
 Epidemiology of dental caries in developmental age

- the level of dental caries, when it is related to the entire study group, the level of
caries = (sum of DMF of all studied) : (number of examined).
Chapter 12 In 2000, Brathall introduced the important caries indicator SiC (Significant
Ca ries Index), which is the average of the OFT values for the respondents with the
h ighest number of teeth affected by caries.
Epidemiology o f dental caries in developmental age
SaC and SiC illustrate the polarity of humus in the population. Caries polarisation is
Dorota Olczak-Kowalczyk the much higher severity of dental caries in a small group of the study population at a
certain age compared to the rest of that population.
In Poland, the caries treatment index is also used. CTI = FT : (DT + FT). CTI values
ra nge from O to l (0 meaning that no tooth with a carious cavity has been filled, 1 mea­
Dehtal caries is one of the most prevalent chronic diseases in children and adoles­ ni ng that all cavities have been filled).
cents worldwide. According to the World Health Organisation, 60-90% of school-aged The indicators increasingly used in epidemiological studies are:
children and almost 100% of adults worldwide suffer from it. The prevalence of dental - pulp-ulcer-fistula-abscess index (PUFA), used to assess the effects of untreated caries,
caries, irrespective of the type of tooth (deciduous, permanent) in children and adoles­ where P/p means pulp involvement (the opening of the pulp chamber is visible or only
cents in Poland based on surveys conducted in 2016-2019 ranges from 4 1 . l % at age 3 to remaining roots or root fragments), U/u (ulceration) - traumatic soft tissue ulceration
98.2 per cent at age 18. (e.g. tongue, buccal mucosa) caused by sharp edges of the crown with pulpal involve­
The the incidence of caries is defined as frequency of caries, i.e. the percentage of ment or root fragments. F/f (fistula) - pus releasing sinus tract associated with a tooth
people with caries in the study population. Caries prevalence (%) = (number of people with pulpal involvement, A/a (abscess) - purulent swelling associated with tooth with
with caries : number of people examined) x 1 00. pulpal involvement; the PUFA/pufa value is the sum of deciduous or permanent teeth
The presence of caries is defined as the presence of a tooth with a carious cavity (D/d) meeting the criteria; for a group of individuals, the PUFA/pufa ratio is calculated to the
or lost due to caries ( M/m), or with a filling (F/f), i.e. DMF/dmf 2: 1. The capital letters number of teeth with untreated caries PUFA ratio: 100 x (PUFA + pufa : PT + pt),
refer to permanent teeth, the small ones to deciduous teeth. - the caries assessment spectrum and treatment index (CAST) covers the entire spec­
The severity of dental caries is assessed using the D MFT/dmft index (so-called tooth trum of caries - from the absence of caries lesion through protection against caries
index) or DMFS /dmfs (so-called surface index), which is the sum of the number of teeth using fissure sealants and treatment (filling) to caries lesions in enamel and dentin,
(T/t) or tooth surface (S/s) with the current caries lesion (P), removed due to caries (U) advanced stages of caries progression including pulp and periapical tissues; it does
and filled (W). W hen calculating the tooth index, a tooth that has a filling and a carious not take into account active and inactive caries lesions.
cavity on another surface qualifies as a tooth with caries. The maximum value of the
D MFT/dmfs index is the number of teeth, while the surface index is the number of sur­ Dental caries in Poland and worldwide
faces (for D MFT - 28, DMFS - 128). At present, there are no significant differences in caries prevalence and Level of se­
When studying population groups, the DMFT can be used to determine: verity of dental caries according to the sex of the respondents and the area of residence
- caries intensity / caries severity when it will be related only to people with caries (urban vs. rural). The highest prevalence of caries is found in people with low socioeco­
(i.e. showing individual D MFT values > 0), nomic status and low health awareness. The prevalence and level of of severity of dental
- Specific Affected Caries Index (SaC), SaC = (sum of DMF in people with DMF > 0) caries in the developmental age population in Poland based on epidemiological studies
: number of people examined with DMF > 0, car ried out in 2016-20 19 are shown in Figures 12.1, 12.2.

160 161
Compendium of Paediatric Dentistry Epidemiology of dental caries in developmental age

M1:-.cd cknt1tion Pcmuncnt dcnt1t1on

_ any carious lesion on the smooth surface of a tooth aged < 3 years, for children aged
100 93,2 3-5 years,
1 or more carious cavities, fillings or smooth surfaces of maxillary incisors lost due
90 R5.2
84
Rl.3
RO 76.7 74,9

to caries
68,1
70
[kc1duous (IJ,7
60 dentition
50
41.1
or
40
dmfs 2: 4 at 3 years of age,

I
30 26.2

20
10.3
_ dmfs 2: 5 at 4 years of age,
10

3 years 5 years
1 ,68
I
6 years 7 years 10 years 12 ycnrs 15 years 18 years
dmfs 2: 6 at 5 years of age.
Jmft > O (deciduous teeth caries) s-ECC in Poland affects one in five children aged 3 years and nearly half of children
■ OMFT > O (pcnnmcnt teeth dcntilion )

aged 5 years.
Fig. 12.1. Prevalence of dental caries in children and adolescents in Poland, There is a clear polarisation of carious disease in deciduous teeth, as evidenced by
based on epidemiological studies conducted in 2016-2019.
the large differences between the mean dmfs of children with S-ECC and the mean dmfs
Pcnmncnt dentition
of other children. At 5 years of age, it is 11 times larger. The prevalence of dental caries
Mixed dentition

6,5
in children aged 5 years in Poland and other European countries is shown in Fig. 12.3.

Poland (20 1 6) 76.7

Czcchia (201 1 ) 55.1

Latvi<1 (2000) 50,3

Wales (20 1 3 ) 41
3 years 5 years 6 years 7 years I O years I 2 years I 5 years 1 8 years
Nothem Ireland (20 1 3 ) 40

Greece (20 1 I ) 36,2

Fig. 12.2. Level of severity of dental caries in children and adolescents in Poland, based on epide­ Uernrnny (2014) 26,2
miological studies conducted in 2016-2019. England (20 1 5 ) 24,7

0 JO 20 30 40 50 60 70 80 90

Deciduous teeth Fig. 12. 3 . Prevalence of early childhood caries in children aged 5 years in European countries.
The prevalence of caries of deciduous teeth in 3-year-old children in Poland is around
40% and increases with age up to 84% at age 7. At the age of three, caries affects an ave­ Permanent teeth
rage of 1.85 teeth, at the age of seven it affects an average of 5 .47. The greatest increase Caries of permanent teeth appears within a short period of time after eruption (as
in caries prevalence and level of severity is observed between the age group 3 and 5 early as 5 years of age) and mainly affects the first molars. Over a period of 4 years
years (Fig. 12.1). (between the ages of 6 and 10), the incidence of permanent dental caries increases more
Carious disease of deciduous teeth occurring in children in the first six years of life than 6-fold. By the age of 12, an average of about three teeth are affected by caries. The
is referred to as early childhood caries ECC (Early Childhood Caries). ECC is defined as greatest increase in caries severity values for permanent teeth (almost 2-fold) occurs be­
the presence of 1 or more teeth with caries, extracted or filled due to caries in children tween the age groups of 12 and 15 years, which is associated with the eruption of second
aged 71 months (5 years and 11 months) or younger. Severe Early Childhood Caries molars. In a child aged 12, the number of permanent teeth affected by caries is close to
(ECC). Severe Early Childhood Caries (S-ECC) is diagnosed with: 3, at 15 it is 5, and in an 18-year-old it reaches 6.5.

1 62 163
Compendium of Paediatric Dentistry Epidemiology of dental caries in developmental age

There is a marked polarisation of caries in those with permanent dentition. In the case
of 12-year-old adolescents, the value of the SiC index reached 5.89 with the DMFT of tn:.11m.:11t u11k� for <kc1<luoust,;�th • Ln,�toi:111 inJc;,,; for 11cnmncnc h;cth (1.(,9
0,7

the entire study group at 2.84. The burden of caries disease varies in different countries

"' I I
around the world. In Eastern European countries it is higher than in Western Europe.
o.S2

Caries prevalence in children aged 12 years in Poland and other European countries is "' (1.37
U.-11

fl,\

shown in Figure 1 2.4.

""I
0.25
O..
:!.\
0.2

I
tl,2
0.15
0.13
0,1 (l.07

J ycu" 5 y.:ani 7 yc.trs t2 y,:; u�

Poland (2016/19) 74,9 6 >.:a11 10 yc;1rs 1 S ycars J 8 la1

Nothem Ireland (2013) 57

Fig. 1 2.5. Mean values of treatment indices for deciduous and permanent teeth in children
and adolescents in Poland, based on surveys conducted in 20 1 6-20 1 9.
Wales (20 I 3) 52

Portugal (2013) 47

Spain (20IO) 45

Switzerland (20 1 1 ) 37

Italy (2012) 35,8

England (2013) 32

Notherland (2002) 32 20

Finland (2009) 26,1

Denmark (2013) 22,3 %

Germany (2014) 18,7
• IOoth,:�ractioJn • cndodo111hk1rcal11,cnt

0 JO 20 30 40 50 60 70 80

Fig. 1 2.4. Caries prevalence in children aged 1 2 years in European countries. Fig. 1 2.6. Percentages of children and adolescents in Poland with a need for endodontic
treatment of pulp disease and tooth extraction, based on the 20 1 6-20 1 9 survey.

50 %
Meeting the dental treatment needs The Treatment Needs I ndex (TNI) values for 46,6
45
deciduous teeth indicate that treatment needs are definitely not being met (Fig. 1 2.5). 40

With regard to deciduous teeth, the percentage of meeting needs for restorative treatment 35 32,5
30
ranges from 7% in children aged 3 years to 31% at age 1 0 years. Almost 30 % of children 25
at the age of 7 years have a need for extraction of a deciduous tooth (Fig. 1 2.6). The per­ 20
14.2
centage of meeting treatment needs for permanent teeth are similar to the percentages of 15 1 3,3 1 3,3 1 2, 5
10
met treatment needs for caries of deciduous teeth during the mixed dentition period. It
is only during the permanent dentition period that they are higher, ranging from 41 % in
L1tvia (2000) Gcnnany Nothem Wales (20 1 3 ) Poland (20 1 6) Englancl
1 2-year-olds to 69% in 18-year-olds. The values of the treatment indices in children aged (20 1 1 ) Ireland (20 1 3) (201 5 )

5 and 1 2 from European countries are presented in Figures 1 2.7, 12.8. Fig. 1 2. 7. Val ue of treatment i ndices in children aged 5 years in European countries.

1 64 1 65
Compendium of Paediatric Dentistry

so

Ch apter 13
75 75
%
70
63.6
60
61.8
58,8
60
54,5
50 47.8
""
The carious process - clinical and radiological diagnosis
4 1 ,7 42,8
41
40

JO

20 Dorota Olczak-Kowalczyk, Anna Turska-Szybka,

10
Jo anna Szczepanska
PoL,nd Italy Wales England llungary Spain Norwcy Nothem France Portugal Dcmnark C-.cnnany
(2016/9) (2012) (2013) (2013) (2008) {20!0) (2004) Ireland (2006) (2013) (2014) (2014)
(2013)

Fi¥ . 12.8. Value of treatment indices in children aged 12 years from European countries. Types of dental caries, classification and diagnosis

References The carious lesion can be:

I . American Academy of Pediatric Dentistry. Policy on early childhood caries (ECC): classifi­ - non-cavities caries (early carious lesion, white opaque spot, white spot lesion) - the
cations, consequences, and preventive strategies. Pediatr Dent 20 1 7; 3 9:59-61. - 2. A nil S, Anand
PS. Early Childhood Caries: Prevalence, Risk F actors, and Prevention. Front Pediatr. 2017;5 : 157. result of demineralisation of the subsurface layer of enamel with a slightly altered
doi: l 0.33 89/fped.20 1 7.00157. - 3. Beneze Z, M ahrouseh N, Andrade CAS, Kovacs N, Varga 0. surface layer, the so-called carious spot lesion,
The Burden of Early Childhood Caries in Children under 5 Years Old in the European Union and
- cavity caries - the result of loss of hard tissue within the enamel and with carious
Associated Risk F actors: An Ecological Study. Nutrients 2021, 13, 455. https://doi.org/10. 3390/
nu 13020455. - 4. Bratthall D. Introducing the significant caries index together with a proposal lesions in the dentin.
for a new global oral health goal for 12-year-olds. lnt Dent J. 2000;50:378-3 84. - 5. Dimitrov A white spot is an opaque, chalky or white lesion with a hard, smooth or rough
E et al. Caries prevalence among 5-7-year-old children in northern Bulgaria. J of lMAB 20 1 7;
23 (3):1633-1636. - 6. Global B urden of Disease Collaborative N etwork: Institute for Health surface. It i_s characterised by an increase in the porosity of the enamel and a change in
M etrics and Evaluation ( l H M E). Global Health Data Exchange. Global B urden of Disease Study light scattering (the ratio of refractive index values for air and enamel is greater than for
2019 (GBD 2019) Results. Available online: http://ghdx.healthdata.org/gbd-resultspulpoctomy.
water and enamel). The greater the porosity of the enamel, the more visible the stain is
(accessed on 30 October 2020). - 7. Grund K et al. Clinical consequences of untreated dental
caries in German 5- and 8-year-olds. BMC Oral Health 2015,4; 15(1): 1 40. Lencova E et al. Early on visual examination. A stain visible on a damp surface is a more advanced lesion (more
childhood caries trends and surveillance shortcomings in the Czech Republic. B MC P ublic Health heavily demineralised) compared to a stain that only becomes visible after drying.
2012 Jui 24; 1 2:547 - 8. Olczak-Kowalczyk D. (ed.) Monitoring the oral health status of the Pol­
ish population 20 1 6-2020. Carious disease and periodontal tissue status of the Polish population.
An early carious lesion on the smooth surface is cone-shaped with the apex pointing
Summary of 201 6-20 1 9 research findings. Editorial and Publishing Department of the M edical towards the enamel-dental junction. On the occlusal ones, the caries is located on the
U niversity of Warsaw, 2021. - 9. Manse B et al. P U FA - an index of clinical consequences of lateral wall of the fissure and has a conical shape with the base facing the enamel-dental
untreated dental caries. Comm Dent Oral Epidemiol 2010; 3 8 : 77.
I 0. N ucca C et al. Prevalence and severity of dental caries in 6- and 12-year-old children in junction, making diagnosis difficult. It is accompanied by dentin changes that are a de­
Constanza District (urban Area), Romania. OHDMBSC 2009, 8: 1 9-24. - 11. Schill H et al. Dis­ fence reaction of the pulp. Starting with the enamel, there are hollow tubules, sclerotic
tribution and Polarization of Caries in Adolescent Populations. lnt J Environ Res Public Health.
(transparent) dentin, healthy dentin and reactive (defensive) dentin. At different depths,
2021; I 8(9):4878. doi: I 0.3390/ijerphl 8094878. - 12. Schmoeckel J et al. I ntroducing a specific
term to present caries experience in populations with low caries prevalence: Specific affected the enamel lesion shows varying degrees of enamel demineralisation. Does not contain
Caries I ndex (SaC) Caries Res. 20 1 9;53:527-53 1 . doi: 10.1159/000496932. - 13. Vadiakas G et bacteria. There are four layers:
al. Oral bealtb and periodontal status of 12- and 15- year-old Greek adolescents. A national path­
finder studies. Eur Arch Paediatr Dent 2012; 13 : 11-20. - surface - mineral loss of approximately 1 % and pore volume of 1 %,
- central - the largest part of the lesion with a loss of mineral substances of about
5-25% and a pore volume from 5% peripherally to 25% in the central part,

1 66 1 67
Compendium of Paediatric Dentistry TI1e carious process - clinical and radiological diagnosis

dark - pore volume of 2-4% with varying pore size (probably the result of multiple Ta b. 13. 1 . Cli nical signs indicating carious lesion activity.
demineralisation and reprecipitation processes), �
transparent - mineral loss of approximately I % and pore volume of l %. ICCMSTM
Signs of active lesions Signs of inactive lesions
caries stage
Progression of demineralisation and enamel detachment leads to macroscopicall y
�
visible tissue loss. In dentin, demineralisation occurs and spreads along the enamel-den ­
Enamel surface whitish or ye!-
tin junction, followed by collagen breakdown. In a cavity extending to dentin, the fol­ lowish, opaque with loss of gloss, enamel surface:
lowing layers are distinguished: decay, bacterial penetration and demineralisation and rough when gently probed; - whitish, brownish or black,
location - plaque retention region, - can be shiny, hard and smooth
sclerotic dentin. In the case of a dynamic carious process (e.g. in immature teeth), the i .e.: with gentle probing;
formation of reactive dentin and a sclerotic dentin layer may not occur. The layer of de­ I niti al and - in the entrance to pits and fissures on smooth surfaces, the carious
moderate - near the gingival margin, lesion is usually located some dis-
mineralization of dentin (slight decalcification) does not contain bacteria and is the lim it
- on contact surfaces below or above tance from the gingival margin;
of cavity preparation. In the total decay layer, dentin is an amorphous mass (a clump the point of contact; may not be covered by a thick layer
of bacteria, mainly Lactobacillus .spp. and broken tissue products) that can be easily can be covered with a thick layer of of plaque.
plaque.
removed with an excavator.
Dental caries is divided into:
soft or leathery den tin with gentle dentin shiny and hard when probed
primary, i.e. occurring on the previously healthy tooth surface, and those associated Advanced
probing gently
with restorations and sealants; caries-associated with restoration is also referred to as
secondary caries;
depending on the location: The international caries detection and assessment system (ICDAS II) takes into ac­
• pits and fissures, count the six stages of the caries lesion. It is based on a visual-tactile examination. Other
• smooth free surfaces (labial-buccal, palatal-lingual), methods used in the diagnosis of dental caries are described in Chapter 4. Codes and
• smooth surfaces bound - proximal (centripetal, distal); criteria for the clinical assessment of caries in pits and fissures according to ICDAS II are
depending on the activity of the course: presented in Table 13.2, and on smooth surfaces in Table 13.3. In addition to the unaided
• acute or wet, chronic or dry, eye, visual assessment uses devices that magnify the image directly (e.g. magnifying
• active or inactive (arested). glass) or indirectly (e.g. intraoral camera). VistaCamiX HD has interchangeable heads:
An active lesion is characterised by high dynamics of mineral displacement and the Cam (for magnified intraoral imaging) and Proof (uses infrared - makes it easier to lo­
likelihood of progression, arrest or regression. In an inactive lesion (retained caries), cate and assess the severity of carious lesions, plaque and calculus). The carious lesion
there is a slow displacement of mineral substance, which results in the lesion remaining is represented by a colour code, where green 0-1 .0 indicates healthy enamel, dark blue
at the same stage (Tab. 1 3.1). The active spot lesion is rough and chalky, while the inac­ 1.0-1.5 - shallow carious lesion in enamel, red 1.5-2.0 - deep caries in enamel, orange
tive spot is smooth, glossy and hard, sometimes discoloured by the penetration of dyes 2.0-2.5 - caries in dentin, yellow > 2.5 - deep caries in dentin.
through the micropores. In the diagnosis of proximal surfaces, it is advantageous to place an orthodontic se­
Within the dentin, an actively progressing carious process is evidenced by a light yellow/ parator in the interdental space for a few days (making the surface to be examined visi­
beige colour, a wet/humid surface, and ease ofremoval with a hand instrument. A lesion with ble), to use waxed dental floss (the floss becomes ragged or retained in a shallow cavity),
to examine radiographs and to perform transillumination.
less activity is darker in colour and drier and more difficult to remove with an excavator.
Inactive (arested) carious altered dentin is dark, d1y and does not yield to hand instruments.

1 68 1 69
Compendium of Paediatric Dentistry The carious process - clinical and radiological diagnosis

Tab. 13.2. Codes and criteria for detecting primary caries of the crown in pitts and fissures A pronounced defect with visible dentin and
according to the I CDAS I I system - clinical picture and VistaCamiX HD camera. overhangs of opaque or discoloured enamel,
after wetting, dark dentin is visible through the
Code Criteria Clinical picture enamel, after drying, a pronounced loss of tooth
5
structure at the entrance or within the cavity/slot
Clearly no dental caries, no change in enamel in the form of demineralization; the presence of
0 a defect in the dentin confirms the penetration of
translucency after 5 seconds of drying
the probe ball into the decay

Noticeable change in enamel limited to pits Extensive cavity with visible dentin on the
and fissures; opacity or discoloration of white walls and floor, loss of tooth structure in depth
6
or brown colour seen after prolonged air drying; and width extends to at least half of the tooth
change not seen on a wet surface surface, or possibly to the pulp

Tab. 13.3. Codes and criteria for the detection of primary coronal caries on smooth free, buccal
A clearly visible change in the enamel beyond
the pits and fissures, visible on a wet surface as an d lingual surfaces, medial and distal proximal surfaces according to I CDAS I I .
2
caries opacity (white spot) and/or brown disco­
Code Criteria Clinical picture
loration; the change is still visible after drying
The surface of the tooth without caries, without changes in
0
the translucency of the enamel after prolonged drying
Localized caries damage to the enamel with­
out dentin exposure or with below lying
darkening, visible on the wet surface as caries Noticeable change in enamel visible after prolonged air dry­
opacity (white spot) and/or brown discoloration ing as caries opacity of white or brown colour; not visible on
exceeding the pits and fissures after drying, vis­ wet surface
3
ible caries loss of tooth structure in the form of
demineralization (white opacity, brown or dark
brown walls), in case of doubt, probing the fur­
row/well causes the instrument to fall into the A pronounced change in the enamel visible on a wet surface
enamel defect as a caries cloudiness or discoloration upon direct viewing,
2 upon a change in the proximal surface seen from the occlusive
Dark shadow of stained dentin with or without direction, is visible as a shadow limited to the enamel on the
localized damage to the enamel, a change seen marginal edge
as a shadow of a discoloured dentin through a
clearly intact surface of the enamel that may not
Initial carious damage to the enamel without revealing den­
4 be or be damaged (loss of surface continuity
tin, after drying, a clearly visible loss ofenamel i ntegrity, when
that does not expose the dentin), visible better
3 the change is seen from the vestibular or lingual side, in case of
after wetting, a darkened area of grey, blue or
doubt, the loss of enamel integrity can be confirmed by gentle
brown colour shows the surface of the caries
surface probing
altered dentin

1 70 171
Compendium of Paediatric Dentistry The carious process - clinical and radiological diagnosis

ta ken using the paralleling technique. Radiological examination reveals carious lesions of
varying severity at the proximal surfaces. On the occlusal surfaces, it does not detect early
Dark shadow of discoloured dentin with or without localized stages of caries; it highlights more extensive lesions. Therefore, radiologically visible demin­
damage to the enamel, the decay appears as a shadow of disco­ eralising lesions should be eligible for surgical treatment. Regardless of the type of surface
loured dentin visible through a clearly intact marginal, vesti­
4 to be assessed, detection of early stages of caries on panoramic radiographs is difficult due to
bular or lingual wall of the enamel, better visible a fter wetting,
the darkened area is an inner shadow of grey, blue or brown the magnification of the image (by about 15 per cent relative to reality) and limited resolution.
colour According to the Manji scale, the following stages of caries disease are distinguished
in the radiological image:

E l - carious lesion covering < ½ of the enamel,

A pronounced defect with visible dentin and overhangs of
opaque or discoloured white or brown enamel, in case of doubt,
5
you can use a ball-ended probe to confirm the bottom of the E2 - carious lesion involving > ½ of the enamel,
defect in the dentin

D1 - carious lesion in dentin, limited to the

Extensive cavity with visible dentin on the walls and the outer ½ of dentin,
floor, significant loss of tooth structure in depth and width,
6
marginal edge may or may not be present, the defect covers at D2 - caries lesion in the middle ½ of the dentine,
least half of the tooth surface or pulp may occur

According to the consolidated ICDAS classification, the following are distinguished:

healthy enamel - ICDAS code 0,
incipient carious lesions - ICDAS code 1-2,
moderate carious lesions / intermediate caries - ICDAS code 3-4, D3 - carious lesion exceeding ½ of the inner dentine.
- advanced carious lesions / deep caries - ICDAS code 5-6.
Radiological examinations can be performed using the classic method (the radiation
An additional examination in the diagnosis of caries at the proximal and occlu­
detector is an X-ray film) or using digital systems (radiography, digital pantomography).
sal surfaces, which is the gold standard, is the radiological examination. With a loss
The use of digital systems makes it possible to reduce the radiation dose, immediately
of at least 20-30% of the mineral substance of the hard tooth tissue occurring in the obtain high-quality radiological images that can be processed (e.g. magnification, con­
course of the carious process, the permeability of the tissue to X-rays is increased, resul­ trast change, rotation, negative and positive acquisition, colour images, 3D imaging) and
ting in darkening. Conventional bite-wing X-rays are used, less often periapical X-rays archived.

1 72
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Compendium of Paediatric Dentistry 'TI1e carious process - clinical and radiological diagnosis

The combined interpretation of the visual-tactile and radiographic findings makes it Ta b . 1 3 .5. Criteria for the diagnosis of caries associated with fillings and fissure sealants.
possible to determine the severity of the carious lesion (Tab. 13.4). Code Symptoms Clinical picture

Tab. 13.4. Degrees of caries based on radiographic and visual examination according to the con­
solidated ICDAS * classification.

0 healthy tooth surface with filling or f issure sealant, healthy

Degrees of progression of caries in the radiological assessment
surface around filling/sealant margin
according to the consolidated ICDAS classification
(and depth of the area of translucency)

a small
lack of a small area moderate extensive
area of
translu- of translu- area of area of first visually discernible change in the enamel, after pro­
translu-
cency cency within translu- trans- longed drying visible as a white or brown opacity (invisible
cency
'· (no the enamel cency lucency
within the on moist surface)
caries) (El and E2) (D2) (D3)
dentin (Dl)

healthy absence of moderate, extensive,

initial initial
enamel caries medium deep pronounced change in the enamel/teeth at the filling/sea­
2 lant margin, opacity visible on the wet surface (more pro­
Degrees of moderate, extensive, nounced after drying)
initial initial initial initial
advancement medium deep
of caries in
visual exa- moderate, moderate, moderate, extensive,
ruination moderate moderate
medium medium medium deep

extensive, extens iv, extensive, extensive, extensive, extensive,

deep deep deep deep deep deep cavity < 0.5 mm with evidence of a code 2, cavity at fi l l ing/
3
clearance margin, opacity or discolouration

Caries associated with fillings and fissure sealants

The caries may be secondary caries or appear around the fissure sealant as a change
around the filling/sealant (caries spot, marginal fissure, tissue discoloration), edge dis­
coloration of the filling/sealant, loss of part or all of the filling/sealant. dental caries in enamel/dentin at the edge of the filling/fis­
sure sealant with translucency of dark colour of carious den­
Discolouration around composite fillings or around sealants is not always a symptom 4 tin, code 2 signs, translucency of discoloured den tin through
of developing caries. Diagnostic criteria for caries associated with fillings and fissure intact enamel or enamel with a slight decay not revealing
sealants are presented in Table 1 3.5. In the presence of enamel malformations, attrition, the dentin

abrasion and erosion, extrinsic and intrinsic discolouration in the caries assessment, the
surface is recognised as healthy.

1 74
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Compendium of Paediatric Dentistry The carious process - clinical and radiological diagnosis

Caries disease affecting deciduous teeth in children in the first six years of life (up to
th e age of 5 years and 11 months) is referred to as early childhood caries (see Chapter
1 2 ). Early childhood caries can be severe (S-ECC), which illustrates caries that is "aty­
cavity adjacent to the filling/fissure sealer, gap between fil­ pical ", "rapidly progressive", "acute", "spreading to the entire dentition".
ling/fissure sealer > 0.5 mm, dentin and signs of caries are In children under 3 years of age, caries affects the maxillary incisal teeth most often
discernible (as in code 4) or if the margins are not visible
5 - discontinuity at the filling/fissure sealant m argin and den­ 011 the labial surfaces, then the medial and occlusal surfaces of the molars. Mandibular
tin detectable when probing along the filling/fissure sealant molars are more prone to caries than maxillary teeth due to the anatomy of the occlusal
margin
surface and the depth of the fissures.
In deciduous teeth, caries lesions usually occur symmetrically on both sides of the
dental arch. In full deciduous teeth (after the eruption of the second molar tooth), caries
often appears on the distal surface of the first molar tooth (proximity of the teeth, flat
distal-proximal surfaces). On the medial surface of the second molar, the carious cavity
extensive cavity with visible dentin, the cavity is wide or appears later. Positioning the deciduous first molar and canine at a certain distance from
6 deep, with clearly visible dentin on the walls and bottom each other facilitates self-cleaning and prevents the development of caries. The surfaces
of deciduous teeth most commonly affected by caries are shown in Table 13.6.

T he carious process in deciduous teeth and immature permanent teeth

Tab. 1 3 .6. Surfaces of deciduous teeth of the mandible and maxilla most commonly affected by
caries.
The stages of caries development in deciduous teeth and immature permanent teeth
are the same as in adults. However, the disease process is more often acute than chronic Teeth Mandible Maxilla
compared to permanent mature teeth. The sooner a carious lesion appears after tooth
Second molars occlusal occlusal
eruption, the more dynamic the disease process.
Caries in the deciduous tooth is characterised by: First molars distal, chewing distal, occlusal

- greater advancement of the carious process compared to the clinical picture (Fig. 1 3 . 1 ), Canine tooth distal distal
poor symptomatology,
Lateral incisors medial medial
rapid transition from one carious stage to another (acute caries process),
- relatively rapid involvement of the pulp in the disease process. Medial incisors medial medial

The early appearance of carious lesions, i.e. within a shortperiod oftime after the erup­
tion of the tooth, is characterised by a rapid progression both in relation to the tooth and
the entire dentition. The disease attacks consecutive erupting teeth and can lead to dental
pulp diseases and destruction of the tooth crown and complete destruction of the deci­
duous dentition. The first lesions are located in the incisal teeth, mainly on the labial and
palatal surfaces, then on the occlusal first maxillary molars. The disease process covers
Fig. 1 3. 1 . Apparent small carious cavity on the occlusal surface of a deciduous first molar.

176 1 77
Compendium of Paediatric Dentistry The carious process - clinical and radiological diagnosis

other surfaces. In the past, milk dental caries occurring in children up to the age of 3 Tab . I 3 . 7 . Stages in the development of ECC occurring within a short time of tooth eruption with
pe rsi stent causative factors.
years was referred to as early caries praecox or suggesting the importance of the method
of feeding the child, as bottle caries, caries associated with feeding, caries associated
,---
Age
Stage Clinical picture Characteristics
(months)
with bottle feeding, caries associated with feeding the infant. The dynamics of the course � - white caries spot on a smooth surface in the
were indicated by the term flowering caries. It is now a severe form of ECC occurring initial reversible area of the tooth neck, sometimes on a pro-
1 0- 1 8
in children under three years of age. The early development of carious lesions in a child
I stage ximal surface,
- pain less
is associated with the early colonisation of the oral cavity by cariogenic microorganisms
- cavities in the maxillary incisal teeth,
linked to the frequent provision of sugars in the diet and lack of oral cleansing and ena­ damages carious - spread of the carious process in the dentin
1 8-24
mel defects. The earlier a child's oral cavity becomes colonised with cariogenic bacteria, [I
stage (yel lowish colour),
the greater the risk of ECC. - pain when eating cold foods
- caries also in molars,
In. addition to the generally accepted (Chapter 12), there are several classifications of
- often complaints of pain,
early childhood caries used in clinical practice. Depending on the severity of the disease - pulpopathies in the maxil lary i ncisal teeth,
and the clinical picture, three forms are distinguished: III deep lesion 24-36 - taking into account the time of eruption of the
teeth, the frequency and cariogenicity of the
I - mild to moderate form: diet, thi s stage can be reached in a period of
- single carious lesions are present in molars and/or incisors, 1 0- 1 4 months
- cause: combination of consumption of cariogenic products and hygiene negligence, - weakening of the tooth structure posing a risk
of fracture under low mechanical forces,
- the number of teeth with caries increases with persistent causes,
IV traumatic stage 36-48 - history of possible coronal fracture,
- usually affects children aged 2-5 years; - dental pulp diseases in molars,
II - moderate to severe form: - pulp necrosis of maxillary incisal teeth
- carious lesions occur on the labial and palatal surfaces of the maxillary incisors
with or without the inclusion of molars, depending on the child's age and stage of During the period of mixed dentition, the teeth most vulnerable to decay are the
the disease, first permanent molars, followed by the incisal maxillary teeth. The sites predisposed to
- mandibular incisal teeth are free of caries, disease in permanent teeth in children with mixed dentition are:
- the disease occurs within a short period of time after a tooth erupts, - pits and fissures on the occlusal surface of molars,
- often caused by factors related to inadequate breast- or bottle-feeding with or with- - fissures on the buccal surface of the mandibular molars,
out hygienic negligence, - fissures on the palatal surface of the maxillary molars,
- untreated passes into a severe form; - depressions on the palatal surfaces of the maxillary incisal teeth,
III - severe form: - medial proximal surface of molars,
- caries lesions affect almost all teeth, including the mandible teeth, - proximal surfaces of the maxillary incisal teeth.
- usually affects children aged 3-5 years. The appearance of carious lesions in permanent first molars is related both to their
In the case of S-ECC appearing in a short time after tooth eruption, with persistent ana tomical characteristics (fissures morphology) and their long eruption time (it can take
causative factors, the stages of disease development over time were distinguished 12-18 months from the appearance of pa1t of the tooth crown in the mouth to contact with
(Tab. 1 3.7). the opposing tooth) and, consequently, to the position of their occlusal surface below that
of th e second deciduous molar (difficult cleaning). The furrows on the occlusal surfaces

178 179
Compendium of Paediatric Dentistry 1l1e carious process - clinical and radiological diagnosis

can vary in shape, e.g. V ( 34%), U ( 1 4%), I ( 1 9%), [K (26%) and inverted Y (7%). The http://www.icdas.org. - 4. Ismail Al et al. The International Caries Classi ication and Manage­
f

shape of the furrows, especial ly the I, [K and inverted Y, and the great depth promote the ment System (ICCMS) An Example of a Caries Management Pathway. BMC Oral Health 2015;
retention of bacterial biofi lm, making cleaning by saliva and toothbrush d i fficult. doi I 0. 1 I 86/ 1 472-683 1 -15-S l -S9. - 5 . Kidd EA, Fejerskov 0. What constitutes dental caries?
Histopathology of carious enamel and dentin related to the action of cariogenic biofilms. J Dent
The caries process in immature permanent teeth i s usual ly characterized by an Res. 2004;83 Spee No C:C35-8. doi: I 0. 1 177/ 1 544059 1 040830 I s07. - 6. Kidd EA. How "clean"
acute cl inical course, greater advancement in dentin, compared to the clinical image - m ust a cavity be before restoration? Caries Res. 2004;38(3):3 05-13. - 7. Lynch RJ M . The primary
a nd mixed dentition, post-eruptive enamel maturation and dental caries: a review. Int Dent J 20 1 3 ·
the bottom of the lesion is located closer to the pulp chamber than in mature permanent 6 3 (Suppl 2): 3 - 1 3 . - 8. Martignon S et al. CariesCare practice guide: consensus on evidence int�
teeth (a thin layer of dentin, a l arge chamber: the lesion in relation to the enamel surface practice. B r Dent J. 20 l 9;227(5):353-3 62. - 9. Pitts NB, Ekstrand KR, I CDAS Foundation. Inter­
qualified as average is deep in relation to the pulp) (Fig. 1 3 .2). national Caries Detection and Assessment System ( ICDAS) and its International Caries Classifi­
cation and Management System (ICCMS) - methods for staging of the caries process and enabling
dentists to manage caries.Community Dent Oral Epidemiol 20 1 3 ; doi: I O. l l l l/cdoe. 1 2025.
I 0. �itts NB et al. From I CDAS to "CariesCare International": the 20-year journey building
international consensus to take caries evidence into clinical practice. Br Dent J. 2021 ;231 ( 12):769-
774. doi: 10. l 03 8/s4 l 4 l 5-02 I -3732-2. - I I . Policy on early childhood caries (ECC): classifica­
tions, consequences and preventive strategies. AAPD References Mannual 2015/ 1 6; 3 7: 50-2.
Policy on early childhood caries (ECC): unique challenges and treatment options. AAPD Refer­
ences Mannual 2015/ 1 6; 3 7 : 5 3-5. - 12. Psoter JW et al. Historical Evolution of Primary Denti­
tion Caries Pattern Definitions. Pediatr Dent. 2004;26:508-5 I I . - I 3. Shoaib L et al. Validity and
Fig. 13 .2. Seemingly small caries decay on the occlusal surface of the fi rst milk molar. reproducibility of l CDAS I I in primary teeth. Caries Res 2009; 43, 6: 442-7.

In permanent mature teeth, the acute course of caries is usually accompanied by

greater pain during cavity preparation ( absence or thin l ayer of reactive dentin, absence
or thin layer of sclerotic dentin closing dentinal tubules and impeding stimulus transmis­
sion). In decidous and permanent teeth with unfinished root development, the sensory
reactivity of the pulp is l ower. I n deciduous teeth, there is no subodontoblastic p lexus
and sensory fibres - myelin-free in the dentine tubules, and during the root resorption
period, there are additionally retrograde changes in the pulp. In permanent teeth, the
Rashkov p l exus does not devel op until after the root is formed.
During the early permanent dentition, i.e. after the second permanent molars have
appeared (according to Avery 1 1 .- 1 3 years of age), caries lesions also appear on the oc­
clusal surfaces of these teeth, less often in the premolar and incisive teeth of the max i l l a,
then in the premolar teeth of the mandible.

References
I . Anil S, Anand PS. Early Childhood Caries: Prevalence, Risk Factors, and Prevention. Front
Pediatr 20 1 7; 5: 157; doi: I 0.3389/fped.20 1 7.00 I 5 7. - 2. Fejerskov, 0 et al. Pathology of dental
caries' Dental caries: the disease and its clinical management. Vol. 2. Oxford, U K: Blackwell
M unksgaard, 2008. 20-48. - 3. I nternational Caries Detection and Assessment System ( ICDAS)
Coordinating Committee. Rationale and Evidence for the International Caries Detection and As­
sessment System ( ICDAS I I) Scotland: Dental Health Services Research Unit; 2005. Access :

1 80
181
 General principles of caries management in children and adolescents

pen tal caries risk assessment

Chapter 14
Caries risk is the probability of developing carious lesions in the near future and the
General principles of caries management probability of progression of existing lesions. The caries risk assessment brings infor­
in children and adolescents m ation about the patient's caries disease activity and causes. It involves determining the
presence and strength of factors influencing the relationship between demineralisation
Dorota Olczak-Kowalczyk and remineralisation (risk factors, protective factors) and prognostic factors (caries indi­
ca tors) (Fig. 14.2). Caries risk assessment allows the causes of caries in a patient to be
diagnosed, discussed and measures planned to eliminate them and thus reduce the risk
The essence of caries management, irrespective of the patient's age, is the preser­
level (personalised dentistry). Caries risk assessments should be carried out regularly
vation of tooth function, vitality and structure using the principles of minimally inter-
d uring follow-up visits. The frequency of visits depends on its level. Follow-up visits for
ventio�al dentistry, i.e. the extensive use of non-invasive methods in the treatment of
a child with a low caries risk should take place every 6-12 months (adults 6-24 months),
non-carious lesions, adherence to the principle of minimal invasion in surgical treatment,
with a high one every 3-6 months regardless of the patient's age.
prevention of the appearance of new carious lesions and prevention of the development
of existing lesions. According to the recommendations of the Management. Internation­
al Caries Classification and Management System (ICCMSTM), caries treatment should
CARIES IUSK FACIORS
be cyclical, and each cycle should take into account the stages enabling the develop­ "BAD"

.. ._.
.. . .....
... .
• bacteria
ment and implementation of an individual treatment plan, i.e. in accordance with the CARD INDICE'I • xcrostomia
" WIIEC" • Incorrect health
patient's needs (Fig. 1 4. 1). The main elements of the cycle are history, classification,

-----
behAliours
• IIIIJl&l < l ye.-.
decision-making, preventive and therapeutic management. The simplified algorithm of • dtllllD CftCIH

the procedure, the so-called 4D cycle according to Caries Care I nternational (CCI™)
WITHOUT CARIES DESEASE
developed on the basis of ICCMS™ , is shown in Figure 14.1. CARIES DEVELOPMENT

Fig. 1 4.2. Factors shaping the level ofrisk according to Featherstone's

concept of balance between demineralisation and remineralisation.
2. D
Dctcctiand asses
lesions Determining the level of caries risk requires an assessment of socioeconomic factors,
general health status, health behaviour (hygiene behaviour, diet, etc.), previous use of
3. D
4D cycle according Decide a
dental care and a clinical examination of the oral cavity (hygiene and gingival status,
to CariesCarc
International
persooaliscdcarc presence of plague and factors favouring plague accumulation, dental status, saliva se­
plan
cretion).
The general medical history should establish whether there are disease-related or
treatment-related factors that increase the risk of caries, e.g. chronic general diseases,
infections, current or past therapies and medications, type and degree of physical or
intellectual disability. Certain diseases or therapeutic approaches:
Fig. 1 4. 1 . Simpl ified algorithm, the so-called 4D cycle accord ing to CariesCare International .

1 82 1 83
 G eneral principles of caries management in children and adolescents
Compendium of Paediatric Dentistry

reduce secretion and alter the physio-chemical parameters of saliva, ro us fillings and active caries indicates the high abundance of cariogenic bacteria in her
cause a decrease in pH (acid reaction of drugs, e.g. �2-sympathomimetics inhalation, 111outh and the risk of their early transmission to the child's oral cavity. Low economic
vomiting caused by disease, e.g. bulimia, or drugs, e.g. cancer chemotherapy, gas­ status and the low level of education of the child's parents are also risk factors for caries.
tro-oesophageal reflux), Properly selected indicators should be used in the clinical evaluation, which allows
f
avour the supply of substrate for bacteria (sucrose content of syrups given to children, their change over time to be assessed (see Chapter 4). There are many tools to help assess
the risk of dental caries, e.g. the Cariogram system, CAMBRA and ICCMS, CCI . Infor­
™
therapeutic high-carbohydrate diets, dietary errors made in conditions with loss of appetite),
favour the presence of plaque through impaired self-cleaning mechanisms (diseases mation on the type of instrument used should be included in the patient's medical record.
with muscular weakness and xerostomia) or difficulties in performing hygiene proce­ The CAMBRA (Caries Management By Risk Assessment) is recommended by the
dures (e.g. neurological diseases, psychiatric illnesses, physical disabilities), A merican Academy of Pediatric Dentistry for caries risk assessment and for infants,
increase the susceptibility of tooth tissue to bacterial acids (diseases during odonto- children and adolescents (CRA) (Tab. 1 4.2, 14.3).
geriesis causing enamel hypomineralisation).
Tab. 1 4.2. Caries risk indicators for children aged 0-5 years i n the CAMB RA system.

E xamples of causes of salivary disorders Medium

Indicators High risk Protective
in children and adolescents according to Walsh risk
Negative fluid balance - insufficient fluid intake or their loss (sports Biological factors
effort, fever, diarrhoea, e.g. Crohn's disease, food allergies), caffe ine

•
consumption, type I diabetes, haemodialysis i n kidney failure, eating Mother/primary caregiver has active dental caries YES
disorders (anorexia) Parent/caregiver has life-time of poverty, low
Side effect of drugs - hypotensive, diuretic, anti-asthmatic and anti­ health literacy
histamines (e.g. used in allergic rhinitis), anti-anxiety, bronchodilators > 3 per day snacks containing sugar or sugary
(�2-sympathomimetics), anti-cancer cytostatics drinks
General diseases - allergic diseases (urticaria, atopic dermatitis), H I V Child uses bottle or non-spi l l cup containing natu-
infection, cGV H D, microcytic anaemia, defi ciency o f iron and B vita­ ral or added sugar frequently, between meals and/ YES
mins, autoimmune diseases, hyperthyroidism, radiotherapy in the head or at bedtime
and neck area, ectodermal dysplasia, puberty disorders
Special health care needs YES
Other - oligodontics, salivary gland diseases (bacterial and viral in­
A recent immigrant YES
fl ammation, calculus, mucosa! cyst, benign and mal ignant tumours, sa­
l ivary gland agenesis), after neurosurgical procedures resulting in da­ Protective factors
mage to the sympathetic and parasympathetic system, genetic diseases Optimal endogenous exposure to fluoride (water,
YES
(Prader-Willi syndrome, syndrome 3A) supplements)
Daily use of fluoride toothpaste Y ES
In children with deciduous teeth, it is also important to collect information about Topical fl uoride from health professional YES
possible diseases, the mother's medications and habits during pregnancy, the course of
Regular dental visits, appropriate home care YES
childbirth (caesarean section - natural birth) and the condition of the newborn (birth
Dental examination
weight, number of points on the Apgar scale) and the method of feeding the child. The dmft > I Y ES
risk of caries of deciduous teeth is higher in babies born by caesarean section, born pre­ Noncavitated (incipient/white spot) active spots or
YES
maturely, with low birth weight and breast- or bottle-fed immediately before bedtime dental enamel defects -- -
1-1 igh levels of Streptococcus mu/ans YES
and at night after the age of 1 2 months without the teeth being cleaned of food debris.
Visible plaque on teeth YES
An assessment of the mother's dental status is also essential, as the presence of 1rnme-

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Compendium of Paediatric Dentistry General principles of caries management in children and adolescents

Tab. 14. 3 . Caries risk indicators for children aged 2'. 6 years and adults in CAMBRA. In the CariesCare International (CCI™) system (Tab. 1 4.4) caries risk is assessed in
Medium tw o stages:
Indicators High risk Protective
risk _ low - recognised at:
Biological factors • the presence of caries-protective factors,
Low socio-economic status • the absence of the risk factors highlighted in red area, present, any other risk factors
During the day > 3 snacks with sugar or sweet
are within a "safe" ranges (e.g. sweet snacks, oral hygiene, fluoride exposure),
drinks
Special health care needs YES _ high, which is recognised in three situations:
• the presence of at least one of the risk factors highlighted in red,
A recent immigrant YES
• a combination of other risk factors suggesting a higher level of risk,
Protective factors
• lack of caries protective factors.
Consumption of optimally fluoridated drinking water YES
In assessing the level of caries risk, it is useful to use commercial tests that allow:
Daily tooth brushing with fluoridated toothpaste YES
- evaluation of saliva secretion (rate of wetting of the lower lip mucosa, amount of sali­
Topical fluoride from health professional (fluoride
YES va secreted after stimulation measured over 5 minutes), its physico-chemical proper­
varnishes, gels)
Home application of preventive measures (xylitol, ties including consistency, pH of resting saliva and buffering capacity (Saliva-Check
YES
M l pastes, antibacterial agents) Buffer test, CRT B uffer and Dentobuff® Strip tests),
Regular visits to the dental office, hygiene proce­ - bacteriological tests requiring bacterial culture for 48 hours (Dentocult® SM Strip
YES
dures at home
Mutans test, Dentocult® LB test, CRT Bacteria test) or based on molecular methods
Dental examination
giving a result within 1 5 minutes (Saliva-Check Mutans test).
2'. 1 interproximal carious lesion
The high risk of caries is evidenced by the level of S. mutans CFU/ml of saliva > 1 05 •
Active white spots on smooth surfaces or enamel The abundance of Lactobacillus spp. reflects the carbohydrate intake of the subject in
defects
the last few weeks.
Apparent reduction in salivary secretion

Defective fillings YES Tab. 14.4. CariesCare I nternational (CCI™) caries risk indicators.
use of fluoride toothpaste min. 1000 ppm twice a day
Orthodontic appliances, prosthetic restorations YES
regular preventive dental visits, including for example appli-
Protective factors cation of topical fluoride
In the CRA system, a patient's caries risk level is assessed as: endogenous fluoridation (where justified)
low - in the absence of any high-risk factor and the presence of risk factors within Hyposal i vation, either drug-, disease-,
"safe" ranges, h ead/neck-radiation or/and age-induced**
moderate - there is no definite low risk or clearly high risk of developing new or Commitment and high intake of free sugars in the form of snacks, drinks, etc.
Risk level of aware- low socioeconomic level, low health literacy, health access
progression of existing caries lesions,
factors ness and medical barriers
high - the presence of any of the high-risk factors or very high caries intensity in ca­ factors inability to comply, low motivation and engagement
rers, or the presence of several lower-risk factors that form a combination likely to lead special health care needs, physical disabilities
to a high-risk level (the number and level of these factors vary according to geogra­ symptomatic-driven dental attendance
phical location and socio-economic conditions).

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Compendium of Paediatric Dentistry General principles of caries management in children and adolescents

active carious lesions or ne,, fillings* *

Signs of carious disease visible on the cleaned, moist tooth surface
prs/PRS indicator (p/P - pulp exposure, r/R - coronal
destruction, s/S - pus-releasing tract/tooth-related pus
Dental containing swelling) NO drying
examination
poor oral hygiene with thick plaque accumulation and reassessment
plaque stagnation areas (higher biofilm retention) cav ity with visible dentine
Risk low salivary flow rate
factors mother/caregiver with active caries lesions
YES
bottle/non-spill cup/pacifier containing natural or added sugar
used frequently or at night (this includes milk and fruit j uices/
Additionally for smoothies) sunsurface shadow
children
\ irregular use of toothpastes with a fluoride content of min.
1000 ppm
Y ES �► drying and reassessment
eruptiing of molars
* Jn t/Je risk assessment, co-occurringfactors favouring plaque accumulation should be assessed,
e.g. braces, enamel malformations. visible micro-cavitation
(discontinuity of the enamel)
** Risk factors hig/Jlighted in red are always t/Je basis for a diagnosis oj"/Jigh caries risk.

Y ES � opacity/discolouration
Dental assessment of the enamel

The next stage of the diagnostic procedure is to assess the presence, activity and
progression of carious lesions (see Chapter 13), the effects of caries (number of fillings
and their condition, number of teeth extracted due to caries, symptoms of dental pulp ICDAS 5-6 ICDAS 4 ICDAS 3 ICDAS 1 -2 ICDAS 0
(extensive caries lesion)
diseases and periapical infections) and diagnostics to differentiate carious lesions from (moderate caries lesion) (initial caries lesion) (sound, no caries)

other pathologies, e.g. lesions of tooth erosion and malformations.

Fig. 1 4.3. A lgorithm for the clinical assessment of carious lesions proposed by
A clinical assessment of the condition of the dentition is made after cleaning the the CariesCare International (CCI™) system.
teeth. In the first stage, wet surfaces are assessed, in the second, dried surfaces (Fig.
14.3). The examination should be complemented by a radiological assessment (Chapter
Treatment planning
1 2, Tab. 13.5).
The determined level of caries risk and the assessment of the patient's dental con­
dition allows decisions to be made regarding management, i.e. the development of an
indi vidual treatment plan and discussion with the patient. This plan should include:
actions concerning both the patient and the tooth,
- elimination of pain,
- stabilisation phase, final tissue reconstruction phase and follow-up visits (Fig. 14.4),
- prevention and treatment methods, the type of measures and materials to be used.

188
189
Compendium of Paediatric Dentistry General principles of caries management in children and adolescents

DIAGNOSIS: In paediatric dentistry, there are many factors that further influence the dental treat­
IDENTIFICATION ment, i.e. the order in which individual teeth are treated, the choice of treatment method,
risk assessment, diagnosis, progno-
sis, management plan the agents and materials used. These include:
�� _ type of dentition (deciduous/mixed/permanent),
_ reason for visit (asymptomatic/symptomatic visit),
FOLLOW-UP VISITS STABILIZATION = lowering the risk - age of the child:
interview - examination - consultation
and stopping caries • the time that has elapsed since the tooth erupted (tissue maturity),
regarding caries: susceptibility, new caries home and professional prophylaxis • the time left to exfoliate a deciduous tooth,
lesions, state of lesions treated with non-operative treatment methods, Interim
non-operative methods and state
Therapeutic Restoration (ITR) _ the child's general state of health,
education and motivation, instruction
offil l ings - the child's dental attitude (cooperation),
- the dental attitude of the parent,
- financial capacity.
FINAL In the case of a child presenting with pain, the priority is to eliminate the pain.
TISSUE RECONSTRUCTION "' Taking into account the child's age and type of dentition, the treatment plan should include:
- during the period of deciduous teeth - start treatment with the teeth that are imp01iant
Fig. 1 4.4. Algorithm for the management of carious disease.
for maintaining correct bite conditions, i.e. the second molars,
- in the mixed dentition, priority is given to the caries prevention and the treatment of
Reducing the level of caries risk requires reducing the impact of bacteria and sup­ permanent teeth; the exception is when there is pain in the deciduous tooth, or the
porting remineralisation. In the case of high caries risk, behavioural changes with regard depth of the cavity threatens to expose the pulp and cause complications.
to oral health are necessary, including brushing twice a day with a fluoride toothpaste When carious lesions are present, it is important to stop carious activity of as many
appropriate to the patient's age and caries risk, without rinsing the mouth after brushing, lesions as possible in the short-term using non-invasive treatment methods and tempo­
the use of fluoride mouthwashes, dietary changes (limiting the amount and frequency of rary cavity fillings.
sugar consumption and introducing sugar substitutes and tooth-protective products), the For uncooperative children, or children with disability, with multiple carious cavities
use of agents that raise the pH in the mouth and provide minerals for ongoing enamel in whom behavioural methods to shape their behaviour have been unsuccessful, treat­
repair (e.g. containing arginine, CPP-ACP), treatment of hyposalivation if necessary, ment under inhalation sedation or general anaesthesia should be considered.
regular dental check-ups. Methods and measures should be selected according to the Minimally interventional dentistry distinguishes between non-invasive/non-opera­
individual patient's needs and age. tive and invasive tooth-preserving operative care.
At the dental office, the patient and his or her parents should receive thorough instruc­ In dental management, it is important to follow the rules:
tions on home prevention and be motivated to change health behaviour. Professional - minimising dental discomfort, pain and anxiety,
treatments to reduce the risk of caries are: professional tooth cleaning, sealing of ana­ - caries prevention,
tomical pits and fissures, use of antimicrobial agents (e.g. povidone iodine), elimination - saving tooth tissue (use of non-invasive or minimally invasive surgical methods,
of active carious lesions (e.g. ITR, impregnation), use of agents containing high con­ repair of fillings),
centrations of fluoride (varnishes, gels every 3 months). The various methods of caries - taking care of the tightness of the completed restoration of lost tissue,
prevention and applied in the treatment of cavitated and non-cavitated caries in children - preserving the vitality of the pulp.
and adolescents are presented in Chapters 1 5, 16.

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Compendium of Paediatric Dentistry General principles of caries management in children and adolescents

Treatment methods for caries in immature deciduous and permanent teeth and the
DEEP CARIES SURFACE CARIES,
medications and materials used are shown in Table 1 4.5. The treatment modalities de­ internal ½ or ¼ dentine MODERATE CARIES
pending on the depth of the cavity and the type of dentition are shown in Figures 14.5 (risk of pulp exposure) does not reach ½ or ¼ of the internal dentin
and 14.6. In cavity caries treated with surgical methods, the priority for medium an d
superficial cavities should be on the longevity of the filling, and for deep cavities on the
i l
Selective caries removal Selective caries removal
protection of the pulp. to "soft" dentine to "firm" dentine

Tab. 1 4.5 Basic methods of treating caries in deciduous teeth and immature permanent teeth.
i A RT
non-operative methods
Deciduous Teeth Two-stage treatment sealing
Treatment method Materials (non-cavitated caries)
teeth permanent A RT

fl uoride agents, calcium-phosphate

Reh{ineralization + + containing agents, sealants: glass-
ionomer cements, fissure sealants Fig. 14.6. Recommended management methods for caries in permanent teeth depending
on the depth of the carious lesion.
I mpregnation + + silver diamine fluoride, silver nitrate
Infiltration + + low viscosity resins
Sealing of fissures and glass-ionomer cements, fissure
+ +
anatomical depressions sealants, resin composites Choice of material for caries restoration
glass-ionomer cements, resin
PRR types I and I I - +
composites
The choice of material for caries restoration depends on the age of the child and the
Atraumatic treatment
+ + glass-ionomer cements quality of cooperation, the phase of treatment (stabilisation/final restoration), the type
of caries (ART)
Hall techn ique + - of tooth to _be treated and the severity and extent of the carious lesion, the possibility of
prefabricated stainless steel crowns
Steel crowns + isolating the treatment area, the number of carious lesions, the type of tooth (deciduous/
F illing cavities treated glass-ionomer cements, resin corn- permanent) and its phase of development, as well as factors related to the parents (e.g.
+ +
with various techniques posites cooperation, financial possibilities).
Selective stepwise calcium hydroxide cements, glass io-
+ + In developmental-age patients, the most common methods for restoring lost tissue are
caries removal, ITR namer or oxide-zinc-eugenol cements
direct restorations using polymeric materials (resin composites, compomers, giomers),
DEEP CARIES SURFACE CARIES, glass ionomer cements (conventional and light-cured) and steel crowns. In permanent
internal ½ or ¼ dentine MODERATE CARIES dentition with loss of > 50% of the coronal ridge, indirect methods or prosthetic treat­
(risk of pulp exposure) does not reach ½ or ¼ of the internal dentin ment should be considered.
i i Glass-ionomer cements are widely used in paediatric dentistry both in the stabiliza­
Selective caries removal Selective caries removal tion phase as materials for temporary use and for the final reconstruction of tissues. The
to "soft" dentine to "firm" dentine
ART
advantages of these materials are:

I I
I,
non-operational methods - biocompatibility,
Hall technique sealing
(non-cavitated caries) - tightness (binds chemically to tooth tissue and base metals; in the first bonding phase,
Fig. 1 4.5 Recommended management of caries in deciduous teeth depending hydrogen bonds are formed between the free carboxyl groups in the cement and the
on the depth of the carious lesion. strongly bound water layers on the tooth, which are gradually replaced by ionic bonds

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Compendium of Paediatric Dentistry General principles of caries management in children and adolescents

involving cations such as tooth calcium and the carboxyl group in the material; th is cement increases, it becomes more translucent (improved aesthetics) and less susceptible
creates a chemically resistant ion-exchange layer for permanent adhesion, which pre­
to water loss.
vents microleakage), The physical properties of RMGI and GIC are similar, but the biocompatibility of
fluoride content and remineralisation of the dentin beneath the filling (release of v a­ R M GI is poorer because they release the H EMA monomer within the first 24 hours.
rious ions over several weeks; fluoride release can continue for at least five years),
fluoride absorption into the enamel adjacent to the filling, Resi n composites
the coefficient of thermal expansion is similar to the tooth structure. Considering the consistency of the material, a distinction is made between conven­
Their disadvantages are low mechanical resistance and sensitivity to acids, which,
tional (medium viscosity), condensable (high viscosity) and semi-fluid (low viscosity)
when exposed to acids and when filling cavities that are too extensive, reduces the du­ composites. They can be cured by light (light-curing), chemically (self-curing/che­
rability of the restoration. In children with a persistent high risk of caries disease, they . mo-curing) or by both (dual-curing).
are u�ed for a shorter period of time than in children with a reduced risk. In the youngest Resin composites are used to fill all classes of cavities in deciduous and permanent
children, a filling in deciduous teeth made of glass-ionomer cements is rarely definitive. teeth. Their are characterised by aesthetics, good mechanical and physical properties,
However, it can be when the time to exfoliation of the physiological tooth is similar to abrasion and fracture resistance, ease of processing and polishing. Their main disad­
the longevity of the filling. In many situations, the use of glass ionomer cement fillings vantages are polymerisation shrinkage, a demanding fitting procedure due to moisture
can be treated as an Interim Therapeutic Restoration (ITR). sensitivity and the need for bonding materials. Light-curing resin composites should be
Due to their remineralising properties, glass-ionomer cements are also used for ce­ placed in the cavity in layers with a thickness not exceeding 2 mm (4-5 mm using con­
menting prefabricated steel crowns and in the treatment of caries in permanent teeth, densed composites and bulk fill type). Each layer requires a separate polymerisation. Ad­
especially for filling small cavities, sealing fissures and filling cavities in incomplete hesion of resin-based materials to the enamel and dentin of deciduous and permanent im­
erupted teeth and in deep caries (sandwich technique), as underlay and ITR restorations mature teeth and the efficiency of orthophosphoric acid digestion are weaker compared
(two-step caries removal method, reducing bacterial impaction by eliminating numerous to permanent teeth. The enamel of deciduous teeth is thinner, less mineralised and has
active caries lesions in a short period of time). a more pronounced aprismatic layer. Dentin is characterised by weaker mineralisation
The most commonly used cements in paediatric dentistry are conventional glass­ and a higher density of dentinal tubules and therefore less intercanal dentin required for
-ionomer cements (GIC), conventional high-viscosity, reinforced glass ionomer cements etching. The enamel of immature permanent teeth also contains more protein and fewer
(HV G IC) and resin modified glass-ionomer cements (RMGI). minerals than mature teeth, dentin - wide dentinal tubules. The efficiency of etching and
Before glass-ionomer cement is inserted into the cavity, the smear layer should be adhesion of the resin composite to the enamel of immature permanent teeth is thought to
removed with a conditioner that is 10-20% polyacrylic acid. The material should be be enhanced by prior deproteinization with 2.5-5% NaOCI.
introduced with a hand instrument or a capsule applicator, pressed with a strip or dental Resin composites for filling cavities in molar deciduous teeth are the least effective
matrix or shaped with a hand instrument. Using conventional cement, the material is of all materials (success rate 1.7- 12.9%). The main cause of failw:e is secondary caries.
shaped a few seconds after application, using a hand instrument with movements from Restorations using prefabricated steel crowns have the highest success rate (96.1%). For
the centre to the edges of the filling (a few touches). Glass-ionomer cement can become newly erupted permanent teeth, the ITR method using glass ionomer cement is benefi­
dry or damaged with excessive exposure to water after placement into a cavity. Its sur­ cial. This allows post-eruptive maturation of the enamel and remineralisation of decal­
face should therefore be protected from moisture by applying a layer of light-curing cifi ed tissues.
resin varnish or Vaseline. Glass-ionomer cements harden within 2-3 minutes, but for The effectiveness of treatment with resin composites depends on the level of caries
4-6 weeks they undergo further changes referred to as maturation. The strength of the risk. They should not be used in patients at high risk.

194 1 95
 General principles of caries management in children and adolescents
Compendium of Paediatric Dentistry

Flowable resin composite are characterized by good adaptati on to the

walls of the ''M i nim um intervention" - M I inspiring future oral healthcare? Br Dent J 2017; 223: 133-135.
n shrinkage.
_ 5 . Bane1jee A. M inimurn intervention oral healthcare delivery - is there consensus? Br Dent J
defect, the ab ility to fil l u ndercuts and partial compensation of polymerizatio 2 020 ;229:393-5 . - 6. Beltran EO et al. Caries classification and management in the context of the
nde nsable com ­
They are used as l i ners before fillin g the cavity w i th conventional or co c a riesCare International (CCI) consensus: a clinical case study. Br Dent J 2019; 227: 3 63-6. - 7.
of class III an d Chisini LA et al. Restorations in primary teeth: a systematic review on survival and reasons for
posite, for filling cavi ti es of all classes i n deciduous teeth, fill ing cavi ti es
nnel method) i n
failures. lnt J Paediatr Dent 20 1 8; 28(2): 1 23 -139. - 8. FOi World Dental Federation. Carious le­
V and small cavities of class 1, as well as the gingival part of class II (tu si ons and first restorative treatment. lnt Dent J 2020;70:5-6. - 9. Ismail AI et al. The International
permanent teeth, repa i rin g composite fillings, as materi als for fixing de
ntal sp lints and c aries Classification and Management System ( I CCMS) An Example of a Caries Management
pathway. BM C Oral Health 2015; DO I : I 0.1186/ 1 472-683 1 - 1 5-S l -S9.
sealing anatomica l caviti es. 10. Ismail A l et al . Caries management pathways preserve dental tissues and promote oral
compos ites
Bioactive composite - Activa™ combines the stren gth and aesthetics of health. Community Dent Oral Epidemiol 2013; DO I : 10. 1 11 1 /cdoe. 1 2024. - 1 1 . Jumlongras D,
ive i on res in , a W hite GE. Bond strengths of composite resin and compomers in primary and permanent teeth.
w i th the ben efits of glass-ionomers. The i ngredi ents are a patented bioact
very good J Clin Pediatr Dent 1997;2 l :223-9. - ! 2. M achiulskiene V et al. Terminology of Dental Caries
patented rubberised resin and a bioactive ionomer glass. Advantages include and Dental Caries Management: Consensus Report of a Workshop Organised by O RCA and Ca­
s calcium, riology Research Group of JADR. Caries Res 2020; 54: 7- 1 4 . - 1 3 . Manhas S et al. Comparative
adhesfon (binds chemical l y to tooth tissue), tolerates moisture an d release
not con tain Eva luation of the Efficacy of Stepwise Caries Excavation vs I ndirect Pulp Capping in Preserving
phosphate and fluoride i ons. It can be used for all types of cavities. It does the Vitality of Deep Carious Lesions in Permanent Teeth of Pediatric Patients: An In Vivo Study.
eness of caries
Bis-GMA or Bisphenol A. However, scient i fic evi den ce for the effectiv Int J Clin Pediatr Dent. 2020;13(Suppl l ) :S92-S97. doi: I 0.5005/jp-journals-10005- 1 874. - 1 4.
Martignon S et al. CariesCare practice guide: consensus on evidence into practice. Br Dent J
treatment with this composite is still sparse.
ability to 2019; 227: 353-362. - 15 . Melo M et al. Current Status and Trends in Research on Caries Diag­
Alcasides are a subgroup of dual-curin g compos i te materials that have the nosis: A Bibliometric Analysis. lnt J Environ Res Public H ealth. 2022; 19(9):5011. doi: I 0.3390/
ce an d aes­
release fluoride, cal ci um an d hydroxide ions, have better mechani cal resistan ijerph 19095011. - \ 6. Melo MA et al. The Use of Bioactive M aterials in Caries Management.
tooth tissue Front Oral Health 2022; doi.org/10.33 89/froh.2022. 832285 . - 17. Nicholson J W. Maturation
thetics than glass-ionomer cements (better translucency), good adhesion to processes in glass-ionomer dental cements. Acta Biomater Odontol Scand. 20 I 8;4( I ):63-71. doi:
oral env i ron­
(both with and w i thout the use of a bon di ng system), less sensitivi ty to the \ 0.1080/233 3793 \ .2018.1497492. - 18. P ires CW et al. ls adhesive bond strength similar in pri­
mary and permanent teeth? A systematic review and meta-analysis. J Adhes Dent 20 I 8; 20(2):
ment than composite materials and glass-ionomer cements.
erised by 87-97. - 19. Pitts N B, Ekstrand K R, J CDAS Foundation. International Caries Detection and
Compomers are composites modified w ith polyacid. They are charact Assessment System ( JCDAS) and its International Caries Classification and M anagement System
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higher mechanical stren gth compared to glass- ionomer cements, good aestheti (ICCMS) - methods for staging of the caries process and enabling dentists to manage caries.
ions. Thei r Community Dent Oral Epidemiol 2013 ; DOI: 10.1111/cdoe. l 2025 .
polishability, contrast on X-ray, ability to release small amounts of fluoride 20. Sidhu SK, Nicholson JW. A Review of Glass-Ionomer Cements for Clinical Dentistry.
abrasiveness
disadvantages include a lack of direct adhesion to tooth ti ssue and a higher .l Funct Biomater. 2016;7(3):16. doi: I 0. 3 390/jfb703 0016. - 21. Schwendicke F et al. M anag­
than compos ites. ing Carious Lesions: Consensus Recommendations on Carious Tissue Removal. Adv Dent Res.
yli c 2016;28(2):58-67. - 22. Schwendicke F et al. Interventions for treating cavitated or dentine
Giomers differ from compomers in the use of a filler pre-bon ded with polyacr carious lesions. Cochrane Database Syst Rev. 2021;7(7):CD013039. doi: I 0.1002/ 1 465185 8.
i ons
acid, whi ch increases the strength of the material and allows the release of fluoride COO l 3039.pub2. - 23. Sheen DI-I, Wang WN, Tarng TH. Bond strength of younger and older
placement permanent teeth with various etching times. Angle Orthod l 993;63 :225-30. - 24. Splieth CH et
similar to glass- i on omer cements. The procedure for comporner an d g i omer
al. How to I ntervene in the Caries Process in Children: A Joint O RCA and EFCD Expert Delphi
is s i milar to that for compos ite placement. Consensus Statement. Caries Res 2020;54:297-305 . - 25 . Sujith R, Yadav TG, Pitalia D, Babaji
P, Apoorva K, Sharma A. Comparative Evaluation of Mechanical and Microleakage Properties of
References Cention-N, Composite, and Glass-ionomer Cement Restorative Materials. J Contemp Dent Pract.
on the Surface 202 0;2 l (6):691-695. - 26. Wang J et al. A comparison of the mechanical proprieties of different
1 . Abdelm egid FY. Effect of Deprotei nization Before and after Acid Etching
nt Enamel. Niger J Clin Pract 2018;2 l :591-6 - 2. Aras S et al. types of primary tooth restorations: an in vitro study. Clin Oral Invest 2022;26, 4419-4426.
Roughness of l mmature Permane
e permanent tooth
Deproteinization treatment on bond strengths of primary, mature and immatur
comparative evaluation
enamel. J Clin Pediatr Dent 20 I 3 ;37:275- 9. - 3 . Bhadra D et al. A I -year
te in Class I I
of clinical performance of nanohyb rid composite with Activa bioactive composi
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Dent. 20 1 9;22( \ ):92-96. -4. Bane1jee A .

carious lesion: A randomized control study. J Conserv

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 Non-invasive methods for treating caries in children and adolescents

The constant, regular use of agents containing low concentrations of fluoride (e.g.
Chapter 1 5
toothpaste 1 000-1450 ppm F) allows a slow but complete remineralisation of the tissues.
The use of agents with high fluoride concentrations results in the deposition of a calcium
Non-invasive methods for treating caries in children fluoride-like compound (fluoride reserve) on the surface of the carious lesion enamel
and adolescents and the closure of micropores that provide diffusion pathways for ions. A so-called tis­
sue scar is formed. Deeper layers of enamel may not remineralise or this will only occur
Joanna Szczepanska, Dorota Olczak-Kowa lczyk after long-term exposure to fluoride and calcium and phosphate ions. In children, the
use of fluoride varnishes, which are safe and can be used from the eruption of the first
deciduous teeth, is important at all stages of treatment of carious lesions. They are well
The success of minimally or non-invasive methods is based on increasing awareness . accepted by children and easy to apply to the teeth by dental staff.
of caries risk factors, detection of early stages of caries, the use of measures to prevent ·
\
CPP-ACP allows the accumulation of phosphopeptide caseinate in the dental plaque,
caries and monitoring of caries for its stopping or progression.
'
+2
which contributes to maintaining the state of supersaturation with ca and PO4- 3 ions.
Non-invasive procedures avoid the preparation of tooth tissue and the use of fillings The addition of 900 ppm or 1 1 00 ppm fluoride ions to this complex further improved the
that will periodically need to be replaced or repaired. However, a prerequisite for their properties of the agents used to remineralise white carious stains. This complex is used
effectiveness is the elimination or reduction of the influence of cariogenic bacteria on the in Recaldent, Tooth Mousse or Curasept Biosmalto Mousse, among others. In addition to
formation and development of the carious process. One of the main non-invasive me­ amorphous calcium phosphate (ACP), the Curasept Biosmalto group of preventive agents
thods used to treat caries is remineralisation and impregnation with silver compounds. contains fluoride ions, e.g. in 1 000 ppm F toothpaste for children up to 6 years of age, and
Remineralization is the repair of demineralized tissue by reincorporating previously carbonates that enhance the bioavailability of calcium, phosphorus and fluoride ions.
lost minerals into the tissues of the tooth. This process occurs thanks to fluoride, calcium Remineralisation is aided by:
and phosphate ions from saliva and plaque, which are supplied with foods, caries pro­ - reducing the influence of the bacterial agent (regular dental cleanings, antibacterial
phylaxis products and some medications. agents, e.g. mouthwashes for use at home, and/or application of an antimicrobial
Fluoride products, phosphopeptide caseinate complex with amorphous calcium phos­ agent in the office, e.g. povidone-iodine,
phate (CPP-ACP, Recaldent), non-stabilised amorphous phosphate (ACP), nano-hy­ - raising the pH of the oral environment (e.g. arginine toothpaste).
droxyapatite (10%) and bioactive glass containing calcium-sodium phosphosilicate (No­ The remineralisation process also occurs in the dentin when using, for example,
vaMin) are used for remineralisation. glass-ionomer materials or those containing the CPP-ACP complex. They cause the
When in contact with the oral environment, fluorine compounds have a twofold effect deposition of calcium phosphate minerals and the formation of hydroxyapatite crystals
_ they inhibit demineralisation and enhance remineralisation. Both of these processes can both in the dentinal tubules, leading to their closure, and around the collagen fibres.
affect both enamel and dentin. I nhibition of demineralisation presupposes the incorpora­ Mineralisation of the cavity floor with the production of tertiary ·dentin is particularly
tion of fluoride ions into the crystal lattice structure of enamel hydroxyapatite, resulting in important in deep caries, as it protects against pulp exposure.
t
a reduction in its acid solubility, by lowering the critical pH value in the oral environmen Agents used for remineralization are bioactive materials because they affect the tissues
for the dissolution of hydroxyapatite crystals from around 5.5 to 4.5. The resulting fluor of the tooth. They can capture calcium, fluorine and phosphorus ions from saliva and incor­
hydroxyapatite or fluoroapatite will then dissolve at a lower pH, so it becomes more re­ porate them into enamel and dentin and release them into saliva and plaque. These materials
sistant to demineralisation. Fluoride ions also lead to an increase in the uptake of calcium con tain fluorine compounds alone, calcium phosphate compounds or all of these components
and phosphate ions, inhibit plaque metabolism by reducing the ability of carious bacteria together. This group includes glass-ionomers (GICs) and bioactive glasses. The powder of
n.
to produce large amounts of acid from carbohydrates and interfere with plaque depositio

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Compendium of Paediatric Dentistry Non-invasive methods for treating caries in children and adolescents

the glass-ionomer materials contains fluoro-aluminosilicate glass, and the bioactive glass is 1 m pregnation with silver compounds
composed ofsodium-calcium phosphosilicate. Modern GIC materials are characterised by an I mpregnation consists in supersaturation of caries altered tooth tissues with com­
increased release of fluoride or other ions such as calcium and phosphate into the oral envi­ p ounds with bactericidal and remineralizing effects. Currently, compounds containing
ronment, thus serving to enhance remineralisation or prevent acid-induced demineralisation. silver are used, such as a 10-40% solution of silver nitrate and 38% silver diamine
The new generations are characterised by improved mechanical properties and resistance to flu o ride (SDF). Their use results in a brown or black discolouration of the tissues (the
demineralisation at the edges of the restoration. The most recent modification of glass-ion­ silver phosphate formed after application discolours when exposed to sunlight or when
omers is the introduction of CPP-ACP compounds into their composition. Other prepara­ exposed to reducing agents). Consequently, their use requires that parents be made aware
tions with remineralising properties, belonging to the bio ceramic cement group, are MTA and informed in advance of such an unsightly effect. They are an effective alternative
and Biodentine. Biodentine is a three-calcium silicate-based cement that releases Ca(OHt for aresting caries in patients with behavioural problems, severe dental anxiety and un­
Mineral trioxide aggregate (MTA) powder consists of tricalcium silicate, dicalcium silicate, . . cooperative patients. SDF is recommended in children undergoing or having undergone
tricalcium aluminate, calcium sulphate dihydrate. radiotherapy. It is minimally invasive agent, has the antibacterial properties of silver
and the remineralising properties of fluoride (contains 44 800 ppm F) and protects the
Sealing pits and fissures collagen structure, preventing its destruction. Applied once or twice a year, it can stop
Sealing of pits and fissures is aimed at creating a mechanical barrier between the active carious lesions involving dentin. No caries removal required. Applied to the caries
enamel and the pathogenic biofilm in places where food residues and bacterial biofilm lesion, it reduces the risk of caries on the adjacent surface of the tooth. Contraindications
are deposited, in places with a particular susceptibility to the development of caries. Indi­ to the use of SDF are deep and extensive cavities (suspected pulpopathy), allergy to sil­
cations include fissures sealing on the occlusal, buccal or palatine surfaces of permanent ver or silver nitrate, lack of parental consent ("black teeth").
molars, premolars and deciduous molars with a good prognosis for retention, foramen SDF is also used in the atraumatic restoration technique. Silver Modified Atraumatic
cecum of the anterior teeth, hypoplastic enamel defects and cavities resulting from ab­ Restorative Technique, SMART) consisting in filling the cavity or sealing the groove
normalities in the anatomical structure of the teeth (e.g. double teeth). with a conventional GIC immediately after the application of SDF.
Sealing healthy fissures is an effective method of preventing caries (primary preven­ SDF can cause irritation of the pulp and oral mucosa. A new agent - silver nano
tion). It can also be used as a non-invasive method of treating incipient non-cavities ca­ fluoride (NSF), effectively inhibits dental caries and does not cause tooth discoloration.
rious lesions, which are characterised by loss of colour, gloss or surface smoothness due Silver nitrate has long been used in the treatment of caries. It exhibits broad-spec­
to demineralisation before macroscopic breakdown of the tooth surface structure occurs. trum antimicrobial activity, lack of bacterial resistance and low toxicity. Inhibits col­
The procedure for fissures and pits sealing is described in Chapter 17. lagen degradation. Similar to SDF, it causes a black discolouration of the impregnated
Glass-ionomer cements, methacrylate-based sealants, polyacid-modified resins tooth tissues (Fig. 15.1 ).
(compomers) or resin-modified glass-ionomers are used for sealing. The choice of ma­ The simultaneous application of 25% silver nitrate solution and 5% NaF varnish
terial depends on the reason for which the sealant is applied and the level of cooperation every six months is as effective in stopping deciduous dental caries as 38% SDF. Apply­
with the child. Resin-based sealers show higher retention rates, while the glass-ionomer ing a 5% NaF varnish after applying silver nitrate and drying prevents contact of AgNO3
application technique is less sensitive to moisture and - importantly - release fluoride with soft tissues hinders washing out of AgNO3 by saliva and enables remineralization,
ions. Therefore, in situations where isolation is difficult, due to the tooth not being fully hinders the elution of AgNO_ through saliva and allows remineralization. The treatment
J

erupted and is unable to stay dry, glass-ionomer would be the better material. is repeated after 2, 4, 8 and 12 weeks.
Both prophylactic and therapeutic sealants should be inspected regularly and repaired
if necessary.

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R eferences
I . Alhowaish L. Non-invasive and Minimally I nvasive Management o f Carious Lesions in
C dre n: A Scoping Review. .I Res Med Dent Sci, 202 1 , 9 (S I ): 1 -8. - 2. Almeida MQ et al. Ther­
hi l
apeutic potential of Brazi I ian fluoride varnishes: an in vivo study. Braz_Dent J . 20 1 1 ;22( 3): 1 93-7.
Fig. 1 5 . 1 . Impregnation of carious le­ _ 3. de Amorim RG et al. Association of chlorhexidine and fl uoride for plaque control and white
sions on the labial surfaces of deciduous spot lesion remineralization in primary dentition. lnt .J Paediatr Dent. 2008; 1 8(6):446-5 1 . - 4. Chu
incisal deciduous teeth of the maxilla C H et al. The effectiveness of the biannual application of silver nitrate solution followed by sodi­
with a 25% silver nitrate solution with a ul11 fl uoride varnish in arresting early childhood caries in preschool children: study protocol for a
varnish coating of 5% NaF. ra ndomi sed controlled trial. Trials 20 1 5 ; 25 ; 1 6:426. doi: I 0. 1 1 86/s 1 3 063-0 1 5-0960-2. - 5. Crys­
ta l YO. Silver diamine fluoride (S DF) : its role in caries management. Caries Management nor-
111al. Dental Update 20 1 9; 46( 1 1 ):I 1 9. doi.org/ 1 0. 1 2968/ denu. 20 1 9.46. 1 1 . 1 O 1 6. - 6. Crystal YO
et al. Evidence-Based Dentistry Update on Silver Diamine Fluoride. Dent Clin North Am 20 1 9
The classical method of impregnation with silver nitrate assumes the use of a 1 0- Jan;63 ( 1 ) :45-68 . doi: I 0. 1 0 1 6/j .cden.20 1 8.08 . 0 1 1 . - 7 . Duangthip D et al. Non-surgical treatment
40% �olution of silver nitrate and precipitator (Lugo! liquid, eugenol, 4-6% pyrogallic of dentin caries in preschool children - systematic review. BMC Oral Health 20 1 5 : 1 5-44. DOI
I 0. 1 1 86/s 1 2903-0 1 5-003 3-7. - 8. Gao SS et al. Caries remineralisation and arresting effect in
acid) or a 30-50% solution of zinc chloride and as a precipitator 1 0% potassium ferro­
children by professionally applied fl uoride treatment - a systematic review. BMC Oral Health,
cyanide. Four treatments at 7-1 0-day intervals are recommended. Treatment cycles are 20 1 6: 1 6- 1 2. 1 6: 1 2 DO I I 0. 1 1 86/s 1 2903-0 1 6-0 1 7 1 -6 - 9. Giacaman RA et al. Evidence-based
repeated every three months. strategies for the minimally invasive treatment of carious lesions: review of the literature. Adv
Clin Exp Med. 20 1 8 ;27(7): 1 009- 1 0 1 6.
Regardless of the type of agent used, performing the treatment requires: I 0. Guideline on Caries-risk Assessment and Management for Infants, Children, and Ado­
isolating the prepared teeth from saliva and protecting the adjacent mucosa from lescents. Review Council on Clinical Affairs. Latest Revision Clinical Practice Guidelines 20 1 4.
contact with the impregnant, - 1 1 . Ferreira JM et al. Therapeutic effect of two fluoride varnishes on white spot lesions: a
randomised clinical trial. Braz_Oral Res. 2009;23( 4):446-5 1 . - 1 2. Sobh EG et al. Effect of CPP­
performing stripping in inaccessible defects on proximal surfaces, ACP modified-G IC on prevention of demineralisation in comparison to other fl uoride-containi ng
mechanical removal of softened carious dentin with an excavator, restorative materials. Aust Den J 2022, 0: 1 - 1 - 1 0.
washing and drying of cavities,
rubbing the impregnator alternately with three swabs soaked in I 0-40% silver nitrate
and three swabs soaked in a suitable precipitant,
dry with a gentle stream of air,
when using silver nitrate with fluoride varnish - application of the varnish.
Specific indications for impregnation with silver nitrate include:
initial and moderate (circular) caries in anterior teeth,
non-retentive, extensive carious cavities on the vestibular and palatal surfaces of mo­
lars.
Contraindications to this procedure, for safety reasons, are very young children who
are completely uncooperative and deep caries, due to the possibility of irreversible pulp
irritation.

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 Invasive methods of caries treatment in children and adolescents

Chapter 16 Allergies to any of the components of the material used and a carious lesion exten­
d ing beyond the outer ½ of the dentin layer are contraindications. The advantages of the
method are:
Invasive methods of caries treatment in children
- single-visit application,
and adolescents - stabilisation of demineralised enamel,
- stopping/delaying the progress of change,
Joanna Szczepanska, Dorota Olczak-Kowalczyk
- closure of superficial micropores and cavities,
- often improving the aesthetic effect,
- non-painfulness and patient acceptance.
In the treatment of cavity caries, minimal preparation of the hard tooth tissues with
modi�ed cavity outline and shape and the use of bioactive adhesive restorative mate� A prerequisite for the infiltration method is the fitting of a cofferdam.
rials is indicated. Continuous improvements in restorative materials are reducing treat­
Treatment technique:
ment steps, shortening treatment times while improving adhesion. The introduction of
self-etching systems has resulted in a combination of etching and infiltration of tooth
tissue with a bonding agent, thus simplifying the procedure. Also, flowable resin com­
posites with self-etching properties could be another advance in reducing working time. - removal of the outer, superficial layer of initial caries
The use of increasingly less invasive dental treatment techniques is of paramount by etching for 2 minutes with 1 5-20% hydrochloric
acid gel (Jeon etch), which is stirred in occasionally
importance when working with the developmental-age patient. Procedures should be as during application with a micro brush,
child-friendly as possible, i.e. short by limited tissue preparation with micro-invasive
techniques on the one hand, and by using saliva-insensitive and fast-bonding materials
on the other. Minimally invasive methods of caries treatment have particular advantages
in paediatric dentistry due to sho1ter treatment times, less painful procedures and the fact
that they are easier to accept and cause less anxiety in children, especially uncooperative
children. - rinsing the acid with water for 30 seconds,
Caries infiltration It involves the use of a low-viscosity light curing resin called infil­
trant with high surface tension to reinforce and stabilise demineralised tissue without the
use of a drill and anaesthesia. The infiltrant penetrates into the tissue structure, fills the
microporosity of the enamel, blocks further bacterial penetration, hinders H" diffusion - drying for 30 seconds with Icon-Dry (if the white
and prevents mineral loss. For this purpose, e.g. Icon® Resin is used. indications for colouration of the carious stain persists, the etching
should be repeated),
infiltration procedures are:
initial carious lesions, involving the entire enamel and crossing the enamel-dentin
jounction and reaching ½ of the outer dentin layer,
demineralisation of enamel after orthodontic treatment, - application of resin (Icon l nfiltrant) to the surface of
developmental enamel and dentin defects or M I H lesions, the lesion using an applicator or micro brush, which
- mild to moderate fluorosis. allows better penetration of the resin,

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Compendium of Paediatric Dentistry Invasive methods of caries treatment in children and adolescents

l esions, together with innovations in materials science, has forced a critical approach to
th e principles of cavity preparation according to Black.
Before starting to prepare the cavity, it is necessary to clean the tooth surface with a
toothpaste that does not contain fluoride compounds and a preventive toothbrush moun­
- allowing the resin to flow into the microporosity for
ted on a micromotor handpiece (slow speed handpieces) or a preventive sandblaster,
about 3 minutes,
and to check the location of occlusal contacts with the use of a carbon paper to avoid
occlusive contact on the edge of the future filling.
Important elements of the proceedings are:
_ proper isolation of the treatment area with the use of a cofferdam or lignin rollers and
- curing the material with a polymerisation lamp for 40
seconds (if necessary, the application can be com- salivary gauze,
1 pleted by leaving the resin added for 1 minute and _ administer local anaesthesia, if necessary,
polymerising for 40 seconds).
_ protection of the gum and the proximal surfaces of adjacent teeth (metal strips, elastic
bands and interdental wedges).
Invasive (surgical) treatment
The opening of the cavity can be performed with different instruments depending
The choice of treatment method for cavity caries and how to restore the lost tissues on the extent of enamel loss and the tooth surface on which the caries develops. It is im­
depends on: portant to open the cavity in such a way as to be able to make a preliminary assessment
the age of the child, of its extent and depth. In children's dentition, caries is undermined, where there is a
type of dentition - deciduous, mixed, permanent, significant disproportion in the course of demineralisation between enamel and dentin.
number of carious cavities, This results in a small entry into the cavity within the enamel and a significant carious
- caries risk level, lesion in the dentin (Fig. 1 6.1).
the extent and depth of the cavity,
the location of the tooth and the type of surface affected by the caries,
- cooperation of the child and parents and compliance with the recommendations.
The most common method of treating a carious cavity is direct preparation and fil­
ling. The carious cavity can be treated traditionally (with drills), manually or with che­
momechanical caries removal, oscillation - sonic or ultrasound, air abrasion or laser.
Mechanical rotation technique - traditional (conventional) involves the preparation Fig. 1 6.1. U ndermining nature of caries on the occlusal surface of a second deciduous molar
(left) and a first permanent molar (right); prominent pulp horns. in both teeth.
of damaged tissues with rotary instruments (burs). Its advantage is that any cavity can
be worked on. Disadvantages include the risk of removal of healthy tissue and thermal
Removal of enamel overhangs should result in access to safe cavity work, but spar­
damage to pulp odontoblasts, soreness, unpleasant sounds and vibrations.
ingly enough so that the loss of healthy tissue is minimised. Hand instruments (enamel
The classic cavity preparation technique according to Black involved filling the ca­
chisels) or diamond burs in the shape of a flame, rounded cylinder (pear) or round on a
vity with amalgam, which showed no connection with the tooth tissue. In order for the
turbine handpiece can be used for this purpose. The approach to the carious lesion should
filling to last, the cavity had to be shaped properly, often with the removal of healthy
start from the area that will provide the best visibility. Carious cavities on the occlusal
tooth tissue. The emergence of new possibilities for detecting and treating early carious or vestibular surface do not pose any major difficulties in their preparation. Jn contrast,

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Compendium of Paediatric Dentistry I nvasive methods of caries treatment in children and adolescents

those on the proximal surfaces of the anterior teeth are opened rather for aesthetic rea­
sons on the palatal/lingual side. Access to cavities in lateral teeth is gained from the
occlusal side if the occlusal-proximal edge is destroyed; from the vestibule or tongue if
the caries is eroding towards the gingiva; from the proximal surface in the absence of an
adjacent tooth.
Removal of carious dentin is carried out with the help of steal round bur on micro­
motor handpiece or by the methods described later in the chapter. This should be started Fig. 16.2. Deep carious cavity on the proximal surface of tooth 75. Preparation of the lateral
walls, cleaning of the cavity floor to a layer of demineralised dentin, slight convergence
from the side walls of the cavity to ensure good adhesion of the filling and its marginal
of the walls towards the occlusal surface, filling with glass-ionomer cement.
tightness. It is crucial to completely remove carious dentin, including demineralised den­
tin' from the enamel-den tin interface to ensure the tightness of the filling.
Atraumatic restorative treatment (ART)
Carious dentin from the bottom of a cavity should be removed with great care, bea-
ring in mind in young teeth in children the large tooth chamber, prominent pulp horns
It generally consists of removing enamel and soft, infected, fully demineralised den­
and the ease with which demineralised, soft dentin can flake off, potentially exposing the
tin with hand instruments until a strong resistance is felt. In shallow cavities, the carious
pulp. The speed of the bur should be low in order to control the bottom of the cavity at
dentin should be removed down to the hard tissue, in deep lesions only the soft dentin.
all times.
For deep cavities that extend to ½ of the dentin on the pulp side, a certain amount of soft
Regardless of the class of cavity, when the carious process drifts towards the pulp, the
carious tissue should be left on the pulp chamber wall to avoid exposing the pulp. Most
cavity floor forms at different levels. The management of deep caries is described later
often, this technique does not require the use of rotary instruments. The ART method
in this chapter.
can be modified - mART (modified art) with the use of slow rotating burs in cases of
Giving a classic outline of the cavity and retaining shape with the currently used
difficulty in removing caries dentin with a hand instrument. Many times it causes less
adhesive materials does not play such a role as in the use of amalgam. The outline of the
discomfort for patients. The cavity is, together with the fissures, filled with an adhesive
cavity is intended to reflect the course of the caries process and its extent is determined
material, usually glass-ionomer cement. The ART method is most effective in Class I
by the direction of caries spread. On the other hand, the resistive shape is currently li­
cavities on the masticatory surface (approximately 93%) because of its good visibility.
mited to the rounding of the angles between the inner walls of the cavity and between
In the Black II class, glass-ionomer cements with high viscosity are better after the use
the inner walls and the surface of the tooth, so that the filling passes gently into the
of the ART technique than ordinary glass-ionomer cements. The ART technique is of­
tissues of the tooth, which reduces the stress of the light-curing material and improves
ten better tolerated by children compared to conventional preparation. It does, however,
its adaptation. It is also possible to leave the enamel unsupported unless it can break off
increase the risk of restoration failure compared to conventional restorative methods,
during chewing.
especially in multi-surface cavities. ART proved to be an appropriate option for the treat­
Giving a retention shape in the era of huge progress in adhesion techniques that
ment of single-surface caries lesions in deciduous teeth.
micromechanically bind to the tooth no longer requires levelling the bottom or forming
The chemomechanical caries removal (CMCR) method involves the removal of
the cavity in such a way that its side walls converge with the bite surface (Fig. 16.2). caries dentin softened with a sodium hypochlorite-based agent (e.g. GK- l 0 J E, Carisolv
In cavities on the occlusal and proximal surfaces of molars and premolars, however, a
and Cariemove) or enzyme-based (Papacarie, Carie-care, BiosolvTM and Brix 3000). Its
parallel or slightly convergent position of the cavity walls towards the occlusal surface
advantages are: painlessness of the procedure, less anxiety for the child, removal of only
is advantageous. The making of retention abutments in the form of grooves or pits only
the infected dentin layer, no irritation of the pulp, no impact on the bonding of adhesive
takes place in limited cases, where there is significant difficulty in retaining the filling.
systems. The disadvantage is the longer time required for cavity preparation.

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CMCR is used for the treatment of open and easily accessible carious cavities. I n r
i n a larger and shallower preparation area. The optimum distance f om the surface of the
selected situations, it may be necessary to open the cavity using a conventional method. perm anent tooth during working is 3-5 mm, in deciduous teeth 2 mm. The speed and ex­
The Carisolv system comprises non-cutting instruments for manual cavity prepara ­ ten t of preparation depend on the type of tissue being sandblasted - hard or soft carious.
tion, as well as a pink gel (containing leucine, lysine and glutamic acid, thickener car­ The insertion of resin-based materials after the use of a sandblaster, however, re­
boxymethylcellulose and dye erythrosine) and a clear liquid (containing sodium chloride quires etching despite the enlargement of the tooth tissue surface . Sandblasting work
and sodium hydroxide to form a 0.5% sodium hypochlorite solution, pH 11). The gel h as to be very careful and requires experience in order not to cause too much hard tissue
and liquid, when mixed immediately before use, form an active carious dentin softening preparation, damage to adjacent teeth, fillings and soft tissues. The advantages of this
preparation. method are: low pain, no negative impact on the pulp, creation of micro retentions, thus
Treatment technique: improving the tightness of the fillings. Disadvantages include the risk of over-prepara­
- gel application, tion . A prerequisite for the sandblaster is the wearing of a cofferdam, the use of goggles
- waiting 30 seconds, for the patient and operator and a suction cup. Contraindications to the use of the abra­
scraping off the lesions with a hand instrument. sive method include: patients with respiratory diseases (e.g. asthma, respiratory failure,
These steps are repeated until the infected carious dentin layer is removed. chronic obstructive pulmonary disease), the presence of unhealed wounds in the oral
The kinetic cavity preparation (KCP) is a blast-abrasive or abrasive-kinetic non-con­ cavity, including post-extraction wounds and after other procedures, as well as inflam­
tact alternative to traditional cavity preparation with rotary instruments. It is one of the mation of the mucosa and periodontium.
techniques in minimally invasive dentistry that uses the kinetic energy of the abrasive Oscillation methods can be of the sonic or ultrasonic type, depending on the fre­
grains through a jet of compressed air or pressurised water. quency of vibrations.
Abrasive sandblasters are designed for cavity preparation, with or without a water Sona-abrasion is an alternative cavity preparation technique to tissue preparation
jacket. In the latter, the air abrasive stream mixed with water forms a homogeneous with a bur. It belongs to the methods of minimally invasive caries treatment. This method
slurry that can improve the visibility of the operating field and lower the temperature. involves the use of a scaler and special tips. The oscillating motion emitted by the scaler
On the other hand, micro-sandblasters, which are less effective, may be advisable for is transmitted to special working diamond coated tips. Unlike the smooth tips used for
developing very small cavities or preparing grooves for sealing. Sandblasters work well calculus removal, those designed for oscillation methods have a diamond coating on one
on the occlusal and cervical surfaces and can be used to clean fissures prior to sealing and side. The ultrasound tips perform high-frequency linear oscillations between 6500 and
extended sealing (prophylactic or abrasive sandblasters), treat small cavities of carious 40 000 Hz. Similarly, sonic tips also perform low-frequency elliptical oscillations (6000
and non-carious origin, remove small glass-ionomer and composite fillings and repair Hz, e.g. the Sonicflex system) generated by the air scaler insert.
fillings. The shape of the instrument tips varies, adapting to the site of the tooth being worked
The following parameters should be taken into account when working with these de­ on. The ball-shaped tip can be used to work on cavities on occlusal surfaces, especially
vices: size, type and quantity of abrasive used per minute, air and water pressure, type of for hard-to-reach areas in molars and on flat surfaces, including· proximal. The hemi­
nozzle and diameter of its outlet, distance from the surface to be treated and processing spherical shape of the tips, with a coating on the convex side, is designed for the prepa­
time. The most common abrasive is sodium bicarbonate or aluminium oxide with a size ration of proximal cavities. A piezoelectric scaler, which generates vibrations of up to
of 27-50 �tm. Bioactive glass is also being used. T he working time and the extent of the 30 000 Hz and can be used to work on the hard tissues of the tooth, is also used in dental
area to be prepared depend on the distance of the nozzle from the tooth surface - the practices. The advantages of oscillating-ultrasound equipment are:
closer the tip of the sandblaster is to the tooth surface, the deeper and narrower the prepa­ - minimally invasive cavity preparation,
ration, and vice versa - increasing the distance of the nozzle from the tooth tissue results - good visibility during caries preparation,

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Compendium of Paediatric Dentistry Invasive methods of caries treatment in children and adolescents

using oscillating angled tips, speed of which should be regulated by secure work in the cavity. At all stages of caries
low noise level, treatment, the rotary instruments used should be water-cooled.
greater acceptability by children, causing them less fear and pain than working with burs. When treating a cavity on the proximal surface of a deciduous tooth, it is important to
Laser cavity preparation methods use gas lasers (CO2 maximum wavelength I 0.6 rem ember that the enamel prisms in this area are directed obliquely towards the occlusal
�un), YAG:Nd (wavelength 1.064 µm), YAG: Er (wavelength 2.94 µm), Excimer system su rface. Therefore, the gingival wall should be directed slightly obliquely towards the
argon:freon ArF and xenon:chlor XeCl in the ultraviolet range (wavelength 0.193-0.308 o c clusal surface .
µm). The laser-emitted pulse, falling on decayed tissues, causes them to heat up rapidly, Glass-ionomer cements are recommended to fill the direct cavity in the deciduous
increase in pressure and explode. The effects of the laser are an increase in surface mi­ tooth . The restoration of cavities with resin composites, compomers is only recommen­
crohardness and acid resistance, the formation of a crystalline barrier due to the fusion of ded once the caries risk level has been reduced to low.
enamel and dentin hydroxyapatites, the removal of carious tissue and the destruction of Disking, or stripping, is used to grind the surfaces of the proximal deciduous front
bacteri'a, making the treated surface sterile. The advantages of the method are obtaining teeth affected by decay, which does not include pulp. I t consists of removing partially
a dentine surface with the appropriate retention pattern, which is free of smear layer and carious tissue and grinding the tooth proximally in the incisal direction, while maintai­
has exposed tubules, antibacterial effect, less painful procedure. Disadvantages include ning the cervical area. Abrasive discs (soft lexes) or thin diamond flame shape burs are
cost, technical difficulties in the preparation of multi-surface carious cavities (generation used for this purpose. The sanded surfaces require fluoride varnish and periodic checks.
of a lot of heat). Disking facilitates cleaning of these surfaces and provides access for saliva and ions

Specific techniques for the treatment of cavity caries in deciduous teeth necessary for remineralisation. The space created also makes it possible to remove ca­
rious dentin with an excavator or impregnation. This method requires additional consent
Caries in deciduous teeth can be treated conventionally, i.e. filled with the direct from parents due to the unsightly effect.
method after after preparation of the cavity, disked or treated with non-invasive methods
such as impregnation (described above) and the Hall technique (HT). Use of celluloid strip crown
For manual removal of caries dentin can be used excavators - with different sizes In the surgical treatment of cavity caries in milk incisor teeth, it is recommended to
and shapes of the working part, which are adapted to the size and location of the cavity. reconstruct with a resin composite using celluloid strip crown (Fig. 16.3).
These are sharp instruments made of stainless steel with a non-slip handle for safe reten­ Treatment technique:
tion in the dentist's hand. These types of instruments are particularly useful in deciduous - select a celluloid strip crown with a size corresponding to the size of the crown of
teeth, especially at the stage of the chi Id's adaptation to treatment or in the absence of the tooth, cut it so that its height corresponds to the height of the crown and the gin­
cooperation when dealing with deep caries or multiple carious cavities. In any case of an gival margin adheres to the surface of the tooth in the cervical region over the entire
extensive cavity with good access to it, excipients can be used for the initial stage of ca­ circumference,
rious dentin removal. Excavators can be used from the initial stage of cavity preparation, - carefully isolate the treatment area from saliva,
use of hand instruments is less painful than mechanical instruments and therefore better - prepare carious cavities and, if necessary, reduce the incisal edge and proximal
tolerated, especially by young children. surfaces,
The use of a specific type and size of burs for slow- or fast-handpieces depends on the - optionally protect the bottom of cavities with glass-ionomer cement,
type of tooth and the location and extent of the cavity. The steps of opening the cavity - etch the tooth surface and apply the bonding system,
and adapting the filling to the occlusion are most commonly carried out with diamond - on the cutting edge of the celluloid strip crown, make holes to allow the excess
burs with a turbine handpiece, while the removal of carious dentin and the smoothing material to flow out,
and polishing of the filling are carried out with burs with slow-speed handpieces, the

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fill the celluloid strip crownpart with a layer of composite material pressed again s t cari es in milk molars to slow the caries process by isolating the microbes present in the
its walls, c a vity from access to saliva and nutrient substrates.
the filled celluloid strip crown is placed on the tooth and polymerised according to the Contraindications to the Hall technique are:
instructions of the manufacturer of the material used, _ clinical and radiological signs of irreversible pulpitis,
remove the celluloid strip crown and polish the restoration after inspection in occlu­ on the X-ray, there is no healthy dentin separating the pulp from the caries lesion,
sion and possible correction. periapical lesions,
In uncooperative children, the procedure can be carried out in two stages. In the first - short time to exfoliation of deciduous tooth (resorption > ½ root length),
stage, use ITR, stripping or impregnation; in the second stage, once the child has adapted - allergy or hypersensitivity to nickel (prefabricated steel crowns are made of
to the dental treatment and his/her behaviour has changed, an aesthetic composite resto­ chrome-nickel steel).
ration can be carried out. The indications for the Hall technique are non- and cavity-causing lesions on the
occlusal surfaces of deciduous molars, if the patient does not accept other methods, and
on the proximal surfaces of deciduous molars. Prefabricated metal crowns are placed
without local anaesthesia.
Specific methods used in the treatment of cavitated caries lesions allowing maxi­
mum preservation of tooth tissues in a patient of developmental age:
- extended sealing (preventive resin restoration type 1),
Fig. 1 6.3. Cosmetic restoration of tooth 5 1 with composite material using a cel luloid shaper.
- preventive filling,
The advantages of this method are: - reconstruction using a prefabricated steel crown,
- parental (guardian) approval, - sandwich reconstruction,
simple technique, - reconstruction of the cavity prepared using the tunnel technique.
easy fit, Preventive resin restoration (PRR) is performed in the presence of a small caries
surface smooth and easy to polish, lesion involving enamel (PRR-l ) or enamel and dentin (PRR-2) in the fissure on the
possible and easy colour selection, occlusal surface (Fig. 1 6.4).
good aesthetic effect,
ease of possible repair.
The restoration of lost incisal tooth tissue is also used:
composite veneered prefabricated steel crowns - do not provide a good aesthetic
result, are easily damaged and require a large reduction in tooth tissue,
zirconium oxide crowns - aesthetically pleasing and biocompatible, but require more
tooth tissue reduction, cannot be clamped for marginal tightness and are expensive.
T he Hall technique is a method of treating deciduous teeth in which a stainless-steel
crown is cemented with glass-ionomer material without tooth preparation and removal Fig. 1 6.4. PRR type I - carious lesion in enamel fi l ied with fissure sealant ( left); PRR type
of decayed tissue. The main concept of the Hall technique is the use of prefabricated 2 - carious lesion in enamel and dentin fi l led with composite material and covered
with fissure sealant (right).
steel crowns (Preformed Metal Crown, PMC, Stainless Steel Crown, SSC) to seal the

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Compendium of Paediatric Dentistry Invasive methods of caries treatment in children and adolescents

Preventive resin restoration type 1 (PRR-1) is also referred to as extended sealing

m aterial, deep - hardening with a calcium hydroxide and/or glass-ionomer cement,
(Fig. 16.5). It is indicated in the presence of caries confined to the enamel and when a composite material) and applying the sealant to the filling surface and other
then with
there are diagnostic doubts about the presence of a carious lesion, especially in those at 1iealthy adjacent fissures (Fig. 1 6.6).
moderate or high risk of caries. Local anaesthesia is not required. T his method is not indicated in teeth with large single- or multi-surface carious le­
Treatment technique: sio ns or with lesions involving the proximal surface of the tooth , where proper isolation
cleaning the tooth surface (brush and fluoride-free toothpaste or air abrasion) and of th e tooth is not possible.
rinsing the cleaned surface,
isolation of the treatment area (lignin rolls and saliva ejector or rubber dam),
removal of caries with a flame-shaped diamond bur of small size and fine grain,
etching of the cavity and fissures on the occlusal surface (sealant - 37% orthophos- .
phoric acid in liquid or gel applied for 20-30 seconds; glass-ionomer cement - 10-20
seconds conditioner), A caries involving
rinsing for 20-30 seconds and drying to obtain a chalk-white surface of the enamel enamel and dentin.
using a cotton ball or a gentle air stream (if contaminated with saliva, repeat etching
for 15-20 seconds),
Prepared cavity with a
using a flow composite and optionally using a fissure sealer - adhesive system, small amount of demi­
application of the sealant into the cavity and adjacent healthy fissures using an appli­ neralised dentin left at
the bottom, etching.
cator, brush or microbrush (spread evenly without forming bubbles),
fissure sealant and flowable composite - polymerisation according to manufacturer's
instructions,
- check for correct distribution of sealant and check in occlusion with possible correc-­ Condition after etching
and application of the
tion (when using glass-ionomer cement 4-6 minutes after application), bonding system.
fluoride varnish aplication.
Cavity fi l led with resin
composite (left), fissure
sealant covering the
composite and sealing
healthy fissures (right).

Fig. 1 6.5. Extended sealant (PRR- 1 ) in tooth 46. Occlusal contacts to be

corrected (left), status
after 1 2 months (right).
Preventive resin restoration type 2 ( PRR-2) consists in removing the caries altered
enamel and dentin (in deep cavities, partially demineralized and uninfected dentin is left Fig. 1 6.6. The next steps in carrying out a P R R type 2.
at the bottom), filling the prepared cavity (with a small depth - only with a composite

2 16 21 7
Compendium of Paediatric Dentistry Invasive methods of caries treatment i n children and adolescents

Steel crowns - selecting and trying on a crown (a well-fitting crown gives resistance and an audible
Caries covering more than two surfaces of the tooth or extensive destruction of click during trial seating),
hard tissues of the tooth may qualify for the installation of ready-made crowns made of - crown adjustment:
stainless steel, also referred to as prefabricated steel crowns. The original sets include
crowns of different sizes for the first and second milk molars and the first permanent
molars divided into upper and lower teeth. They have a modelled occlusal surface ac­ • trimming the crown along the edge while maintaining
its intraoral contour using special scissors (causes an
cording to the anatomical structure. The crowns are very thin and can be easily adjusted
increase in the circumference of the crown edge),
by bending and shortening.
• bending of the trimmed crown along the entire gingi­
Indications for the use of steel crowns are:
val edge (if loose) with the crown crimping forceps to
- restoration of deciduous teeth with vital pulp with carious cavities on multiple sur- . ensure a marginal fit (the convex beak of the crimping
fa�es and proximal surfaces, forceps is placed 0.5 mm from the crown margin in­
extensive destruction of the crown of a permanent tooth with uncompleted root de- side the crown; the crown margin is bent inwards by
0.5 mm),
velopment,
restoration of deciduous and permanent immature teeth after endodontic treatment, • try on and check in the bite (deciduous tooth - it is allowed to raise the height
restoration of teeth affected by local or general developmental disorders (e.g. MIH, by 1 - 1 .5 mm, permanent tooth must be adjusted in the bite before cementing,
hypoplasia, amelogenesis imper:fecta, dentinogenesis imperfecta),
restoration of traumatised teeth, • contouring the transverse edge of the crown with for­
restoration or protection of teeth at risk of tissue loss due to attrition, abrasion or ceps in order to smooth the bends created during ben­
erosion, ding (the convex beak of the forceps is placed inside
- creating an attachment for certain orthodontic appliances, e.g. space maintainers, the crown), smoothing the edges of the crown,
patients at high risk of caries,
lack of cooperation from the child or difficulty in keeping the treatment area dry ma­ - cementation of the crown with glass-ionomer cement (excess cement that flows out
king it impossible to place a conventional restoration. from under the crown is removed with a dental probe or dental floss before it hardens).
Crowns are not used in cases of resorption > ½ the root length of a deciduous tooth, in
nickel allergy or hypersensitivity, on living teeth with suspected pulpopathy and periodontitis. Sandwich technique
Treatment technique: The sandwich technique used in deep carious cavities involves a two-layer cavity
depending on the indication, prepare a carious cavity or ca1Ty out a pulp treatment filling. The inner layer, restoring the dentin, is glass-ionomer cement, the outer layer is
and fill the chamber/ cavity with a suitable drug and material, resin composite. A distinction is made between open sandwich fillings (the cement is
- tooth preparation: not covered with composite material in the gingival area in the case of a cavity at the
• grinding the occlusal surface by about 1.5 mm while maintaining the inclinations proximal surface) and closed sandwich fillings (the glass-ionomer cement is completely
of the nodules, covered with composite material).
• elimination of proximal points by grinding these surfaces with a I mm diamond When using chemically cured glass-ionomer cement, the surface of the cement must
flame (proximal walls should be parallel, not tapering towards the occlusal surface), be etched after hardening (micromechanical bonding) before placing the resin composite.
• rounding of the edges in the occlusal-buccal and occlusal-lingual line, Light-curing cement should not be etched as it chemically combines with the resin composite.

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Compendium of Paediatric Dentistry Invasive methods of caries treatment in children and adolescents

Tunnel cavity preparation is used to treat primary caries involving 1/3 of the outer part An open tunnel cavity, after placing a contoured metal matrix strip and stabilising it
of the dentin located at the proximal surface of permanent premolars and molars with the with a wedge, is filled with glass-ionomer cement within the dentin, then with composite.
marginal edge preserved (Fig. 1 6.7).
[\1anagement of deep caries
Treatment technique:
- isolation of the treatment area, Deep caries in immature deciduous and permanent teeth, due to the large tooth pulp
- setting a diamond round bur for high-speed handpiece on the occlusal surface at chambers, poorly mineralised inter- and peritubular dentin and wide dentinal tubules,
a distance of 2 mm from the marginal edge (obliquely towards the carious lesion on poses a great threat to the pulp. The rapid spread of the carious process results in
the proximal surface) and preparation (the entrance to the cavity should ensure ade­ a limited defence response from the pulp in the form of sclerotic dentin produced in the
quate visibility and access to the carious dentin), dentinal tubules by odontoblasts or tertiary dentin formed at the pulp/dentin interface
- re.moval of caries dentin with a steel round burs for slow speed handpiece. in response to harmful stimuli. Therefore, there is usually limited reversible pulpitis in
a deep carious cavity, which can heal with properly undertaken treatment. Hence, when
there is clinical doubt as to whether we are dealing with medium or deep caries in
a child's tooth, it is always safer to make a "hyperdiagnosis".
The aim of deep caries management is to preserve the vital pulp and inhibit further in­
flammation in order to avoid more complicated and less promising root canal treatments.
In these cases, during the patient's history, the patient complains of pain provoked by
a low temperature, e.g. fluid intake, or a mechanical factor - residual food in the cavity.
Discontinuing the cold stimulus or carrying out thorough hygienic procedures results in
the cessation of the ailment. A similar patient reaction occurs during a clinical examina­
tion with ethyl chloride, causing brief, transient pain.
Dentin in a carious lesion can be divided into 4 layers due to the extent of tissue
removal, each of which can be characterised by the ability to scratch with an instrument
Fig. 1 6. 7. Tunnel preparation of a cavity on the distal surface of tooth 45, and the force used to do so as follows:
filling with glass-ionomer cement with sealing of the adjacent fissure. - soft dentine - it will be deformed under the influence of the instrument and can be
easily removed from the cavity with a small force, e.g. with an excavator,
As a result of the preparation, a tunnel may be formed connecting the entrance in - leathery dentine - does not deform under the influence of the instrument, but it can be
a healthy enamel on the occlusal surface with the exit on the proximal surface at the site easily degreased without using a large force,
of caries - external or open tunnel method. In the case of mature permanent teeth, in the - firm dentine - it is resistant to removal by hand instruments and a certain force must
absence of a cavity in the enamel at the surface (demineralised enamel), the carious den­ be exerted on these instruments,
tin can be removed, leaving the demineralised enamel at the proximal surface, hoping to - hard dentin - can be removed with high force using only a sharp instrument or bur.
repair it (the cavity is filled with glass-ionomer cement). In the case of immature teeth, Clinically, it is difficult to determine whether the contaminated dentin tissue has been
due to the ongoing post-eruptive maturation of the enamel and frequent negligence in completely removed and this layer that is visible in the cavity is just demineralised den­
cleaning these surfaces, leaving the enamel decalcified carries the risk of progression of tin. One must therefore be guided by subjective tactile assessment and the appearance of
the lesion.

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Compendium of Paediatric Dentistry Invasive methods of caries treatment in children and adolescents

the tissue during excavation of the carious dentin. It is nowadays considered that wh e n
working on a deep carious cavity, where the dentine layer separating the cavity fl oor
from the pulp chamber does not exceed to '/4 of the thickness of this tissue, onl y th e
Fig. 16.8. Radiological image of deep
�1

f
irreversibly damaged, in ected, soft dentin layer should be selectively removed. On th e caries - occupied inner 1/,, of dentin with
other hand, demineralised dentin (affected dentin), which is considered "pre-cario us", a zone of dentin impermeable to radia­
tion on the pulp side (left), very deep ca­
should be left in place, is not infected by bacteria and remineralisation is possible. F i­ ries covering the entire dentin thickness
nally, the cavity is closed tightly with a filling, which will inactivate the microorganism s and exposing the pulp (right).
left behind due to the lack of access to nutrients, facilitating the arrest of decay. The use
of restorations with remineralising properties allows the necessary ions to be supplied to In the second variant - stepwise caries excavation is less invasive and takes place in 2
the demineralised layer, causing the dentinal tubules and inter- and pericanalicular de11� stages. During the first stage, the soft carious dentin is paitially removed with hand instru­
tin to. seal, thus protecting the pulp from bacterial penetration. In addition, the fluoride ments or rotary instruments, leaving enough soft tissue at the bottom of the cavity to make
and calcium ions released from the fillings will be able to contribute to the prevention space for the placement of a temporary filling with tissue remineralising properties (Fig.
of secondary caries. The widely used adhesive materials provide a peripheral seal of the J 6.9). The demineralised carious tissue left on the chamber wall avoids iatrogenic pulp
cavity and isolate the carious lesion from the oral environment, which is an additional exposure. The sidewalls need to be cleaned to hard dentin. After 6 to 12 months, a perma­
argument for not having to completely remove the demineralised dentin. nent filling can be placed into the compact dentin layer after the caries has been removed.
There are several management techniques for the minimally invasive treatment of
deep caries: selective removal, stepwise removal or non-selective removal of carious
tissue into the hard dentin. Excavation of dentin during the preparation of carious cavity
can take place in two variants: selective caries excavation (SE) or stepwise caries exca­
vation (SW) z. Selective caries excavation is a low-invasive, ultra-conservative 1-step
procedure. This is the indirect pulp capping (IPC) technique. In the case of deep caries in
immature permanent teeth, it consists of the excavation of the soft carious dentin, leaving
only a thin layer of demineralised tissue on the chamber wall, which is covered with
a lining layer. It is possible to leave soft dentin in the deciduous teeth. Findings indicate
that complete removal of soft dentin is not always necessary or desirable. The sidewalls
should be cleaned to hard, healthy dentin. The final restoration takes place at the same Fig. 16.9. The preparation of a deep carious cavity in a permanent molar with an incompletely
visit. The main disadvantage of IPC is its proximity to the pulp and the possibility of its formed root; light colouring of the carious tissue, high moisture content of the affected dentin
exposure. indicating the acute course of the disease; dentin left demineralised and spot soft; filling with
glass-ionomer cement.
To help decide whether to use selective caries excavation in a deep cavity, deep and
extra-deep cavities are distinguished. On X-ray, deep caries penetrates the inner '/4 of the
The two-stage treatment method is also called ITR from the so-called interim the­
dentin, but is demarcated by a zone of dentin impermeable to radiation on the pulp side.
rapeutic restoration, in which to stimulate the process of healing-remineralization of
Very deep caries, i.e. with radiographically visible caries covering the entire thickness th e dentin at the bottom of the cavity, it is temporarily filled with calcium-hydroxide,
of the dentin and exposing the pulp, excludes the possibility of using this method, as the g lass-ionomer, glass-ionomer resin-modified or zinc-eugenol oxide materials. ITR is ap­
bacteria are located in the pulp (Fig. 1 6.8).
plie d:

222 223
Compendium of Paediatric Dentistry Invasive methods of caries treatment in children and adolescents

for stopping or preventing the progression of carious lesions in young patients unc 0_ 1.,a test Revision 2017 - 12. Saber AM et al. Recent Advances in I ndirect Pulp Treatment Mate­
operative or with special health needs and multiple active carious lesions, ri a ls for Primary Teeth: a Literature Review. lnt J Clin Pediatr Dent. 2021; 14(6): 795-80 I . - 13.
Sath y aprasad S et al. Research article. Resin infiltration in paediatric dentistry - a review. Int J
when it is not possible to treat and fill a cavity in the same visit, for safety reasons in c u r Res 2020; 12 ( 12): 15298-1530 4. - 14. Schwendick e F. Managing carious lesions: consensus
relation to the pulp and the need to postpone it, reco111111 endations on carious tissue removal. Advances in Dental Research 2016; 28, 5 8-67. _ 15 .
in the case of caries of an incompletely erupted tooth (Fig. 16.10). seale NS, Randal l R. The use of stainless-steel crowns: a systematic literature review. Pediatr
oent. 2015 ;37(2): 145-60. - 16. Wright JT et al. Evidence-based Clinical Practice Guideline for
To be successful, the risk of caries should be reduced (home and professional prophy­ th e U se of Pit-and-Fissure Sealants. American Academy of Pediatric Dentistry, American Dental
laxis) and regular check-ups should be carried out. Associ_ation_- Pediatr Dent 20 1 6;3 8(5): 1 20-136. - 17. Wright JT et al. Sealants for Preventing and
Arrestmg Pit-and-fissure Occlusal Caries in Primary and Permanent Molars. A systematic review
of ra ndomized controlled trials - a report of the American Dental Association and the American
Academy of Pediatric Dentistry. JADA 2016; 147(8):631 -45.

Fig. 16.10. Acute primary caries in an incompletely erupted permanent molar, reparation leavi ng
a demineralized layer at the bottom of the cavity, filling with glass-ionomer cement.

Non-selective removal to hard dentin - formerly known as complete caries remo­

val, together with the demineralised layer from the lateral walls and cavity floor, is not
a technique currently recommended, in both deciduous and permanent teeth.

References
I . Alhowaish L. Non-invasive and Minimally I nvasive Management of Carious Lesions in
Children: A Scoping Review. J Res Med Dent Sci, 2021, 9 (S I ): 1 -8. - 2. American Academy of
Pediatric Dentistry. Pediatric restorative dentistry. Pediatr Dent. 2017;3 9(6): 312-24. - 3. Bj0rndal
L et al. Management of deep caries and the exposed pulp. I nt Endod J. 2019; 52(7):949-973. - 4.
Clarkson JE et al. Selective Caries Removal in Permanent Teeth (SCRiPT) for the treatment of
deep carious lesions: a randomised controlled clinical trial in primary care. BMC Oral H ealth
2021;21, 3 3 6. doi.org/l 0.1186/s l2903-02 1 -01637-6. - 5 . Cianetti S et al. Sonic and ultrasonic
oscillating devices for the management of pain and dental fear in children or adolescents that
require caries removal: a systematic review. BMJ Open 20 1 8;8:e020840. doi : I O. l 1 36/bmjop­
en-2017-020840. - 6. Desai H et al. Minimally I nvasive Therapies for the Management of Dental
Caries - A Literature Review. Dent. J . 2021, 9, 147. https://doi.org/10.3390/ dj 9120 1 47. - 7. I nnes
NPT et al. Managing Carious Lesions: Consensus Recommendations on Terminology. Adv Dent
Res. 2016;28(2) :49-57. - 8. Jain S et al. Principles and Practice of Conservative Adhesive Resto­
rations: A brief review. U DR 2020; 5(2): I 10-116. - 9. Jose CS. Bioactive glass material and its
applications in dentistry. lnt J Dent Sci 2019, 2, 3: 1 -5 .
I 0. K her M S , Rao A. The Posterior Preformed Metal Crown (Stai nless Steel Crown).
In: Contemporary Treatment Techniques in Pediatric Dentistry. Spri nger, Cham. 20 1 9. doi.
org/ 1 0.1007/978-3-030- 1 1860-0_4. - 11. Ntovas P et al. Evidence provided for the use of osci l­
lating instruments in restorative dentistry: A systematic review. Eur J Dent 2017; 1 1 : 268-73 - 12.
Policy on Interim Therapeutic Restorations ( ITR). The Re ference Manual o f Pediatric Dentistry .

224 225
 Prevention of dental caries

Chapter 1 7 _ reducing the impact of bacterial biofilm - reducing microbiological burden and
cariogenicity (oral hygiene, antimicrobial agents, diet and accessibility to dental
plaque sites - sealing of fissures and anatomical cavities),
Prevention of dental caries _ supporting remineralisation - influence on saliva secretion, supply of calcium,
phosphate and fluoride ions (diet, prophylactics, chewing gum).
Anna Turska-Szybka, Dorota Olczak-Kowalczyk
Prevention in the postnatal period may be of the nature of primary prevention,
co nsisting in maintaining a balance between demineralization and remineralization in
the absence of symptoms of dental caries, or secondary, which consists in eliminating
the symptoms of the disease and restoring the balance between demineralization and
The essence of dental caries prevention is to eliminate or reduce the effect of the remineralization.
cau_s�tive factors, i.e. the cariogenic biofilm and the susceptibility of tooth tissue to the Caries prevention strategies can target the whole population, subgroups of the popu­
acids produced by bacteria, and to enhance the action of protective factors. The aim is lation or specific individuals (e.g. those at high risk of caries). In practice, a combination
to provide a balance between the constantly recurring processes of demineralisation and of these three approaches is needed to reduce caries, with individual care built on popu­
remineralisation. lation-based preventive strategies.
Prevention of caries should begin in the prenatal period and continue throughout a Depending on the role and responsibilities of those involved, these strategies can
person's life. be divided into three groups:
In the prenatal period, the activities include: I - community-based strategies,
influence on the susceptibility of dental tissues - ensuring proper odontogenesis, II - strategies based on dental professionals (professional tooth cleaning, varnishes,
duration of pregnancy, fluoride gels and foam, fissure sealants, antibacterial agents),
- shaping the child's taste preferences - diet, III - individual strategies involving self-care (fluoride agents: toothpastes, mouthwa­
delaying the colonisation of the child's mouth with cariogenic bacteria (primary­ shes, gels, supplements, gels and mouthwashes with chlorhexidine, diet, non-car­
primary prevention) by reducing the number of cariogenic bacteria in the mother's iogenic sweeteners).
mouth (oral hygiene, elimination of active lesions, antimicrobial measures, non­
cariogenic diet).
During pregnancy, it is necessary to reinforce preventive and therapeutic measures Health education
due to factors that increase the risk of oral diseases, including dental caries (lowering
of the pH and buffering capacity of saliva, reduced saliva production, mouth brea­ Health education is the process of shaping the habit of caring for one's own and
thing, hygiene negligence, dietary mistakes (frequent snacking, including those contai­ others' health and the ability to create a healthy environment, which enables the
ning sugar), gastrointestinal disorders (reflux, vomiting). acquisition of competences (skills, knowledge and health attitudes) that are necessary
In the postnatal period, the activities directly concern the child and take into ac- for responsible participation in social life. Health education is a lifelong process. It is an
count: integral part of health promotion. Its effectiveness depends on the active participation
delayed colonization of the oral cavity by cariogenic bacteria (primary prevention), of all sections of the community, including parents, carers and pre-school and school
effect on the susceptibility of dental tissues to acid produced by bacteria in the pre­ educators, children and young people.
eruptive and post-eruptive periods,

226 227
Compendium of Paediatric Dentistry Prevention of dental caries

Health education should address: well-being, a good quality of life, an attractive, aesthetically pleasing smile, no pain or
- nutrition and the promotion of non-cariogenic eating habits, discomfort when eating. The educator should be empathetic, willing to explain and help,
- hygiene procedures and their systematic implementation, motivating and supportive.
promotion of fluoride compounds and other measures and approaches in the Motivational interviewing was proposed to improve the effectiveness of oral hygiene
prevention of caries disease, education. It is a patient-centred counselling strategy aimed at improving the patient's
f
- the beneficial ef ects of healthy and aesthetically pleasing dentition on physical healt h intrinsic motivation and changing their oral health behaviour.
and mental and social well-being, as well as the detrimental effects of diseases of the
masticatory organ, including loss of dentition, on general health and, in the case of Methods of caries prevention in the post-eruptive period
pregnant women, on the health of the child,
the importance of preventive examinations and treatment of deciduous and perman ent. The essence of prevention is to maintain the mineral composition of the hard den­
te�th, periodontal disease, dental maxillary defects and others. tal tissues by maintaining a demineralisation-remineralisation balance. Dental caries is
In health education, we can distinguish three stages: speaking, showing, performing. therefore prevented by creating conditions in the mouth that weaken the deminerali­
The patient should be listened to before any action is taken in order to assess knowledge, sation process and strengthen the remineralisation mechanisms. The remineralisation
then review what the patient is already doing and has done in terms of prevention, so that process is also used to treat early carious lesions. Suppression of demineralisation is
only possible changes can be made later. The recommendations or procedures presented by an essential function for promoting tooth rernineralisation. Remineralization involves
the teacher should be uncomplicated. The final stage is to give the patient the opportunity to capturing calcium (Ca+2 ), phosphate (PO/) and fluoride (F·) ions in slightly saturated
do what was previously recommended, what they have learned, providing help and support. saliva and directing these ions to the demineralization sites where they are deposited.
It requires the presence of partially demineralised crystals which, when exposed to su­
Motivation persaturated fluids, comparable to the minerals present in hydro xyapatite, can enlarge to
The prerequisites for the patient to implement health-pro moting behaviours are: their original size. Remineralization occurs at pH values in the range of 7.5 to 8.5, in the
awareness of the fact that they are (may be) susceptible to caries disease, presence of Ca+2 and PO/ ions, in liquids surro unding enamel crystals or derived from
recognition that the advice given to him is useful in real life and practical, partially demineralized dentin.
understanding that prevention is better than treatment, The conditions for supporting remineralisation and weakening demineralisation are:
the benefits obtained from a particular action are higher than the costs of providing - reducing the impact of the cariogenic bacterial biofilm and its effects on the tooth
the advice, so that the patient does not feel a loss, surface (mechanical cleaning of the tooth surface, use of fluoride agents and other
the feeling that the person giving them advice is competent and reliable, inspiring bacterial metabolic inhibitors, stimulation of saliva secretion, restriction of sugar
confidence. intake, use of pre- and probiotics, antimicro bial agents, sealing of pits and fissures
Despite the above conditions, the patient may still not feel motivated to take and anatomical cavities),
health-promoting action. It is helpful in these cases, for example, to show deminera­ - neutralisation of acids produced by bacteria and acceleration of the mineral-saturated
lisation and decay or bleeding gums using an intraoral camera. Encourage the patient state of the fluids surrounding the enamel by raising the pH of the oral enviro nment
in a way that is clear and understandable to him/her and present the possible conse­ through, among other things, the stimulation of saliva secretion, the use of arginine,
quences. Often, it can be more convincing to be told, for example, about the risk of bad - supplying the ions necessary for remineralisation.
breath or the loss of an aesthetically pleasing and healthy appearance of the teeth. It is The basic method of limiting the impact of the bacterial biofilm is mechanical clea­
worth outlining the benefits of health-promoting behaviour, such as self-confidence and nin g of teeth and the use of antibacterial agents.

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 Prevention of dental caries
Compendium of Paediatric Dentistry

Oral hygiene, antimicrobials

soft bristle plastic toothbrush:
The most common oral hygiene practice to mechanically control plaque is teeth cleaning. tooth brushing using the Fones
- manual or electric,
method:
lt is recommended to brush the teeth twice - in the morning and in the evening. Morning - with a small, rounded head,
From the eruption of - with circular movements of the
brushing should take place after breakfast and evening brushing after supper. No food or li­ - with a wide handle for
the first deciduous teeth vestibular surfaces of the teeth,
comfortable holding by the
quids should be consumed after evening brushing due to a reduction in the natural cleaning of to the age of 5 years or - horizontal/scrubbing movements
parent and then by the child,
in children with special of the occlusal surfaces of the
the teeth with the tongue and facial muscles, as well as less saliva production at night. possibly with a disc (to
needs teeth,
prevent the toothbrush from
Before brushing, the mouth should be rinsed with water and spit out, removing food - sweeping movements of the
being pushed too far into the
residues. The minimum brushing time required to effectively remove plaque is appro­ lingual surfaces of the teeth
mouth)
ximately 2 minutes.
After brushing, spit out the excess paste without rinsing to prolong the protectiv e teeth cleaning using the sweeping
method (roll):
effectlOf the fluoride from the paste. - with rotary and sweeping
After use, the toothbrush should be thoroughly rinsed under running water and set in movements on the lingual and
soft bristle plastic toothbrush:
vestibular surfaces of the teeth,
a cup with the "head" upwards to dry. Do not store toothbrushes in airtight packaging, as - with a head size adapted to
From the age of 6 brushing at a 45 ° angle to the
a moist environment promotes the multiplication of bacteria. the child's mouth,
tooth surface,
- manual or electric
The toothbrush should be replaced regularly every 2 to 3 months ( unless it has pre­ - with a horizontal (scrubbing)
motion on the occlusai surfaces
viously worn out). After infectious diseases, it is advisable to replace the toothbrush of the teeth, the brush perpen-
previously used, as a period of upper respiratory tract infection favours colonisation of dicular to the tooth surfaces
the toothbrush with pathogens.
moving the scraper from the back
Both e lectric and manual toothbrushes are effective at removing plaque, although
to the front of the tongue, cleaning
power toothbrushes are superior to manual toothbrushes in both short-term and long- the root and then its lateral sur-
faces,
term plaque control.
From 6-8 years of age brushes and tongue scrapers rinse the scraper after each move-
To clean the spaces between the teeth more thoroughly, dental floss, bands or inter- ment,
tal
dental brushes and irrigators are used. The irrigator allows you to clean the interden cleaning the base of the tongue
after a night out
spaces and massage the gums, thanks to a stream of water under pressure. and before going to bed
The type of sanitary utensil and method of plaque removal recommended for use with
a child of different ages is shown in Table 1 7 . 1 . From 4-5 years of age;
for children with dis- a spray containing suitable sub-
abil ities or who cannot stances cleans teeth, interdentai
Tab. 1 7. 1 . Accessor ies and oral cleansing methods according to the age of the child. use toothbrushes at the dental irrigators spaces and massages the gums;
Age Accessories Method time due to the risk of the water jet should not be directed
increased bleeding of towards the gums
baby accessories rol led up or the gums
placed on the index finger:
- rubber or silicone brush, cleaning and massaging the gingi-
From 0 to 6 months - special m icrofibre thimble, rinsing the mouth for 30 seconds
val folds From the age of 6 rinses
- a piece of gauze or a cotton and then spitting out the liquid
handkerchief,
- wipes with xylitol

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Compendium of Paediatric Dentistry Prevention of dental caries

before brushing to make it more For the youngest, up to 3 years of age, it is recommended that the parent (caregiver)
effective; applies a toothpaste with a concentration of l 000 ppm fluoride in smear or rice-size amount
the thread, which is stretched
between the index fingers, is i ntro- to the toothbrush. Remove excess paste with a damp gauze pad. It is not necessary to teach
From 8- 1 0 years of age duced into the space between the young children to rinse their mouth after toothbrushing, as the child usually does not under­
or earlier; after eruption dental floss, tapes teeth in an upward and downward
motion along the tooth surface and stand this activity and will usually swallow the water along with the toothpaste. Systematic
of second deciduous
molars applied to the cleans their contact surfaces; sw allowing of fluoride toothpaste at around 2 years of age can result in white spots on the
child by the parents do not perform sawing move- front permanent teeth. Brush your teeth in the morning and evening. If the child is breast­
ments. Floss gently to avoid da-
maging the gums fed or formula-fed, the teeth should also be brushed after a night feeding.
cleaning interdental spaces with
interdental brushes
horizontal movements Pre-school child - 3.-6'" year
The amount of 1000 ppm F paste applied to the toothbrush should be increased to
Youngest child, up to 3 years of age the equivalent of a pea size. Children should gradually be made aware that toothpaste
Oral care should start in the first months of a child's life, no later than the eruption of should not be swallowed but spit out. Children up to around the age of eight have not yet
the first deciduous tooth. Parents should clean the mucosa and gingival folds regularly developed sufficient manual dexterity to clean their teeth themselves, so it is the parents'
from early infancy - every evening before bedtime. The aim of the hygiene routines started responsibility to clean their children's teeth effectively. Particular attention should be
during this period is to keep the mouth clean and to get the child used to oral manipulation. paid to cleaning the occlusal surfaces of the not yet fully erupted first permanent molars.
The baby may bite the mother's finger when trying to put it in the mouth and may not The end bristles (elongated in some brushes) should be placed at such an angle as to
want to open the mouth. The mother can then inse1t her finger around the angle of the sweep food remains from under the overhanging gingiva.
baby's mouth and then slide her finger along the inner surface of the cheek to the back of
the mouth. Then insert a finger gently between the upper and lower gingival folds or the Children > 6 years of age and adolescents
upper and lower teeth and, when the child opens the mouth, the whole mouth can be wiped. Recommendations:
A soft toothbrush should be used to clean the teeth to remove food debris from the teeth and - toothbrushing with a fluoride toothpaste with a concentration of 1450 ppm up to 2 cm,
gently massage the gums. From this point onwards, the child should be taught to hold the - using dental floss to clean the interdental spaces,
brush in his or her hand, place it in the mouth and carry out simple cleaning movements. - using a fluoride rinse or chewing sugar-free gum for 10 minutes no more than three
Toothbrushes for oral hygiene of young children can be manual or powered by elec­ times a day if the child is unable to brush after meals during the day. Fluoride rinses
tricity (electric and sonic). There are sonic/electric toothbrushes on the market for even should be used at a different time than brushing teeth with fluoride toothpaste.
the youngest children. They have soft bristles and, thanks to their gentle vibrations, al­ A dentist may recommend a toothpaste with a higher fluoride content (5000 ppm) to
low the surfaces of the teeth and gums to be thoroughly cleaned. They are equipped with a patient over 1 6 years of age if he or she identifies an increased i-isk of caries disease,
a timer that signals every 30 seconds to move to the next quadrant of the dental arch. The e.g. in patients with braces, xerostomia.
effectiveness of brushing depends on the correct use of the toothbrush, not the type of In addition to the fluoride compound and substances that facilitate cleansing, tooth­
toothbrush. Electric toothbrushes require a different brushing technique - their heads, pastes may also contain ingredients that promote remineralisation (calcium compounds,
by performing rotating and oscillating-pulsing movements, remove plaque from the sur­ hydroxyapatite) or neutralisation of the oral pH (arginine).
face of the tooth with which they are in contact, so each tooth surface should be cleaned It is also a good idea to use accessories to help clean the teeth, especially cleaning the
separately, without leaving out any tooth. The brush should not have hard bristles. in tcrdental surfaces. To do this, use dental floss, an interdental brush or an irrigator.

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Prevention of dental caries

Dental floss is waxed or unwaxed, available in different scents and thicknesses. Floss, The disadvantage of traditionally used products such as chlorhexidine is the short
in addition to mechanically cleaning the surface between the teeth, can provide sub­
retention time in the mouth. Recently, a mineral-binding micellar system has been deve­
stances with anti-caries (fluoride or xylitol) or antibacterial effects (e.g. chlorhexidine) .
loped that not only binds quickly to the tooth surface, but also releases the encapsulated
They can be multi-fibre (nylon, waxed) or single-fibre (polytetrafluoroethylene - PTFE). medication over a longer period of time. This was achieved by covalently attaching the
PTFE floss is softer than traditional nylon floss and hence easier to move between teeth .
tooth-binding molecules to the ends of the pluronic copolymer.
They are also less likely to break or fray. For those with fixed braces, floss with a stiff end The plant extracts that have been shown to inhibit S. mutans are the water-soluble
is recommended, which is easier to insert into hard-to-reach interdental spaces.
in gredient of the Labiatae family, the juice of the Vaccinium berry plant, the essential oil
T he use of antibacterial agents is increasingly raising concerns about long-term
composition of Co/eusforskohlii.
antimicrobial resistance and the negative impact on the ecology of oral microbes. Anti­ Antibacterial peptides - show strong action against a wide spectrum of bacteria,
microbials used to prevent dental caries are presented in Table 1 7.2.
penetrating the inside of the cell and disrupting metabolic mechanisms.
�
Tab. 17 .2. Antimicrobial agents used in the prevention of dental caries.
Other technologies supporting remineralization include: iontophoresis (transfer­
Mechanism ring the appropriate amount of the drug in a specific area of the tooth surface), UV rays
Active substance of action Means Side effects
and effectiveness (initiating some chemical reactions, e.g. hardening of the varnish, bactericidal action),
discolouration of the teeth laser (increasing the content of calcium and phosphate ions and reducing carbonate ions
and tongue, soreness and in hydroxyapatite), ozone (bactericidal action, supporting the removal of proteins from
peeling of the mucous
the demineralized tooth structure and diffusion of calcium and phosphate ions into the
cationic bis-biguanide membranes, temporary
varnish, gel, spray,
with a wide spectrum taste disturbance, swelling tooth), photodynamic therapy (uses light to activate the photosensitizing agent in the
toothpaste, mouth-
of action, including of the parotid gland and presence of oxygen, which results in the formation of reactive radicals inducing cell
Chlorhexidine wash and chewing
against S. mutans; hypersensitivity;
(CHX) gum. 0.05% C HX death; exhibits antibacterial action; erythrosine is a photo-sensitizer suitable for S. mu­
advantageous sirnul- the risk of altering the corn-
mouthwash and 1 %
taneous use of C l-IX position of the oral micro- tan.s).
Cl-IX in gel form
and fluorine flora by mass destruction of
bacteria and the develop-
rnent of other antimicrobi-
Isolation (limiting the access of cariogenic bacteria and the build-up of food residues)
al-resistant bacteria
pastes and rinses Sealing of fissures and pits creates a protective layer preventing further proliferation
broad spectrum anti-
Triclosan ( currently withdrawn of cariogenic bacteria, as well as a barrier preventing the acquisition of
bacterial action nutrient sub­
from use)
strates by bacteria present in anatomical fissures. I t is recommended to use
consists of an iodine (I) 10% PVP-1 solution resin-based
molecule and polyvi- rubbed (1-2 ml of
sealant as the first-choice material, while in cases of difficulty maintaining
the dryness of
nylpyrrolidone (PVP). preparation) into the treatment area - sealants based on glass-ionomers.
PVP itself has no anti- tooth surfaces or I ndications for sealing:
microbial activity, it has applied to trays; iodine allergy must be
Iodine povido- - all deciduous and permanent teeth susceptible to caries of anatomical fissures,
an affinity for the bacte- I % mouthwash ( 10 excluded before starting
nate (PVP-1)
rial cell membrane, thus ml PVP-1 for I min.); treatment - in children and adolescents with systemic diseases and physical and
delivering the active PVP-1 with fluoride
intellectual
disabilities,
iodine molecule directly varnish for rernine-
to the surface of the ralisation and caries - all caries-prone fissures and pits in patients at high risk of caries,
rnicroorganisrn prevention

234
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Compendium of Paediatric Dentistry Prevention of dental caries

- narrow and deep fissures with a high degree of plaque retention due to the high r i sk Glass-ionomer material:
of caries development, _ cleaning of the tooth surface (as mentioned above),
only teeth without carious decay. isolation of the treatment area (as above),
Bis-GMA resin-based materials (resin composite fissure sealants or flowable res i n - does not require etching and an adhesive system; possibly a conditioner for
composites and compomerics) require orthophosphoric acid etching prior to app lica­ I 0-20 s,
tion of the sealant. Materials based on glass-ionomer cements combine chemically wi th - drying the tooth with a gentle stream of air to obtain a slightly damp surface of the
enamel and dentin (or conditioner), used when it is impossible to maintain the dryness enamel,
of the treatment area (erupting or freshly erupted tooth, non-cooperative patient), release - preparation of the material mixing the capsule in a shaker or plastic spatula (powder
fluoride that has a bacteriostatic effect on the adjacent enamel. and liquid in a ratio of 1 : 1 ),
- rapid placement of the material on the tooth surface to be sealed using a dispensing
cannula or mixing tip and even distribution of the material '
Sealing procedures
- light-cured bonding/varnish or glazing of the applied glass-ionomer material,
- material binding (total setting time: 4-6 min.),
Resin-based sealants
cleaning the tooth surface with a prophylactic toothpaste with pumice (fluoride­ - correction of the occlusion height (as above) and possibly correction of the sealing
free) and a rotary brush or air abrasion and rinsing the cleaned surface, surface,
isolation of the treatment area from moisture and saliva (lignin rolls, cofferdam and - re-coating of the material with varnish.
salivary gauze),
etching of the enamel within the wells and furrows (37% orthophosphoric acid in Flowable composite resin or glowable compomer:
the form of liquid or gel) for 20-30 s, Procedures as above.
rinsing the etching gel with a strong water stream (20-30 s) and drying the tooth Note! Adhesive systems are recommended.
with a gentle air stream to obtain a chalk-white surface of the enamel; in the case Some materials after the use of an etching gel (37% phosphoric acid) require the use
of salivation onto the etched surface, repeat etching ( 1 5-20 s), of a "dry" agent, which is a special primer-dryer for enamel
- application of the sealant with an applicator, brush or brush, dispensing cannulas, A glass-ionomer sealant can provide a "transitional" sealant until the tooth erupts and
directly from the microtips and spreading the sealant, is replaced with a composite sealant. Follow up sealant checks should take into account
before applying the sealant, an adhesive system (low viscosity hydrophilic coupling the retention assessment and possible re-application at total loss or repair of the lost part
system) can be used, of the sealant, in accordance with the procedure presented.
waiting 15 s to allow the sealant to penetrate deep into the pits and fissures,
- polymerisation (time according to material manufacturer's recommendations: Sugar substitutes

20-40 s),
adjustment of the contact points between the maxillary and mandibular teeth using Non-cariogenic sweeteners can be divided into two categories: high-intensity sweet­
eners such as saccharin, sucralose, acesulfame-K and aspartame, and polyols, low-calorie
a articulating paper; in the case of excess material, removing it with diamond bur
sugar replacers such as xylitol, stevia, erythritol, sorbitol (Tab.17.3). They occur naturally
checking the retention of the sealant on the tooth surface using a probe.
or are chemically synthesized. Sugar alcohols (polyols) are found in many plants. They are
Do not use in patients with an allergy to methacrylates!
not fermented by micro-organisms and are therefore considered non-cariogenic.

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Prevention of dental caries

Chewing gum with polyols should be used in children and adolescents twice a day , f
growth of bene icial organisms at the expense of cariogenic organisms, disrupting the
after about 10 minutes. Adverse reactions to higher doses of polyols include abdomin al
e xtracellular polysaccharide matrix of oral biofilms. The aim of the measures should be
pain, bloating and diarrhoea.
to try to move the biofilm from a state of dysbiosis to a state of symbiosis with the tooth.
Oth er strategies against demineralization include neutralizing bacterial acid using cal­
Tab. 1 7. 3 . Sugar substitutes. f
cium carbonate as the buf ering effect of plaque pH and sodium bicarbonate to provide
Sugar Mechanism of action an alkaline oral environment. Alternatives include calcium-containing agents such as
Means
substitute and effectiveness lactate, calcium glycerophosphate and calcium phytate, as well as ammonia toothpastes,
inhibits the growth of cariogenic bacteria, re- chlorophyll-containing toothpastes and anti-enzymatic toothpastes. SensiStat techno­
duces the cariogenic potential of plaque, stimu-
!ates the secretion of saliva with a high content logy (calcium carbonate carriers) - contains bicarbonate, arginine, amino acid complex
of minerals (remineralization), and calcium carbonate molecules. The arginine complex is responsible for the adhesion
I inhibits the dissolution of enamel in acids
of calcium carbonate particles to the surface of the enamel and dentin, allowing slow
(reduces the diffusion of Ca+2 and PO/-ions), food products, chewing gum,
Xylitol affects the bioavailability of calcium in saliva jellies, toothpastes, mouthwa- dissolution and release of calcium.
(remineralization of subsurface enamel lesions), shes, tissues with xylitol The therapeutic approach should focus on understanding key aspects:
toothpaste with F and 10% xylitol reduces
l . the importance of factors influencing the oral biofilm in health and disease, including
the incidence of caries by 13% compared to a
paste containing only F, the role of sugars and diet, healthy and dysbiotic microbiome profiles, the role of
daily dose in the prevention of caries: 7- 1 0 g transmission and the acquisition of microbiome profiles throughout life,
of xylitol/day (min. 4 g/day), 3-5 times a day
2. ways to manage the oral microbiome associated with carries, including strategies to:
anti-plaque activity, reducing the formation
of biofilm and the growth of S. mutans and food products, increasing the number of beneficial species and changing their balance in the biofilm,
Lactobacilli, toothpaste, - inhibiting the key functions of harmful species (rather than killing them),
Stevia
reduction of the formation of extrace l l ular mouthwashes,
design and testing of beneficial probiotic phenotypes,
polysaccharides, increasing the rate of saliva chewing gums
secretion and salivary pH - intervention at the onset of the disease with an extended duration
. ,
- increasing the host's defence
inhibition of biofilm formation, lower adhe- against pathogenic microbes,
sion of S. mutans, S. sobrinus and Scardovia - increasing saliva function to promote symbiosis;
wiggsiae bacteria to the surface of teeth in food products,
3. the importance of diagnostics - including dysbiosis markers - and explorin
plaque and saliva, lower expression of bac- toothpaste, g their role
Erythritol in strengthening caries risk assessment pulpectomy.
terial genes involved in the production of mouthwashes,
transferases, chewing gums The use of prebiotics and probiot ics is a complementary method of prevent
reduces the risk of caries more effectively ing ca­
than sorbitol and xylitol ries. A prebiotic is "an indigestible food ingredient that benefits the host
by selectively
anti-plaque activity, reducing biofilm forma-
stimulating bacterial growth and thereby improving the health of the host".
Sorbitol
Prebiotics are
food products, chewing gum arginine, dietary fibre and oligosaccharides.
tion and the growth of cariogenic bacteria
Arginin e is an amino acid that occurs naturally in low concentrations
in saliva.
Impact on the bacterial biofilm Health-associated bacteria in the oral biofilm can act as arginolytic via
the arginine de­
Oral biofilm homeostasis is a key element in maintaining oral health, which is why a minase system (ADS). Arginine promotes the growth of arginoly
tic commensals (i.e. S.
it is recommended to limit the cariogenicity of the bacterial biofilm by modulating sanguinis, S. parasanguinis, S. gordon ii etc.), producing an ammon
ia metabolite that is
its composition by manipulating the oral environment in order to selectively favour the hig hly alkaline and causes an increase in pH in the oral environm
ent (Fig. 17.1 ).

238
239
Compendium of Paediatric Dentistry Prevention of dental caries

Arginolytic m icroorganisms tains more bicarbonates, which raises its pH and significantly increases its buffering
Arginine
(S. sang11is, S. gordo11ii i Lactobaci/li spp.) capacity, and more calcium and phosphate ions than resting saliva.

!
Many factors determine saliva secretion, such as the time of day (most saliva is se­
creted in the late afternoon, least during sleep), the sight, taste and smell of food, chewing
\ Ammonia activity, body hydration, nutritional status and general health. The salivary glands are
neutralisation of acids produced by other stimulated by the very act of chewing and the taste of food, especially acidic food. It is

!
bacteria
therefore important to ensure that the child eats resilient foods.
Chewing sugar-free gum causes a 10- 12-fold increase in saliva secretion (from a
Increased pH resting value of 0.4-0.5 ml/min to about 5-6 ml/min). Secretion decreases to 2 ml/minute
after about 5 minutes and gradually to 1.2-1.5 ml/minute after 20 minutes. Increased
F ig. 1 7 . 1 . Mechanism of action of arginine. salivary secretion may persist for up to 2 hours. Chewing gums may additionally provide
antibacterial ingredients, e.g. xylitol.
This promotes remineralisation and modifies and reduces the cariogenicity of the It has been shown to reduce the incidence of caries in people who chew sugar-free
bacterial biofilm. Toothpastes containing 1.5% arginine, insoluble calcium carbonate gum for twenty minutes after a meal and reduce the burden of oral S. mutans bacteria up
and 1450 ppm F in the form of sodium monofluorophosphate are more effective than to five years after two years of using xylitol-containing gum.
fluoride-only toothpastes in preventing dental caries. However, long-term use of arginine Cheeses:
poses a risk of increased plaque alkalisation and excessive growth in the mouth of - stimulate saliva secretion and acid neutralisation,
anaerobes such as Porphyromonas gingivalis. Foods rich in arginine are: seeds (sunflower, - they are a source of calcium and phosphate ions, because casein phosphopeptides
pumpkin, squash), nuts, beans, soya, watermelon, tuna. released by cheese proteolysis after its consumption lead to the formation of casein
Probiotics are defined as "live micro-organisms that, when administered in adequate phosphopeptide complexes with calcium phosphate (CPP-CP), which increase the
amounts, confer health benefits to the host". Lactobacilli spp. probiotics have been ex­ level of calcium and phosphates in the dental plaque, thus increasing its pH,
tensively studied clinically with empirical caries prevention effects. However, probiotic - reduce the adhesion of S. mutans to the tooth surface,
colonisation in the mouth is transient, so probiotic survival enhancers are needed to - the lipids in cheese can reduce demineralisation by forming a coating on the surface
provide long-term caries prevention benefits. of the enamel and through the antibacterial action of fatty acids.
Synbiotics are defined as "mixtures of probiotics and prebiotics that benefit the host
by improving the survival and implantation of live microbiological dietary supplements". Prophylactic remineralizing agents can be classified as fluoride and non-fluoride.
Such a mixture can compensate for the disadvantages of the individual components, while Fluoride prophylaxis is addressed in Chapter 18.
giving a synergistic effect of caries prevention. In vitro studies highlight the possibility
of using the synbiotics L-arginine and L. rhamnosus GG in the prevention of caries. The Non-fluoride remineralization systems are divided into:
combination of oral prebiotics (arginine) and probiotic arginolytic strains (S. dentisani and - endogenous systems for the utilization of calcium phosphate, e.g. proteins,
S. A 12) is potentially promising in preventing caries and poses a challenge for the future. peptides, dendrimers, which are capable of adsorption to specific sites (subject to
Stimulation of saliva secretion can be achieved by eating resilient and aromatic rernineralization) and accumulation of calcium and phosphate present in saliva.
foods, cheese, chewing gum (to strengthen sugar-free prophylaxis), the use of CPP-ACP Accumulation of ions leads to supersaturation of calcium and phosphate and
preparations. Facilitates oral cleansing and acid neutralisation. Stimulated saliva con- ultimately to remineralization of enamel,

240 24 1
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Compendium of Paediatric Dentistry Prevention of dental caries

exogenous systems for the utilisation of calcium phosphate, e.g. nanocrystalline and p hate ions to the oral cavity. During toothbrushing, intra-oral agitation causes ACP to
amorphous calcium phosphates, which are delivered to remineralised sites via external precip itate immediately on the tooth surface. This precipitate dissolves easily in saliva,
sources. The supplied solid calcium phosphates are either dissolved and remineralise m aking it available for remineralisation. Recommended for remineralisation of early
the HA prisms, or they adsorb to the enamel prisms and combine with the crystal prisms . cari ous lesions after orthodontic treatment. Calcium and phosphate are not stabilised,
Depending on the patient's treatment needs, for example, fluoride and other com- all owing the two ions to mix into insoluble precipitates before they are available for
pounds can be added. According to Walsh et al, the requirements for an ideal reminera­ contact with saliva or enamel.
lising agent are:
diffusion into subsurface lesions or delivery of calcium and phosphate, Systems containing stabilised calcium phosphate
does not provide excess calcium,
-- is not conducive to the formation of calculus, Casein, the phosphorus protein of cow's milk, is known to interact with calcium

works at an acidic pH, and phosphate and is a natural food ingredient (milk and dairy products). Its techno­
works in patients with xerostomia, logical name is casein phosphor-peptides-amorphous calcium phosphate (CPP-ACP).
- increases the remineralising properties of saliva, CPP s have the ability to bind and stabilise calcium and phosphate in solution and bind to
shows advantages over fluoride for novel materials. plaque and enamel, maintaining a supersaturated state to tooth enamel, reducing demi­
It is recommended to use topical non-fluoridated remineralizing agents: neralisation and increasing remineralisation. The combination of fluoride and ACP with
as a complementary therapy in patients with a high or very high risk of caries, CPP-ACP can produce a synergistic effect of enamel remineralisation. Also, CPP-ACP is
for the reduction of tooth erosion in patients with gastro-oesophageal reflux or other effective in reducing the depth of lesions better than fluoridated toothpaste.
dental diseases of mixed aetiology, The CPP-ACPF complex is used in the treatment of white spot caries lesions, during
for the reduction of demineralisation in people undergoing orthodontic treatment and after orthodontic treatment, enamel hypomineralisation, fluorosis treatment, after
with fixed braces, tooth whitening, tooth hypersensitivity, after scaling, for erosion treatment, for caries
- for enamel regeneration in early carious lesions, stabilisation, for root caries treatment and for patients with special needs. CPP-ACP can
for enamel regeneration after aggressive whitening techniques, be used in the form of toothpaste, mouthwash, lozenges, chewing gum and mousse.
- in cases of fluorosis or tooth hypersensitivity. The ability of CPP-ACP to deliver high concentrations of stabilized ca+2 and PO -3 4

Fluoride-free remineralisation therapies have been classified according to their mode ions may be particularly important in highly cariogenic environments, where fluorides
of action as: and saliva homeostatic mechanisms alone are not enough to repair developing lesions.
- agents affecting tooth enamel (calcium phosphate products, unstabilised amorphous Dicalcium phosphate dehydrate (DCPD) - is added to toothpaste to protect against
caries (in this case it is combined with compounds containing F such as NaF and/or Na
calcium phosphate systems, stabilised amorphous calcium phosphate systems, crys­ 2'

talline calcium phosphate systems), PO3 , F). Increases free calcium ion levels in plaque fluid (remains elevated for up to 1 2
- anti-biofilm agents, hours), enhances calcium incorporation into enamel.
agents neutralising bacterial acids. Alpha & Beta tricalcium phosphate (TCP) - is considered one of the possible ways
to increase the level of calcium in plaque and saliva. Products containing TCP are tooth­
Systems containing amorphous unstabilized calcium phosphate: ACP (Amor­
pastes with NaF (5000 ppm F) and varnishes with 5% NaF. TCP provides better surface
phous Calcium Phosphate) technology.
and subsurface remineralisation compared to 5000 ppm fluoride and CPP-ACP. The po­
The two-phase delivery system is a non-stabilised calcium phosphate system incor­
tential of TCP is promising, but more research is needed to confirm its effectiveness in
porated into a two-chamber fluoride toothpaste to separately deliver calcium and phos-
e nhan cing remineralisation.

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Compendium of Paediatric Dentistry Prevention of dental caries

Alkaline earth polyphosphates (metals), e.g. sodium trimetaphosphate(STMP) , Self-assembling peptides ( peptides that self-aggregate as cellular carriers) - enable
calcium glycerophosphate or hexametaphosphate are agents with the abi lity to i nhi b i t i ncreased mineral gain and inhibit mineral loss. Curolox® technology uses self-assem­
demineral ization and enhance remineralization. bl ing peptides (P 1 1 -4) for the regenerative treatment of early carious lesions. The remi­
ne rali sation process of the treated lesion takes 8- 1 2 weeks.
Bioactive glass materials Herbal components can influence mineral saturation and precipitation, act as an­
B iogl ass(i<' is a multi-component inorgan ic compound composed of elements (si li­ ti m icrobial agents or stabilise col l agen, which can function as a scaffold for mineral
con, calcium, sodium and phosphorus) naturally occurring in the body. NovaMi n'� i s deposition. They have demonstrated the abi l ity to positively shift de- and remineralisa­
described as an inorgani c amorphous sodium calcium phosphate (CSPS) material th at tion processes. Among the most promising are Galla chinensis, hesperidin, gum arabic,
has been designed based on materials known as bioactive glasses. A lthough it is widely exudate - a liquid from acacia.
used in dentinal hypersensitivity, studies indicate its abi l ity to act as a biomimetic re- .
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Compendium of Paediatric Dentistry

- 1 9. N asseripour M, Newton .IT, Warburton F et al. A systematic review and meta-analy sis o r
the role of sugar-free chewing gum on Streptococcus mutans. BMC Oral Health 2 1 , 2 1 7 (202 J ).
20. Pukallus M L, Plonka KA, Barnett AG, Walsh LJ, Holcombe TF, Seow WK. A ranclom i secI,
C hapter 18
controlled clinical trial comparing chlorhexicline gel and low-close fluoride toothpaste to p revent
early childhood caries. l nt J Paecliatr Dent. 20 1 3 ; 23: 2 1 6-224. - 2 1 . Riley P, Moore D, A h med
F, Sharif MO, Worthington HY. Xylitol-containing products for preventing dental caries in ch il­ Fl u oride in prevention o f dental caries
dren and adults. Cochrane Database Syst Rev. 20 1 5 ; 26:CD0 I 0743 . - 22. Stein C, Santos N M L,
Hilgert JB, Hugo FN. Effectiveness of Oral Health Education on Oral Hygiene and Dental Car­ An n a Turska-Szybka, Dorota Olczak-Kowalczyk
ies in Schoolchildren: Systematic Review and Meta-analysis. Community Dent. Oral Epiclernio l.
20 1 8 ;46:30-37. - 23. Sitthisettapong T, Phanturnvanit P, H uebner C, De Rouen T. Effect of CPP ­
ACP Paste on Dental Caries in Primary Teeth: A Randomized Trial. Dent Res. 20 1 2; 9 1 : 847- 85 2.
- 24. Stoleriu S, Andrian S, Pancu G, Nica I, lovan G. The use of arginine-containing toothpaste s
Why Fluoride is Important
in dental hard tissues reminera l ization. Rom J Oral Rehab. 20 1 6; 8( 4): 1 2-6. - 25. Tayab T, Rai
K, Kumari V, Thomas E. Effect of chewing paneer and cheese on salivary aciclogenicity: a corn- ·
parati\\e study. J nt J Clin Pediatr Dent. 20 1 2;5( 1 ):20-4. - 26. Twetman S, Keller M K . P robiotics Fluoride plays an important role in caries prevention, acting in several ways. Two pe­
for caries prevention and control. Aclv Dent Res. 20 1 2 Sep;24(2):98- I 02. - 27. Walsh T, Olivei­
ra-Neto J M, Moore D. Chlorhexicline treatment for the prevention of dental caries in children an d riods are distinguished in the anti-carious effect of fluoride: pre-eruptive and post-eruptive.
adolescents. Cochrane Database Syst Rev. 20 1 5 ; 4:CD008457. - 28. Wolff MS, Schenkel AB. Th e In the pre-eruption period, fluoride participates in the primary mineralization of
Anti caries Efficacy of a 1.5% Arginine and Fluoride Toothpaste. Aclv. Dent. Res. 20 1 8, 29, 93-9 7.
enamel and maturation of enamel before tooth eruption:
- 29. Yu OY, Lam WY-H, Wong AW-Y, Duangthip D, Chu C-H . Non-restorative Management of
Dental Caries. Dent. J. 202 1 , 1 8;9( 1 0): 1 2 1 . - acts as a catalyst for the formation of the mineral phase of enamel, hydroxyapatite -
Ca i oCPO4)/OH\,
replaces hydroxyl ions (OH"), resulting in the formation of fluoroapatite,
fluorohydroxyapatite - Ca/PO4)3 OH 1 -xFx,
- promotes the correct formation of the crystal structure,
- promotes the formation of larger apatite crystals with lower carbonate content,
- is involved in pre-eruptive maturation of the enamel (removal of water and organic
substances), which promotes less acid solubility of the enamel,
- results in favourable morphological changes - more rounded cusps and shallower
fissures on the occlusal surface.
In the post-eruption period, fluoride affects:
- demineralisation and remineralisation processes (Fig. 17. I ),
- the deposition of bacterial plaque and the formation of changes in the bacterial flora,
- lowering the carbohydrate metabolism of plaque bacteria.

Methods of fluoride prevention

Fluoride prophylaxis methods are divided into:

- systemic (endogenous): active and passive,
- local (exogenous): group and individual - home or professional.

246 247
Compendium of Paediatric Dentistry Fluoride in prevention of dental caries

Systemic fluoride prophylaxis methods Fluoridated salt

The fl uoridation of table salt is recomm ende d by the W HO whe n wate r fluoridation
Collective, passive interventions cann ot be introduced. Studies on the e ffect of fluoridated salt on the prevention of dental
caries have found similar results to water fluoridation, and wh en the majority of salt for
Fluoridated water h ul11an consumption is fluoridated, the e ffi cacy of fluoridate d salt on a community scale
Th e optimal le ve l of fluoride in drinking wate r in relation to dental health has been is similar to that of water fluoridation. The study also showed social acce ptability, no in­
e stimate d to be around 0.7 mg/I (0.5-1 mg/I). According to the World H e alth Org ani­ crease in individual salt intake, no prove n increas e in enamel fluorosis, no other reported
sation (WHO), it should not exceed 1 .5 mg F/1. Currently, it is e stimated that aro und n egative health effects.
380 million p e ople worldwide r e gularly consume artificially fluoridate d water and The optimum fluoride content of salt depe nds on the ave rage salt intake and, accor­
50 million consum e drinking water containing the optimum concentration of fluoride . ding to th e W HO, should be at le ast 200 mg F/kg - wh en both table salt and salt supplied
from, natural sources. Artificially fluoridate d water is us ed by people in I reland, the to bakeries, restaurants, cantee ns are fluoridated, and 400 mg F/kg - when only table salt
UK, Spain, S erbia, the USA, Australia, N ew Ze aland and Canada. I n Poland, the vast is fluoridated. The iodisation of salt does not preclude the addition of fluoride to it. Fluo­
majority of the population us es water containing less than 0.5 mg F/1. In many re gions ridated salt is available in Peru, Colombia, Uruguay, M exico, Jamaica, and in Europe in
of the world whe re the natural wate r fluoride conte nt is spars e or low, fluoride com­ Austria, the Czech Republic, France, Ge rmany, Slovakia, Spain and Switze rland, wher e
pounds are adde d to the water to cariostatica\ly optimal lev els. Water fluoridation has approximately 250 mg F/kg is added.
b een proven to be an effe ctive and safe me thod of pre ve nting dental caries in childr en The reduction in caries associate d with the use of fluorinate d salt is 5 0%.
and adults. It was also found that the be n efits of wate r fluoridation with regard to caries
re duction far outweigh any possible n egative aesthe tic effe cts, i.e. the occurre nce of Individual fluoride supplementation, active
v e ry mild or mild de ntal fluorosis. Oral fluoride supplements are of limited use as a public h ealth measure. R ecommen­
The caries r e duction associate d with water fluoridation is estimated to be 30-59% for dations for dosage and the age at which oral fluoride supplem entation should b e started
deciduous teeth and 40-49% for p ermane nt teeth. are bas ed on s everal factors, including the level of fluoride in the wate r consumed, and
can the re fore vary from dep ending on the environment. Fluoride supplementation should
Fluoridated milk be conside red in children at high risk of caries, but improving the quality of toothbru­
Diffe re nt amounts of fluoride (NaF) are adde d to milk, but the most common con­ shing or using toothpaste with higher fluoride content is more be neficial. Howev er, it
centration is 5 ppm F/1. The pres ence of fluoride -binding calcium and protein in milk is not advisable for caries risk assesse d as low. B e fore its implementation, potential
results in l ess fluoride de livery to the body compared to fluoridated water. Th e use sources of fluoride supply should be assesse d, as well as the possibility and quality of
of fluoridate d milk is imple me nte d in the form of pre ve ntiv e programmes for school coope ration with the child's pare nts (caregivers), as the administration of fluoride tablets
children, who are give n 200 ml of fluoridate d milk (5 mg F/1) for 200 days a y e ar. Milk must take place systematically and ove r a long p eriod of time mider close supervision.
fluoridation programm es have been implem e nte d in Russia, Chile, the U K, Bulgaria It is beneficial to suck or chew fluoride tablets be fore swallowing to take advantage of
and Thailand. the local cariostatic effect of fluoride . Suppleme ntation is not re comme nded for children
The caries re duction associated with the use of fluoridated milk depe nds on the age under the age of 3 years and for young children with regular twice daily toothbrushing
of the child and the duration of use and is 40-50%. Afte r 3 years of drinking fluoridated with fluoride toothpaste.
milk, a 31% re duction in deciduous dental caries was observed compare d to non-fluori- With a fluoride content in water < 0.3 mg/I, it is recomme nded to consider fluoride
suppleme ntation after the age of 6 months at moderate or high caries risk (AAPD and
date d milk.

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Compendium of Paediatric Dentistry Fluoride in prevention of dental caries

ADA) or in children after the age of 3 years at high caries risk (Polish experts panel) w ith Brushing twice a day with fluoride toothpaste, in the morning and in the evening after
the involvement and cooperation of parents and dentist (Tab. 1 8. 1 ). Fluoride supplementa­ th e last meal (immediately before bedtime) is the primary method of preventing caries.
tion should be considered in children with bronchial asthma if there are contraindications to Th is treatment should be performed from the appearance of the first tooth in a child's
topical application of fluoride-containing agents and in children with intellectual disabilities. mouth , regardless of the level of caries risk. Up to the age of 8, children's teeth should be
brushed by their parents (carers). They, too, should apply the right amount of toothpaste
Tab. 1 8. 1 . Dosage of fluoride tablets/drops recommended by a Polish experts panel. to their toothbrush. In older children, adult supervision is recommended when the child
-
Age Recommended fluoride dose/day is brushing their teeth.
0-35 months 0 mg If left unattended, the child runs the risk of applying too much toothpaste and
3-6 years 0.25 mg sw allowing it, and of ineffectively removing plaque (biofilm), due to insufficiently
7- 1 6 years 0.5 mg developed manual skills. In children under 6 years of age, toothbrushing with a flu­
\
oride-containing toothpaste is the only form of fluoride home prophylaxis. In older
In Poland, tablets with sodium fluoride only are not available, Zymafluor D 500 can children and adolescents, especially with an increased risk of caries, mouthwashes
be ordered ( 1 tablet contains 1 2. 5 µg of cholecalciferol, equivalent to 500 LE of vitamin containing 1 00-225 ppm F to 900 ppm F may additional ly be used at home, and in
D3 and 0.553 mg of sodium fluoride, equivalent to 0.25 mg of fluoride). adolescents over 1 6 years of age, toothpastes with a high fluoride content (5000 ppm
The reduction in caries of permanent teeth in children aged 6- 1 6 years is 24%. There F) may also be used.
is no strong evidence demonstrating the efficacy of fluoride supplementation in the pre­ To increase the anti-carious effect of the fluoride contained in the toothpaste, it is ad­
vention of caries in deciduous teeth. visable to spit out the excess toothpaste after cleaning instead of rinsing the mouth with
water. It is advisable to demonstrate to the children's caregivers the appropriate amount
Methods of fluoride prevention local (exogenous): individual and group - home or uf toothpaste applied to the toothbrush.
professional
T he optimal dose of F is 0.05 mg/kg b.w, per day. Using a pea-sized amount of
paste, relative to a smear or rice-size amount, increases by more than 2 times the po­
Topical fluorides are defined as "systems that deliver fluoride to exposed surfaces of
tential amount of fluoride ingested by the child. A 2-year-old child weighing 1 5 kg
deciduous and permanent teeth at elevated concentrations to provide a topical protective
who brushes his teeth twice a day with a trace amount of paste and swallows the whole
effect and are therefore not intended for consumption". They can be used individually
amount, will take in 0.2 mg F, which is a dose of 0.0 1 3 mg F/kg b.w. If the same child
(toothpastes and mouthwashes) and professionally (gels, varnishes, foams, lotions).
brushes his or her teeth 2 times a day with a pea-sized amount of paste and swallows
the whole amount, he or she will take in 0.5 mg F, which is a dose of 0.033 mg F/kg
Topically applied fluorides individually
b.w. Children are also exposed to fluoride contained in food and drinks. Taking into
account additional potential sources and the risk of developing fluorosis at the time of
Home prevention
tooth formation, it is recommended to use a toothpaste (1000 ppm F) in a smear or
rice-size amount from the first tooth eruption to the age of 3 years, and then at the
Toothpaste age of 3-6 years - in the amount of pea grain (Tab. 1 8.2). This regimen is expected
The use of toothpaste containing fluoride compounds, either independently or in to maximise the anti-carious effect of F, while reducing the risk of developing fluoro­
conjunction with water fluoridation, has been recognised as one of the world's greatest sis compared to the previous recommendation of using a pea-sized amount of fluoride
public health achievements. The FDl call s on all countries to ensure universal access to paste from the age of 2 years.
fluoride toothpaste to combat dental caries and improve oral and overall health.

250 25 1
Compendium of Paediatric Dentistry Fluoride in prevention of dental caries

Tab. 1 8.2. Evidence on the safety of fluoride toothpastes. ....-- 6- I 0 I 000- 1 500 1 500
.---
I 0-12 1 500 2800*

--
Amount of F Daily dose Optimurn .--- 1 -2 c m, up to ful l
Amount of of F sup- daily 12-16 1 500 2800*
supplied with length of brush �
Paste quan- supplied F Body
toothpaste plied with dose of F 16-1 8 1 500 5 000
Age tity 1 000 with paste weight
ppm F for single
use
when bru-
shing teeth
(kg)
toothpaste
(brushing
per body
weight 0,05 - > 18 1 500 5 000

-
2 times a day 2 x daily) mg/kg/day •pas tes not available in Poland, pastes up to 1 500 ppm F are recommended.

6 footprint < 0.05 mg/

0.1 mg 0.2 mg 6 0.033 mg/kg
months (0.1 g) kg/day Pastes with high fluoride content contain 2800 ppm (not available in Poland) and
12 footprint < 0.05 mg/ 5000 ppm F. In the country there are pastes containing 1.1% sodium fluoride, i.e. 5000
0.1 mg 0.2 mg 10 0.02 mg/kg
months (0.1 g)
footprint
kg/day
--
< 0.05 mg/
ppm F or 0.5% F (5 mg Fig). The high fluoride concentration in the toothpaste increases
the concentration of fluoride in the oral environment, which reduces demineralising pro­
2 years
\
0. 1 mg 0.2 mg 15 0.0 1 3 mg/kg
(0.1 g) kg/day
cesses and increases remineralising ones, producing a clinically proven cariostatic effect.
pea-size < 0.05 mg/ These toothpastes are recommended for use at home in people over 16 years of age
2 years 0.25 mg 0.5 mg 15 0.033 mg/kg
(0.25 g) kg/day
with a high risk of caries who require intensive fluoride prophylaxis, including:
-- in patients treated with fixed orthodontic appliances,
For adult patients with a low caries risk, the use of a minimum of twice-daily fluo­ - in patients with an increased risk of caries, where existing oral hygiene practices are
ride toothpaste containing 1450 ppm F is considered a basic, sufficient model of caries proving inadequate,
prevention. In patients with an increased caries risk, additional application of fluoride - in case of the presence of incipient carious lesions in the crown and root area of the
preparations or the use of toothpaste with increased fluoride content is indicated. teeth, despite regular daily use of standard fluoride toothpastes,
Current FDI recommendations also recommended by Polish experts regarding the - when exposing dentin after scaling and other dental procedures,
use of fluoride toothpastes in areas with a content :S 1 mg F in drinking water are pre­ - in people with xerostomia.
sented in Table 18.3. Using toothpastes with a high fluoride content makes it possible to provide increased
amounts of fluoride without having to change daily hygiene habits. According to the
manufacturer, these toothpastes should be used every day, three times a day, at 2 cm,
Tab. 18.3. FDI recommendations for the use of fluoride toothpaste according to caries risk level.
for at least three to six months, instead of conventional fluoride toothpaste. Studies on
Fluoride content of the paste toothpastes containing 5000 ppm F show their beneficial effects on the teeth already
(ppm F)
Age
Amount of paste Caries risk
when used twice a day. Among other things, remineralisation of carious lesions after 2
in years
low high weeks of use, a reduction in the loss of enamel minerals and a protective effect on tooth
enamel in patients treated with fixed braces have been confirmed. The use of toothpastes
0,5-3 rice grain 1000 containing 5000 ppm F without rinsing after brushing results in a twofold increase in the
�
fluoride concentration in saliva and further reduces the accumulation of new bacterial
plaque compared to toothpastes containing 1450 ppm F. In adolescents aged 14-16 years
3-6 pea-size 1000 1450
�
with active caries, the use of toothpastes containing 5000 ppm F results in 40% less
caries progression than with conventional toothpastes.

252 253
Compendium of Paediatric Dentistry Fluoride in prevention of dental caries

Preventive efficacy of toothpastes containing at least 1 000 ppm F has been proven. for the use of fluoride preparations in children at increased risk of caries are included in
The efficacy of toothpastes containing 440/500/550 ppm F is questionable. It is believed Table 1 8.5. For patients using fixed orthodontic appliances, fluoride varnish is allowed
that toothpastes with concentrations lower than 1000 ppm F may have some benefi ci a l every 6- 1 2 weeks.
effect and can only be taken into account in children with a low risk of caries when there
Tab . 1 8.5 . Recommendations from Polish experts on the use of gels, foams and varnishes.
is a risk of fluorosis.
Age Risk of caries Gel, foam Varnish
�
Mouthwashes moderate no twice a year
Children under 6 years
The use of fluoride-containing mouthwashes also enhances anti-carious protection: high no 4 times a year
sodium fluoride (NaF), acidulated phosphate fluoride (APF), stannous fluoride (S11F0 ) Children c: 6 years and moderate twice a year twice a year
and amine-fluoride (AmF), sodium monofluorophosphate (SMFP) and ammonium flu- . adolescents high 4 times a year 4 times a year
oride (NHl), Studies show that mouthwashes with a higher fluoride content are more
effective in remineralising carious stains. Fluoride mouthwashes are recommended for Fluoride gels and foams
people over 6 years of age with caries risk assessed as moderate to high (Tab. 1 8.4). Due to the risk of overexposure to fluoride ( e.g. a child swallowing the gel or foam),
they should only be used in children over 6 years of age.
Tab. 1 8.4. Polish experts' recommendations on the use of mouthwashes. During the procedure, an appropriate amount of prophylactic agent should be used on
Age Risk of carious disease Rinse an individual spoon (up to 2-4 ml or about 40% of the spoon capacity), a saliva ejector
moderate no should be used, the child's head should be tilted forward along with the spitting of saliva
Children under 6 years of age
high no for 30 seconds after application. Application time 4 minutes. The patient should not eat
Children c: 6 years of age and moderate yes or drink for 30 minutes after application. In the case of the foam, an amount equivalent
adolescents high yes to \ of the- gel weight is sufficient to cover the teeth.
The reduction in caries in permanent teeth with fluoride gels was estimated at 28%. It
They are particularly recommended for children using braces, adults with prosthetic was also assessed that the use of gels in children with deciduous teeth in the prevention
restorations and in cases of reduced saliva secretion. There are no uniform recommenda­ of deciduous dental caries could result in a 20% reduction in dmf, but the evidence was
tions regarding the timing of their use in relation to toothbrushing. The greatest benefit described as low quality.
comes from rinsing with them at times other than brushing. It is recommended to use The prophylactic efficacy of fluoride foams is estimated at 24% for deciduous teeth
about 1 0 ml of the rinse for 1 -2 minutes. Mouthwashes containing about 1 00 ppm F are and 4 1 % for the smooth surfaces of permanent first molars (weak scientific evidence).
used twice a day, about 225 ppm F once a day, about 900 ppm F once a week. Rinses can
be used by children under parental supervision until they are sure they are not swallowed. Fluoride varnishes
The prophylactic efficacy of fluoride rinses is estimated to be around 26%. Fluoride varnishes have been developed to extend the contact time of tooth tissue
with fluoride. Varnishes usually contain a high concentration of fluoride and are avai­
Fluoride topical individual, professional applications (gels, foams and varnishes) lable in both low and high viscosity formulations. Formulas of fluorine compounds and
the ir concentrations used in varnishes available on the market include 5% NaF, 0.9%
Professional agents containing fluoride compounds (so-called professional fluoride difluoro silane and 6% NaF in combination with 6% CaF2 (56 300 ppm F). In countries
prophylaxis) are used for people at increased risk of caries. Fluoride gels, foams and with widespread fluoridation of drinking water, fluoride varnish is only recommended
varnishes should be applied in the dental office. Recommendations from Polish experts

254 255
Compendium of Paediatric Dentistry Fluoride in prevention of dental caries

for patients at increased risk of caries, whereas in countries with limited or no wa te D ental fluorosis is diagnosed on the basis of a proven more than optimal fluoride sup­
r
fluoridation, fluoride varnish is recommended for all children and adolescents, wit h th e the body during enamel development. A number of enamel developmental, genetic
pl y to
frequency of application increasing to four times a year for those at high risk of carie s. a nd environmental disorders can cause a misdiagnosis of mottled enamel. The clinical
The use of varnishes does not require age restrictions if the recommended dose s are pic ture of dental fluorosis depends on the dose received, the duration of exposure and the
adhered to (Tab. 18.5). individ ual age at which the dose is received.
The largest sources of fluoride exposure include toothpastes and other exogenous
Safety of Fluoride fluoridation preparations, supplements, fluoridated water and infant formulae based on
it, tea, certain juices and bottled waters, and seafood and chicken meat due to the fee­
Single doses of fluoride varnish containing 5% NaF (22 600 ppm): ding of poultry with fishmeal. In order to reduce the risk of developing dental fluorosis
0.10 ml for infants, in form ula-fed infants, it is recommended to prepare water-based modified milk with
o.;5 ml (= 5.65 mg F) for children over 1 year of age in deciduous dentition, a fluoride content of less than 0.3 ppm.
0.40 ml (= 9.04 mg F) during mixed dentition, The application of 0.50 ml of 5% NaF varnish provides 3-1 1 mg of fluoride,
- 0.50-0.75 ml (16.95 mg F) during the permanent dentition. the probable toxic dose (PTD) of 5 mg/kg of body weight. Fluoride varnish is the most
Toxic doses: concentrated fluoride preparation used in Europe, it contains almost 2 times more flu­
1 mg F/kg b.w. - early signs of poisoning, oride than the APF gel, but it does not pose a threat to health. It has been shown that
5 mg F/kg b.w. - likely toxic dose, the peak in serum fluoride concentration after application of 5% NaF varnish in young
- 14-28 mg F/kg b.w. - lethal dose (LD), children is only ½ peak values occurring after application of 1.25% APF gel. According
32-63 mg F/kg body weight - a certain lethal dose (CLD). to the results of the study in children aged 12 to 15 months, the baseline plasma fluoride
Mild gastrointestinal symptoms occurring after one hour are observed after ingestion concentration was 13 ± 9 µg/1 immediately after application of the 5 % NaF varnish
of 1 mg F/kg b.w. (nausea, excessive salivation, stomach pain, vomiting, diarrhoea), and 21 ± 3· �tg/1 5 hours after varnish application. The mean estimated peak plasma flu­
while they are more severe after an intake of about 5 mg F/kg b.w. oride after treatment was 57 ± 22 µg/1 and an average of 20 ± 4 µg/kg was retained. The
Early signs of intoxication (1 mg F/kg b.w.) may occur after a 2-year-old child amount of fluoride retained, not excreted in the urine, was 253 times lower than the acute
weighing 10 kg of 20 fluoride tablets containing 0.5 mg of fluoride (or 10 tablets of 1 mg toxic dose of 5 mg/kg. This is due to both the more precise amount of varnish applied,
of fluoride), while in older children with higher body weight, these symptoms will occur as well as its adherence to the tooth surface and slow breakage from the tooth surface,
after a proportionately higher intake of tablets. Toxic symptoms can occur as a result of loosening and swallowing. Fluoride is mainly excreted by the kidneys, and less than 1 0%
careless topical application of fluoride preparations. is excreted in the faeces and less than 1 % - with sweat and saliva.
The development of dental fluorosis can occur during the first eight years of a child's Fluoride varnish applied to children under 6 years of age 2 to 4 times a year at
life. Later on, tooth enamel is not sensitive to excess fluoride, as its pre-eruptive maturation 3- to 6-month intervals does not cause the development of dental fluorosis or symp­
is complete. The critical period for the development of fluorosis of the permanent central tom s of acute poisoning. In addition, unintentional swallowing of the varnish is un­
incisors in the jaw is the first three years of life. Ingestion of elevated doses of fluoride in likely compared to other fluoride preparations with a high concentration of fluoride
early childhood can therefore lead to mineralisation disorders and structural defects in the (gels, foams). Therefore, its use is safe in young children. Analysis of the number of
most aesthetically important permanent anterior teeth. ln the course of this condition, the adverse events reported to the US Food and Drug Administration has confirmed that
production of the enamel matrix by ameloblasts is impaired, the removal of amelogenins the use of fluoride varnish should be considered safe (the AE rate is between 0.099
from maturing enamel is reduced and there is subsurface hypomineralisation of the enamel. a nd 0.105 per million).

256 257
Compendium of Paediatric Dentistry Fluoride in prevention of dental caries

Applying a varnish containing 5% NaF is easy and very fast, without the need fo r The first generation of fluoride varnishes are varnishes containing 5% NaF, i.e. 2.26% F
saliva suction and professional plaque removal. Routine brushing of the teeth and dry i ng (22 600 ppm F), the second - based on Recaldent technology, i.e. additionally containing a
of the tooth, e.g. with a cotton ball, is sufficient. Drying the tooth is not absolute ly n e­ caseinate phosphopeptide complex and amorphous calcium phosphate (CPP-ACP) or amor­
cessary, as the varnish hardens on contact with saliva. Do not rinse the mouth afterwards . phous calcium phosphate (ACP). This complex formula of fluoride preparations increases
The patient can immediately close the mouth and leave the surgery. The applicati o n of the release and absorption of fluoride, intensifies remineralization and closes dentinal tubules,
the varnish ensures that a high concentration of fluoride is maintained in contact with the whi ch is also used in the therapy of dentin hypersensitivity. Fluoride coatings based on Re­
enamel for a period of 1 to 7 days, and therefore much longer than after application of caldent technology may also contain chlorhexidine, acting as an antibacterial and remineral­
the gel or fluoride foam, i.e. for 1 0- 1 5 minutes. It is recommended that for 4 hours after izing agent, or arginine and chlorhexidine, exerting an antibacterial and remineralizing effect
application, the patient does not eat hard food and does not brush his teeth on the day of and stabi lizing the pH level. Varnishes containing tricalcium phosphate (TCP) and the active
application. form of tricalcium phosphate (fTCP), sodium calcium phosphate (CSPS), sodium triphos­
Many varnishes contain colophony mastic (e.g. Duraphat). A child who has been phate (TMP) or calcium glycerophosphate (CaGP) are also available on the market. These
hospitalised for severe asthma or allergies in the past 1 2 months, or who is allergic to varnishes are currently undergoing clinical evaluations to determine their effectiveness. Pre­
the patches, may be at risk of an allergic reaction to colophony mastic. In such cases, vious studies indicate that fluoride varnishes with ACP, TCP, CSPS inhibit demineralisation
consideration should be given to the use of colophony mastic-free varnish (authorised and initiate enamel remineralisation. There is insufficient scientific evidence for the effective­
for use in the prevention of caries in the UK) or to the use of age-appropriate alternative ness of fluoride varnishes containing 0.9% difluorosilane (0. 1 % F, i.e. 1 000 ppm F) in caries
fluoride fonnulations ( e.g. fluoride mouthwash or toothpaste with a higher concentration prevention. However, the effectiveness of a varnish containing 1 .5% ammonium fluoride (i.e.
of fluoride). Contraindications: hypersensitivity to sodium fluoride or to any of the ex­ 7700 ppm F) in the prevention of caries of deciduous teeth. When dry, this varnish provides
cipients, ulcerative gingivitis, stomatitis, bronchial asthma. Duraphat contains 27.9 g of a level of approximately 30 000 ppm F. The effectiveness of this varnish in preventing caries
Ethanol 96% per 1 00 ml of suspension (each dose contains up to 0.2 g of alcohol) and in permanent teeth is confirmed by unpublished randomised studies.
should therefore be considered for use in pregnant and lactating women. However, lite­ The prophylactic efficacy of fluoride varnishes containing 5% NaF (22 600 ppm) is
rature data indicate a negligible rate of adverse reactions following varnish application. estimated to be about 37% caries reduction for deciduous teeth and about 46% for per­
In the case of application of a varnish containing 1 .5% ammonium fluoride (i.e. manent teeth.
7 700 ppm fluoride) it is recommended that the teeth are cleaned of p laque, isolated from
saliva and dried with an air spray. After application, it is necessary to let the varnish dry Topically applied to fluoride group
for 1 minute and not to rinse the mouth. The patient is advised to refrain from eating or The World Health Organisation, in order to prevent caries disease, recommends the
drinking for 1 hour. Do not take fluoride tablets or apply other topical products contai­ use of rinses in the form of school-based prevention programmes in children living in
ning high concentrations of fluoride for the next 2 days after varnish application. non-fluoridated areas. The fluoride in the rinses, like that from toothpaste, is retained in
Following varnish application, more fluoride is retained on the demineralised than on plaque and saliva, preventing the development of caries. Solutions containing 0.2% so­
the healthy tooth surface. In addition to the incorporation of fluorine into the hydroxy­ dimn fluoride (900 ppm F) are most commonly used in school prevention programmes.
apatite crystal structure and the formation of fluoroapatite, calcium fluoride is formed The reduction in caries resulting from the use of a fluoride solution mouthwash is 30%.
on the enamel in the form of granules. At the neutral pH of the oral cavity, it stabili­ In kindergarten, children are covered by daily supervised toothbrushing with flu­
zes the acquired membrane proteins(pellicles) and secondary calcium phosphates. With oride toothpaste.
a decrease in pH, calcium fluoride dissolves and releases fluoride ions, so it acts as a re­ In primary schools, brushing is carried out 5- 1 0 times a year every 2 weeks - 30 ml of
servoir - a prolonged source of fluoride after application. NaF 0.5- 1 %, 6-9 drops of AmF or 1 cm of AmF gel and rinsing 1 5-30 times a year l O ml

258 259
Compendium of Paediatric Dentistry

of 0.2% NaF. For many years, at the request of the Minister of Health and through a
nurse or hygienist, a program of supervised tooth brushing has been implemented in PART IV
grades I-V I pupils (after consent by their parents), which is carried out 6 times a school
year at intervals of 6 weeks.
Dental pulp diseases
References
I . Alexander SA, Ripa LW. Effects of self-applied topical fluoride preparations in orthodontic
patients. Angle Orthod. 2000 Dec;70(6):424-30. - 2. Al-Mui la A, Karlsson L, Kharsa S et al. Com­
bination ofhigh-fluoride toothpaste and no post-brushing water rinsing on enamel demineralisation Chapter 19
using an in-situ caries model with orthodontic bands. Acta Odontol Scand. 20 I O Nov;68(6): 3 23 -
8. - 3 . American Dental Association Council on Scientific Affairs. Fluoride toothpaste use for
young chil dren. J Am Dent Assoc. 2014 Feb; 1 45 (2): 190-1. doi : 10.14219/j ada.2013 .47. Erratum ··. Dental pulp diseases and changes in the periapical tissues of
in: J Am Dent Assoc. 2014 Mar;145(3) :236. - 4. Ekstrand J , Koch G, Lindgren LE, Petersson teeth in children and adolescents - diagnosis, causes, course
LG. Pharmacokinetics of fluoride gels in children and adults. Caries Res. 1981; 15(3):213-20. _
5 . Heifetz SB, Meyers RJ, Kingman A. Comparison of the anticaries effectiveness of daily and of the disease process
weekly rinsing with sodium fluoride solutions: findings after three years. Pediatr Dent 1983 ; 4:
300-303. - 6. Jui l ien S. Prophylaxis of caries with fluoride for children under five years. B MC Joanna Szczepanska, Dorota Olczak-Kowalczyk
Pediatr. 2021 Sep 8 ;21 (Suppl I ):351. - 7. Kaczmarek U. Cariostatic mechanisms of fl uoride. Czas
Stomatol 2005; 6: 404-413 - 8. Li J, Dallas S, McBride-Henry K. U se of full-strength fluoride
toothpaste among preschoolers i n New Zealand, and factors determining toothpaste choice. N z
Med J. 2016 Jun 1 0;129(1436):44-51. - 9. Marinho YC, Chong LY, Worthington H Y, Walsh T. Conducting an accurate interview and the physical examination and the selection of
Fluoride mouthrinses for preventing dental caries in children and adolescents. Cochrane D atabase
Syst Rev. 2016 Jui 29;7(7):CD002284. appropriate additional examinations allow a correct diagnosis to be made and the method
I 0. Marinho YC, Worthington H Y, Walsh T, Chong LY. Fluoride gels for preventing dental of treatment to be applied, which should take into account the child's age, and thus the
caries in children and adolescents. Cochrane Database Syst Rev. 2015 Jun 15 ;20 l 5(6):CD002280. type of dentition and stage of its development. The original diagnosis may be modified,
- 1 1 . M arinho YC, Worthington H Y, Walsh T, Chong LY. Fluoride gels for preventing dental car­
ies in children and adolescents. Cochrane Database Syst Rev. 2015 Jun I 5 ;2015(6):CD002280. - depending on the progress of treatment or the emergence of complications.
12. Marinho YC, Worthington HY, Walsh T, Clarkson JE. Fluoride varnishes for preventing dental An interview related to pulpitis should be collected first from the patient. However,
caries in children and adolescents. Cochrane Database Syst Rev. 2013 Jui 11 ;(7):CD002279. - 13.
in the case of younger children, with whom age-related communication and ailments
Marinho YCC. Cochrane fluoride reviews: an overview of the evidence on caries prevention with
fluoride treatments. RCS 2014; 5 (2): 78-83. - 14. Nordstrom A , Birkhed D. Preventive effect of found may be difficult, obtaining precise information is sometimes impossible. Often he
high-fluoride dentifrice (5 000 ppm) in caries-active adolescents: a 2-year clinical trial. Caries Res. is unable to describe the complaints accurately and answer questions about the duration
20 I 0;44(3):323-3 I . - 15 . Petersen PE, Ogawa H . Prevention of dental caries through the use of
fluoride - the WHO approach. Community Dent Health. 2016 Jun;33(2): 66-8. P M I D: 2735246 1 . of the pain now or in the past. Therefore, indirectly, the child's complaints should be
- 1 6. Petersen PE, Ogawa H . Prevention of dental caries through the use of fluoride - the WHO out from the parent. Although pain is a subjective sensation, it is the first indication and
approach. Community Dent Health. 2016 Jun;33(2):66-8. - 17. Toumba KJ, Twetman S, Splieth C
a very important symptom of an ongoing pathological process, including inflammation.
et al. Guidelines on the use of fluoride for caries prevention in children: an updated EAPD policy
document. Eur Arch Paediatr Dent. 2019 Dec;20(6):507-5 l 6. - 18. Tubert-Jeannin S, Auclair C, A history directly focused on pulpitis should start with information on chronic sys­
Amsallem E et al. Fluoride supplements (tablets, drops, lozenges or chewing gums) for preventing temic diseases, the stage of treatment of the disease and the medications used, the pre­
dental caries in children. Cochrane Database Syst Rev. 2011 Dec 7;20 l1(12) :CD007592. - 1 9 .
sen ce of which may influence, among other things, the choice of the appropriate treat­
Walsh T, Worthington H Y, Glenny AM et al. Fluoride toothpastes of di fferent concentrations for
preventing dental caries. Cochrane Database Syst Rev. 2019 Mar 4;3(3):CD007868. ment method or the need to consult the child's dentist. I t should be resolved whether the
20. Wong MC, Clarkson J, G lenny AM et al. Cochrane reviews on the benefits/risks of fluoride presence of fever in the child is related to local inflammation or to an ongoing general
toothpastes. J Dent Res. 2011 May;90(5):573-9.
infection. When taking a dental history, it is important to establish the history of current

260 261
 Dental pulp diseases and changes in the periapical tissues of teeth in children
Compendium of Paediatric Dentistry and adolescents - diagnosis, causes, course of the disease process

and past complaints and their previous treatment. When analysing the history of pain, i t
is important to determine whether it is primary pain or has occurred before, which may
indicate a chronic inflammatory process. It is important to assess the course and impac t
of pain based on the following characteristics: Fig. 19. I . Deep carious ca­
vity in tooth 47 - c l i nical
circumstances of appearance (spontaneous - without any stimulus, provoked - influ­ image on the left, radio­
enced by food, temperature, biting), graphic image on the right
- duration (short or long, intermittent or continuous), - carious exposure of the
medial pu lp horn.
- intensity (strong, moderate, weak - depends on individual sensitivity),
character (sharp, dull, pulsating),
- location (localised, diffuse, radiating),
time of occurrence ( during the day, also during sleep).
It is important whether painkillers were applied, including the type of agent, dose
and duration of use, relieving the discomfo1t. All these pain parameters can be indicative
of the severity of the inflammatory process. Acute, primary, localised pain may indicate
reversible pulp inflammation. Dull, diffuse, recurrent pain is indicative of an irreversible
process.
Fig. 19.2. Deep carious cavity with exposed pulp necrosis in the tooth 54 (left), grey discolo­
Extraoral clinical examination for dental pulp diseases should consist in first as­ ration and carious defect in the tooth 74 (middle), destruction of tooth crowns 84 and 85
sessing disorders in facial features that may be caused by swelling. Palpation should be with pulp necrosis and tooth abscess on the vestibular side (right).
examined for warming of the skin and the condition of the surrounding submental and
submandibular lymph nodes - size, soreness, displacement with respect to the skin and In additional examination of the pulp, a thermal and possibly electrical test should
bone substrate. T he intraoral examination begins with the identification of the tooth be used, starting with a healthy homonymous tooth on the opposite side of the arch,
causing the pain, i.e. the tooth: adjacent or opposing, then the causal tooth should be assessed. A horizontal and verti­
with a deep carious cavity in which the pulp is exposed; if pulp exposure is visible in cal tapping test (percussion test) is used to assess the periapical tissues, as well as the
the cavity, this provides an opportunity to assess the appearance of the pulp (polyp, Smreker test in more advanced destruction of the bone structure in the apical region
presence of exudate - serous, bloody, purulent, necrotic masses) (Fig. 19.1 ), of the root. A radiological examination is then advisable, in the first instance a dental
with extensive or leaking filling, radiograph. Radiologically, the size of the tooth cavity, the stage of development of
with fracture, breakage, abrasion/erosion of hard tissues, the root and the degree of narrowing of the apical opening, the extent of inflammation
with altered colour (pink colour - resorption, grey or brown - pulp necrosis) (Fig. in the periapical tissues and the presence, position and development of the permanent
1 9.2), successor of the causative deciduous tooth are assessed. In situations of diagnostic
with a swelling or fistula present on the alveolar mucosa. difficulty, it is possible to refer the patient for CBCT in justified cases, e.g. when there
Tooth mobility is assessed by touch, as well as the texture of the excessive elevation is a significant discrepancy between the medical history and clinical examination and
on the oral mucosa. the radiological image.

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Compendium of Paediatric Dentistry and adolescents - diagnosis, causes, course of the disease process

Causes of pulp disease and course of the disease process in deciduous pulp horns and the thin layer of poorly mineral ised hard tissues of the tooth (in immature
and permanent immature teeth permanent teeth mainly primary dentin) increase the risk of early involvement of the
p ul p in the disease process.
I nfectious agents (usually associated with untreated caries), trauma (mechanical, In deciduous teeth, the response of the pulp to the stimulus is related to the deve­
thermal, chemical and physical) and ischaemia can cause inflammation or necrosis of l opmental phase of the tooth. I n the period before root resorption, the pulp contains
the pulp, followed by complications in the periapical tissues. n um erous cells and vessels. The response to the noxious stimulus is massive deposition
Depending on the defensive capacity of the pulp and the intensity and duration of of tertiary dentin and a strong inflammatory response. During the root resorption phase,
pathological factors, pulpitis can be partial or complete, acute or chronic, reversible or retrograde, atrophic and degenerative changes occur, leading to a gradual weakening of
irreversible. Reversible pulpitis is caused by short-acting harmful factors of slight inten­ defence and reparative functions.
sity, i.e. mechanical (acute and chronic injuries), thermal (preparing a cavity or grinding Compared to mature permanent teeth, the pulp of a deciduous tooth has less ability
a tooth), chemical (dental medicines). The same factors acting for a longer period of to localise inflammation, and the presence of chamber-periodontal canals favours the
time, more intensely or repeatedly can cause irreversible inflammation with an acute or spread of infection to the area of the root furcation. The predisposition to pathological
chronic course. The main cause of pulpitis is dental caries. resorpt ion following the use of calcium hydroxide materials, the absence of sub odon­
Dental pulp cells (odontoblasts, fibroblasts, neurons, endothelial cells and stem cells) toblastic plexus and sensory fibres in the dentinal tubules are also characteristic, which
have receptors capable of detecting bacterial components. Their exposure to bacte­ may be associated with less discomfort during cavity preparation.
rial antigens (e.g. bacterial DNA, cell wall lipopolysaccharides) results in the release The pulp of the immature permanent tooth is characterised by a high defensive ca­
of pro-inflammatory cytokines, including TNFa, IL- 1, I L-8, IL- 1 2, IL-6 and IFNo. The pacity (good vascularisation, numerous cells, high activity of cylindrical odontoblasts
level of cytokines in the pulp reflects the severity of the inflammation. The response arranged in a single layer). Due to the immaturity of the nerve tissue, it responds less
to cytokines and other chemotactic signals released by cells in the pulp is vasodilation well to stimuli (Rashkov plexus develops after the root is formed, numerous myelin-free
and migration of immune cells (e.g. monocytes, macrophages, dendritic cells, mast cells C-fibres and fewer A-type myelin fibres than in mature permanent teeth).
and neutrophils). Inflammation is also accompanied by a local release of neuropeptides Factors unrelated to tooth type and developmental stage are:
(neurogenic inflammatory response), resulting in an amplification of the pain sensation. - developmental abnormalities of the teeth, e.g. tissue intrusion, enamel hypoplasia,
Neuropeptides play a role in the regulation of blood flow in the pulp, angiogenesis (they enamel and/or dentin hypomineralisation,
facilitate healing) and have an antibacterial effect. Pulpitis aims to limit infection and - systemic diseases, including:
allow healing. The result is the formation of reactive dentin (if there was no damage to • causing less blood flow in the pulp (e.g. sickle cell anaemia due to blockage of
the odontoblasts) or repair dentin (formed by odontoblast-like cells). vessels by stiff and sticky red blood cells),
In deciduous, permanent immature teeth, the carious process is usually dynamic, • congenital hypophosphatemia (large pulp chamber with prominent horns,
making it difficult for the pulp to produce secondary and reactive dentin. Inflammatory covered by a thin layer of tissue).
changes in the pulp of a permanent tooth with uncompleted root development already Untreated dental pulp diseases are the cause of periapical tissue involvement. The
occur with deep caries and in the pulp of a deciduous tooth with most carious lesions spread of infection is favoured by:
exceeding half the dentin thickness. - in the deciduous tooth - short roots, a thin layer of root cement, wide apical holes,
The tissues of immature deciduous and permanent teeth are characterised by greater often additional channels ended apical foramen and chamber-periodontal canals,
permeability to harmful agents (low mineralisation of enamel and dentin, wide dentinal - in a permanent tooth with incomplete root development - wide connection to peri­
tubules, in deciduous teeth mostly straight). The size of the pulp chamber with prominent radicular tissues and thin root wal ls.

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 Dental pulp diseases and changes in the periapical tissues of teeth in children
and adolescents - diagnosis, causes, course of the disease process
Compendium of Paediatric Dentistry

Inflammatory lesions in the periadicul ar tissues can have an acute or chronic co urse a mild and transient response, lasting no more than one to two seconds after the stimulus
that may be exacerbated (Fig. 19.3). is removed. Normal periapical tissues are not sensitive to percussion or palpation, and
the radiograph of space of periodontal ligament (PDL) is not altered.
Inflammation, pulp necrosis The pulp with reversible inflammation, also called congestion, is characterized
by the ability to heal (Tab. 19.1). After appropriate causal treatment, the inflammation
periapical tissue inflammation should resolve and the pulp should return to normal, maintaining vitality. On the basis of
both the history and clinical examination, there are no symptoms typical of irreversible
pulpitis. The pain is provoked, short-lived and relieved with over-the-counter painkillers.

r
acute chronic
They most often arise during the consumption of food and decrease when the stimulus is
removed, and hygiene procedures are properly carried out. Reversible pulpitis should be
periapical abscess
differentiated from dentin hypersensitivity, which is not itself an inflammatory process,
subperiosteal abscess �I submucosal abscess I� although the symptoms are similar.
The irreversible pulpitis may be asymptomatic or symptomatic, including part or
Fig. 1 9.3. Development of inflammation in the periapical tissues due to dental pulp diseases. all of the pulp chamber (partial pulpitis) or the entire cavity of the tooth (total pulpitis)
(Tab. 19.1 ). The development of this condition renders the pulp largely or completely
The immaturity of the child's immune system, the rich vascularisation of the periden­ unable to heal. In the earlier stages of inflammation, pain occurs when provoked during
tal tissues and the structure of the bone structure (predominance of spongy over compact the consumption of food, especially hot or cold food. It is characterised by a significant
bone, thin bone lamellae, numerous bone canals) favour the rapid spread of the disease prolongation of the response after withdrawal of the stimulus, e.g. cold. In the symptom­
process. The purulent exudate can penetrate through the bone, periosteum and mucosa atic form, the pain is more often spontaneous, i.e. it is felt by the patient independently
into the oral cavity and even through the skin on the outer face. It can form a submucosal of the irritant. If the inflammatory process is acute and does not last long, the amount
abscess or fistula _ active (secreting purulent contents) or passive (not secreting purulent
of accumulated exudate in the tooth cavity is not yet large, the pain can be weak, opaci­
contents, which can open when purulent exudate accumulates). A pathological process fying and tolerated by the patient. During clinical examination, pain induced by a thermal
in the root region of a deciduous tooth can damage the permanent tooth's root germ. The stimulus (e.g. ethyl chloride) is severe and of longer duration. At this stage, there are no
enamel-forming organ (Turner's teeth) is most commonly affected. changes in the apical periodontium, so neither the percussion test nor the radiological
In children, dental inflammation is an indication for rapid intervention due to general assessment is helpful in the diagnosis. In such cases, the dental interview and additional
immunological immaturity and the construction of anatomical structures in the head and
examination with a thermal test are necessery basic tools for assessing the pulp con­
neck, and due to the proximity of the respiratory tract and brain. Especially dangerous dition. When using pulp viability tests in multi-rooted teeth, false-positive results can
are abscesses within the maxilla, where the continuity of the space promotes the move­ sometimes be obtained, when in one root canal the pulp reacts positively, but in the other
ment of inflammation towards the maxillary sinuses and orbit and through the connec­ there is already necrosis.
tion of the angular and facial veins even with the cavernous sinus. As the inflammation continues, the discomfort may worsen as the amount of exudate
increases. The pain can then be pulsating and radiating to other areas of the face, making
Classification of dental pulp diseases of decidous and immature permanent teeth it difficult to locate. Remissions may be getting shorter. It can be felt when bending over,
a nd it can occur at night, i.e. when lying down, when the blood supply to the head area
Clinically, a healthy pulp is asymptomatic tissue, although it may not be histolo- increases. Over-the-counter painkillers are usually ineffective. If the irreversible acute
_
gically normal. Healthy pulp normally responds to cold stimulus testing in the form of

266 267
 Dental pulp diseases and changes in the periapical tissues of teeth in children
Compendium of Paediatric Dentistry and adolescents - diagnosis, causes, course of the disease process

inflammation of the pulp turns into a chronic phase, the ailments may decrease a little. permanent teeth with uncompleted root devel opment. It is a lesion either originally
W hen further treatment is not given, the inflammation can spread to the periradicular chronic or a descent of acute pulpitis. A polyp is a pulp tissue that undergoes hyperplasia
tissues. It often happens that after more destruction of the hard tissues of a deciduo u s and often escapes from the open tooth chamber into the carious cavity. It is shaped like
tooth or an exacerbation of the inflammatory process, the attention of the carer is draw n an amorphous formation - beaten or with a smooth surface, light or dark red in colour.
to the child, who only then goes with the child to the dentist. At any time, irreversib le It can bleed spontaneously, but profusely when touched with an instrument, without gi­
chronic pulpitis can be exacerbated by various local factors or systemic immune decli ne. ving any discomfort as a result of very weak innervation. A long-lasting polyp can cause
Studies show that in the case of pulpitis of deciduous teeth inflammation, chronic or periapical lesions. The polyp should be differentiated from a swollen gingival papilla
chronic exacerbated conditions are most often observed. This is because the acute phase or gingival polyp, outlined with a probe, and must be located in the tooth cavity/pulp
of inflammation is short-lived. chamber and not extend into the gingival space.
In the case of a visible tooth pulp (intraoperative assessment), an important indicator
of its condition is its appearance, i.e. the presence of bleeding, pus, the time of bleeding
and the colour of the blood. It is commonly believed that strong, prolonged bleeding and
dark blood staining indicate irreversible inflammation. However, recent observations in­
dicate that bleeding time and blood colour are not fully reliable indicators. B iomarkers of
inflammation are being sought to facilitate diagnosis and treatment selection.

Tab. l 9. l . Symptoms and methods of treatment of reversible and irreversible pulpitis.

Review and physical

Reversible Irreversible partial Irreversible total
examination + O
J no 111° Fig. 1 9.4. Pulp polyps Fig. 1 9.5. Internal resorption
treatment method
in teeth 6 l and 62. in the distal canal of tooth 75.
spontaneous
Anamnesis 110 asymptomatic/symptomatic inflammation
pain

pulp exposure no yes yes A specific type of dental pulp disease is also an inflammatory internal resorption,
pulp bleeding 110 yes - moderate no/yes - strong the so-called internal pulp granuloma (Fig. 1 9.5). Its essence is the destruction of dentin
Clinical by multinucleated giant cells, so-called osteoclast-like cells. It can affect the coronal or
pulp response yes - weak or
Findings yes yes - extended root portion of the pulp and lead to perforation of the tooth wall. It is diagnosed radio­
to stimuli prolonged
graphically (oval widening of the chamber or canal). In the case of resorption located in
response to no - acute inflammation
tapping
no
yes - chroni c inflammation
the chamber part, it can cause a pink discolouration (so-called pi11k spot) caused by the
shining of well-vascularised granulation tissue through a thin layer of dentin and enamel.
root cana I treat-
indirect pulp partial or It does not cause pain.
Treatment ment or extraction
capping total p u lpothomy The final stage of acute or chronic irreversible inflammation is pulp necrosis. It ari­
of a tooth
ses as a result of impaired blood circulation in the confined volume of the tooth cavity.
The course of necrosis is often asymptomatic. On clinical examination, a deep carious
A specific type of chronic granulomatous inflammation is hypertrophic pulpitis,
also called pulp polyp (Fig. 1 9.4). It occurs more frequently in deciduous molars and cavity with pulp exposure that does not respond to probing. The tooth is usually dull,

268
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 Dental pulp diseases and changes in the periapical tissues of teeth i n children
and adolescents - diagnosis, causes, course of the disease process
Compendium of Paediatric Dentistry

Tab. 19.2. Differentiation of pulp in lammation of deciduous teeth.

f
grey in colour. Necrosis can sometimes be diagnosed accidentally when there is a lack of
response during cavity preparation. A dull sound is detected by percussion examination Pulp condition
of the tooth. At this stage, radiological examination is unlikely to show periadicular pa­ Diagnostic reversible
thology. Irreversible pulpitis in chronic or asymptomatic form cannot always be clearly factors inflamma- irreversible inflammation pulp necrosis
distinguished from pulpitis necrosis. tion

Currently, all classifications of pulp disease, including those recommended by the Clinical
mostly acute acute or chronic
course
American Academy of Pediatric Dentistry (AAPD) and the American Association of
provoked:
Endodontics (AAE), divide pulpitis into reversible, irreversible, necrosis. Each of these provoked: no - asymptomatic,
acute,
asymptomatic form - yes - symptomatic:
inflammatory conditions can have an acute or chronic phase and an asymptomatic or short-lasting,
persisting, after removal of the when periapical tis-
symptomatic form. Therefore, due to the similarities in symptoms between the two, there Pain disappears
stimulus sue is affected (reac-
quickly after
can sometimes be difficulties in making a precise diagnosis (Tab. 19.2). spontaneous: symptomatic form - tion to heat, pain on
removal of
acute or dull, of varying severity biting)
Caries that does not expose the pulp is usually the cause of mild to moderate in­ the stimulus
flammation that resolves when the causative agent is removed. Curable inflammation is Colour of the normal or grey,
correct correct
considered reversible. crown brown, gloss loss
In deep caries (the bottom of the carious lesion is located in the ¼ of the dentin layer Excessive
110 often none
but is separated from the pulp by a distinct zone of hard dentin) and very deep caries pulp bleeding
(the carious lesion covers the entire thickness of the dentin) bacteria may enter the pulp, Response yes: with yes: with periapical
110
causing a more intense inflammatory reaction. Pulpitis is generally considered irrever­ to percussion periapical tissues inflammation tissues in flammation

sible. According to the principle of minimal intervention, in cases of deep caries, selective Increased
no no/yes no/yes
mobility
removal of carious dentin and observation is possible. In very deep caries, the pulp in
yes: decrea-
a state of irreversible inflammation should be removed.
Response to ses soon after
The inflammatory process in the tooth pulp does not progress linearly. The dental yes: strong and prolonged none
cold stimulus stimulus
pulp has mechanisms (high blood flow in the pulp, the presence of arteriole-ve­ withdrawal
nous interconnecting vessels, an extracellular matrix that limits the increase in pulp Pulp electric
acute inflammation - decreased,
excitability reduced none
pressure to the site of irritation and inhibits the spread of microorganisms and toxic chronic inflammation - increased
threshold
products) that allow healing and also limit infection and inflammation to a specific Swelling
site in the pulp. The condition of the pulp in different parts of the pulp can vary, often no/yes
Fistula
making it impossible to make a single and unequivocal diagnosis. Inconsistencies
no/yes: if inflammation of the periapical tissues is present,
between the clinical diagnosis of the pulp state and the histopathological diagnosis translucency in the furcation area or root apex
were also noted, as well as the possibility of repair (dentin formation) even in teeth R adiologi-

f(II: �;
110
with carious pulp exposure and bacterial infection. Therefore, the choice of invasiv e cal changes
in periapical
therapy (amputation, pulp extirpation) should only concern irreversible inflamma­ tissues · · ,
·
�-•
tions. The classification of pulpitis as reversible or irreversible i s increasingly being -0 ' · ,
�
\
it !

questioned. .· _ :· . :�::

270 271
 Dental pulp diseases and changes in the periapical tissues of teeth in children
Compendium of Paediatric Dentistry and adolescents - diagnosis, causes, course of the d isease process

Failure to treat dental pulp diseases may cause the spread of inflammatory chan ges Ta b. 19.4. Diagnosis of peri implantitis.
to periapical tissues, primarily involving the periodontal ligament, with the formation
Clinical and radiologi­ Inflammation of the periapical teeth
of periapical abscess (Tab. 19.4). The patient then experiences severe, throbbing pai n '
cal symptomatology
which worsens when lying down. On clinical examination, the tooth responds positively acute chronic
to horizontal or vertical percussion and may show increased mobility, which must be yes - of varying degrees of se­
verity, a feeling of tooth eruption
Spontaneous pain
r
differentiated f om physiological resorption. Pressure pain is noted in the area of the root yes - for exacerbations
from the alveolus or elongation of
apex (Owinski test). If the process progresses further, due to unimplemented treatmen t, the tooth
the inflammation enters a clu·onic phase. With prolonged chronic purulent inflammation, Pain on biting, reaction
yes yes
the exudate may move through the bony structure of the periapical region and a fistula to percussion
may form. In the case of deciduous teeth, the emerging pathological canal connects the . subperiosteal abscess - mucosa I
space nround the root apex with the fistula, most often located in the vestibule of the Alveolar process redness, hard swelling, painful
in the area of the active or passive purulent
submucosal abscess - enlarge­
oral cavity. If the fistula is active, purulent or bloody-purulent contents may come out of fistula
causative tooth ment of swelling, palpation fluc­
its canal. Once the fistula has formed, the pain becomes even less intense, which often tuance
reassures parents and they do not go to the dentist.
no change in periapical tissues
Involvement of a larger area of bone tissue in the inflammatory process is manifested or widening of the periodontal radiolucencyin the apical or
by the appearance of oedema, which, destroying the bone, locates under the periosteum, space furcation area

forming a subperiosteal abscess. In the acute inflammation phase, local pain increases
Radiological picture
significantly, the causative tooth is very tender on pressure, reacts strongly to biting,
and there is a feeling of the tooth blowing out of the socket. Heat and the lying position
increase discomfott, while cooling down relieves pain. A soft, painful elevation on the
alveolar process is detected. The accompanying systemic symptoms are clearly exacer­
bated in children. Fever, chills, malaise, sleep disturbances or loss of appetite may occur. Lymph nodes non-painful, hard movable
painful, soft, non-movable rela­
surrounding areas to the ground and skin
With the further spread of inflammation, the abscess forms under the mucous mem­ tive to the skin
(painful in exacerbations)
brane, then the swelling increases more, but the clinical symptoms decrease. Fluctuance
is felt on palpation. The surrounding lymph nodes are enlarged, soft, mobile and painful, References
and the skin in the area is hotter and red. Laboratory examination shows leucocytosis and I . American Academy of Pediatric Dentistry. Pulp therapy for primary and immature perma­
nent teeth. The Re ference Manual of Pediatric Dentistry. Chicago, I l l ; 2020: 399-407 - 2. Amer­
elevated C-reactive protein test. ican Academy of Pediatric Dentistry. Guideline on Pulp Therapy for Primary and Immature Per­
The transition process of peridental tissue inflammation from the acute to the chronic manent Teeth. Originating Committee Clinical Affairs Committee - Pulp Therapy Subcommittee.
phase in deciduous teeth is often shott due to the looser spongy bone structure, less mine­ 20 1 4. - 3. Duncan H F. Present status and future directions - Vital pulp treatment and pulp pres­
ervation strategies. lnt Endod J. 2022;55 (Suppl. 3):497-511. - 4. El Karim IA et al. Deciphering
ralised alveolar bone and thilmer alveolar lamina than in the permanent dentition. In chronic
� eparative Processes in the Inflamed Dental Pulp. Front. Dent. Med, 2021; 31; doi .org/ 1 0.3389/
periapical tissue inflammation, the radiological picture shows inflammatory changes not only tdmed.2021.6512 1 9. - 5. Mohammad G et al. Pulpal Diagnosis of Primary Teeth: Guidelines
for Clinical Practice. Bangladesh J Dent Res Edu 2012, 2, 2: 66-68. - 6. Piekoszewska-Ziytek
in the apical area, but also at the furcation site. The presence of translucency at the root bifur­
P et al. Alveolar infections - a review of the literature. New Stomatol 2016, 2 : 1 20- 1 34 I DOI :
cation site in deciduous molars is the result of the spread of infection from the tooth chamber 10.5604/142669 1 1 .1208252 - 7 . Taha N A et al. Full Pulpotomy with Biodentine in Symptomatic
through the canals, running from the pulp chamber to the periodontal ligament). You ng Permanent Teeth with Carious Exposure Journal of Endodontics, 2018; 44: 932 -937.

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 Treatment of dental pulp diseases and periapical lesions in deciduous teeth

Examples of systemic diseases that require postponement or temporary endodon­

tic treatment to prepare against the risk of complications when, for example, tooth ex­
Chapter 20 traction is indicated, also performed under general anaesthesia:
- diabetes,
Treatment of dental pulp diseases and periapical lesions - haemorrhagic diathesis, leukaemia,
- heart defects, cystic fibrosis,
in deciduous teeth
- immune deficiencies,
Joanna Szczepanska, Dorota Olczak-Kowalczyk - hyperthyroidism,
- herpes or infectious diseases.
Local factors to consider in the choice of treatment for pulpitis:
Genert1I indications and contraindications for endodontic treatment - clinical and radiological diagnosis,
of deciduous teeth - degree of development, root resorption - duration of presence of the tooth in the
mouth,
The aim of endodontic treatment of pulp inflammation of deciduous teeth, depending - presence of a permanent successor - a relative condition,
on the severity of the process, is to maintain all or part of the pulp viability. These proce­ - the possibility of restoring the crown of a tooth,
dures are referred to as vital pulp therapy and include indirect pulp capping, direct pulp - crowding in the deciduous dentition - removal, especially of a molar, can have
capping and pulpotomy. If the pulp has to be removed in its entirety, root canal treatment a negative impact on maintaining space for permanent teeth.
is carried out to preserve the function of the tooth based on healthy periradicular tissues. Local contraindications to endodontic treatment of deciduous teeth:
The choice of the appropriate method of management of pulp disease in deciduous - tooth in the period of physiological resorption, with a retained root length of less
teeth depends firstly on the age of the child, i.e. the stage of development of the tooth, than ½;
the length of time it has remained in the mouth, including the presence and progression - significant tooth mobility resulting from advanced pathological root resorption, pre-
of physiological resorption. Another criterion is the clinical symptoms present and the vious trauma or from destruction of the periodontium by an inflammatory process,
diagnosis made. It is also important to consider the child's general condition, which will - crown of a tooth not suitable for permanent restoration,
determine the use of a specific treatment method - temporary or definitive, depending on - caries causing perforation of the chamber bottom,
the results of the consultation with the with the doctor treating the systemic disease. An - foci of thinning of the bone structure in the furcation or periapical region visible on
example are children with immune disorders, including cancer, in whom, with certain X-ray,
treatments, there is no guarantee of full eradication of the infection and hence, in doubt­ - swelling or fistula,
ful cases, there are broad indications for tooth extraction. Another situation is the use of - orthodontic needs,
interim treatment and deferred extraction in children with coagulation disorders, who - poor oral hygiene.
need to be adequately prepared for this procedure. Important factors that can influence In some cases, the presence of one of the above-mentioned contraindications preju­
the treatment of pulp inflammation are: dices the inability to undertake treatment; in other situations, more circumstances need
- the possibility of cooperation with the child, taking into account the duration of the to be taken into account in order to decide on tooth extraction.
entire treatment and the precision of the procedures performed, General medical contraindications to conservative treatment of pulp disease in
contact with the child's parent, who should follow the dentist's instructions and at­ deciduous teeth:
tend regular follow-up visits, on which the success of the treatment also depends.

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Compendium of Paediatric Dentistry Treatment of dental pulp diseases and periapical lesions in deciduous teeth

difficult cooperation with the child and carers, Mineral trioxide aggregate ( MTA) is a material from the group of synthetic bio
no guarantee of achieving the kind of infection elimination that will protect against ceramics. It is characterised by its bioactivity and biocompatibility, showing odonto­
bacteraemia in cases of cardiac defects, immune decline (cancer, chemotherapy, tropic - remineralising properties. lt is a strongly alkaline preparation whose pH is ini­
bone marrow or other organ transplants), infective endocarditis and many others. tially 10.2 and becomes even higher after a few hours. In addition, the content of metal
The correctness of the diagnosis for pulp disease should be based on: tri oxides inhibits the growth of microorganisms and thus inflammatory processes. The
general medical history for contraindications to a particular treatment method, reaction of MTA with water produces calcium hydroxide, which binds in the presence
dental treatment history and in relation to the current case (treatment period and of tissue fluids (e.g. saliva) and hardens after 3-4 hours. Quick-setting formulations are
subjective effects assessed by the patient), now also available. MTA is not resorbed and also shows good tightness, unlike Ca(OH\,
current systemic (fever) and local complaints (location, intensity, duration, aggra­ which reduces the risk of bacterial microleakage. Therefore, when placed at the bottom
vating/relieving factors), of a cavity, it does not need to be removed when a final filling needs to be replaced. It
extNt- and intraoral examination, also has considerable mechanical strength. The dentin bridge formed under the influence
additional clinical (pulp and periapical tissues assessment tests) and radiological ofMTA is thicker and more uniform and forms more quickly than under calcium hydrox­
examinations. ide. The disadvantage of MTA is the possibility of discolouration of the tooth crown and
the composite material with which the tooth is eventually filled.
Preparations used in the endodontic treatment of deciduous teeth MTA is used for sealing the exposed pulp in direct capping and amputation procedures,
The most commonly used preparations in the endodontics of deciduous teeth are cal­ filling root canals, repairing perforations in the root and chamber floor. It is used speci­
cium hydroxide (CH), mineral trioxide aggregate (MTA), Biodentine (BD), formocresol fically in paediatric dentistry in the apexification and revascularisation procedure. Many
(FC), ferrous sulphate (FS), and iodoform. Each of these materials has different proper­ authors believe that MTA is now the gold standard for pulpotomy of deciduous teeth.
ties in relation to the pulp. Materials that show odontotropic properties, stimulating the Biodentine, like MTA and Ca(OH\, has odontotropic activity. It stimulates the for­
formation of tertiary dentin - reactive as a response of the pulp to harmful stimuli (caries, mation of reactive and reparative dentin and is therefore called dentin substitute. Both
cavities of non-carious origin, dental drugs) or reparative, also known as restorative, in­ MTA and B iodentine are bioactive endodontic cements but differ in their chemical com­
clude calcium hydroxide, MTA and Biodentine. The mummifying properties has formo­ position. B iodentine is a bio ceramic because it has calcium silicates in its composition.
cresol, the haemostatic and antibacterial properties - iron sulphate, and the antimicrobial The tricalcium silicate and calcium carbonate contained in the powder provide good
properties - iodofonn. mechanical properties, while zirconium dioxide is responsible for the contrast on the
Calcium hydroxide and materials containing it exhibit strong alkalizing and bacteri­ X-ray. The liquid also contains calcium chloride, which reduces the setting time of the
cidal properties. The disadvantage of these preparations is, among others, the creation of material, as well as a soluble polymer and water. The combination of powder and liquid
an irregular, porous dentin bridge, which may result from the failure to fully release hy­ results in a cement with a high calcium hydroxide content and a high pH, resulting in
droxyl ions. Jn addition, Ca(OH)2 is dissolved and absorbed by the dental tubule fluid and the antibacterial effect of Biodentine. It has the advantage of creating a good marginal
shows no adhesion to the hard tissues of the tooth, causing bacterial microleakage. This seal to prevent bacterial microleakage and an adequate dentinal bridge thickness. Unlike
can become problematic when used in direct pulp capping. Calcium hydroxide can, on the MTA, it does not discolour the hard tissues of the teeth and has a shorter setting time of
one hand, initiate calcifying processes in the pulp but, on the other hand, weaken the den­ about 12 minutes but achieves complete hardness after about 30 days. Therefore, after
tin structure during long-term use in root canal treatment. Studies show that it is the least the application of Biodentine, the final filling should be performed at the next visit.
clinically and radiologically effective material in pulpotomy of deciduous teeth compared Biodentine is used in deep or large carious cavities, for direct pulp capping, in pul­
to formocresol, ferrous sulphate and MTA. Tn addition, it can cause internal resorption. potomy and apexification, in regenerative endodontic procedures, for restoration of root

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Compendium of Paediatric Dentistry Treatment of dental pulp d iseases and periapical lesions i n deciduous teeth

and furcal perforations, internal and external resorptions. It is a good alternative to MTA treatments methods of diseases of pulp and periapical tissues in deciduous teeth
for pulpotomies of deciduous molars.
Formocresol is made up of 35% tricresol, 19% formaldehyde, 1 5% glycerol, an d The main aim of pulp therapy, according to modern endodontics, is to preserve the vi­
31% water, according to Buckley's formula. It exhibits potent bactericidal activity and tality of the pulp and the healthy supporting tissues of the tooth, which is to be achieved
inhibits many enzymes in the inflammatory process. lt is used in vital and mortal pulpo­ through the widest possible use of vital methods (Tab. 20.1 ).
tomy of deciduous teeth in the form of a 20% solution. A cotton wool tampon is inserted The effectiveness of pulp disease treatment lies not only on the part of the dentist,
into the chamber for five minutes or several days, depending on the number of stages in but also good cooperation with the patient is important. A prerequisite for effective treat­
the procedure. It is recently believed that a contact time of a few seconds with the pulp is m ent is:
equally effective. This can limit both the dose and the contact time with the pulp tissue. - a thorough general medical history, in order to take into account contraindications
It has mummifying properties for the pulp. The shorter residence time cotton wool with when deciding on the method of treatment,
formooresol in the chamber is intended to achieve only a superficial layer of mummifica­ - correct clinical examination to qualify the tooth for a specific treatment or to
tion, while preserving the viability of the deeper root pulp. For irreversible inflammation exclude the possibility of keeping the tooth in the mouth,
or other indications, leaving the preparation in the chamber for 5-7 days results in deeper - proper selection and evaluation of the pulp condition on the basis of additional
mummification. The preparation should only be applied to the pulp cut off at the level of examinations for a more precise diagnosis,
the canal orifices once haemostasis has been achieved. - the correct technique for carrying out the treatment with the appropriate treatment
The use offormocresol in dentistry is within the short-term exposure limits for form­ preparation,
aldehyde. A retrospective analysis of the use of formocresol in pulpotomy in deciduous - observing the principles of asepsis,
teeth showed that the preparation is effective and allows the deciduous tooth to remain in - compliance of the patient and the child's caregiver with the dentist's recommenda-
the mouth after the procedure for an average of 2.5 years. tions, including reporting to follow-up visits.
Iron sulphate is a haemostatic agent, which in a 15.5% solution has become one of
the preparations used in the treatment of pulpotomy of molar deciduous teeth. In addi­ Tab. 20.1. Treatment methods for pulp diseases of deciduous teeth.

tion, ferrous sulphate, has a pH of 1 , shows antimicrobial activity against oral micro-or­ Conditions for carry-
Methods Quality of the preserved Technique of
ganisms, comparable to 0.2% chlorhexidine. Although the exact mechanism of action ing out the treatment pulp treatment
is still unknown, it is believed that on contact with the blood, ferrous sulphate forms an
biological methods -
iron-protein complex that agglutinates and mechanically closes the blood vessels. In a preservation of part or all indirect capping,
pulpotomy, once iron sulphate haemostasis of the root pulp has been achieved, the cham­ of a clinically healthy pulp direct capping,
ber floor is covered with a layer of zinc oxide with eugenol, followed by a lining material using Ca(OH)2, MTA, B io- pulpotomy
Vital local anaesthesia dentine
and definitive filling or steel crown.
Iodoform exhibits bactericidal and bacteriostatic activity against many oral micro­ non-biological methods
preservation of canal pulp
organisms. It is used in a mixture with Ca(OH\, e.g. in pastes for root canal fillings of pulpotomy
with impaired function us-
deciduous teeth (e.g. Vitapex and Metapex) or with zinc oxide with eugenol. Iodoform ing FC or FS
is a more easily resorbable material than zinc oxide with eugenol when pushed past the pulpotomy,
Mortal devitalising agent Pulp necrosis
root apex. lodoform is also thought to have a weak anaesthetic effect and may inhibit pulpectomy
bleeding.

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Compendium of Paediatric Dentistry Treatment of dental pulp diseases and periapical lesions in deciduous teeth

Indirect pulp capping abnormal

pulp response to cold
The purpose of indirect capping is to mineralise the layer of demineralised carious den­ correct (significantly pro-
stimu lus
tin left behind and to produce secondary pathological dentin. The indication for interme­ longed or absent)
diate capping is deep caries without symptoms indicative of pulp inflammation. Reversibl e Additional tests
response to percussion 110 yes
partial inflammation of the pulp may also be diagnosed, as the pulp chamber in the deep
pathological changes on
cavity may be very thin, which promotes the penetration of bacteria into the pulp, desp ite 110 yes
X-ray
the lack of clear exposure, by poorly mineralized inter- and perianal dentin and a larger
diameter and simple course of the dental tubules in the deciduous tooth. In order to apply When a one-step protocol is chosen, the deep cavity is treated and fil led definitively
indirect pulp capping, an assessment based on clinical and radiological criteria, shoul d at the same visit. However, this method in young teeth may risk exposing the pulp. In
indicate that its irritation caused by the depth of the defect is capable of healing (Tab. 20.2) . the case of two-stage treatment based on so-cal led interim therapeutic restorations (ITR),
Th() indirect pulp coating procedure is widely used in deciduous teeth due to the gradual excavation of the carious dentin with temporary fi l ling of the cavity to stimulate
signi ficant prevalence and intensity of caries and often untreated caries. In children w ith the pulp to produce sclerotic, tertiary dentin is indicated. During the first visit, the sof­
early childhood caries who are found to have multiple active cavities, these need to be test, outer, infected layer is removed, and a thin layer of demineralised carious dentin is
treated in the short term to prevent carious lesions from progressing, w ith the risk of pulp left at the bottom of the cavity, the excavation of which would risk exposing the pulp.
complications. This objective can be achieved through caries stabil isation. It involve s This method is appl icabl e when caries progression needs to be controlled, especially in
the careful removal of carious dentin with hand instruments such as excavators or the use deciduous teeth that show signs of reversible partial pulpitis. The cavity is fi lled with a
of round burs on a slow speed handpiece. The basic principle when treating a cavity with calcium hydroxide preparation, chemo- or l i ght-cured glass-ionomer cement, reinforced
deep caries is to avoid exposing the pulp. Regardless of the treatment protocol chosen, with zinc oxide with eugenol to stimulate the healing process. In some cases, a second
the infected layer of soft, irreversibly damaged carious dentin should be selectively re­
stage of treatment is carried out after 1 -6 months. The decayed tissue is then completely
moved first from the walls, then from the bottom of the cavity. At the bottom, a demine­ removed, a·n d the cavity is finally fil led permanently. However, if the filling placed at the
ral ised dentin layer with preserved collagen network structure and apatite crystals can be
first visit is air-tight and the tooth shows no complaints or pathological changes, there
left near the pulp, which should be supplied with a suitable material with remineralising
is no indication to re-enter the cavity. Regardless of the number of stages, establ i shed
properties. It is also currently acceptable to leave a smal l amount of soft dentin. fillings should be inspected periodically for repair or replacement.
The ITR method of treating deep caries is widely used especially in children who
Tab. 20.2. Diagnostic criteria for indirect pulp capping in a deciduous tooth.
are anxious, uncooperative or have disabi lities. At the same time, fluoride prophylaxis
Diagnostic Indications Contraindications and appropriate home oral hygiene measures will serve to reduce the number of carious
Symptoms
components
bacteria in the sal iva, thereby in fluencing not only the inhibition of demineralisation
Provoked pains yes/no -
processes in tooth tissue, but also the maintenance of the quality of established fi l lings,
Rev iew �
spontaneous pains 110 yes including temporary ones, protecting them from secondary caries.
crown of tooth unsuit-
deep carious cavity yes able for permanent Technique for carrying out the procedure:
C linical restoration
- cleaning the tooth of dental deposits,
examination pulp exposure no yes
- possible admin istration of local anaesthesia,
swelling, fistula 110 yes
- removal of overhanging enamel with the turbine bur,

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Compendium of Paediatric Dentistry Treatment of dental pulp diseases and periapical lesions in deciduous teeth

isolation of the tooth from access by saliva, - abnormal (signifi-

removal of carious dentin from the lateral walls of the cavity and a layer of soft pulp response to cold stimulus correct cantly prolonged or
Additional tests absent)
infected dentin from the cavity wall with round bur on slow-speed handpiece,
response to percussion no yes
- washing the cavity with physiological saline solution or chlorhexidine and drying pathological changes on X-ray yes
no
,_
with a sterile cotton wool swab,
in the 1-step treatment method, the application of a layer of odontotropic prepara­ Technique for carrying out the procedure:
tion and the final filling of the cavity (in the 2-step carious dentin removal method, _ cleaning the tooth of dental deposits,
the cavity is cleaned after 2-3 months if the cavity is filled with zinc oxide with - isolation of the tooth from access by saliva,
eugenol, or after 6 months if glass-ionomer cement is used and the final filling is _ assessment of the extent of exposure and condition of the pulp (colour of blood,
placed), intensity of bleeding),
- pulp check-up and filling tightness after 3 and 6 months.
assessment of oral hygiene status,
- the performance of anaesthesia,
Direct pulp capping - isolation of the tooth from saliva access (recommended use of cofferdam),
The aim of direct capping is to initiate pulp healing with the formation of a reparative - washing the cavity in the treated tooth with sterile cotton wool balls with 0.9%
den tin, or dentin bridge, at the site of exposure and to preserve the viability of the coronal NaCl, 3% Hp2 , 1-2% NaOCl, Ca(OH)2 suspension in 0.9% NaCl and gentle drying
and root pulp in its entirety. The indication for this procedure is only non-carious pulp with a sterile cotton swab,
exposure, i.e. occurring as a result of trauma when the patient presents within 24 hours, - application of non-hardening calcium hydroxide, MTA or Biodentine to the site of
or iatrogenic, which can happen accidentally during the final cavity preparation stage. exposure,
A positive prognosis can be expected if, in addition, the size of the exposed pulp is no - tight, temporary or final filling of the cavity,
more than 1 mm (point), and oral hygiene is very good (Tab. 20.3). MTA or Biodentine - control of the condition of the pulp and periapical tissues and the tightness of the
are used in this method. As experience has shown, direct pup capping in deciduous teeth filling after 3 weeks and 3, 6 and 12 months.
is very rarely used.
Pulpotomy
Tab. 20.3. Diagnostic criteria for direct capping of the pulp in the deciduous tooth.
The purpose of pulpotomy (pulp amputation) is to eliminate bacterial infection by re­
Diagnostic
Symptoms Indications Contraindications moving the inflamed coronary pulp while maintaining the vitality of the root pulp or with
components
provoked pains yes - impaired function (mmmnification). Pulpotomy is the most widely used and promising pulp
Anamnesis procedure in the deciduous dentition. It allows the preservation of deciduous teeth up to their
spontaneous pains no yes
crown of a tooth un- natural exfoliation, avoiding the more difficult and less promising pulpectomy procedure.
trauma or deep carious lesion in
yes suitable for permanent The indication for this procedure is extensive caries complicated by reversible pulpitis
the final stage of preparation
restoration
minimum size significant or irreversible partial pulpitis, without features of periapical pathology. The cause of these
Clinical
pulp expo-
inflammatory conditions is pulp exposure occurring spontaneously as a result of the ongoing
examination blood colour bright red dark red
sure carious process, during mechanical cavity preparation or as a result of trauma, when the
bleeding non-intensive severe or no bleeding
patient presents after 24 hours (Tab. 20.4). The pulpotomy procedure makes it possible to
swelling, fistula no yes establish an intraoperative diagnosis of the pulp based on the pulp status image and the pos-

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Compendi u m of Paediatric Dentist ry Treatment of dental pulp diseases and periapical lesions in deciduous teeth

sibility of controlling bleeding. The greater the exposure and intensity of the pulp bleedin g, In the case of deciduous teeth, only total pulpotomy is performed due to the dynamics
which cannot be controlled within a few minutes, and the darker the colour of the blood, the of the inflammatory process resulting from the limited defensive capabilities of the pulp,
greater the likelihood of an advanced inflammatory process. The essence of pulpoto111y is especia lly during the resorption period, which can last from 2 to 4 years, and a lower
the removal of the inflamed chamber pulp, leaving a vital canal pulp that is healthy or in a a bil ity to reduce inflammation compared to the pulp of permanent teeth. To ensure hea­
state of reversible inflammation (bleeding from the canal pulp stumps can be stopped with in ling of the root pulp, the coronal pulp should be cut away in such a way that the surface
minutes) (Fig. 20. 1 ). If it is not possible to stop the bleeding within 3-4 minutes, it is neces­ Jeft is as smooth as possible. The next step is haemostasis and removal of a possible
sary to choose another treatment method, i.e. pulp extirpation or tooth extraction (Fig. 20.2). clot from the bottom of the chamber, which, being a breeding ground for bacteria, can
Similarly, the presence of oedema or a fistula disqualifies against the use of pulpotomy. provoke an inflammatory response of the pulp, cause difficult healing and complications.
A suitable preparation is then applied to the tooth chamber. The pulp amputation method
in deciduous teeth uses formocresol, zinc oxide with eugenol, iron sulphate, MTA. As
studies show, the efficacy of these preparations is similar in most cases, although MTA
is increasingly considered the gold standard in pulpotomy of deciduous teeth. Recently,
Biodentine has also been recommended for this purpose. Calcium hydroxide, on the
F ig. 20. 1 . Stopped bleeding and
I ight-coloured surface of canal other hand, is not recommended for use in the pulpotomy procedure as it can cause
pul p stumps after amputation of the internal resorption. The procedure with MTA and Biodentine is similar.
chamber pulp.
I n the deciduous teeth, the bottom of the chamber is formed by a thin layer of tissues,
the duct canals have a funnel-shaped inlet below the highest point of the chamber's bot­
Positive pulp response to stimuli tom, and the distance between the lowest point of the chamber's vault and the highest
point of its bottom is small (Fig. 20.3). Therefore, when performing pulp amputation, it
local anaesthesia is important to bear in mind the risk of perforation of the chamber floor and the need to
+ remove pulp also from the corners of the chamber (smooth out the overhangs).
pulp amputation After pulpotomy, follow-up examinations are indicated: clinical every 6 months and
antibiotic-steroid radiological immediately after surgery, then annually. Complications may be evidenced
paste
for 1 -2 weeks
l
by pain, the appearance of fistulas or soft tissue swelling, increased tooth mobility. Ra­
HAEMOSTA S I S ( Ledermix )
diological signs may include: thinning in the periapical region or root furcation, patho­
logical resorption, canal obliteration.
root canal treatment
the child's cooperation

+
swab with FC / ferrous sulphate / NaOCI
Fig. 20.3 . Thin chamber floor, the duct
canals have a funnel-shaped inlet, short
amputation paste distance between the lowest point of the
FC tampon for 5-7 days
chamber vault and the highest chamber
Fig. 20.2. Choosing a treatment method in the case of inflammation Aoor in teeth 64 and 65.
of the pulp of the deciduous tooth.

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Compendium of Paediatric Dentistry Treatment of dental pulp diseases and periapical lesions in deciduous teeth

f
Tab. 20.4. Diagnostic criteria for pulpotorny in a deciduous tooth. - cutting of the chamber pulp at the level of the duct canals with a sharp excavator,

i
Diagnostic
a round bur with slow-speed handpiece or a round diamond bur with high speed
Symptoms Indications Contraindications
components handpiece,
provoked pains yes - - chamber preparation,
Review - washing the chamber with physiological NaCl solution or chlorhexidine and drying
spontaneous pains no/short-term long-term
with a sterile cotton wool swab,
crown of a tooth un-
deep carious cavity or - stopping the bleeding with a cotton wool ball moistened with 2.5% NaOCI solution,
yes suitable for permanent
trauma
restoration - introduction of an MTA or Biodentine layer with a thickness of 2-3 mm into the
size greater than I mm very h igh chamber and gentle condensation,
Clinical
exam ination pulp ex- blood colour bright red dark red - after binding the material, tight, temporary or final filling of the cavityor cementing
\ posure severe bleeding or of the steel crown at the next visit.
bleeding non-intensive inflammatory exudate
or no bleeding
swelling, fistula 110 yes Technique forcarrying out the procedure with the use of formocresol or iron
pulp response to cold necrosis of the sulphate:
correct/ incorrect
stimulus canal pulp - cleaning the tooth of dental deposits,
Additional tests response to percussion no/yes yes - performing local anaesthesia (in the case of pain despite the anaesthesia, the so-
pathological changes called amputation can be performed after reducing the sensitivity of the pulp (de­
no yes
on X-ray sensitization), i.e. after placing in the defect a few days before the amputation of the
antibiotic-steroid paste),
Technique for carrying out the procedure of vital pulpotomy in the deciduous - isolation of the tooth from access by saliva,
tooth with the use of M TA or Biodentine: - preparation of the carious cavity with a bur with high speed handpiece to provide
cleaning the tooth of dental deposits, access to the cavity,
performing local anaesthesia (in the case of pain despite the anaesthesia, the so­ - change of instruments to sterile,
called amputation can be performed after reducing the sensitivity of the pulp (de­ - washing the cavity with physiological saline solution or chlorhexidine and drying
sensitization), i.e. after placing in the decay a few days before the amputation of the with a sterile cotton wool swab,
anti biotic-steroid paste), - removal of the chamber vault with round bur with slow-speed handpiece or a round
isolation of the tooth from access by saliva, diamond bur with high speed handpiece,
preparation of the carious cavity with a bur with high speed handpiece to provide - cutting off the ventricular pulp at the level of the canal orifices with a sharp excava­
access to the cavity, tor, round bur with slow-speed handpiece or a round diamond bur with high speed
change of instruments to sterile, handpiece
washing the cavity with physiological saline solution or chlorhexidine and drying - chamber preparation,
with a sterile cotton wool swab, - introduction to the chamber:
removal of the chamber vault with a slotted drill or round bur with slow speed • a cotton wool swab moistened and drained on a formocresol swab according to
handpiece, Buckley's recipe and then removing the cotton wool from the chamber after 5

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Compendium of Paediatric Dentistry Treatment of dental pulp diseases and periapical lesions in deciduous teeth

minutes (in the event of a longer treatment or lack of cooperation with the ch il d, - chamber preparation,
the formocresol swab can also be left for 5-7 days), - placing a cotton wool swab moistened with formocresol according to Buckley's
or recipe in the chamber for 5 minutes ( or for 5-7 days with the III-visit procedure in
• using an iron sulphate syringe applicator for 1 5 seconds and then rinsing the the case of persistence of pulp sensitivity),
chamber with distilled water, - removal of the wool swab from the chamber,
tight application to the bottom of the chamber of a 3-4 mm thick ZnO amputation - applying tightly to the bottom of the chamber a 3-4 mm thick amputation paste of
paste made with drops of eugenol and formocresol in a ratio of 1 : 1 or a paste only ZnO made with 1 : 1 drops of eugenol and formocresol,
of zinc oxide with eugenol, - installation of a glass-ionomer or carboxyl cement as a liner and final fill ing or ce­
the application of a glass-ionomer or carboxyl cement as a liner and the final fil l ing mentation of the steel crown,
or cementation of the steel crown (Fig. 20.4), - regular clinical and radiological follow-up.
- reg11lar c linical and radiological follow-up.
Pulpectomy
The aim of performing a pulpectomy is to remove the entire inflamed coronal and
root pulp. The indication for this procedure is irreversible total inflammation or necrosis
of the pulp. In favourable circumstances, endodontic treatment can be carried out in
Fig. 20. 4. Successive layers of materials deciduous teeth. However, due to the difficulty of accurately shaping the canals ( curved,
placed in pulp amputation with formocresol, thin wall ed) and filling them precisely, problems in establishing the working length, the
a - formocresol paste covering the chamber possibility of perforation and the risk associated with the proximity of the permanent
floor and canal pulp stumps, b - liner mate­
rial, c - final fi l ling. tooth bud, root canal treatment in deciduous teeth is not often performed.
When traditional root canal treatment is problematic, another procedure in the treat­
P ulpotomy procedure in a deciduous tooth using formocresol after pulp devita­ ment of pulp necrosis in deciduous teeth may be Lesion Sterilization and Tissue Repair,
lization (2-3 visits) : (LSTR). This method takes advantage of the natural defence and regenerative properties
I visit: of the host tissues, having first eliminated bacteria from the root canals. It consists of
cleaning the tooth of dental deposits, disinfecting the canals with a paste - a mixture of 3 antibiotics ( e.g. ciprofloxacin, met­
isolation of the tooth from access by saliva, ronidazole and clindamycin), without prior mechanical instrumentation. A ready-made
partial or complete preparation of a carious cavity, paste is also Ledermix containing a steroid and demeclocycline, or Pulpomixine. After
- washing the cavity with physiological saline solution or chlorhexidine and drying it preparation of the cavity and chamber, the canal orifices are widened with a diamond
gently with a cotton wool swab, round bur to improve penetration of the antibiotic paste. The bottom of the chamber is
application of a devitalizing agent and dry wool on the exposed pulp for 7- 1 4 days, then covered tightly with paste, a glass-ionomer material and final filing or steel crown
- application of a tight temporary fi ll ing; is filled or cemented is placed
II visit: The prerequisite for p lanning a pulpectomy procedure is not only the specific local
- isolation of the tooth from access by saliva,
indications. Good cooperation with the child, a certain age and therefore stage of deve­
removal of temporary filling, lopment of the deciduous tooth (no or minimal resorption) and good general health of
complete preparation of the carious decay and the chamber with a bur with high-speed the child are essential.
handpiece, together with cutting off the chamber pulp at the level of the duct canals,

288 289
 Treatment of dental pulp diseases and periapical lesions in deciduous teeth
Compendium of Paediatric Dentistry

From the point of view of the development of a particular group of teeth, root canal
treatment can be performed:
in an incisal tooth in a child under 4.5 years of age,
in a canine below 7-8 years of age,
in the second molar before the eruption of the fi rst permanent molar, i.e. under 7-8
Fig. 20.6. N umerous root canals
years of age. and a chamber periodontal canals
Indications for pulpectorny, in addition to conditions based on the history and clinical in a deciduous molar.
and radiographic examination of the causative tooth, include the importance of keeping
the tooth in the mouth (malocclusion, hypodontia of the permanent successor, location in
the vicinity of a cleft palate, and haemophilia). However, these factors are not an abso­
lute condition for retaining a deciduous tooth in the mouth. They should be taken into ac­
count among other elements such as the clinical condition or the expected retention time
of the tooth due to the degree of root resorption or significant destruction of the crown. Fig. 20.7. Progressive root resorption and zinc oxide with eugenol filling the canals of tooth 85 .
The difficulties in root canal treatment of deciduous teeth are related to their anatomy.
The thin layer of mineralised root tissue (arched in the case of molars) and physiological Contraindications to pulpectomy surgery include:
resorption, which is difficult to identify radiographically, pose a risk of root wall perfora­ advanced physiological and pathological internal or external resorption,
tion during mechanical preparation (Fig. 20.5). The wide apex opening, further widened - perforation of the chamber bottom,
by resorption, makes it difficult to determine the working length and risks overflowing - approaching physiological exfoliation (Tab. 20.5).
the canal. Long, narrow, often medially and distally flattened root canals, sometimes di­
vided by secondary dentin into two thin and often obstructed, the presence of additional Tab. 20.5 . Indications and contraindications for extirpation in relation to the condition of the tooth.
canals terminated with apex foramen, numerous connections between the canals, often
Examination Evaluation criteria lndications Contraindications
with a pronounced root delta, hinder the complete extirpation of the pulp and create
provoked pains yes no
the need to fill the canal with material with antibacterial properties (Fig. 20.6). Due to Review
spontaneous pains yes no
progressive physiological resorption, the root canal filling materials should also resorb destruction of the
(Fig. 20.7). These include pastes containing combinations of zinc oxide with eugenol, crown that makes its
deep carious cavity yes
iodoform and calcium hydroxide. reconstruction im-
possible
size small or larger -
Clinical
examination pulp ex- blood pink or dark red -
posure
more intense or no bleeding that cannot
Fig. 20.5. Root canal filling bleeding
bleeding be controlled
material visible through the
pulp response to stimuli incorrect correct
thin root wall of a deciduous
swellinQ no ves
molar at the initial stage of
response to percussion no/yes
root resorption.
Additional pathological changes on
no no/yes
tests X-ray

290 291
 Treatment of dental pulp diseases and periapical lesions in deciduous teeth
Compendium of Paediatric Dentistry

The positive course of root canal treatment is evidenced by the absence of pain. I n - definitive filling of the canals with resorbable material, i.e. slowly hardening zinc
a clinical examination, there i s no swelling, fistula, positive reaction to percussion, the oxide with eugenol, non-hardening calcium hydroxide, iodoforrn paste or a mixture
tooth does not show mobility. Radiographs do not show periapical lesions and those of iodoform paste with calcium hydroxide (e.g. Vitapex), manual filling with a root
previously present should have healed. The process of physiological resorption togethe r canal instrument or with an applicator is recommended,
with the root canal filling material is proceeding well. The eruption of the permanent - referral for a follow-up X-ray,
tooth should be seamless. Root canal treatment must be carried out with great care, both - filling the chamber with glass-ionomer or carboxyl cement,
during the mechanical preparation and flushing of the canal, due to the presence of the - placement of a final filling or steel crown,
permanent tooth bud. - regular clinical and radiological follow-up every 12 months.
Stages of pulpectomy in the deciduous tooth:
References
- referral for a dental radiograph (assessment of the development and shape of the
I . American Academy of Pediatric Dentistry. Pulp therapy for primary and immature perma­
rooti and determination of the working length; the wide apical foramen makes it nent teeth. The Reference Manual of Pediatric Dentistry. Chicago, I l l ; 2020: 399-407 - 2. A mer­
impossible to measure with an endometer), ican Academy of Pediatric Dentistry. Guideline on Pulp Therapy for Primary and I mmature Per­
manent Teeth. Originating Committee Clinical Affairs Committee - Pulp Therapy Subcommittee.
possible administration of local anaesthesia, 2014. - 3. Bossu M et al. Diffrent Pulp Dressing Materials for the Pulpotomy of Primary Teeth :
- isolation of the tooth from saliva access (use of a cotferdam is advisable), A Systematic Review of the Literature. J. Clin. Med. 2020, 9, 838, doi: 10.3390/ jcm9030838.
complete preparation of a carious cavity with wide access to the chamber due to its -- 4. (:i nar C et al. Antibacterial effect of haemostatic agents. J Clin Exp Dent. 2012;4(3): 151-
5. doi: I 0.43 l 7/jced.50750. - 5. Cordell S et al. A Randomised Controlled Trial Comparing the
large size in a deciduous tooth, Success of Mineral Trioxide Aggregate and Ferric Sulfate as Pulpotomy Medicaments for Primary
chamber opening, Molars. J Dent Child 2021 ;88(2): 120-8. - 6. Coll JA et al. Use of Non-Vital Pulp Therapies in Pri­
- removal of the chambered pulp with a sharp excavator or a diamond roun bur with a mary Teeth. Pediatr Dent 2020,4,(5 :337-49. - 7. Dhar V et al. Use of Vital Pulp Therapies in Pri­
mary Teeth with Deep Caries Lesions. Paediatr Dent 2017, 39, 5: 146E-l 59 - 8. Kolasa M i wsp.
slow-speed handpiece or high-speed handpiece, Direct pulp coverage in permanent teeth in children - formation of tertiary dentin, materials used.
chamber preparation, Part I I . Nowa Stomatol 20 1 8, 2: 78-84 I DOl : 1 0.25 1 21/NS.2018.23.2.78. - 9. Kozubska A et al.
Efficacy of formocresol amputation in the treatment of pulp of deciduous molars - a retrospective
removal of the canal pulp using pulp extractors, Hedstrom files, paper points or gen­ study. New Dentistry 2018; 2 3(3): 95-10 1 DOI : https://doi.org/ 1 0.25 1 21/NS.2018 .23.3.95 .
tle syringe flushing of the pulp and exudate from the canals, 10. Mohammad G et al. Pulpal Diagnosis o f Primary Teeth: Guidelines for Clini­
sparing mechanical preparation of canals to a length of less than 2 mm from the cal Practice. Bangladesh J Dent Res Edu 2012, 2, 2: 66-68. - 11. Piekoszewska-Ziiytek p
et al. Alveolar infections - a review of the literature. New Stomatol 2016, 2: 1 20-134 I DOI:
radiological length of the tooth using endodontic files ("K", Hedstrom or NiTi), I 0.5604/ J 4266911.1208252 - 12. Pulp Therapy for Primary and Young Permanent Teeth: Foun­
careful but generous irrigation of the canal with 0.9% NaCl, 3% hydrogen peroxide dational Articles and Consensus Recommendations, IAPD 2021. Therapeutic. - 1 3 . Saber AM
et al. Atraumatic Restorative Treatment and Interim Restoration : A Review of the Literature.
solution, 0. 1 -1-2.5% sodium hypochlorite solution, 0.2-0.4% chlorhexidine solu­
Dent .I 2019, 7, 28; doi: I 0.3390/dj70 I 0028. - 1 4. Sain S et al. Lesion Sterilization and Tis­
tion, 6% citric acid, distilled water (also using ultrasound). sue Repair-Current Concepts and Practices . Int J Clin Pediatr Dent. 2018 Sep-Oct; 1 1 (5): 446-
thorough drying of the canal with paper points, 450. doi: I 0.5005/jp-journals- I 0005-1555. - 1 5 . Sokotowska K i wsp. Direct covering of pulp
111 permanent teeth with the use of Bioclentine® material - 3-year observations. New Stomatol
in the event of exudation in the canal or major ailments, a disinfectant insert should 20 I 7, 3: 1 1 2-1 1 9 - 1 6. Taha NA et al. Full Pulpotomy with Biodentine in Symptomatic Young
be used in the antiseptic chamber for 7- 10 days (e.g. camphorized monochlorophe­ Permanent Teeth with Carious Exposure Journal of Enclodontics, 2018; 44: 932-937.
nol, camphenol, Cresophene),

292 293
 Specificity of pulp disease treatment of immature permanent teeth

plying a biological dressing of odontotropic material to the bottom of a prepared carious

cavity or to a dentinal wound in the case of a post-traumatic crown fracture. In carious
Chapter 21 cavities, the aim of management is to remove the most infected dentin and stimulate the
pulp to form reactive dentin.
Specificity o f pulp disease treatment of immature Currently, calcium hydroxide or zinc oxide with eugenol are most commonly used

permanent teeth as biological dressings with odontotropic and bactericidal properties. These materials
should be covered with glass-ionomer or carboxyl primer cement, followed by a tight
Lidia Postek-Stefanska, Joanna Szczepanska, filling.
Dorota Olczak-Kowalczyk
Indirect Pulp Capping - one-stage treatment:
- local anaesthesia,

Biological pulp treatment of immature permanent teeth - isolation of the tooth from saliva access (recommended rubber dam; when unable to
use a rubber dam, other effective isolation may be considered),
The main goal of treatment in the case of immature permanent teeth is to preserve the - opening the cavity (with a bur with high speed handpiece),
living pulp tissue - all or part of it - to ensure apexogenesis, i.e. the proper formation - removal of the main mass of soft, necrotic, infected carious dentin (with a round bur
of the root at a full, genetically programmed length with the formation of the apex. In with slow speed handpiece ),
a situation where there is simple pulp necrosis or complicated by inflammation of the - removal of carious dentin from the walls and bottom of the cavity, leaving it in the
periapical tissues and the Hertwig epithelial sheath is destroyed, the aim of treatment is area closest to the pulp,
to apexify, i.e. stimulate the further development of the root, the formation of a root apex - washing the cavity with disinfectant (e.g. 2% chlorhexidine, 1 -2.5% sodium hypo­
or only a mineralized barrier in the apex without the participation of the pulp; sometimes chlorite) and physiological saline (0.9% NaCl),
also without the participation of the Hertwig sheath. - dehumidification of the prepared cavity (recommended sterile cotton balls),
In immature permanent teeth, the methods of choice to ensure apexogenesis are: - covering the decalcified dentin left on the bottom with a biological dressing (with
in-direct pulp capping, direct pulp capping, partial pulpotomy, complete pulpotomy. a formulation Ca(OH\ hardening liner type: Dycal, Life, Calcimol LC, Calcipulpe),
a non-hardening material (Biopulp, Calcicur, Calxyl), zinc oxide eugenol (ZnOE)
Indirect pulp treatment (IPT) / Indirect Pulp Capping (IPC) and a cement liners,
- placement of a tight final filling.
The indirect pulp capping method is used in the following cases:
- deep carious cavities, in teeth with a healthy pulp or reversible pulpitis, where com­
plete cleaning of the bottom would expose the pulp, Indirect Pulp Capping - two-stage treatment
I visit:
- post-traumatic crown fracture without pulp exposure.
The absence of spontaneous pain, possibly moderate pain provoked by chemical and - local anaesthesia,
- isolation of the tooth from saliva access (recommended rubber dam; when unable to
thermal stimuli, which disappears spontaneously after cleaning the teeth or taking an
analgesic (e.g. paracetamol, ibuprofen) is important in the assessment of the pulp con­ use a rubber dam, other effective isolation may be considered),
- washing the tooth with a mild disinfectant,
dition. On clinical examination, the pulp responds positively to vitality tests and there
are no pathological changes in the periapical tissues on X-ray. This method in-volves ap- - opening the cavity (with a bur with high speed handpiece),

294 295
Compendium of Paediatric Dentistry Specificity of pulp disease treatment of im mature permanent teeth

- removal of the main mass of soft, necrotic, infected caries dentin (with round bur D irect Pulp Capping
with slow speed handpiece), Indications for this method include permanent teeth with unformed roots in the case
- removal of residual carious dentin from the cavity walls, particularly in the ena­ of:
mel-dentin junction and the bottom, leaving it in the area closest to the chamber so - slight pulp exposure within healthy dentin (< I 1111112) during excavation of a carious
as not to expose the pulp, cavity in a tooth with healthy pulp,
- washing the cavity with disinfectant (e.g. 2% chlorhexidine, 1-2% sodium hypoch lo­ - small post-traumatic pulp exposures (< I mnl) if the patient presents for treatment
rite) and 0.9% NaCl, within a short period of time after the injury (1-2 days).
- dehumidification of the prepared cavity (recommended sterile cotton balls), Currently, it is considered that the size of the surface area of the exposed pulp, as
- covering of the decalcified dentin left at the bottom of the cavity with a biological well as the time elapsed since accidental exposure, do not have a significant impact
dressing (Ca(OH\ hardening liner: Dycal, Life, Calcimol LC) or a non-hardening on the outcome of biological treatment (direct pulp cap, partial and complete pulpo­
dressing (Biopulp, Calcipulpe), or zinc oxide-eugenol (ZnOE), tomy), because the pulp is only superficially infected. The success of the treatment
- tight coverage of the biological dressing with glass-ionomer or ZnOE-reinforced ce­ is determined primarily by ensuring sterile conditions for pulp wound healing. The
ment (IRM material); fill the whole cavity for 3-12 months. exposed pulp should be bright red in colour and there may be slight bleeding, easily
I I visit: stopped.
- pulp assessment: clinically (no hypersensitivity, no provoked pain, no spontaneous Contraindications for the use of this method are: spontaneous pain, nocturnal pain,
pain), radiographically (no pathology on X-ray, visible reactive dentin), increased mobility of the tooth, significant, not easily stopped bleeding (lasting several
- local anaesthesia, minutes) from the pulp after pulp exposure, serous or purulent exudate from the pulp
- isolation of the tooth from saliva access (as above), chamber after pulp opening, on the X-ray: widening of the periodontal sulcus, patholo­
- removal of the temporary filling and biological dressing from the cavity, gical changes in the area of root furcation and in the periapical tissues.
- removal of the remaining caries dentin (a round bur with a slow speed hndpiece); I n the case of post-traumatic damage to the healthy pulp, the prognosis is signifi­
work carefully so as not to remove the newly formed dentin (poorly calcified, white), cantly better than in teeth with carious pulp exposure, where the pathological changes
- washing the cavity with disinfectant (e.g. 2% chlorhexidine, 1 -2.5% sodium hypo­ in the tissue are greater as a result of bacterial infection in the course of caries. This
chlorite) and 0.9% NaCl, method makes use of the high biological potential of the pulp to form reparative dentin,
- dehumidification of the prepared cavity (sterile cotton wool balls), particularly marked in immature teeth. The aim of treatment is to stimulate progenitor
- covering of the bottom of the cavity with liner (Ca(OH\, glass-ionomer cement, cells located in the pulp to differentiate into odontoblasts capable of forming the basic
bonding system) and cement liner, substance (dentin matrix) of reparative dentin.
- the placement of a tight final filling. For direct pulp cup, materials based on Ca(OH)2 or calcium silicate - MTA, Bioden­
The determinants of a positive treatment outcome are: tine are recommended. Among the preparations based on Ca(OH)2 ; non-hardening mate­
- preserved living, healthy pulp, rials are preferred, which show a greater ability of antibacterial and stimulating odonto­
- correct formation of the root apex (apexogenesis), blasts to produce reparative dentin than hard-binding liners. A prerequisite for successful
- absence of symptoms such as tooth sensitivity, pain, swelling, treatment is the tight protection of the pulp wound against bacterial microleakage. W hen
- in the radiographic image, there are no signs of internal and external resorption and placed on the pulp of Ca(OH\, necrosis develops at the point of contact, with limited
pathology in periapical tissues. inflammation underneath. In this area, a dentinal bridge is formed, which undergoes

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Compendium of Paediatric Dentistry Specificity of pulp disease treatment of immature permanent teeth

mineralisation. ln some cases, despite the formation ofa calcified dentinal bridge, chronic Pulpotomy
pulpitis or even pulp necrosis occurs. In these situations, internal resorption or oblitera­ The procedure involves cutting away part (partial pulpotomy) or all (complete pulpo­
tion of the pulp cavity may develop. Therefore, the mineralised dentinal bridge visible on tomy) of the inflamed coronal pulp.
the X-ray cannot be the only indicator of a successful treatment outcome.
Alternative materials for direct pulp coverage include calcium ceramics - hydroxy­ Pulpotomy is indicated in cases of:
apatite, tricalcium phosphate and tetra-calcium phosphate, bone morphogenetic proteins - reversible, asymptomatic pulpitis with carious exposure of this tissue,
(BMPs). - reversible symptomatic low-grade pulp inflammation,
- post-traumatic pulp exposures:
Direct Pulp Capping - management: • < 4 mm2 - having contact with the oral environment over 1-2 days - partial pul­
clinical and radiological pulp assessment, potomy,
loca} anaesthesia, • > 4 mm2 - having longer contact with the oral environment - complete pulpotomy.
- isolation of the tooth from saliva access (recommended rubber dam; when unable to In the case of inflammation limited to a place near the carious lesion, partial pulpoto­
use a rubber dam, other effective isolation may be considered), my is recommended, and in inflammation involving coronal pulp i n a larger area - com­
opening the cavity, plete pulpotomy. In trauma exposures, the lesser importance of the time elapsed since the
- complete removal of caries dentin from the walls, then from the bottom of the cavity, injury is increasingly emphasised. Some authors consider a delay of less than nine days
- opening of the chamber (pulp exposure, accidental - pulp injury), between the onset of injury and the treatment administered to be a safe period.
- assessing the condition of the pulp by its colour (pinkish red), bleeding (slight, easy Contraindications to the use of this method are:
to stop, blood bright red), - irreversible pulpitis involving both the coronal and root portion,
washing with disinfectant, removal of possible clot, inhibition of bleeding (2% chlor- - significant hypersensitivity of the tooth to thermal stimuli (heat, cold),
hexidine, 1-2.5% NaOCl, aqueous suspension Ca(OH)2 ) and 0.9% NaCl, - chronic· pain (originating in the dental pulp),
drying the prepared cavity with sterile cotton wool balls, - positive response to percussion,
covering the exposed pulp with a selected biological dressing - Ca(OH)2 , MTA or - on the X-ray, pathological changes in the furcation area and periapical tissues,
B iodentine, - obliteration of the pulp chamber and/or root canal, calcification in the dental cavity.
- covering the bio-dressing with a sealed base cement (glass-ionomer or IRM), In post-traumatic pulp exposure, this tissue is cut off to a depth of approximately 1-3 mm
- the placement of a tight final filling (usually composite). (partial pulpotomy to Cvek); in teeth with carious exposure, the pulp must be cut off deeper, as
Teeth treated with direct pulp coverage should be checked periodically clinically and it is infected over a larger area. In caries-exposed teeth, irreversible inflammation of the pulp is
radiographically. The positive outcome of the treatment is evidenced by: often confined to the area ofthe pulp under the caries lesion. Difficulties in obtaining haemosta­
positive pulp viability test, sis after removal of the smface patt of the pulp indicate more extensive inflammation and are an
no hypersensitivity or pain, indication for complete pulpotomy. In the case of complete pulpotomy, the whole coronal pulp
- reparative dentin visible on the X-ray (calcified dentinal bridge), is cut off, leaving only the root pulp. The remaining healthy patt of the pulp is provided with
root formation (formation of the apex, wall growth in thickness), a biological dressing - a non-hardening preparation based on Ca(OH\, MTA or Biodentine.
no signs of internal or external resorption, obliteration of the canal lumen, foci of The mechanism of pulp wound healing after amputation is identical to that of the
calcification, direct pulp capping method for this tissue. The biological dressing initiates the processes
no pathological changes in periapical tissues. leading to the formation of a mineralised dental bridge and reparative dentin.

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Compendium of Paediatric Dentistry Specificity of pulp disease treatment of immature permanent teeth

Pulpotomy, like other endodontic procedures, should be performed with rubber dam to - the placement of a tight final filling or restoration of the tooth crown in the event of
protect the pulp from infection. For cutting off the pulp, it is best to use a round diamond bur its traumatic fracture,
with high-speed handpiece with sterile water cooling or 0.9% NaCl (gentle technique). The - control of the procedure performed on the X-ray,
resulting smooth wound surface provides the best healing conditions. In the case of partial - periodic clinical and radiological checks.
pulpotomy, heavy bleeding that cannot be stopped with a sterile ball of cotton wool or, on
the contrary, the absence of any bleeding at all, indicates a more advanced pathological pro­ Complete pulpotomy - management:
cess in this area of the pulp, so the pulpotomy should be carried out deeper and, in selected - clinical and radiological examination (assessment of pulp condition, degree of root
cases, up to the complete cutting off of the whole coronal pulp (complete pulpotomy). The formation, possibly pathology in periapical tissues, furcation area),
same measures are used to stop bleeding and disinfect the wound surface as described in the - local anaesthesia,
direct pulp capping method. After d1ying with sterile cotton wool balls on the wound surface, - isolation of the tooth from saliva access (recommended rubber dam),
gently, without pressure, apply a biological dressing - a non-hardening preparation based on - disinfection of the treated tooth and adjacent teeth with a mild disinfectant,
Ca(OH)z, MTA or Biodentyne and tightly cover it with adhesive dental cement. - complete removal of caries from the walls and bottom of the cavity (ifthere is carious
pulp exposure),
Partial pulpotomy - management: - removal of the chamber vault (with a slotted burr with high seed handpiece),
clinical and radiological examination (assessment of pulp condition, degree of root - complete pulpotomy of the pulp up to the level of the canal orifice (with a sharp
formation, possible pathology in periapical tissues, furcation area), excavator or a round bur with slow speed handpiece),
local anaesthesia, - suppression of bleeding from pulp (sterile cotton wool balls soaked with 0.9% NaCl)
- isolation of the tooth from saliva access (recommended rubber dam), and its disinfection (1 -2.5% NaOCl, 2% chlorhexidine or an aqueous suspension of
- disinfection of the treated tooth and adjacent teeth with a mild disinfectant, Ca(OH)z),
complete removal of caries from the walls and bottom of the cavity (if there is carious - covering the duct pulp with a biological dressing - non-hardening material Ca(OH)z,
pulp exposure), MTA or Biodentine (with a layer of at least 1 .5 mm thick),
partial removal of the pulp at the place of its exposure to a depth of at least 1-3 mm, - sealing the biological dressing with glass-ionomer cement (preferably reinforced
depending on the cause of the exposure; the pulp should be removed together with with resin),
the surrounding dentin (diamond round bur with high speed handpiece with cooling - the placement of a tight final filling or restoration of the tooth crown in the event of
with sterile water administered from a syringe), its traumatic fracture,
inhibition of pulp bleeding (0.9% NaCl sterile cotton wool balls), possible disinfec­ - control of the procedure performed on the X-ray,
tion (1-2.5% NaOCl, 2% chlorhexidine, Ca(OH\ suspension in 0.9% NaCl); if after - periodic clinical and radiological checks.
amputation the bleeding cannot be stopped within a few minutes, and the blood is
dark red, the pulp should be amputated deeper, until the bleeding is stopped effective­ Apexification in non-vital teeth with immature roots:
ly, and the outflowing blood - bright red, The indication for this method is pulp necrosis or irreversible pulp inflammation due
- covering the pulp with a biological dressing based on Ca(OH\, MTA or Biodentine to caries or post-traumatic damage in teeth with unformed roots. Treatment is aimed at
(with a layer of at least 1.5 mm thick), completing root formation or stimulating the mixed pulp-periodontal tissue to form a
- sealing the biological dressing with glass-ionomer cement (preferably reinforced mineralised barrier to close the canal lumen, allowing the canal to be finally filled. This
with resin), requires chemo-mechanical preparation of the canal and the placement of a preparation in

300 301
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the canal to stimulate healing and the formation of an apical barrier (apexification). D u e JU visit:
to the thin canal walls, mechanical canal preparation should be very sparing, compen­ - final filling of the canal with thermos - plasticised gutta-percha,
sated by abundant rinsing with chemical disinfectants (1-3% NaOCl, 2% chlorhexidine, - X-ray control of the correctness of the root canal filling,
17% EDTA, 1 -50% citric acid, 10% urea peroxide) and 0.9% NaCl. Physical factors - placing a filling in a cavity in the crown of a tooth.
such as ozone, ultrasound, temperature (NaOCl heating), laser light or LED (light-acti­ Follow-up visits after 3, 6 and 12 months (then at annual intervals for several years)
vated disinfection) can be used to enhance the effectiveness of decontamination. to assess by X-ray the formation of the root apex or possible pathology (periapical tissue
CmTently, MTA is recommended for the apexification procedure, in addition to Biodentine cha nges).
with similar propetties. Prior to MTA placement, it is recommended to pre-apply a calcium Radiological criteria for correct closure of the canal lumen with MTA material in­
hydroxide paste for 2-4 weeks to eliminate infection, control exudate or bleeding from the peri­ clude:
apical area. If it is technically impossible to close a wide apical opening with MTA, it is recom­ - no pushing of material into the periapical tissues (overfilling) or underfilling of the
mended, to place a resorbable collagen sponge (e.g. Spongostan, Colla Cote), followed by the canal greater than 3 mm from the apical opening,
introduction of the MTA. The advantage of the MTA material is that it can be used in a one-step - no gap between the material and the canal wall,
apexification treahnent method. The MTA placed in the apex area of the unformed root in the - no sign of displacement of the MTA material during the final filling of the canal
form of a layer about 4 mm thick is a hard barrier effectively sealing the canal light so that it can (difference in the control X-ray image after placement of the MTA layer and after the
be finally filled without displacing the obstructive material to the periapical tissues. final filling of the canal),
- no signs of pushing sealant or root canal filling material (gutta-percha) into the peri­
Apexification with MTA (or Biodentine) apical tissues.
I visit: In clinical practice, calcium hydroxide, hydroxyapatite pure or in combination with
- endodontic treatment as in the Ca(OH)2 method, Ca(OH)2 , is also still used in the apexification procedure. Since initiation of apex healing
- placement of Ca(OH)2 paste in the canal for 1-2 weeks (can be inserted into the canal with the use of Ca(OH)2 takes a minimum of 3-4 months, and the period necessary to
with a Lentuo needle). achieve apexification is from 6 to 24 months, the course of treatment with these prepara­
II visit: tions requires multiple visits to replace the canal filling, on average every 3 months. It is
- local anaesthesia, therefore a multi-stage, long-term treatment. The reason for the failure of this treatment
- fitting of a rubber dam, may be the loss of marginal tightness of the temporary filling in the crown as well as the
- removal of Ca(OH)2 paste from the canal, filling in the canal, leading to reinfection. Another serious problem associated with the
- rinsing with disinfectant (if MTA is used, the canal cannot be rinsed with chlorhexi- long duration of apexification treatment with calcium hydroxide is the low strength of
dine, as this interferes with the binding of the preparation), thin root walls - long treatment can lead to root fracture.
- drying the channel with paper points,
- placing the MTA preparation in the canal in the apical end of the canal using an Apexification using Ca(OH)z_based pastes
adequate plugger and the back end of sterilised paper points (layer of about 4 mm), l visit:
X-ray control of correct MTA placement, - taking of X-rays (determination of root development, condition of periapical tissues,
- insetting a ball of moist cotton wool into the canal mouth (MTA binds in a moist preliminary determination of working length),
environment for several hours), - local anaesthesia, rubber dam isolation, disinfection of crown,
sealing the tooth with glass-ionomer cement or ! RM. - preparation of endodontic access (much wider than in mature teeth),

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Compendium of Paediatric Dentistry Specificity of pulp disease treatment of immature permanent teeth

extirpation of necrotic pulp,

- measurement of the working length on the X-ray with the endodontic instrument I Pulp treatment methods for immature permanent teeth

in the canal (a safety margin of 0.5-1.0 111111 from the radiographic apex should be
considered), necrosis or irreversible pulpitis

sparing mechanical preparation of the canal alternating with rinsing with disinfec­ entire healthy pulp,
after indirect, direct
l
tants (1 -2.5% NaOCl, 2% chlorhexidine, 10% urea peroxide, 17% EDTA) and 0.9% apex ification with
stimulation
covering or after vital revascularisation
NaCl, amputation spontaneous Ca(OH), i MTA or Bio- using polyantibiotic
revascularisation dentint + thermally

l
- drainage of the canal (with paper septic points), paste or Ca(OH)/
after total plasticised gutta-per-

I I
MTA/
placement ofCa(OH)2 paste in the canal (some authors recommend prior filling of the luxation cha + Gl-cement + B iodentine+ GI-ce-
apexogenesis or avulsion composite
canal with Ledennix or other antibiotic paste for 1-2 weeks), ment + composite

- fillipg of the cavity (IRM, glass-ionomer cement). Fig. 2 1 . 1 . Endodontic treatment methods for immature permanent teeth.
Next visits:
control of the apexification (X-ray examination of the progress of root formation or
Pulp revascularisation/revitalization
formation of the apical barrier), clinical examination of the forming barrier (gentle
Regenerative endodontic procedures can be performed in patients with ASAI or
probing with an endodontic instrument),
ASA2 for immature permanent teeth diagnosed with pulp necrosis when the diameter
replacing the Ca(OH\ paste with a fresh one.
of the apical foramen is greater than 1 mm, the final restoration does not require a root­
Last visit:
crown post.
control X-ray (evaluation of the apical barrier, correctness of the canal filling),
This method involves removal of dead tissue, thorough disinfection of the root ca­
- final filling of the canal (thermally plasticised gutta-percha method recommended).
nal, insertion of an antibiotic or calcium hydroxide pad into the canal, followed by me­
Follow-up visits after 3, 6 and 12 months (then at annual intervals for several years)
chanical bleeding of the periapical tissues (access through the canal) and closure of the
to assess (by X-ray) the formation of the root apex or possible pathology (periapical
entrances (orifices) to the root canal with MTA material. The use of antibiotic toothpaste
tissue changes).
has good results, nevertheless side effects such as discolouration of tooth tissue, cyto­
A thermally plasticised gutta-percha technique (Obtura, System B) is preferred as
toxicity, sensitisation, development of antibiotic resistance and problems with removal
a definitive root canal filling after apical treatment. Lateral condensation of the studs
of root canal material must be taken into account. The results of current research recom­
increases the risk of root wall breakage. An alternative to gutta-percha and sealant is to
mend the application of calcium hydroxide. Based on the blood clot found in the canal,
fill the canal with glass-ionomer cement or chemo-light-curing composite resin (using
pulp-like tissue is formed from stem cells. The pulp regeneration process involves stem
a dentine bonding system) and use a fibreglass post. The thin root walls of teeth after
cells from the dental papilla (the target dental pulp) of the fonning root and stem cells
apexification need to be reinforced in such a way that root fracture or crown breakage
from the tissues surrounding the root (bone, periodontium). Eventually, pulp-dentin-like
does not occur. If the apexification procedure is performed with MTA, the entire length
tissue is formed in the canal, the woven tissue of which may also contain dentin-, cemen­
of the canal can be filled with this preparation.
tum- and bone-like cells. Apexogenesis occurs as a result of this procedure. A significant
advantage of the method is the growth of the root wall not only in length, but also in
thickness, which cannot be achieved (or only in rare cases) with a Ca(OH\ or MTA­
based preparation in the apical method. Success is determined by the microbial-free
environment in the canal and periapical tissues.

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Pulp regeneration by tissue engineering techniques using stem cells, growth factors - placement of MTA or Biodentine on the clot in the canal mouth or on top of the
and gene therapy is also possible. Research in this area is currently underway, but it will collagen matrix (the material should be approximately 3 111111 below the enamel­
take time to apply it to everyday clinical practice (Fig. 2 1 . 1 ). dental junction),
- fi lling the cavity with an adhesive composite material (final filling) or IRM or glass­
Revascularisation - management procedure: ionomer cement (temporary fil ling if a moist ball of cotton wool is placed in the
I visit: chamber).
taking of X-rays. (determination of root development, assessment of periap ica l If symptoms of infection persist after disinfection of canal, the antimicrobial medica­
tissues), ment should be reintroduced into the canal.
local anaesthesia, application of a rubber dam, disinfection of the tooth crown (e.g . The procedure can also use platelet-rich plasma (PRP) or platelet-rich fibrin (PRF) in
1 0% iodopovidone - Betadine), p lace of a blood clot.
creating access to the tooth cavity, The c linical evaluation of the outcome of endodontic treatment of teeth with un­
abundant rinsing of the canal with 1 .5-3% NaOC! ( 1 0-20 ml, 5 min) and 0.9% NaCl formed (also formed) roots should take into account the absence of symptoms such as
without mechanical preparation of the canal with fi les, tooth hypersensitivity, pain on biting and tapping, swelling, fistula, pathological tooth
drying the channel with paper points, mobility. In immature teeth treated with indirect and direct pulp capping, the pulp should
- insertion into the canal, up to the level below the enamel-dental junction: respond correctly in tests to assess its viability.
• a three-antibiotic paste ( ciprofloxacin, metronidazole, minocycline: l : 1 : 1 , or al­ Radiological control of immature teeth after endodontic treatment should be carried
ternatively a two-antibiotic paste without minocycline or containing amoxicil lin, out after 3, 6 and 1 2 months and then at annual intervals until root develop-ment is
clindamycin, or cefaclor instead of minocycline) or complete (4 years is recommended). In teeth treated with biological methods (indirect,
• calcium hydroxide paste - ready-made or Ca(OH\ diluted with distil led water direct pulp capping and pulpotomy - paitial and total), a calcified dentine bridge should
(3 : 1 ); be visible on the X-ray and the root should be properly formed including the apex. In the
inserting a bal I of cotton wool into the chamber, case of teeth with necrotic pulp treated by apexi fication, the treatment results on X-ray
- filling of the cavity (IRM, glass-ionomer cement). according to Weine can be as follows:
I I visit (after 2-3 weeks): - normal root development, well-developed apex, convergent root walls with a proper­
- local anaesthesia without a vasoconstrictor, rubber dam isolation, disinfection of the ly formed root canal lumen,
tooth crown, - formed apex, no root wall growth in thickness, divergent or parallel wal ls (as at the
removal of the temporary filling, start of treatment),
removal of antibiotic or Ca(OH)2 paste, near or in front of the apex (in the lumen of the canal), a mineralised barrier of va­
irrigation of the canal with l .5-3% NaOC!, followed by 0.9% NaCl ( 1 0-20 ml), then rying degrees of saturation is visible,
20 ml EDTA for 5 min, - no features of root development, no visible calcified barrier in the apical region, but
drying the channel with paper points, a barrier is palpable on clinical examination after insertion of the endodontic instru­
inducing bleeding from the periapical tissues by injuring them with a 1 5K. or 40H fi le ment into the canal lumen.
and producing a blood clot - its level should reach at least 3-4 mm below the enamel­ Failure of apexification is evidenced by the absence of a visible mineralised barrier in the
cement junction (a stable clot forms within 1 5 minutes), a fibrin sponge can be placed apical part of the root, which is also not perceptible on direct endodontic examination, or the
on top of the clot (Spongostan, Colla Cote), occurrence of pathological changes in the periapical tissues, external resorption, root fracture.

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Compendium of Paediatric Dentistry Speci ficity of pulp disease treatment of immature permanent teeth

The European Endodontic Society has defined guidelines for the radiological asse s s-
ment of the quality of endodontic treatment ( 1 994). These are as follows:
success of the treatment: correct outline, structure and width of the periodontal
space, reduction in the size of pathological changes in periapical tissues compared to
the picture on the X-ray before the treatment, no signs of inflammation external root
resorption; in the event that extensive pathological changes in the periapical tissues
have healed, and the widening of the periodontal space persists on a limited area, Fig. 2 1 .4. Apexi fication performed in tooth 2 1 using MTA: a) - diagnostic X-ray
_
this should be interpreted as a scar rather than persistent inflammation; this case is (patient aged 1 0 years), b) - MTA injected i nto the root canal, c) - control photo
(root canal fi lled with thermo-plasticised gutta-percha - Obtura I I system).
considered a success of the treatment,
uncertain (doubtful) treatment outcome: the periapical translucency has not
Pa thological resorption of mineralized tooth tissues
changed, nor has the size of the lesion decreased,
treatment failure: visible new lesion that appeared after endodontic treatment, after
Resorption of a tooth is the process of destroying its mineralised structures - dentin
root canal filling, signs of progressive resorption or hypercementosis.
and root cementum. Under physiological conditions, resorption only affects deciduous
The final result and duration of endodontic treatment of immature permanent teeth
teeth (before they are replaced by permanent teeth). Pathological resorption occurs in
depends on the type of material used, as wel l as on factors related to the treatment proce­
permanent teeth and can also affect deciduous teeth. Pathological resorption of hard den­
dure, removal of bacteria and protection against their invasion, correct diagnosis, selec­
tal tissue involves inflammatory reaction cells, osteoclasts, odontoclasts, cementoclasts
tion of the appropriate treatment method and, in the case of teeth with dead pulp, on the
depending on the tissue affected, in addition to monocytes and macrophages. These cells
quality of preparation and sterility of the canal and its tight closure. The patient's gen­
are stimulated by cytokines and pro-inflammatory enzymes. The resorption process is
eral health is also important, as it determines the regenerative capacity of the pulp and
initiated when there is damage to the dentin ( layer of odontoblasts and prodentin) or the
peridental structures. The results of treating pulp necrosis of immature permanent teeth
root cementum (osseornucoid and cementoblasts).
with MTA are shown in Fig. 2 1 . 2, 2 1 .3, 2 1 .4.
Pathological factors cai.1sing resorptions are:
- acute mechanical inj uries (partial luxation, avulsion with late tooth replantation),
chronic mechanical inj uries (pressure of the retained tooth or tumour, orthodontic
treatment), thermal , mechanical iatrogenic inj uries ( during the development of cavi­
ties and grinding of teeth under the prosthetic crown) and chemical (internal whiten­
ing of the dead tooth 30% H 2 O2 ) '
pulpal or periodontal biological factors leading to local inflammatory reaction (pulp
infection caused by caries, periodontal infection, endodontic infection caused by
F ig. 2 1 .2 . Procedure of apexification in tooth Fig. 2 1 .3 . The procedure of apexification in trauma - damage to the root cementum and pulp death with its infection as a result of
1 1 after trauma with the use of MTA tooth 2 1 after trauma with the use of MTA tooth luxation), radiotherapy of tumours,
in a 9-year-old boy. in a 9-year-old girl.
- systemic factors - systemic diseases, endocrine disorders,
- unknown (idiopathic) factors.

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Compendium of Paediatric Dentistry Specificity of pulp disease treatment of immature permanent teeth

The classification of resorption proposed by Andreasen (1970) takes into account: hyperplastic (invasive) resorptions:
internal resorptions: inflammatory and replacement, invasive internal replacement,
external resorptions: surface, inflammatory and replacement. • coronal invasive (internal),
Division of pathological resorptions taking into account their location: • invasive cervical (internal) :
1. internal resorptions (occurring in the tooth cavity, starting in the dentin): - Class l - includes enamel and a thin layer of coronal dentin,
• Type A - crown resorption, - Class 2 - located close to the pulp within the coronal dentin only,
• Type B - root resorption, - Class 3 - comprising the coronal dentin and ½ of the root dentin,
• Type C - resorption with perforation of the canal wall, - Class 4 - comprising the coronal dentin and over ½ of the root dentin.
• type D - resorption with ventricular perforation ( distinguished by some clini­
cians) ;
Tab. 21.1. Classification of resorption according to Heithersay and Lindskog and treatment
2. exterual resorptions (of the root, starting in the root cement) :
management.
inflammatory apical root resorption in the course of chronic periapical tiss ue
Division of resorption
inflammation, Procedure
according to Heithersay and Lindskog
• inflammatory lateral root resorption (as a result of post-traumatic pulp necrosis),
Resorptions due to injury (non-infectious)
• cervical resorption,
l - surface (external) I - due to slight, reversible damage to periodon­
• replacement resorption, ankylosis (osteosarcoma), tal fibres and root cementum - radiological ob­
• resorption caused by chronic mechanical trauma, servation recommended, endodontic treatment
only in case of signs of infection,
• resorption accompanying systemic diseases.
2 - transitional apex 2 - due to slight, reversible post-traumatic da­
Due to the extent of the pathological process, resorptions can be superficial (often (internal) mage (on X-ray "blunting" of the root apex, wi­
self-healing, the resorption process is accompanied by cementum or dentin apposition) dened periodontal gap) - radiological obser­
vation recommended (changes resolve sponta­
or deep (progressive, leading to perforation of the root wall, penetrating into the alveolar neously up to 1 2 months after trauma), endodon­
bone). Resorptions can be acute or chronic. tic treatment recommended only in case of signs
The current division of resorptions proposed by Heithersay and Lindskog considers of infection or discolouration,
3 - compression and orthodontic 3 - removal of the cause - surgical treatment
three groups of resorptions based on their aetiology and indicates the clinical manage­ (external) ( e.g. dentigerous tumour), orthodontic/surgical
ment for each group: treatment ( e.g. retained jaw fang),
4 - replacement, replacement, ankylosis 4 - mature teeth, normal occlusion - observation
trauma-induced resorptions: - when more than 20% of the periodontal for future implant restoration,
• surface (external), fibres are damaged as a result of trauma (if 4 -- Mature teeth in infraocclusion - surgical re­
• transient apical internal, the osseomucoid and root cementum are not positioning (selected cas·es) and application of
damaged, replacement does not occur) Emdogain to the root surface,
• pressure and orthodontic(external), 4 - i mmature teeth in infraocclusion - decon­
• replacement, ankylosis (external) ; struction (according to B. M algrem) and pros­
thetic provision with a removable prosthesis.
infection induce dental resorption:
Surgical repositioning (selected cases) and ap­
• internal inflammatory (infective) root: apical and intra-radicular, plication of Emdogain to the root surface. Im­
• external inflammatory, plant prosthetics - once alveolar bone growth is
complete.
• communicating internal-external;

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Compendium of Paediatric Dentistry Specificity of pulp disease treatment of immature permanent teeth

Resorptions caused by infection (inflammatory) 3 - cerv ical (internal) 3 - Class I , 2: topical application of 90% trichlo­
l
I - internal inflammatory resorption (apical I - apex resorption - channel treatment - acc u-1 roacetic acid, curettage (with a bur embedded in
and intra-root) rate disin fection of 5.25% NaOCI and 3% H o the contra-angle), procedure to be carried out as
and channel instrumentation, preferably usin� described above, filling of the resorption cavity
ultrasonic files to the resorption level, long-ter n1 with glass-ionomer cement,
( 6- 1 2 months) use of Ca(OH)2 , final fil l i ng of 3 - Class 3 : topical application of 90% trichloro­
the channel (thermally plasticized gutta-perch a acetic acid (for 1 -2 min) to the resorptive tissue,
technique, MTA preparations), curettage (with a bur embedded in the curette),
I - intra-root resorption - endodontic treatment procedure to be carried out as described above,
over the full length of the canal according to the possibly pulpectomy, antibiotic-steroid paste,
scheme described above, root canal filling, filling of the resorptive cavity
2 - external in flammatory resorption 2 - root canal treatment, intracanal insert with with glass-ionomer cement or MTA-type materi­
antibiotic-steroid preparation (e.g. Ledermix) or al, orthodontic extrusion if necessary,
long-term application of Ca(OH)z, the fi nal fil­ 3 - Class 4: poor prognosis, initial observation is
ling of the canal after inhibition of resorption, recommended, if clinical signs of progression ap­
2 - prophylactically after replantation of the mature pear - tooth extraction and prosthetic restoration
tooth - pulp extirpation, antibiotic-steroid paste ap­
plied as soon as possible, final root canal filling, References

3 - perforating (internal/external) 3 - channel treatment according to the scheme I . Aeinehchi M et al. Mineral trioxide aggregate (MTA) and calcium hydroxide as pulp-cap­
given above to the level of resorption, inducing ping agents in h uman teeth: preliminary report. Int Endod J 2003 ; 36: 225-23 l . - 2. AAE.
calcification by using Ca(OH)z alone or after Clinical considerations for a regenerative procedure. In: Clinical resources. Regenerative
prior topical application of 90% trichloroacetic endodontics. 4 January 201 8 . Chicago, IL: American association of Endodontists; 20 1 8 .
acid, the perforation is closed with M TA type https ://www.aae.org/specialty/wp-con tent/up I oads/si tes/2/20 1 8/06/ConsiderationsF orRe­
material, the channel is filled with plasticized gEnd�_AsOfApri12018 . pdf. - 3. American Academy of Pediatric Dentistry: Pulp Therapy
gutta-percha for Primary and I mmature Permanent Teeth . The Reference Manual of Pediatric Dentistry.
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Hyperplastic (invasive) resorptions Chicago, A1ner Acad of Pediatric Dent 202 1 :3 99-402 - 4. Bahns F et al. Revascularization
I - internal replacement I - endodontic treatment - pulpectomy and che­ of immature permanent teeth with apical periodontitis: new treatment protocol? J Endod
(located in clinical crown) mo-mechanical canal preparation, final filling of 2004; 30. 196-200. - 5. Bimstein E, Rotstein I. Cvek p ulpotomy - revisited. Dental Trau­
the canal with plasticised gutta-percha, thorough matol. 2 0 1 6;32(6): 43 8-442. - 6. Bj0rndal L. Indirect pulp t herapy and stepwise excavation.
cleaning of the post-resorption cavity and fi l ling J Endod 2008; 34, 7: 29-3 3 . - 7. B ose R et al. A retrospective evaluation of radiographic
with glass-ionomer cement, outcomes in immature teeth with necrotic root canal systems treated with regenerative end­
2 - crown (internal) 2 - careful application of 90% trichloroace­ o?ontic procedures. J Endod 2009; 3 5 : 1 343- 1 349. - 8. Camp J H . Diagnosis dilemmas in
tic acid (for 1-2 min) to the resorptive tissue vital pulp therapy: treatment for the toothache is changing, especially in young, immature
(surrounding tissues protected with glycerol), teeth. J Endod 2008; 34: 6-1 2 . - 9. Darcey J, Qualtrough A. Resorption: part 1 . Pathology'
curettage of the resorptive tissue (with a drill classification and aetiology. Br. Dent. J. 2013;214:439-45 1 .
embedded in the caecum), this procedure should 1 0. Darcey J, Qualtrough A. Resorption: part 2. Diagnosis and management. Br. Dent.
be repeated until the granulation is completely J. �013 ;214:493-509. - 1 1. Dominguez-Reyes A et al. Study of calcium hydroxide apexifi­
removed. I f the pulp is also involved - recom­ _
cat1 �n 111 26 you�g permanent incisors. Dent Traumatol 2005 ; 21: 141 - 1 45 . - 1 2 . Eggmann,
mended pulpectomy and definitive root canal Flonn, et al. Partial pulpotorny without age restriction : a retrospective assessment of perma­
fi lling after antibiotic-steroid intraluminal inlays, nent teeth with carious pulp exposure. Clinical Oral Investigations 26. 1 (2022): 365-373. -
filling of the resorption cavity with glass-iono­ 1 3 . E uropean Society of Endodontology developed by: Galler KM, Krastl G, Simon S, Van
mer cement, orthodontic extrusion if necessary, Gorp G, M eschi N, Vahedi B, Larnbrechts P. European S ociety of Endodontology position
statement: Revitalization proced ures. I nt Endod .J. 2016;49: 7 1 7-723. - 1 4. Garcia-Godoy
F, M urray PE. Recommendations for using regenerative endodontic procedures in perma­
n ent immature traumatised teeth. Dent Traumatol 2012; 28, 1: 33-41. - 1 5 . H eithersay GS.

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M anagement of tooth resorption . A ust Dent J 2007;52( I suppl): l 05- 1 21. - 16. J eeru pha n P art V
T et al. M ahidol study I : comparison of radiographic and survival outcomes of imm ature
teeth treated with either regenerative endodontic or apexification methods: a retrospec tive
study. J Endod 2012; 3 8 : 1 3 3 0-13 36. - 17. Jodlowska A et al. Use o f C alcicur material in the
endodontic treatment of permanent teeth w i th u n formed roots. J Stoma 20 1 1 ; 64, 1 1 : 8 23- Acquired tooth damage of non-carious origin
837. - 18. Kher, M . S . , Rao, A. Strategies for Pulp Therapy in l mmature Permanent Teeth. l n :
Contemporary Treatment Techniques in Pediatric Dentistry. Springer, Cham . 2019; https ://
doi.org/10.1007/978-3 -03 0 - 1 1860-08 - 1 9 . Malmgren B . Decoronation of an ankylosed tooth
for preservation of alveolar bone prior to implant placement. Dent. Traumatol. 200 I ; 17 :93-95 . Chapter 22
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pulpotomy agents in young permanent teeth (apexogenesis). Pediatric Dent 2006; 21: 1-8. - 21.
Parirokh et al. M ineral trioxide aggregate: a comprehensive literature review. Part I . Chemical,
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Traumatic dental injuries - epidemiology, causes,
method f)f treating pulp necrosis in teeth with an un formed apex - pulp revascularisation. Part J . classifications, complications
New Dentistry 2014, I : 37-40. - 2 3 . Pazera R et al. A modern method o f treating pulp necrosis in
teeth with an unformed apex - pulp revascularisation. Part 11. New Stomatol 2014; 2: 1 6-20. - 24. Dorota Olczak-Kowalczyk
Pazera R, Szczepai'lska J. Resorption as a sequela of dental trauma - diagnosis and management.
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management of teeth with unformed apices with mineral trioxide aggregate and calcium hydrox­
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Traumatic dental injuries (TOI) and their consequences are a health, economic and
review. Dent Traumatol 2005; 21: 1-8. - 28. Sapir S, Shapira J . Decoronation for the management psychosocial problem for people of developing age. They account for about 5% of trau­
of ankylosed young permanent tooth. Dental Traumatol. 2008;24: 131- 1 35 . - 29. Srinivasan V et matic injuries to the body in all age groups. The prevalence of trauma to deciduous teeth
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- hypotonia of the orbicularis oris muscle,
dental caries,
- previous history of TDI,
- tongue piercing,
- male gender (the importance of gender is declining due to mo;e frequent participa-
tion in sports by girls),
- practising contact sport,
- age (the incidence of dental trauma is higher in three age ranges, i.e. 1-3-year-olds,
7- 10-year-olds and 16-18-year-olds),
- systemic diseases, e.g. asthma, neuromuscular diseases, cerebral palsy, intellectual
disability, epilepsy.

3 14 315
Compendium of Paediatric Dentistry Traumatic dental injuries - epidemiology, causes classifications, complications

Traumatic damage occurs as a result of a rapid transfer of energy to the tooth and its 3. Complicated crown fracture. A fracture involving enamel and dentin and
supporting structures, through direct contact of the teeth with a hard surface or indirect exposing the pulp.
action, i.e. contact of opposing teeth caused, e.g. by impact on the face. The result can 4. Uncomplicated crown root fracture. A fracture involving enamel, dentin and
be fracture and/or displacement of the tooth with complete rupture or crushing of the cementum but not involving the pulp.
supporting tissues (gingiva, periodontal ligaments and bone). 5. Complicated crown root fracture. A fracture involving enamel, dentin and
The type of traumatic damage and its extent depends on: the energy of the impact, cementum and exposing pulp.
the characteristics of the causative object (hardness, elasticity, shape), the direction of 6. Root fracture. A fracture involving dentin, cementum and the pulp.
the impact force and the type of tooth (deciduous, permanent). The result of being struck B. Injuries to the periodontal tissues:
by a low-weight object at high speed or being struck by a sharp-edged object is usually 1. Concussion. An injury to the tooth supporting structures without abnormal loo­
fractures of the crowns of the teeth. The causes of damage to the periodontal tissues are sening or displacement of the tooth, but with marked reaction to percussion.
usually, impacts with a heavy object at low speed, a resilient object or an object with 2. Subluxation. An injury to the tooth supporting structures with abnormal loose­
rounded edges. Luxation injuries are more common in deciduous teeth and crown frac­ ning but without displacement of the teeth.
tures in permanent teeth. 3. [ntrusive luxation (central luxation). Displacement of the tooth into the alveolar
Traumatic damage to teeth can be the result of accidental events (sp01ts, traffic acci­ bone. This injury is accompanied by comminution or fracture of the alveolar
dents, falls and collisions, e.g. on playgrounds) or non-accidental (violence, beatings). In socket.
the youngest children, falls or violence are common causes, at school age, falls from bicy­ 4. Extrusive luxation (peripheral luxation partial avulsion). Partial displacement of
cles, scooters, accidents in playgrounds, and in adolescents, fights, accidents during sports the tooth out of its socket.
and traffic accidents are common causes. Tooth injuries - both deciduous and permanent, 5. Lateral luxation. Displacement of the tooth in a direction other than axially. This
most often occur at home, then at school, at playgrounds, in spo1ts facilities, on the streets. is accompanied by comminution or fracture of the alveolar socket.
Most traumatic dental injuries involve a single anterior tooth, most commonly the 6. Exarticulation (complete avulsion). Complete displacement of the tooth out of
medial incisors, followed by the lateral maxillary tooth. The likelihood of damage to its socket.
multiple teeth has been linked to some causes of trauma (sporting activities, violence and C. Injuries of the supporting bone:
traffic accidents). Traumatic damage to the teeth may be accompanied by injuries to soft 1. Comminution of alveolar socket. Crushing and compression of the alveolar
tissues, most often the lips, then the gums, least frequently the tongue. socket. This condition is found together with intrusive and lateral luxation.
There are a number of classifications of traumatic dental injuries. The currently ap­ 2. Fracture of the alveolar socket wall. A fracture contained to the facial or lingual
plicable classification is the Andreasen clinical classification, which takes into account socket wall.
both traumatic damage to the teeth, periodontium, bone tissue, as well as the gingiva and 3. Fracture of the alveolar process. A fracture of the alveolar process, which may or
oral mucosa. It applies to post-traumatic damage to both permanent and deciduous teeth. may not involve the alveolar socket.
Andreasen 's classification: 4. Fracture of the Mandible and Maxill a. A fracture involving the base of the man­
A. Injuries to the hard dental tissues and pulp. dible or maxilla and often the alveolar process (jaw fracture). The fracture may
1. Crown infarction. An incomplete fracture (crack) of the enamel without loss of or may not involve the alveolar socket.
the tooth substance. D. Damage to the gingiva or oral mucosa:
2. Uncomplicated crown fracture. A fracture contained to the enamel or involving 1. Laceration of gingiva or oral mucosa. A shallow or deep wound in the mucosa
enamel and dentin, but not exposing the pulp. resulting from a tear and usually produced by a sharp object.

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Compendium of Paediatric Dentistry Trau matic dental injuries - epidemiology, causes classifications, complications

2. Contusion of gingiva or oral mucosa: A bruise usually produced by an impact Factors that may increase the risk of complications are:
from a blunt object and not accompanied by a break of the continuity in the mu­ - completed root development (in immature teeth, a wide apical opening provides
cosa, causing submucosal haemorrhage. better pulp vascularisation and greater healing capacity in cases of post-traumatic
3. brasion of gingiva or oral mucosa: A superficial wound produced by rubbing or pulp exposure and root fractures, as well as the chance ofr evascularisation when
scrapping of the mucosa leaving a raw bleeding surface. the blood supply vessel to the pulp is interrupted),
Classification according to Ellis has limitations because it only applies to teeth, all - traumatic damage:
damage to deciduous teeth is grouped in one class and does not include all types of • favouring bacterial invasion into the pulp ( e.g. fractures with a fracture fissure
traumatic damage. Includes nine classes: close to the pulp chamber or exposing the pulp),
Class I - simple crown fracture with little or no dentin affected, • those causing pulp ischaemia, i.e. causing interruption, compression of the ves­
Class II - extensive crown fracture with considerable loss of dentin, but with the pulp sel supplying blood to the pulp (e.g. partial and complete luxations),
not affected, • causing rupture or crushing of the periodontal fibres (e.g. partial and complete
Class Ill - extensive crown fracture with considerable loss of dentin and pulp exposure, luxations);
Class IV - a tooth devitalized by trauma with or without loss of tooth structure, - coexistence of traumatic damage in the same tooth,
Class V - teeth lost as a result of trauma, - repeated trauma to the same tooth,
Class V I - root fracture with or without the loss of crown structure, - general diseases impairing healing,
Class V II - displacement of the tooth with neither root nor crown fracture, - lack of or inadequate temporary protection of the tooth, inadequate storage of a
Class V III - complete crown fracture and its replacement, completely avulsed tooth or the crown fragment that could be used for restoration,
Class IX - traumatic injuries of primary teeth. too late reporting to the dentist (especially in the case of complete tooth avulsion),
Dental inj uries are at risk of many local complications, including: early, i.e. occurring incorrect diagnosis and choice of treatment.
immediately after the injury (e.g. pain, swelling, increased tooth mobility, tooth dis­ Traumatic damage to the tooth (mainly in the nature of luxations and root fractures
placement) or late, including: concerning the tooth with traumatic damage (resorptions, with fragment displacement) can also result in pulp canal obliteration (PCO), which is
pulp necrosis, inhibition of root development, discoloration) (Tab. 22.1 ), relating to the not currently considered a complication. It involves the deposition of hard tissue in the
permanent successor of an injured deciduous tooth. lumen of the chamber and root canal. It can be partial or total. It occurs more frequently
The consequences of traumatic injury also include medical costs, deterioration in in immature teeth (Fig. 22. 1). The tooth takes on a yellowish colour. Endodontic treat­
quality of life and facial aesthetics, which can negatively affect the patient's psychoso­ ment may be considered for planned prosthetic or orthodontic treatment.
cial development.
The occurrence of complications concerning the traumatised tooth and the type
of complication depends on a number of factors related to the trauma itself (type of
traumatic damage, coexistence of traumatic damage in the same tooth), the type of
dentition (deciduous, permanent), the developmental stage of the tooth, the quality of
the first aid given, the time elapsed between the trauma and the dental appointment Fig. 2 2 . 1 . Progressive cavity
and the therapeutic management, the patient's general state of health and the patient's obliteration of laterally luxated
cooperation. tooth 1 1 . R ight - status 6 months
after inj ury.

318 319
Compendium of Paediatric Dentistry Traumatic dental injuries - epidemiology, causes classifications, complications

Tab. 22.1. Complication related lo the injured tooth. External inflammatory

resorption
Type of complication Diagnosis
] frequent in cases of severe tooth

I
a negative vital signs luxation (lateral luxation, intrusion,
can occur at different times after clinically, it may be asym­
test and at least 2 other avulsion), more frequent in im­
trauma, so the condition of the pulp ptomatic, cause pain on
signs from interview and mature permanent teeth (the more
is assessed at the initial ex-amina- vertical or horizontal per­
physical examination, e.g. immature the tooth, the faster the
tion and each follow-up examina- cussion, depending on the
fistula, progression of resorption), can lead
tion; location of the resorption,
X-ray - periradicular tissue to complete root loss in a short time;
Pulp necrosis - more often in luxated teeth than in or in acute cases, produce
changes, inhibited root the result of superimposing infec­
crown fractures; symptoms of peri radicular
development; tion on damage to the root cement;
- high risk: tooth avulsion, intrusion, infection (e.g. swelling,
pulp response to stimuli damage to the cement causes surface
lateral luxation ; it is una-voidable tooth sensitivity, fistula);
may not be normal un- resorption, followed by exposure
in the case of perma-nent tooth on X-ray radiolucencies:
til 4-6 weeks or even 3 of the dentin, which contacts the
intrusion with a fully shaped root along the root surface and
\
months after injury dead pulp and provides a route for
in the adjacent alveolar
usually asymptomatic, bacteria and bacterial toxins to move
bone
possibl e pink discoloration outwards, thus sustaining the resorp­
in the crown of the tooth tion process
(pink spot), when the
result of metaplasia of the inflamed
inflammatory resorption
pulp into tissue: the essence is the replacement of re­
concerns the ventricular Replacement resorption sorbed root tissue with bone tissue;
Internal surface - granulation tissue containing os-
pulp, detected accidentally
resorption (JSR): teoclasts that destroy dentin (inter- the cause is the death of the cells of
in X-rays: clinical signs: metallic
inflammatory, nal inflammatory resorption), the periodontal ligament, usually
- inflammatory: oval en- percussion sound, lack of
replacement - bone-like or cement-like, depos- as a result of lateral tooth luxation,
largement of the tooth physiological tooth mo­
ited at the site of damaged dentin intrusion or avulsion;
cavity, bility;
(internal replacement resorption) ankylosis may occur;
- interchangeable: irregular no visible periodontal
widening of the tooth during developmental age, there
may be gradual intrusion of the an­ space on X-ray
cavity or tunnel led re-
sorption kylotic tooth and inhibition of bone
growth in its area
transient condition; shallow re-
Inhibition of root deve­
sorption of cementum as a result of
lopment
E xternal surface local trauma to the periodontium
on X-ray subtle changes in
resorption, (ESR), or cementum (minor luxation, e.g.
the contour of the root the cause is simple pulp necrosis or
non-infectious subluxation, root fractures), healing
through deposition of new repair complicated by inflammation of the
no progress of root forma­
cementum periapical tissues and destruction of
the Hertwig epithelial root sheath tion
(HERS)

320 32 1
Compendium of Paediatric Dentistry Traumatic dental injuries - epidemiology, causes classifications, complications

The most frequently observed complications concerning a tooth that has suffered Reducing the frequency of traumatic damage to teeth and associated complications
an injury in relation to deciduous teeth are: discoloration of the crown, pulp necros is, requires preventive measures to reduce the risk of a causal event of injury and the risk
periradicular tissue inflammation, premature resorption of the tooth root, ankylosis, ab­ of tooth damage (primary, primary prevention) or its severity in the event of an event, as
scess formation and fistulae. The risk of ankylosis in deciduous teeth is lower than in well as the correct provision of first aid (secondary prevention) and therapeutic treatment
permanent teeth, which is most likely due to greater elasticity of the alveolar bone and (tertiary prevention).
greater healing ability in the youngest children. The key elements of prevention are:
Injuries to deciduous teeth can also cause disorders of the eruption of permanent teeth - education addressed to children and young people, as well as adults responsible for
(e.g. retained eruption, ectopic eruption), the separation of the tooth germ in the form chi Id safety and first aid at the scene of an accident ( especially parents, carers, pre­
of sequestrum and developmental abnormalities of the permanent successors, including school educators, teachers, trainers), which should provide knowledge on how to
discoloration and enamel hypoplasia, coronal dilaceration, root dilaceration, spliting, or avoid injuries and how to provide assistance if they occur,
tearing of the roots, inhibition of the root development. The most common complica­ care to ensure the child's safety at home, when using transport, in playgrounds and
tion affecting permanent incisors after luxation of deciduous teeth is white or yellow­ during group activities,
ish-brown discoloration and enamel hypoplasia. Very rare complications are odonto­ elimination of the influence of local factors favouring tooth injury (e.g. treatment of
ma-like malformations and an dentigerous cyst. malocclusion, caries),
The consequences of an injury to a deciduous tooth on the successor permanent tooth - the use of facial and dental protection (face shields, mouth guards) for traumatic
depend on the type and severity of the injury and the developmental stage of the perma­ sports ( contact sports, motor sports, sports where there is a risk of fal ling or being
nent tooth germ. Injury to a deciduous incisor tooth in the first two years of life can affect hit by e.g. a knee, elbow or an object (e.g. ball, stick, disc) and by people who have
the crown of the developing permanent tooth and, in older children over four years of suffered facial trauma.
age, the developing root of the successor tooth. The risk of disruption to the permanent For the youngest children, it is important to secure the sharp edges of furniture, re­
tooth is highest with intrusion or avulsion of the deciduous tooth, fol lowed by extrusion strict access to stairs (gates), prevent the child from climbing on the furniture and move
and lateral luxation. Intrusion and avulsion of deciduous incisors in children under two around with an object in the mouth (e.g. a cup or bottle). Toys, sports equipment, play­
years of age is considered the greatest threat to developing permanent teeth. Damage to ground equipment should meet safety standards.
the permanent tooth root can occur regardless of the degree of resorption of the root of Face and teeth protectors aim to reduce the impact of blows by preventing the blow
the traumatised deciduous tooth. The impaction of a deciduous tooth induces stresses from reaching the mouth area or by cushioning, absorbing or distributing the forces of
in the permanent tooth's pulp and surrounding hard and soft tissues, regardless of the impact. Face protection devices are masks made of thermoplastic materials or metal
direction of the force and the stage of resorption of the deciduous tooth. gratings attached to helmets. Devices with a built-in chin section to protect the teeth in
A serious complication of a tooth injury can be tetanus, which occurs in people who the event of a chin impact are advisable. Protective mouthguards are applied to the up­
are insufficiently immunized (the last dose of primary or booster vaccination was for per dental arch. The exception to this is people with a Class III malocclusion, for whom
more than 1 0 years) or not vaccinated at all. Even a small cut when contaminated with the mouth guard should cover the lower arch. Mouthguards can be standard (without or
soil, dust or faeces can be a gateway to infection. If the wound or knocked-out tooth has with the possibility of being moulded by the user) and customised (single-layer or multi­
been in contact with the ground and tetanus protection is uncertain, tetanus prophylaxis, -layer) prepared in the prosthetic laboratory. In addition to sports people, mouthguards
i.e. the administration of a vaccine, possibly combined with the administration of tetanus are also recommended for patients with neurological disorders that favour dental injuries
antitoxin, is used. (e.g. children with cerebral palsy).

322 323
Compendium of Paediatric Dentistry

References
Chapter 23
I . Agouropoulos A et al. A 5-year data report of traumatic dental injuries in children and ado­
lescents from a major dental trauma centre in Greece. Dent Traumato I . 202 1 ;37(4):63 1 -638. - 2.
Andreasen J O et al. Textbook and colour atlas of traumatic injuries to the teeth. 4th ed. Wiley-Black­
well 2007 - 3 . Azami-Agbdash S et al. Prevalence, etiology, and types of dental trauma i n chi ldren Specifics of the dental examination of the traumatised child
and adolescents: systematic review and meta-analysis. Med J Islam Repub Iran. 20 1 5 ;29(4):23 4.
- 4. Borges TS et al. I mpact of traumatic dental i njuries on oral health-related quality of life of Joanna Szczepanska
preschool children: A systematic review and meta-analysis. PLoS ONE 20 1 7; 1 2(2): e0 l 72235 ;
doi .org/ 1 0. 1 37 1 /journal.pone.0172235. - 5 . Bossu M e t al. Evaluation o f the Application of Ital­
ian National Guidelines for Prevention and Management of Dental I njuries in Developmental
Age. Int J Envi ron Res Public H ealth. 2020;17(8):2875 . doi: I 0.3390/ijerph 1 7082875. - 6. Child­
Tooth injuries in children require a visit to the dentist as soon as possible. Depending
hood Asthma Management Program Research Group (CAM P). Long-term Effects of Budesonide
or Nedocromil in Children With Asthma. N Engl J Med 2000;343 ( 1 5): I 054-63 . - 7. Carla M on the type of injury, i.e. the degree and extent of damage to the hard tissues of the tooth,
et al. Consequences of dental trauma to the primary teeth on the permanent dentition. RSBO pulp, periodontium, bone structures and soft tissues, the patient will need immediate,
20 1 2;9(4J:457-462. - 8 . de Aguiar Santos BO et al. Root resorption after dental traumas: classifi­
cation and clinical, radiographic and histologic aspects RSBO (Online) 20 1 1 ; 8(4). - 9. Dubey A delayed or late treatment.
et al. Assessment of traumatic dental injuries in patients with cerebral palsy. J I ndian Soc Pedod The interview begins with a question about the age of the child, that is, determining
Prev Dent 20 1 5;33:25-7.
what type of teeth we are dealing with (deciduous or permanent) and at what stage of
I 0. El-Kalla 1 H et al. impact of Dental Trauma on Qua!ity of Life Among 1 1 - 1 4 Years School­
children. Contemp Clin Dent. 2017;8(4):53 8-544. - 1 1. Feliciano KM et al. A systematic review development are individual dental groups. On this basis, we obtain preliminary informa­
of the diagnostic classifications of traumatic dental injuries. Dent Traumata] 2006; 22(2):7 1 -6. - tion about the stage of development of the root in length, the convergence of its walls and
1 2. Flores MT, Onetto J E. H ow does orofacial trauma i n children affect the developing dentition?
Long-term treatment and associated complications. Dent Tramtol. 20 1 9; 35(6): 312-323. - 1 3 .
the width of the apical foramen, but also about the degree of mineralisation of the tooth
H ergi.iner A et al. Attention-deficit/hyperactivity disorder symptoms in children with traumatic tissues and the size of the chamber.
dental i njuries. Dent Traumatol 20 1 5 ; 3 1 (2): 1 40- 1 43 . - 1 4. Glendor U . Epidemiology of traumatic We then proceed to obtain information about the patient's general health and current
dental injuries - a 1 2-year review of the literature. Dent Traumatol 2008; 24(6): 603-61 1 . - 1 5 . Lam
R. Epidemiology and outcomes of traumatic dental i njuries: a review of the l iterature. Australian treatment. It is important to ask the child's caregiver about conditions such as congenital
Dent J 20 1 6;(61,Special Issue: The Management of Dental Trauma):4-20. - 16. Levin L, Zadik and acquired heart defects, immunosuppressive diseases (cancer, bone marrow and other
Y. Education on and prevention of dental trauma: it's time to act! Dent Traumatol . 20 1 2 ;28( 1 ):49-
organ transplants), blood and blood-fo1ming diseases, kidney and joint diseases and the
54. - 1 7. Levin L et al. International Association of Dental Traumatology guidelines for the man­
agement of traumatic dental injuries: general introduction. Dent Traumatol 2020;36(4): 309-3 1 3 . stage of their treatment and medication used, and whether the child is under tetanus vac­
- 1 8 . Magno MB et al. Associations and risk factors for dental trauma: A systematic review of cination protection. Knowledge should also be obtained from the child and parent about
systematic reviews. Community Dent Oral Epidemiol. 2020;48(6):447-463 . - 1 9. Miamoto CB
et al. Dental trauma in individuals with severe cerebral palsy: prevalence and associated factors. possible general symptoms following an impact, fall, etc. These include questions: "Was
Braz. Oral Res. 2011; 25 (4); doi .org/10. 1 590/S 1 806-8324201 1 000400007. there loss of consciousness or was there retrograde amnesia?", "Were there or are there
20. Nonato ER, Borges MA. Oral and max i l lofacial trauma in patients with epilepsy prospec­ headaches and dizziness, nausea, vomiting?".
tive study based on an outpatient population. Arq Neuropsiquiatr 20 1 1 ;69(3 ): 49 1 -5 . - 2 1 . Ohman
C et al. Compressive behaviour of child and adult cortical bone. Bone. 20 1 1 ; 49: 769-776. - 22. These symptoms may indicate a concussion, which consists of temporary loss of con­
Petti S et al. World traumatic dental injury prevalence and incidence, a meta-analysis-One billion sciousness and orientation, short-term cardiac and respiratory disorders or balance. Such
l iving people have had traumatic dental injuries. Dent Traumatol 20 I 8;34(2):71-86. - 23. Slayton
R L, P almer EA. Prevention of Traumatic Dental Injuries. I n : Traumatic Dental I njuries in Chil­
symptoms can appear immediately after the accident, but also after a shorter and longer
dren Springer, Cham. (2020), https://doi .org/10. I 007/978-3-030-25793-4_ l 0. - 24. Soares AJ et period of time afterwards. The questions asked by the dentist will bring these abnorma­
al. Pereir Frequency of root resorption following trauma to permanent teeth. J Oral Sci 20 1 5 ; lities to the attention of the parents, as they may occur after a certain period and should
5 7(2):73-78. - 25 . Yilela A B F et al. Dental trauma on primary teeth at different root resorption
stages - A dynamic finite element impact analysis of the effect on the permanent tooth germ Dent then be associated with an earlier event. The presence of such symptoms will require the
Tramtol. 20 1 8; 35(2). - 26. Xiang H et a l . Nonfatal I njuries Among US Chi l dren With Disabling patient to be referred to a GP, paediatrician or neurologist for specialist investigations for
Conditions. Am J Public Health 2005; 95( 1 1 ): 970-5 .
craniofacial fractures or intracranial bleeding.

3 24
325
Compendium of Paediatric Dentistry Specifics of the dental examination of the traumatised child

T he dental interview begins with questions to gather information about the date and Clinical examination
circumstances of the injury. It must be resolved whether the injuries sustained are indeed When proceeding with the clinical examination, we start with an extraoral assess­
accidental or whether they may be the result of violence and crime: ment of facial symmetry, the presence of swelling, bruising, injury in the face, neck and
I . "When did the accident occur?" (20-30 minutes, 1 hour, a few hours ago, yesterday, a head. We examine by palpation whether there is any mobility of the bone fragments. We
few days or a few weeks ago). The timing of the appointment particularly plays a role analyse in the context of the interview whether these are fresh or old changes and deter­
in avulsion, extrusion, lateral luxation, root fracture or alveolar fracture. mine the shape of the change, which can indicate the cause. In the case of multiple skin
2. "Where did the accident take place?" (at home, at school, on the street, during sports lesions, it is important to assess the stage of healing. In the intraoral examination, we
activities). At pre-school age, these are most often falls at home or in the playground; also look for injuries, hematomas or swelling on the mucous membrane of the atrium,
at school age, it may be a bump or fall at school, e.g. down the stairs or during sports cheeks, palate. When assessing a child under the age of five with oral soft tissue injuries
activities. Young people most often suffer facial injuries as a result of falling, hitting involving the l ips, palate, gums, tongue and severe dental injuries, it is important to con­
or booting, but also during sports. sider the potential for harm to the child.
3. "What happened?" (impact with a hard object, fall from height, traffic accident, sports We assess possible occlusal abnormalities, symmetry of mouth opening, pain in the
exercise, assault, abuse, violence). It is important for the dentist to assess the com­ temporomandibular joint.
patibility of the relationship of the carer and the child with the inj uries suffered. The In the scope of the examination of the condition of teeth after injury, the following
extent of the injuries should be analysed in relation to the reason given - whether the are assessed:
account is plausible and not questionable. Explanations of the causes of the trauma extent of fracture or breakage of hard tissues,
inconsistent with the facts and the differences between the parents' and the child's size of pulp exposure and colour of blood,
indicate violence against the child. Knowledge of the cause of the injury - contact of the colour of the crown,
the dentition with a hard, immovable object (e.g. a wall), with a moving object (e.g. response to percussion,
a ball, a fist) makes it possible to analyse force dissipation. - tooth mobility and displacement,
4. "Has your child previously suffered a dental injury?" (if so, ask about the circumstanc­ - pulp response to stimuli.
es). Repeated trauma can be indicative of violence. All these results should be recorded in a special patient examination card after injury
The next questions will be directly dental related - was first aid given (where - both initial and control ones, which allows a comprehensive and objective look at the
and when?); have there been previous inj uries to thi s tooth/teeth? (worse prognosis course and effectiveness of the treatment process. Transillumination or diaphanoscopy can
with repeat trauma); has any occlusal disturbances appeared?; was a tooth or chipped be used to diagnose enamel fractures, which are not always visible under the light of a den­
tooth fragment found? (aspiration into the respiratory tract or entrapment in soft tal lamp. The fracture within the crown can only involve enamel, enamel and dentin, and
tissues, and where the fragment or whole tooth i s stored). The latter question i s par­ further expose the pulp. The fracture of the tooth tissue is usually oblique, sometimes even
ticularly relevant in the case of avulsion of a permanent tooth and the possibil ity of a subgingival ( crown-root fracture with or without pulp exposure). Next, you should analyse
replantation procedure. In the case of a broken fragment of the crown, i t is possible the color of the tooth to see if it is altered compared to the adjacent tooth. The pink color
to use it to re-store the tooth if its size and storage after the injury were appropriate. of the crown may be transient and indicate extravasation in the pulp. Usually, after some
It should be emphasised that delayed reporting for first aid may be indicative of time, the clot is absorbed, and the col or of the tooth returns to its original state. In contrast,
violence against the child. darkening and matting of the tooth indicates pulp necrosis, which can be confirmed by
assessing the appearance of the pulp when exposed and testing it for vitality.

326 327
Compendium of Paediatric Dentistry Speci fics of the dental exam inatio n of the traum atised child

Evaluation of percussion response is not warranted in acute injuries where periap i­ The final stage of the patien t's examination after the injury
is to make a diagn osis
cal lesions are not expected to occur. At this point, you can only cause additional tooth and plan therapy. Both components will depend on the age
of the child and the associated
trauma. On the other hand, in "old" injuries or during follow-up visits, the assessment of type of teeth and the stage of tooth development, but also
on concomitant general dis­
the tooth for tapping in a horizontal and vettical direction is one of the basic and neces­ eases. The initial diagnosis may change during the course
of treatment as teeth respond
sary examinations, using a finger in young children or the handle of a metal instrument positively to management or compl ications arise. Diagnosis
of deciduous teeth after
in older children. A pathological reaction to percussion may indicate damage to the peri­ trauma can be carried out on a more limited basis due to difficu
lties in younger children
odontal ligament and periapical region of the tooth. or a more radical procedure (tooth extraction) in older childr
en when the tooth is close
The mobility of the tooth is classified on the basis of, for example, a 3-degree scale: to physiological exfoliation. In addition, in this decision,
great importance should be
1 - horizontal mobility < 1 111111, l l 0 - horizontal mobility < l mm, I I I0 - vertical mobi­
°
attached to the effects that the deciduous tooth has had on
the correspondi ng permanent
lity. A complete lack of physiological mobility is found in the case of significant intru­ tooth after trauma. The management plan should be presen
ted to the parents - taking into
sion, latebl luxation or ankylosis (+ metallic opaque sound). Increased tooth mobility is account the stages and presumed length of treatment, the
possibility of compl ications
observed after partial luxation, root fractures especially in the ½ cervical region, while and the follow-up visits, on which the success of the treatm
ent largely depends.
groups of teeth are observed after alveolar fractures. Luxation of the tooth can occur
with dis-placement indifferent directions - with protrusion, retrusion or lateral luxation. Refere nces
I . Andreasen FM, Kahler B. Diagnosis of acute dental trauma
In contrast, the mobility of a deciduous tooth may be due to physiological resorption. : the importance of standardized
documentat ! on : a review. Dent Traumatol 2015; 3 1 (5): 340-34
Thermal and electrical stimulation is used to assess the condition of the nerve fi­ _ 9. - 2. Cairns AM, Mok JYQ, Weil­
bur� RR. lnJune s to the head, face, mouth and neck in physic
_ ally abused children in a community
bres of the pulp. Increased sensitivity of the tooth to low temperature is reported by setting. l nt J Paed1a tr Dent. 2005; 15 : 310-8. - 3 . Kellogg N.
Oral and dental aspects of child abuse
and neglect. Pediatrics.20 05; I 1 6(6): I 565-8 . - 4. Moule
the patient during the history and is associated with the consumption of cold foods and A, Cohenca N. Emergency assessment
and treatment plann1 11g for traumatic dental injuries. Austra
lian Dent J 20 1 6; 6 1 :( J Suppl) 21-38.
results from clinical examination with e.g. ethyl chloride. On the other hand, hot drinks - 5 . Myers GL. Evaluation and diagnosis of the traumatised
dentition. Dent Traumatol 2019· 35
(6): 3 02-308,
or foods will induce pain in inflammation of the pulp and periapical tissues. A short-term
reversible reaction to a cold stimulus indicates a normal pulp condition. Faradic current
examination is recommended in permanent teeth with a closed root apex, in which case
pulp assessment is most reliable. In teeth with an open apex, when the pulp is not fully
mature, its response to an electrical stimulus may be impaired. The second pulp structure
that should be examined is the blood vessels. Real-time assessment of vascular flow
using laser Doppler flowmetry is a non-invasive, objective and most reliable method.
Another group of additional examinations is the radiological assessment of the con­
dition of the root and periodontal tissues. Depending on the type and extent of the inju­
ry, dental radiographs, possibly in addition to pantomography or cone beam computed
tomography (CBCT), should be used for this purpose. The stage of development of the
root and the type of damage - traumatic or resorptive, inflammation of the periradicular
area and the healing processes - reparative and regenerative during treatment - should
be analysed.

328
329
 Deciduous tooth injuries - diagnosis, treatment, prognosis
according to the International Association of Dental Traumatology

In examining a child after a deciduous tooth injury, it is important to assess tooth mobility,
Chapter 24 tooth position, contact with opposing teeth, pressure sensitivity and tooth colour. Due to the
low reliability of the results, pulp sensitivity tests are not recommended. It is also recom­
Deciduous tooth injuries - diagnosis, treatment, prognosis mended that radiological diagnostics be kept to a minimum. ln the absence of fragments of
according to the International Association of Dental fractured teeth, it is imp011ant to establish their location (history, examination) because of the
Traumatology risk of their being forced into the soft tissues, swallowed or aspirated into the respiratory tract.
Trauma to a deciduous tooth, especially luxation, can cause discolouration of the
Dorota Olczak-Kowalczyk, Piotr Sobiech tooth crown, which may disappear within a few weeks or months, persist, produce no
clinical or radiographic signs, or be indicative of pulp necrosis. Discolouration of a de­
ciduous tooth after trauma is not an indication for root canal treatment. Root canal treat­
General .principles for the management of deciduous teeth injuries ment can be initiated at the onset of clinical or radiological signs of dental pulp diseases.
During the deciduous dentition period, replantation of an extracted tooth is not re­
and 6 years of age. They
I njuries to deciduous teeth most commonly occur between 2 commended due to the excessive burden on the child of the treatment procedure, the pos­
is due to the high elasticity
are usually in the nature of periodontal tissue damage. This sibility of damaging the permanent tooth or disturbing its eruption process and aspiration
r attachment area of the
of the surrounding bone and periodontal ligament and the smalle of the replanted tooth.
collagen fibres (short root). Traumatic injuries, especially extensive injuries with associated soft tissue injuries
to a deciduous tooth
The diagnostic and therapeutic management of traumatic injury or requiring invasive surgical treatment, may require general antibiotic therapy (amo­
age of the child, the deve­
depends on the type and severity of the traumatic injury, the xicillin, penicillin, in case of allergies, consider other antibiotics). It is also essential to
y of cooperation with the
lopmental stage of the affected deciduous tooth and the qualit consider tetanus prophylaxis.
disorders of the permanent
child and parents. Treatment should not cause developmental Parents should always be informed ofpossible management options, h·eatment techniques
related to a tooth injury is
teeth or develop dental anxiety in the child. Sometimes a visit and early and long-term complications, as well as the need to report promptly to the surge1y
the anxiety of the child
a child's first visit to the dental office. It is important to reduce if symptoms suggestive of complications occur, e.g. swelling, increased tooth mobility, the
anaesthesia) and to act as
and their parents, to ensure that the procedure is painless (local appearance of a fistula. Recommendations for home care should also be given to them and
, e.g. in intrusion and lateral
an analgesic when pain is expected (ibuprofen, paracetamol) the importance of home care for the healing of damaged tissue should be explained:
tooth trauma are:
luxation, root fracture. Treatment methods used in deciduous avoiding repeated injuries, including caution when eating food (in severe luxation,
with minor displace-
observation _ shock, subluxation of laterally dislocated teeth soft foods are preferred for a minimum of a week),
ment, tooth intrusion, oral hygiene: cleaning the region of injury with a soft toothbrush or cotton swab
g,
attention to oral hygiene - prevents infection and promotes healin soaked in an alcohol-free mouthwash containing 0. 1 to 0.2% chlorhexidine gluco­
al trauma, extrusion
tooth repositioning - lateral luxation of a tooth causing occlus nate twice a day for one week,
< 3 mm of a tooth with an open apex, limiting the use of a pacifier.
necrosis, no pos­
extraction of the tooth or the crown part of a broken tooth - pulp The child should be encouraged to drink from an open cup, and in the case of a non spill
fractures, serious
sibility of restoration of the tooth in the case of crown and root cup - to use it without pressure on the teeth.
ion of the tooth with
lateral luxation, extrusion > 3 mm of the mature tooth, extrus Damage to the hard tissues of the tooth and pulp
le, tooth extraction
parafunctions, e.g. suction of the pacifier or finger. If possib Fractures within the crown of a deciduous tooth can involve:
should be avoided on the child's first visit.

33 1
330
 Deciduous tooth i njuries - diagnosis, treatment, prognosis
accordi ng to the I nternational Association of Dental Traumatology
Compendium of Paediatric Dentistry

only enamel: breakage, fracture, Tab. 24.2. Diagnostic and therapeutic management of uncomplicated and complicated crown
fractures of deciduous teeth.
enamel and dentine: enamel- dentine fracture, uncomplicated crown fracture,
Coronal fracture Coronal fracture
enamel, dentine and pulp: enamel-dentine fracture with pulp exposure, complicated
uncomplicated complicated
coronal fracture.
- loss of enamel and dentine - loss of enamel and dentine with
The cause of a fracture of the crown of a deciduous tooth is trauma acting straight an- Oral examinations
without exposing the pulp pulp exposure
gular to the crown of the tooth. The diagnostic and treatment management of post-trau­
matic damage to the crowns of deciduous teeth is presented in Tables 24.1 and 24.2. - lack of sensitivity to percussion (if present, indicates the coexistence
of a luxation or root fracture),
Tab. 24. 1 . Diagnostic and therapeutic management of post-traumatic damage to the enamel of - physiological mobility,
deciduous teeth. - pulp viability tests usually positive (test unreliable in deciduous teeth)

Enamel rupture Enamel fracture

- visible loss of enamel and
\
(enamel rupture without (fracture limited X-ray examination - visible loss of enamel and dentine
dentine,
tissue loss) to enamel with tissue loss) extending into the pulp chamber
- optionally performed
force acting straight angular force acting at an angle
Cause - photo in apical view,
to the crown of the tooth to the tooth crown Recommended
- in case of missing tooth fragment and present soft tissue injuries,
loss of enamel, other symptoms as X-ray examinations
fracture lines on the surface of the inspection of the lip, tongue and/or cheek is indicated
enamel without loss of tissue, reaction in enamel f acture
r
- minor exposure - partial pulp
to tapping - no (in pain, necessa1y amputation,
oral examina- diagnosis for luxation or fracture of - temporary protection of ex­
- large exposure - amputation of
tion the root), no increase in mobility, pulp posed dentine with glass­
coronal pulp
response to the vitality test normal -ionomer cement or compo­
- once the pulp has been secured:
(not reliable in deciduous teeth) site material,
Treatment. - temporary protection of exposed
- immediate or postponed
is recommended in case of suspected is recommended in case of suspect- dentin with glass-ionomer cement
X-ray examina- (after temporary restoration)
root fracture ed root fracture or composite material,
tion final restoration of a tooth
- final restoration of a tooth crown
no treatment, no recommendation restoration or smoothing of sharp crown with composite ma­
with composite material,
to the patient and no follow-up re- edges; when the lip or cheek is in- terial
- in case of pulp necrosis, consider
quired jured, eliminate the presence of a
root canal treatment or extraction
broken tooth crown or foreign body
in the soft tissue; - after I week,
recommendations for the patient in - after 6-8 weeks, - after 6-8 weeks,
case of soft tissue injury - non-al- - X-ray examination - in case - after I year,
Follow-up (clinical
coholic mouthwash containing 0. 1 - of clinical symptoms sugges­ - X-ray examination - one year
and radiological)
0.2% chlorhexidine gluconate ap- ting complications (e.g. pulp after pulp amputation or root canal
Treatment plied topically (on a cotton swab or necrosis symptoms) treatment, and when symptoms
soft brush) 2 times a day for a week; suggesting complications occur
control tests not required; - symptoms,
possible complications: crown dis- - crown discolouration,
colouration, dental pulp disease, - pulp necrosis and infection and periradicular tissue inflammation
Negative treatment
periapical infections (fistula, ab- (fistula, abscess, increased tooth mobility, persistent grey disco­
outcomes
scess, increased mobility and other louration of the crown),
signs of infection), retention of the - on X-ray, inhibited further development of the root of the immature
root of an immature tooth tooth, signs of periapical tissue inflammation

332 333
 Deciduous tooth injuries - diagnosis, treatment, prognosis
according to the International Association of Dental Traumatology
Compendium of Paediatric Dentistry

Crown-root fractures may concern enamel, dentin and cement, the so-called uncom­ Clinical and radio- - after I week,
plicated coronary-root fracture without pulp involvement, or enamel, den tin, cement and logical follow-up - after 6-8 weeks,
assessments are - after I year,
pulp, the so-called crown-root fracture with pulp involvement, complicated crown-root necessary in the case X-ray examination is performed I year after pulpotomy or root canal
fracture (Tab. 24.3). The cause is usually trauma acting straight angular to the crown of of a retained tooth treatment, as well as in the case of symptoms suggesting complications
the tooth. - symptoms,
- crown discolouration,
- pulp necrosis and infection and periradicular tissue inflammation (fis-
Tab. 24. 3 . Diagnostic and therapeutic management of crown-root fractures of deciduous teeth. Negative treatment
tula, abscess, increased tooth mobi lity, persistent grey discolouration
outcomes
Uncomplicated/complicated crown-root fracture of the crown),
- on X-ray, inhibited further development of the root of the immature
- the fracture of the crown runs below the gingival margin, tooth, signs of periapical tissue inflammation
- the coronal fragment is usually present and mobile

A fracture of the root of a deciduous tooth involves the cementum, dentin and pulp
Oral examination and can occur with or without displacement of the fragment broken off. It is usually
caused by trauma acting in the cervical part of the crown in a direction from the top at
an angle to the long axis of the tooth. The diagnostic and treatment management of root
fractures of deciduous teeth is presented in Table 24.4.
- the coronal part of the fracture is usually visible, while the apical
course of the fracture is not visible, Tab. 24.4. Diagnostic and therapeutic management of root fractures of deciduous teeth.

- the crown fragment can be mo­

vable and displaced,
Oral examination
- temporary discolouration of the
X-ray examination
crown (pink or grey) may occur

- in case of missing tooth fragment and present soft tissue inj uries, X-ray examina­ - fracture gap usually located in the
inspection of the lip and/or cheek is indicated tion mid-root or apical region
Recommended - a periapical radiograph and the paralleling technique
X-ray examinations
- remove the mobile fragment and consider whether reconstruction is Recommended
possible, X-ray a periapical (paralleling technique) or occlusal radiograph
when reconstruction is possible: examinations
- uncovered pulp - protect dentin, e.g. with glass-ionomer cement,
Treatment - exposed pulp - pulpotomy or root canal treatment, depending on the coronal fragment:
stage of root development and the degree of fracture, - not displaced - no treatment required,
when reconstruction is not possible: - d isplaced without excessive mobility - leave to reposition spontaneous-
Treatment
- remove all loose fragments leaving a fragment of the root so as not to ly, even with abnormal occlusal contact,
damage the permanent tooth germ or remove the entire tooth - displaced with high mobility and causing abnormal occlusal contact:
• removal of the coronal fragment, leaving the apical one,

334 335
 Deciduous tooth injuries - diagnosis, treatment, prognosis
according to the International Association of Dental Traumatology
Compendium of Paediatric Dentistry

Tab. 24.5. Diagnostic and therapeutic management of alveolar fracture in deciduous dentition.
• repositioning of the crown fragment, in the absence of stability after
repositioning, flexible immobilization for 4 weeks - Frequent mobility and displacement of the fractured segment with
Oral examination several teeth,
- occlusal disorders
- Fracture lines can be at any level from the alveolar margin to the apex
X-ray examination of the root, and may i nclude deciduous tooth germs,
- the fracture may not be visible
- a periapical ( paralleling technique) or occlusal radiograph,
Recommended
- lateral radiograph (relationship between the upper and lower dental
coronal fragment not displaced: X-ray examina-
arch, displacement of the fractured segment towards the labial direc-
- after 1 week, tions
tion)
- after 6-8 weeks,
- after I year, then annually until permanent teeth erupt; - manual or forceps repositioning,
after repositioning and splinting: Treatment - stabilisation with an flexible splint for 4 weeks,
\
- protection (suturing) of gingival wounds if present
Clinical follow-up - after I week,
assessments are - after 4 weeks (removal of the splint), - after I week,
needed - after 8 weeks, - after 4 weeks (removal of the splint),
- after I year; Necessary - after 8 weeks,
after removal of the coronal fragment: follow-up - after I year,
- after I year; assessments - at the age of 6 years to monitor the eruption of permanent teeth,
X-ray examination is performed when there are symptoms suggestive of radiological control: after 4 weeks and after I year (additional X-ray
complications examinations on suspicion of pathology)
- symptoms, - symptoms,
- pulp necrosis and infection and periradicular tissue inflammation (fistu- - necrosis and pulp infection,
la, abscess, increased tooth mobility, persistent grey discolouration of Negative treat-
- crown discolouration,
Negative treat­ the crown), - inflammation of the periapical tissues,
ment outcomes
ment outcomes - further development of the root of the immature tooth, symptoms of - no further formation of the root of the immature tooth,
periradicular tissue inflammation and inflammatory resorption inhi­ - little or no improvement in the position of the displaced segment,
bited in X-ray, - abnormal development and eruption of a permanent tooth
- maintained abnormal tooth position
Tab. 24.6. Diagnostic and therapeutic management of dislocated deciduous teeth.
The cause of alveolar fracture and lateral luxation is trauma acting straight angular
Injection, intrusion Lateral luxation Extrusion
to the crown of the tooth in the central part. It can cause damage to the permanent tooth
- axially displaced - displaced tooth, usually - the tooth appears
socket. In lateral luxation, there is a fracture of the labial or palatal/lingual lamina of the
tooth into the alveo­ in a palatal/li ngual or elongated,
alveolar process, the zone of compression is usually in the cervical area, less often in the lar bone labial direction, - increased mobility,
periapical area. Most often, the apex is pressed into the bone (lack of mobility) accom­ - lack of mobi I ity, - possible abnormal
Oral exa­ - possible abnormal occlu- occlusal contact
panied by disruption of the periodontium and damage to the nerves and vessels. If the sal contact
mination
bone fracture occurs on both sides of the alveolus, an alveolar fracture is diagnosed. The
diagnostic and therapeutic management of alveolar fracture in the deciduous dentition is
shown in Table 24.5, in lateral luxation, intrusion and extrusion in Table 24.6. In case of
tooth concussion or subluxation, no treatment is needed. Observation and control exam­
ination after 1 and 6 weeks are recommended.

336 337
 Deciduous tooth injuries - diagnosis, treatment, prognosis
Compendium of Paediatric Dentistry according to the International Association of Dental Traurnatology

- at the age of 6 years

- lip-sh i1led apex -
widened periodontal - with the risk of compl i- - with the risk of compli-
space in the apical re­ to monitor the erup- cations, clinical obser-
visible apex, ab­ cations, clinical observa-
gion (best seen on the tion of a permanent vation every year until
breviated image of tooth, tion every year until the
occlusal radiograph, es­ permanent teeth appear, the permanent teeth ap-
the tooth compared pecially with labial dis­ - X-ray examination pear,
to the homony­ - X-ray exami nation only
placement of the tooth) only in the presence
mous tooth on the of symptoms sug- in the presence of symp- - X-ray examination only
- widening of the peri­ toms suggestive of cam- in the presence of symp-
X-ray exa- opposite side (Fig. gestive of compli-
odontal crevice in the plications toms suggestive of cam-
mination 25 .1), cations
apical region plications
- apex displaced to­
- ankylosis - ankylosis -
wards the perma­
nent tooth bud, - pulp necrosis and infection and periradicular tissue inflammation (fistula, ab-
apex invisible, Negative scess, i ncreased tooth mobility, persistent grey discolouration of the crown),
tooth i mage elon­ treatment - further development of the root of the immature tooth, symptoms of periradi-
gated ( Fig. 25 .2) outcomes cular tissue inflammation and inflammatory resorption in X-ray,
- maintained abnormal tooth position,
Recom­ - i mpaired development or eruption of a permanent tooth
mended - periapical (paralleling technique) or occlusal radiograph
X-ray
- no abnormal occlusal Fig. 24.1. The apex of
contact or slight occlusal the punctured tooth
disorder - spontaneous 62 is lip-shi fted - the
- spontaneous repo­ repositioning (usually visible apex, the ab­
- no abnormal bite con­ breviated image of
sitioning regardless occurs within 6 months),
tact - spontaneous repo­ the tooth compared to the
of the direction of - large displacement:
sitioning, homonymous tooth on the
Treatment tooth displacement • extraction at risk of
- excessive mobility, ex­ opposite side.
(usual l y occurs swallowing/aspiration
trusion > 3 mm - tooth
within 6 months, of the tooth,
extraction
sometimes a year) • repositioni ng, in case
of tooth instabi l i ty
flexible immobilisa­
tion for 4 weeks Fig. 24.2. Point of pierced
tooth 51 shifted in the di­
- after I week, rection of the permanent
- after 6-8 weeks, tooth bud - image of the
- after 6 months, tooth elongated.
- a fter I year;
- a1ler I week, after repositioning and
- after I week, Avulsion of a deciduous tooth requires localisation of the erupted tooth due to the
- after 6-8 weeks, rai l ing:
Followups - a fter 6-8 weeks, risk of the tooth being driven into the soft tissues, as wel l as swal lowed or aspi rated
- a1ler 6 months, - after I week,
- after I year
- after I year, - after 4 weeks (removal into the respiratory tract. In the absence of information about the knocked-out tooth, the
of the splint),
chi l d should be referred to a medical diagnosis, especially in the event of respiratory
- a fter 8 weeks,
- after 6 months, symptoms. If a deciduous tooth is avulsed, a dental radiograph should be taken in the
- after I year, periapical or occlusal proj ection (to exclude intrusion) . Treatment management is based

338 339
Compendium of Paediatric Dentistry

on the parents' compliance with care recommendations. Follow-up examinations after Chapter 25
6-8 weeks and at 6 years of age to monitor the eruption of the permanent tooth are re­
commended. Follow-up radiological examination is performed only with the occurren ce
of symptoms suggestive of complications, which are disorders of development and erup­ Trauma to permanent teeth - diagnosis, treatment, prognosis
tion of the permanent tooth . according to the International Association of Dental Trauma­
tology
References
I . Andreasen JO et al. Textbook and colour atlas of traumatic inj uries to the teeth. Wiley-Black­ Dorota Olczak-Kowalczyk, Piotr Sobiech
well 2007 - 2. Assuncao LR et al. Luxation injuries in primary teeth: a retrospective study in chil­
dren assisted at an emergency service. Braz Oral Res. 20 1 1 ; 25: 1 50-6. - 3. Eissa MA et al. Dental
trauma characteristics in the primary dentition in Greifswald, Germany: a comparison before and
after German unification. Eur Arch Paedi atr Dent 22, 783-789 (202 1 ). https://doi.org/ I 0. 1 007/ General p rinciples for the management of traumatic injuries of permanent teeth
s40368-0211 -00606-5. - 4. Day PF et al. I nternational Association of Dental Traumatology guide­
lines for the management of traumatic dental injuries: 3. Inj uries in the primary dentition. Dental
Traumatol 2020; 36(4): 343-359. - 5. Kaczmarek U. D iagnosis and treatment of traumatic lesions The dental management of traumatic injuries of permanent teeth, regardless of the
of deciduous teeth according to Andreasen. - 6. Lauridsen E et al. The risk of healing compl ica­ type of injury, always requires that every effort be made to preserve the tooth, restore its
tions in primary teeth with intrusive luxation: A retrospective cohort study. Dent Traumatol 20 1 7;
3 3 : 329-36. - 7. Shah S. Traumatic dental inj uries in the primary dentition - a review. J Pak Med function and aesthetics and, above all, preserve the pulp vitality in both the tooth with
Assoc. 2020;70(Suppl I )(2):S76-S82. P M I D: 3 I 98 1 34 1 . - 8. Slayton RL. Management of prima­ an incomplete root and the mature tooth. The success of treatment depends on many
ry tooth luxation inj uries. Clin Dent Rev 2020;4, 1 2. doi.org/ I 0. 1 007/s4 I 894-020-00075-x. - 9. factors related to the injury itself, the type and maturity of the tooth, the diagnostic and
Spinas E et al. Root Fractures in the Primary Teeth and Their Management: A Scoping Review.
Dent. J. 2022, 1 0, 74. doi .org/ I 0.3390/dj I 0050074. treatment procedure, as well as the cooperation of the patient and parent. It is essential to
implement medical recommendations and follow-up appointments.
Important elements of the proceedings are:
preventing invasion of bacteria into the pulp (from the dentine tubules at the frac­
ture of the crown, along the blood clot in the case of periodontal tissue injury, along
with blood - anachorosis),
proper and regular evaluation of the pulp condition (absence of pulp reaction does
not rule out necrosis, pulp reaction to stimuli may not be normal until 4-6 weeks or
even 3 months after injury),
initiation of root canal treatment at necrosis and first signs of inflammatory resorption,
flexible stabilisation of teeth without exceeding the recommended time,
use of splints that do not traumatise the periodontal tissues.
Pulp necrosis is diagnosed with a negative vitality test result and the presence of at
least two additional signs of necrosis resulting from history, physical examination (e.g.
fistula), radiographic examination (e.g. periapical tissue changes, arrested root develop­
ment). Root canal treatment is usually necessary in traumatic damage to mature teeth,
such as crown fracture (with or without pulp exposure) with associated luxation, intru­
sion, extrusion, lateral luxation.

340 341
 Trauma to permanent teeth - diagnosis, treatment, prognosis according
Compendium of Paediatric Dentistry to the International Association of Dental Traumatology

In teeth with unfinish ed root developme nt, it should be remembered that th e Type of injury 2 weeks 4 weeks 4 months
pulp can rema in v iable and heal or undergo spontaneous revascularization. There­ *
Subluxation
( i f railed )
fore, root canal treatment is avoided. In luxation of the i mmature tooth with in ­
Extrusion *
complete root formati on with rupture of the vessels, new vessel ingrowth beg ins
Avulsion *
approxi mate ly 4 days after inj ury and progresses at a rate of approximately 0 . 5 ...
mm/24 hours. Revascularisation i s to b e expected espec ially with a n apical fora­ Lateral luxation *
men diameter � 1 . 0 mm. As the diameter decreases, the chance of revascul arisation Intrusion .,.

j
also decreases (very rare in teeth with a narrow apical opening, i .e . < 0 . 5 mm) . Root f acture
r
*
(apical third, mid-third)
Pulp necrosis usua lly occurs when the crown of a i mmature permanent tooth is
Alveolar fracture *
fr actured with intrusion.
Root fracture (cervical third) *
Stabjlization of teeth should be:
short-term (after about 1 week after luxation or replantation of the tooth, the new Fig. 25. 1 . Duration of stabilization depending on the type of inj ury.
collagen begins to join the broken periodontal fibres; after 2 weeks, the main colla­
gen fibres are repaired to a degree that provides about one-third of the mechanical
strength of the periodontium),
passive and flexible (al lows physiological tooth mobility),
easy to set up and remove,
preferably made of 0.3-0.4 mm stainless steel wire fixed to the teeth with com­
posite material, nylon fibre (0. 1 3-0.25 mm) or fibreglass (without bonding); Rib­
Local Cutting and adjusting the Replantation of a tooth.
bond-THM splints and titanium splints are also used, · anaesthesia. wire to the shape of the
positioned: dental arch.
• on labial surfaces (occlusal conditions, access for endodontic treatment),
• away from the gingiva and proximal areas to avoid p laque retention and secon­
dary infection.
Figure 25. l shows the recommended duration of immobilization depending on the
type of inj ury, Figure 25.2 shows the method of immobilization of dislocated teeth with
the use of a rai l made of wire fixed with composite material.
Parents and children should be given instructions on oral care to ensure proper hea­ Point etching Application of bonding The end results.
ling conditions (oral hygiene and rinsing with an antimicrobial agent, e.g. 0. 1 2% chlor­ of enamel. resin, then flow composite
(traumatically damaged
hexidine gluconate solution) and about the need to prevent further injuries and about tooth is fixed last).
follow-up appointments.
Fig. 25 .2. Method of stabilization dislocated teeth using a steel wire fixed
to the teeth with composite material .

342 343
 Trauma to permanent teeth - diagnosis, treatment, prognosis according
Compendium of Paediatric Dentistry to the International Association of Dental Traumatology

Traumatic injuries to teeth have a high risk of complications. Follow-up visits are Follow-up
aimed at early detection and initiation of treatment, which significantly improves the examinations - there is no need if there are no - after 6-8 weeks,
(clinical and other damages - after I year
prognosis. radiological)
- symptoms,
Fractures of the crown of a permanent tooth - necrosis and pulp infection,
Negative treat- - inflammation of the periapical tissues,
Traumatic enamel damage can be an enamel infraction, i.e. a crack or crazing of the ment outcomes - lack of further root development in immature teeth
enamel without loss of tooth structure, or an enamel fracture, i.e. a fracture limited to - - loss of recovery
the enamel with loss of tooth structure. The diagnostic and therapeutic management is
shown in Table 25. 1 . Enamel and dentine fractures may cause loss of only hard tissues of the tooth and
do not reach the pulp, the so-called uncomplicated enamel and dental fracture, uncom­
Tab. 25 . 1 . piagnostic and therapeutic management of enamel damage. plicated crown fracture or loss of enamel and dentine with pulp exposure, the so-called
Enamel infraction Enamel fracture enamel and dental fracture with pulp exposure, complicated crown fracture (Tab. 25.2).
- f acture Ii ne( s) on the tooth sur­
r - loss of enamel without exposure of The cause is trauma acting at a slight angle to the crown of the tooth. Uncomplicated
face dentin enamel-dentine fractures account for approximately 60-70% of traumatic injuries to per­
manent teeth.

Intraoral Tab. 25 .2. Diagnostic and therapeutic management of fractures of the crown of a permanent
examination tooth.

Coronal fracture Coronal fracture

- lack of sensitivity to percussion (if present, indicates the coexistence of uncomplicated complicated
a luxation or root fracture), - loss of enamel and dentin with ex­
- physiological mobility, - loss of enamel and dentine posure of the pulp,
- pulp vitality tests usually positive without exposing the pulp - sensitivity of the exposed pulp to
- recommended image in periapical projection, stimuli (e.g. cold)
Intraoral
- additional radiographs if other damage is suspected examination - lack of sensitivity to percussion (if present, indicates the coexistence of
- visible loss of enamel, a luxation or root fracture),
X-ray - in case of missing tooth fragment - physiologica l mobility,
examination and present soft tissue injuries, - pulp viability tests usually positive (a negative test indicates temporary
- no abnormalities
inspection of the lip and/or cheek is pulp damage)
indicated - visible enamel and dentine loss ex­
- the available tooth fragment can be tending into the pulp chamber
- fluoride preparations can be used;
fixed with an adhesive system,
in case of severe damage, consid­ depending on the extent and location
er etching and sealing with bon­ X-ray
of the fracture: - visible loss of enamel and dentine
Treatment ding resin to prevent discoloura­ - smooth the sharp edges, make an examination
tion and bacterial infection, aesthetic correction (grinding) and
- in other cases no treatment is nec­ apply a fluoride preparation,
essary - restore the crown with composite

344 345
 Trauma to permanent teeth - diagnosis, treatment, prognosis according
Compendium of Paediatric Dentistry to the International Association of Dental Traumatology

Recommended
- recom111ended parallel periapical radiographand additional radiographs if
other lesions are suspected,
l
X-ray - in case of 111issing tooth frag111ent and present soft tissue injuries, inspec-
examinations
tion of the lip and/or cheek is indicated

teeth with an incompletely formed

- an accessible and intact tooth
root - important to keep the pulp
fragment (after irrigation for 20
alive:
min i n water/saline) can be fixed
- direct capping
using the adhesive syste111,
- partial pulpotomy (Fig. 26.3); Local anaesthesia
- temporary protection of exposed Cofferdam applied Pulpotomy
mature teeth:
dentin with glass-ionomer cement
- direct capping,
or composite material,
- total pulpotomy,
- final restoration of a tooth crown
- root canal treatment when a
with composite material
\
root-canal post is required;
Treatment
once the pulp has been secured:
- accessible and undamaged part of
the tooth (after hydration for 20
minutes in water/saline) can be
fixed using an adhesive system,
note: at the thickness of dentin ad­
- temporary protection of exposed
jacent to the pulp :S 0.5 mm (pink Visible
dentin with glass-ionomer cement Pulp capping with MTA Temporary resto­
colour without bleeding), a calcium root pulp
or composite material, ration of a cavity with
hydroxide preparation should be ap­
- final restoration of a tooth crown glass-ionomer cement
plied
with composite material

- after 6-8 weeks,

Follow-up tests
- after 6-8 weeks, - after 3 months,
(clinical and
- after I year - after 6 months, On the left - the condi­
radiological)
- after 1 year tion after complete am­
- symptoms, putation of the pulp.
- necrosis and pulp in fection, Right - status after 5
Negative treat­ months: dentine bridge,
- i nflammation of the periapical tissues,
ment outcomes further tooth root for­
- further root development inhibited,
- loss/da111age of restoration of lost tooth tissue mation.

Fig. 25 . 3 . Pulp amputation in a permanent tooth with an unerupted root

with complicated coronal fracture.

Complicated fracture of
Crown-root fractures include enamel, dentin and cement without exposing the pulp,
the crown of tooth 21
with an incompletely the so-called uncomplicated crown-root fracture or with its exposure, the so-called com­
formed root - extensive plicated crown-root fracture (Tab. 25.3). The fracture is in the horizontal or oblique plane
exposure of the pulp.
and below the gingival margin. The cause is an injury acting at an angle to the crown of
the tooth in the area of the cutting edge.

346 347
 Trauma to permanent teeth - diagnosis, treatment, prognosis according
to the International Association of Dental Traumatology
Compendium of Paediatric Dentistry

Tab. 25.3. Diagnostic and therapeutic management of fractures of the crown-root of a permanent tooth. the plan of further action depends on the age of the patient and his coope-
ration,
Uncomplicated Complicated
opportunities:
crown-root fracture crown-root fracture
- orthodontic extrusion of a apical or immovable fragment and subsequent
- the f acture of the crown runs below the gingival margin,
r
reconstruction (all types of fracture - provided that the appropriate length
- percussion test - positive, of the root is obtained after extrusion),
Intraoral - pain on tapping, Further - surgical extrusion (a l l types of fracture - provided that the appropriate
examination - the coronal fragment is usually present and mobile, therapeutic length of the root is obtained, except for the crown and root fracture in the
- pulp viability test - usually positive for apical fragment options tooth with unfinished development of the apex),
- usually the visible coronal part of the fracture, while the apical course of - root canal treatment in cases of pulp necrosis and infection,
the fracture is invisible, - decoronation (root submergence),
- replantation with or without root rotation,
- extraction,
- autotransplantation

X-ray - a fter I week,

examination Clinical and - after 6-8 weeks,
radiological - after 3 months,
assessments - after 6 months,
are required - after I year,
- then annually for at least 5 years
- in case of missing tooth fragment and present soft tissue inj uries, inspec­
tion of the lip and/or cheek is indicated - symptoms,
- a parallel periapical radiograph, two additional radiographs from different - discolouration,
vertical and/or horizontal angles and a occlusal radiograph, Negative - necrosis and pulp infection,
Recommended
- when standard X-ray diagnostics is insufficient consider CBCT (visua­ results of treat- - inflammation of the periapical tissues,
X-ray
lisation of fracture gap, determination of fracture extent and crown/root ment - inhibition of root development in a tooth with an incompletely formed root,
examinations
ratio) - loss or damage to the reconstruction,
- marginal bone loss and periodontitis
pending the establishment of the treatment plan, the loose fragment � n the
.
adjacent tooth or on a stationary fragment should be temporarily stabilized
( Fig. 25.4) Root fractures
- teeth with an incompletely The root fracture is caused by a direct injury acting from above at an angle to the
formed root - aim to pre­
crown in the cervical region, usually a hard object - a small one with sharp edges on
- consider the removal of the crown or serve the pulp by partial
Treatment movable fragment and subsequent re­ pulpotomy; impact at the root site or with rounded edges - on the crown of the tooth.
construction, - mature teeth - usually pulp Root fracture involves cementum, dentin, pulp. The tooth pulp and periodontal liga­
- protect exposed dentin, e.g. with extirpation and subsequent
root canal treatment, ment can be damaged to varying degrees depending on whether or not the coronal frag­
glass-ionomer cement or composite ma­
terial - protect exposed dentin, e.g. ment of the root is displaced (Fig. 25.5). The apical portion of the tooth root is usually
with glass-ionomer cement not affected by trauma and is not displaced, and the neurovascular connection in the
or composite material
apical opening is not disrupted. Similarly, the periodontium around the apical fragment
Recommenda­ soft food for I week, tooth brushing with a soft brush, rinsing with 0.1 %
tions for the
is not damaged. Periodontal tissues in the fracture line and surrounding coronal f ragment
chlorhexidine solution
patient are damaged, and the extent of the damage depends on the region of the root and the
coexistence of other inj uries (e.g. concussion, subluxation, luxation). The alveolar bone,
most often adjacent to the root fracture line, may also be damaged.

348 349
 Trauma to permanent teeth - diagnosis, treatment, prognosis according
to the International Association of Dental Traumatology
Compendium of Paediatric Dentistry

Root fractures are classified according to:

the location of the fracture of the root: apically, in the middle part of root, cervically
(apical fractures have the best prognosis, and the cervical fractures have the worst
prognosis, especially those located above the alveolar crest, due to the lack of peri­
odontal tissue, bones and the risk of infection),
the course of the fracture line: horizontal, oblique, vertical,
number of fragments: single or multiple,
displacement of the coronal fragment: with or without displacement.
Prognostic factors such as the degree of displacement of the fracture fragment, the
age of the patient, the stage of root development, the mobility of the coronal fragment
and the diastasis of the fragments should be taken into account when planning the treat­
ment of a root fracture (Tab. 25 .4).
Andreasen et al. distinguish between four types of tooth and periodontal reaction
after root fracture:
1. healing with hard tooth tissue - dentine and cement (most likely with no or mini­
mal displacement of the coronal fragment after correct repositioning, possible with
significant displacement after immediate assistance and stabilisation of the coronal
fragment),
2. healing with periodontal-derived connective tissue (response to root fracture with
displacement of the coronal fragment if the pulp is repaired by revascularisation),
Fig. 25.4. Management of crown-root fracture complicated by pulp necrosis 3. healing with bone and connective tissue (possible in case of root fracture before
with preserved coronal fragment. alveolar bone growth is complete) (Fig. 25.6),
4. lack of healing - inflammatory granulation present in the fracture line, caused by
necrosis and pulp infection in the coronal fragment.
Displacement of a coronal fragment of a fractured root

pulp in the coronal fragment

localised acute inflammatory response stretched or torn at the fracture site: educed or
at the fracture site or haemorrhage absent blood supply can lead to pulp necrosis
Fig. 25.6. Root fractures: tooth 21 (left) - healing with bone
Fig. 25.5. Pulp condition in the coronal fragment of the fractured root. and connective tissue, tooth 1 1 (right) - no healing.

351
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 Trauma to permanent teeth - diagnosis, treatment, prognosis according
to the I nternational Association of Dental Traumatology
Compendium of Paediatric Dentistry

Tab. 25 .4. Diagnostic and therapeutic management of root fracture. Fracture of the alveolar process may or may not involve the alveolus (Tab. 25.5 ). Its
cause is trauma acting perpendicular to the crown of the tooth in its central part.
Root fracture
lntraoral examination: mobility and sometimes displacement of the
coronal segment, possible transient discoloration of the crown into Tab. 25 .5. Diagnostic and therapeutic management of alveolar fracture.
reddish or grey and bleeding from the gum pocket; pain on tapping;
pulp viability test may be initially negative, indicating transient or per­ - often mobility and displacement of the fractured segment with with
manent damage to pulp innervation. several teeth moving together,
Intraoral examina-
X-ray examination: parallel periapical radiograph, two additional ra­ - occlusal disturbances,
tion
diographs of the tooth taken with different vertical and/or horizontal - most often the response of the tooth pulp to stimuli in the fractured
angulations, and a occlusal radiograph; when standard X-ray diagnos­ segment is negative
tics is insufficient, consider CBCT ( Fig. 25. 7). - fracture lines can be at any level - from the marginal bone to the root
Treatment: repositioning of the coronal fragment under X-ray con­ apex,
X-ray examination
trol, flexible stabilization for 4 weeks for fractures in the apex part and - fracture of the tooth root may coexist,
4 months in the coronal part. - the fracture may not be visible
Recommendations for the patient: soft food for I week, brushing - parallel periapical radiograph,
teeth with a soft brush and rinsing with a 0. 1 % chlorhexidine solution - two additional radiographs from different vertical and/or horizontal
to prevent the accumulation of plaque and sediment. Recommended angles,
Clinical and radiological examinations (monitoring of pulp condi­ X-ray examinations - occlusal radiograph,
tion and healing): after 4 weeks (or removal of stabilization photo), - when standard X-ray diagnosis is insufficient, consider CBCT (loca-
after 6-8 weeks, after 4 months (or removal of stabilization photo), tion, extent, direction of fracture)
after 6 months, after 1 year, then every year for at least 5 years.
- manual or forceps repositioning,
Important:
- stabilisation with an elastic splint for 4 weeks,
A false negative pulp response to viability tests is possible for several
- protection (suturing) of gingival wounds, if present,
months, so endodontic treatment should not be initiated solely on the Treatment
- root canal treatment should not be started at the first visit; the decision
basis of their results.
on root canal treatment should be based on the assessment of the pulp
Pulp necrosis usually occurs only in the coronal fragment, in the apex
condition at the first visit and the follow-up visits
there are rarely pathological changes requiring treatment.
Negative treatment results: pain, extrusion and/or excessive mobili­ - after 4week (removal of the splint),
ty of the corona fragment, widening of the X-ray fracture line, necrosis - after 6-8 weeks,
and infection of the pulp with inflammation in the fracture line. Follow-up examina- - after 4 months,
tions (clinical and - after 6 months,
radiological) - after I year,
- then observe bone and soft tissue healing every year for at least 5
years
- symptoms,
Negative treatment - necrosis and pulp infection,
outcomes - inflammation of the periapical tissues,
- insufficient healing of soft tissues

Periodontal tissue damage is:

- concussion - damage to the supporting structures of the tooth without increasing
Fig. 25.7. Image of a root fracture suggesting a horizontal fracture in the central part mobility and without displacement, there is pain on knocking,
of the root (left); an oblique fracture extending to the edge of the bone palatally
on CBCT (centre and right). - subluxation - damage to the supporting tissues of the tooth leading to an increase in
mobility without displacement of the tooth with bleeding from the gum pocket,

352 353
 Trauma to permanent teeth - diagnosis, treatment, prognosis according
Compendium of Paediatric Dentistry to the International Association of Dental Traurnatology

intrusive luxation, intrusio displacement of the tooth in apical direction combined Tab. 25.7. Diagnosis and management of intrusion, lateral luxation and extrusion of a permanent
with fragmentation or f racture of the socket, tooth.
extrusive luxation, extrusion - partial axial displacement of the tooth from the Intrusion Lateral luxation Extrusion
socket in the occlusive direction with often accompanying protrusion or retrusion,
- apically displaced - displaced tooth, usual­ the tooth appears elon­
lateral luxation - displacement of the tooth in any lateral direction, associated with tooth into the alveo­ ly in a palatal/lingual gated,
fragmentation or fracture of labial or palatine/lingual lamina of the alveolar process, lar bone or labial direction increased mobility
avulsion, tooth loss - complete tooth loss from the socket, clinically the socket is
empty or filled with a clot. no mobility,
a high-pitched metallic sound when tapping, usually a negative
The diagnostic and therapeutic management of periodontal tissue injuries is present- usually a negative response of the pulp to vitality response of the pulp to
lntraoral
ed in Tables 25 .6, 25.7. tests vitality tests
examina­
tion
Tab. 25.6. Diagnostic and therapeutic management of dental concussion and subluxation.

Concussion Subluxation
- increased tooth mobility,
- physiological tooth mobility, - the response of the pulp to vitality tests
- pulp response to vitality tests may be temporarily negative,
Intraoral exam- usually positive - bleeding from the gingival crevice may
ination occur
widening of the peri­ widening of the peri­
- no displacement of the tooth, the periodontal odontal space in the api­ odontal space in both
- sensitivity to percussion and touch space may not be cal region is best seen on the apical and l ateral
X-ray visible along the en­ radiographs taken with regions
- without radiographic abnormalities
examination tire length or part of horizontal angle shifts or
- parallel periapical radiograph, two the root (especially occlusal exposures
Recommended - parallel periapical radiograph X-ray exa­
additional images at different vertical mination the apical part),
X-ray and additional photos with enamel-cement
and/or horizontal angles,
examinations suspicion of other damage junction displaced
- occlusal radiograph
- usually unnecessary, apically compared
- in case of excessive mobility or ten- to an adjacent
Treatment - not required non-injured teeth
derness when biting the tooth, elastic
splinting for 2 weeks
Follow-up - after 2 weeks (removal of the splint),
assessment - after 4 weeks, - after 3 months,
Recom­
(clinical and - after I year - after 6 months,
mended - parallel periapical radiograph, two additional radiographs from different ver­
radiological) - after I year
X-ray exa­ tical and/or horizontal angles and an occlusal radiograph
- symptoms, minations
Negative - necrosis and pulp infection,
results of treat- - inflammation of the periapical tissues,
ment - inhibited further root development
- - external inflammatory resorption

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Compendium of Paediatric Dentistry to the International Association of Dental Traumatology

teeth with an incom­ < 3 mm - allow spon­

pletely formed root: taneous reeruption, if
enable spontaneous not within 8 weeks -
re-eruption regard­ surgical reposition ing
less of the degree of and stabilization! for
injection, 4 weeks, alternatively
if this does not orthodontic to avoid
occur, start ortho­ ankylosis,
dontic repositioni ng 3-7 mm - tooth reposi­
within 4 weeks, tioning surgical (prefe­
pulp revascularisa­ tooth reposition ing - rably) or orthodontic,
tion may occur, tooth repositioning: inserting the tooth back > 7 mm - surgical re­
root canal treat­ freeing the apex from a into the alveolus under positioning,
ment - in the case bony blockage and gen­ local anaesthetic, mature teeth:
of pulp necrosis tly moving it back to its stabilisation with elastic - the pulp usually under­
or symptoms of original position under splint for 2 weeks (in goes necrosis,
external resorption, local anaesthesia, the case of a marginal - initiate root canal
start as soon as the stabilisation with elas­ bone fracture, splinting treatment (steroid-anti­
position of the tooth for an additional Treatment
tic splint for 4 weeks, biotic paste or calcium
allows it after approx. 2 weeks, 4 weeks), hydroxide) to prevent
pulp assessment is with pulp necrosis - the development of
Treatment necessary; root canal treatment inflammatory external
teeth with an incom­ resorption
pletely formed root:
the pulp almost
- possible revasculari­
always undergoes
sation,
necrosis,
- with pulp necrosis or
start root can a I
signs of inflammato1y
treatment after 2
external resorption, sta1t
weeks or as soon as
root canal treatment as
the position of the
soon as possible;
tooth permits (ste­
roid-antibiotic paste
or calcium hydrox­
ide) to prevent in­
flammatory external
resorption
- after 2 weeks,
- after 4 weeks,
Spontaneous re-erup­ Follow-up - after 8 weeks,
tion of an erupted tooth assessment - after 12 weeks,
21 within 6 weeks; (clinical - after 6 months,
mature teeth - injec­ and radio­ - after I year,
tions: logical) - then annually for at least five years,
- patients (and parents) should be informed about the need for checks and
symptoms indicating the need to see a dentist

356 357
 Trauma to permanent teeth - diagnosis, treatment, prognosis according
Compendium of Paediatric Dentistry Lo the International Association of Dental Traumatology

- symptoms, maintaining the contour, width and height of the alveolar bone. Parents and the patient
symptoms, - symptoms,
- blocked tooth,
marginal bone should be informed of their risk and further treatment options.
atrophy, - marginal bone atrophy
- ankylosis Replantation cannot always be performed, e.g. due to unconsciousness. Contraindi­
Negative results - ankylosis
treatment cations to tooth replantation also include: extensive caries, lack of patient cooperation,
- necrosis and pulp infection,
- inflammation of the periapical tissues, severe general illnesses, e.g. immunodeficiencies, conditions with a high risk of infective
- external inflammatory resorption endocarditis. The decision to replant a tooth in a patient with a general disease burden
should be taken on an individual basis.
Avulsion is one of the most serious traumatic dental injuries. The prognosis of a After tooth replantation, general antibiotic therapy is indicated due to the risk of oral bac­
completely dislocated tooth largely depends on how it is dealt with immediately after the terial infection and subsequent inflammatory resorption of the root. The drug of first choice is
injury at the scene. The treatment of choice is tooth replantation, which should be carried amoxicillin or penicillin. In patients over 12 years of age, tetracycline may be used.
out as sooh as possible, as the state of the periodontal cells responsible for healing is Replanted permanent teeth should be stabilised for 2 weeks with a flexible splint. In
closely related to the length of time the tooth has been outside the alveolus and the con­ case of traumatic contact with the opposing tooth or displacement of the replanted tooth
ditions under which it has been stored. If an erupted tooth is kept "dry" for 30 minutes, after removal of the splint, immobilisation can be extended by one week.
about 50% of the periodontal cells die, and after 60 minutes they all die. Storing the tooth Root canal treatment of the mature tooth should be started within two weeks after
in a suitable transport medium increases the survival time of the periodontal cells: replantation. Calcium hydroxide for 4 weeks or steroid-antibiotic paste for 6 weeks is
in physiological saline solution and after wrapping in plastic film for up to 1 hour, used as a temporary canal filling. In teeth with uncompleted root development, apexi­
in saliva for up to 2 hours, fication or pulp regeneration is carried out only after it is ascertained that pulp necrosis
in pasteurised milk for up to 6 hours, has occurred.
in tissue culture medium for up to 24 hours. After replantation, the patient and his or her parent should be advised to avoid contact
Note: it is not recommended to store in water, but it seems to be a better solution than sports, eat soft foods for a fortnight, brush with a soft toothbrush after every meal and use
leaving the tooth "dry". a 0.12% chlorhexidine solution twice a day for a fortnight, and follow-up visits: after two
Depending on the risk of loss of viability of the periodontal cells, there are 3 groups weeks (after removal of the splint), after four weeks, after three and six months, after one
of replanted teeth: year, then annually for at least five years.
tooth replanted immediately or within a very short time (up to 15 minutes) of the Possible complications after tooth replantation are the presence of symptoms, swel­
event - high probability of survival of periodontal cells, ling, fistula, excessive or no mobility (ankylosis), radiographic signs of external inflam­
tooth stored in storage medium, i.e. milk, tissue culture medium, saliva or saline, matory resorption, exchange resorption or both at the same time. During the develop­
total time in dry environment outside the mouth < 60 minutes - threat to viability of mental period, there is a risk of infraposition of the tooth in case of ankylosis. After
periodontal cells, replantation of a tooth with an incompletely formed root, further root development may
tooth stored in a dry environment outside the mouth for > 60 minutes, regardless of additionally be inhibited.
whether the tooth was subsequently stored in any of the above measures - high pro­ The consequences of tooth ankyiosis are alveolar growth abnormalities (Fig. 25.8).
bability of periodontal cell death. At developmental age, in order to preserve the existing bone volume and allow vertical
Replantation of of avulsed permanent tooth, especially stored in a dry environment growth, a decortication may be performed, which involves removing the crown of the
outside the mouth > 60 minutes, is at high risk of complications (ankylosis or inflam­ ankylotic tooth and leaving part of the root.
matory resorption). However, it allows aesthetics and function to be restored while

358 359
 Trau ma to permanent teeth - diagnosis, treatment, prognosis according
to the International Association of Dental Traurnatology
Compendium of Paediatric Dentistry

Tab. 25.8. Management of the replanlation of an avulsed tooth outside the surgery.

Mature tooth Tooth with incompletely formed root

- clean the wounded area with water, physiological NaCl solution or chlorhexidi ne,
- veri fy the correct position of the replanted tooth cli nically and rad iographically,
- when a tooth is misaligned, correct it by applying gentle pressure with your finger,
- i f necessary, administer local anaesthesia, preferably without a vasoconstrictor,
Fig. 2 5.8. l nfraposition of replanted
tooth 2 1 due to ankylosis. - if the tooth or teeth have been embedded in the wrong socket or rotated, consider
correction up to 48 hours a fter the injury,
- flexible spli nt for 2 weeks,
Decoration: - with alveolar or maxillary/mandibular fracture - splint for approximately 4 weeks,
in early mixed dentiti on (7- 1 0 years of age) is carried out within 2
years of the iden- - suture gum wounds, if present,
- begin endodontic treatment if pulp revascularisation
tificati Qn of ankylosis, - start root canal treatment within 2
ed rather earlier, does not occur, once pulp necrosis has been con-
in the late period of the mixed dentiti on (10-1 2 years) to be perform weeks after replantation,
fi rmed,
sition of the
as there is a rapid progression of ankylosis and associated rapid infrapo - system ic antibiotic,
tooth once the patient has reached puberty, - possible tetanus prophylaxis, recommendations, controls.
infrapo sition,
in the early period of permanent dentition, due to the slow growth of
it may not be necessary (continuous monito ring is important). Tab. 25.9. Treatment of a ful ly d islocated tooth stored in a storage medium, total time in a dry
environment outside the mouth < 60 minutes.

Diagnostic and treatment regimens for tooth eruption

If a tooth is avulsed at the scene of the accident:
Mature tooth I Tooth with incompletely formed root
- remove any visible contamination of the tooth by gently rinsing the surface with 0.9% NaCl
reassure the patient, or a physiological storage medium, e.g. milk,
- evaluate the root surface, remove any contam ination by gently moving the tooth inside for
find the tooth, avoid touching the root, place it back in the alveolus. storage or rinse the surface with sal i ne,
NaCl solution
if the tooth is contaminated, rinse it gently with milk, physiological - place the tooth or leave i t in a storage medium during the col lection of the interview, clinical
or the patient's saliva, and radiological examination of the patient and preparation of the patient for replantation,
after tooth replantation, the positio n of the tooth should be maintained,
e.g. by bit- - administer a local anaesthetic, preferably without a vasoconstrictor,
ing on a gauze pad, tissue or napkin, - rinse the alveolus with sterile 0.9% NaCl solution, assess whether the alveolar wall has been
that is available fractured; if so, recompose the fractured fragment, remove the clot with a stream of sal i ne,
if replantation is not possible - place the tooth in a storage medium
- replant the tooth slowly, pressing l ightly with your finger, do not use excessive force,
to avoid drying of the root surface and death of the periodontal cells,
- verify the correct position of the replanted tooth clin ically and radiographical ly,
refer the patient to a dentist. - apply flexible split for 2 weeks,
is shown in
The management of a patient who presented after on-site replantation - in the case of a fracture of the alveolar process or jaw/mandible - a splint for about 4 weeks,
with a tooth kept - suture gum wounds, if present,
Table 25.8, with a tooth kept dry for less than 60 minutes in Table 25.9,
dry for more than 60 minutes in Table 25. 1 0. - start root canal treatment within 2 - endodontic treatment should be started ifthere is no pulp
1 _
weeks after replantatlon, revasculanzatlon, after confirmat10n of its necrosis,
- systemic antibiotic,
- possible tetanus prophylaxis, recommendations, controls.

361
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Compendium of Paediatric Dentistry

Tab. 25 .1 O. Management of a fully dislocated tooth stored in a dry envi ronment outside the
mouth > 60 minutes.
Chapter 26
Mature tooth Tooth with incompletely formed root
- remove loose residues and vi- Abrasions, attrition, abfraction and erosion
sible impurities by shaking the - remove any impurities by gently agitating the storage
tooth in the storage medium or medium with a tooth, or briefly and gently rinse the sur-
with a gauze pad soaked in 0.9% face with a stream of 0.9% NaCl,
Dorota Olczak-Kowalczyk, A nna Turska-Szybka
NaCl,
- place the tooth or leave it on the support during the collection of the interview, c linical
_ _
and radiological examination of tbe patient and preparation of the patient for replantat1on, The causes of non-carious tooth lesions can be chronic or repeated mechanical and/or
administer a local anaesthetic, preferably without a vasoconstrictor,
chemical factors. Depending on the type of causal factor, a distinction is made:
- rinse the alveolar socket with sterile 0.9% NaCl solution, assess whether the alveolar wall has
been frac\ured; if so, recompose the fractured fragment, remove the clot with a 0.9% NaCl
abrasions - the effect of repeated contacts of the tooth with foreign objects or mate­
stream, rials (e.g. with excessively hard bristles of the toothbrush, with excessive force ex­
replant the tooth slowly, pressing lightly with your finger, do not use excessive force, erted during b rushing or improper brushing technique, with abrasive toothpaste, with
verify the correct position of the replanted tooth clinically and radiographically, objects held or bitten by the teeth, e.g. a pen, nail biting (non-fitting paraphrases),
- apply flexible splint for 2 weeks, playing a wind instrument or contact of the teeth with jewellery inside and around the
in case of alveolar or maxillary/mandibular fracture - for approximately 4 weeks,
mouth); the placement of the lesions indicates a causal factor (Fig. 26.1),
suture gum wounds, if present,
pathological attrition - the consequence of improper two body wear, usually due to
- start root canal treatment within - begin endodontic treatment if pulp revascularisation
2 weeks after replantation, does not occur, once pulp necrosis has been confirmed, bruxism, i.e. short-circuit parafunction; they occur on the surfaces of functionally ac­
systemic antibiotic, tive teeth, i.e. primarily on the incisal edges of anterior teeth and occlusal sur-faces of
possible tetanus prophylaxis, recommendations, controls. lateral teeth, less often on the palate surfaces of the anterior teeth of the maxilla and
labial surfaces of the anterior teeth of the mandible, and in people with malocclusion
References
also on the buccal and tongue surfaces (Fig. 26.2); they require differentiation from
1. Abbott P Y. Diagnosis and management of transverse root fractures. Dent Traumato I 20 I � ;
35(6): 3 33-347. - 2. Andreasen FM et al. Root fractures in Textbook and Color Atlas of Traumatic physiological attrition,
Injuries to Teeth, F. M. Andreasen and J. 0. Andreasen, Eds., pp. 3 37-371, Blackwell, Copenha­ abfractions - the effect of repeated, excessive occlusal load of the tooth, which caus­
gen, Denmark, 2007 - 3 . Bourguignon C et al. International Association of Dental Traumatolo­
gy guidelines for the management of traumatic dental injuries: 1 . Fractur�s and lu��t10ns. Dent
es tooth flexure, triggering stresses in the cervical region, leading to the destruction
Traumata! 2020;36(4): 3 14-330. - 4. Einy S et al. Immediate post-operative rehabil1tat1on after of connections between the crystals of tooth tissues, microcracks and fractures of the
decoronation. A systematic review. Dent Traumatol 2020;3 6(2): 141-150. - 5. Fouad A F. Inter­ enamel, and then dentin; the contributing factor is bruxism,
national Association of Dental Traumatology guidelines for the management of traumatic dental
injuries: 2. Avulsion of permanent teeth. Dent Traumata] 2020; 36( 4): 3 31-342. - 6. Lawson JA et dental erosion - the effect of acids of external origin (mainly from food and beve­
al. Decoronation of ankylosed teeth: An Overview. Dental Update 202 1 ; 48 ( 4), do1 .org/l 0.12968/ rages, acidic drugs such as vitamin C, certain anti-asthmatic drugs, iron preparations,
denu.2021.48.4.289. - 7. Malmgren B. Decoronation: how, why and when? Je California Dental
from acidic saliva substitutes and saliva stimulants, as well as from oral hygiene
Association, 2000; 28: 846-854. - 8. Ong D et al. Autotransplantation: a viable treatment option
for adolescent patients with significantly compromised teeth. Australian Dent J, 2016;.61 (4):3 96- products acidified or containing chelators) or internal (vomiting, acid reflux, urae­
407. - 9. R angareddy MS et al.M anagement of Root Fracture: A Novel, Noninvasive Treatment mia, ketoacidosis). The most common risk factor for tooth erosion in children is the
Approach. Case Reports in Dentistry Volume 20 1 3 ; doi.org/1 0.1155/20 1 3/653261.
frequent consumption of drinks and foods with erosive potential. With intrinsic acid
effects (reflux, vomiting), lesions most commonly appear on the palatal surfaces of
the maxillary anterior teeth and on the occlusal and buccal surfaces of the mandibular

362
363
Compendium of Paediatric Dentistry Abrasions, attrition, abfraction and erosion

lateral teeth (Fig. 26.3). The action of the acid causes softening and subsequent loss of causal factors. The most common causes of non-carious lesions in children are expo­
of tissue on the tooth surface and subsurface mineral dissolution. The loss of hardness sure of tooth tissue to acids (internal or external), occlusal parafunctions, e.g. bruxism,
of the enamel makes it vulnerable to mechanical damage. Enamel can already erode and non-occlusal parafunctions, such as nail biting. The risk of tooth tissue loss and the
at pH < 5.5 and dentin at pH < 6.0. degree ofloss depends on the degree of mineralisation of enamel and dentin, the defence
function of saliva and the duration of exposure to damaging factors. The deciduous den­
tition, due to the low degree of mineralisation of the enamel and its greater permeability,
as well as the weaker defence function of saliva related to the immaturity of the salivary
Fig. 26. I . Abrasion of the glands, is more vulnerable to mechanical and erosive factors than permanent teeth.
incisal edge and buccal sur­ The diagnosis should assess:
face of tooth 2 1 caused by
intraoral jewellery. - the age of the child and the type of dentition, especially the length of time the tooth
has been in the mouth (freshly erupted permanent teeth in a child may have minimal
Basic information on bruxism changes despite exposure to damaging factors, whereas deciduous teeth present for
Definition: non-functional, habitual, unconscious clamping and grin­
a long time may have very advanced changes) (Fig. 26.5),
ding of teeth; during episodes of bruxism, rhythmic activity of the mus­
cles of the masticatory organ may occur (with a frequency of approx. 1 - the presence of potential causative factors, including systemic diseases and drugs
Hz) or prolonged isotonic contractions (even a few m inutes); the forces used, diet (type and frequency of food and beverages consumed, consistency of
generated during grinding and clamping usually exceed those occurring
during chewing food, method and speed of drinking), hygienic behaviours (method of brushing
Forms of bruxism: teeth, type of toothbrush, prophylactic agents, etc.), the presence of parafunctions
- awake bruxism (AB) and other mechanical factors,
- sleep bruxism - (SB) : 80% N REM phase, 5-1 0% REM, the condition of the dentition (presence, location, appearance and degree of non-ca­
- combined bruxism (in the waking and sleeping states);
- primary (idiopath ic) - unknown cause, rious lesions, presence of hypomineralisation, occlusal conditions) and the presence
- secondary - accompanies certain diseases ( e.g. cerebral palsy, asthma, of dentin hypersensitivity to thermal, dehydration, mechanical and chemical stimuli,
depression), use of certain medications (e.g. selective serotonin inhibi­
tors, psychotropic drugs, amphetamines, L-dopamine) and stimulants, condition of the mucosa (presence of lesions of a mechanical trauma nature, e.g.
snoring, psycho-emotional disorders (e.g. chronic stress) bite marks on the buccal or tongue mucosa, indentations on the lateral edges of the
Children: in younger children, it may be associated with the immaturity tongue),
of the musculo-neural system of the masticatory organ, and during the condition of the gingiva (recessions).
period of tooth replacement - with occlusive instability; often disap­
pears at the age of several years I t is also beneficial to assess saliva secretion, its pH and its ability to buffer acids.
Pathological attrition is manifested by a flattening of the occlusal surfaces, usually
Lesions of attrition, erosion or abrasion can occur separately, as single manifesta­ similar in both dental arches. Characteristically, the wear facets of the lower and upper
tions, but most commonly occur simultaneously and are referred to as erosive wear or teeth match exactly, the incisal edge facets are uneven, the edges of the clashes are sharp,
tooth wear. It is very difficult to differentiate them, especially in the early stages. Tooth and the surfaces of the facets are shiny (physiological attrition - incisal edge clashes are
tissue loss caused by the coexistence of erosion and attrition is clearly visible on the even, the edges of the clashes are smooth, and the surfaces of the facets are dull) (Fig.
incisal edges and/or occlusal surfaces of teeth. Lesions on the buccal or lingual surfaces 26.2). In pathological attrition, tissue loss progresses more rapidly than in people of the
are usually the result of erosion or, less commonly, abrasion. The assessment of the same age group.
presence of individual components of tooth tissue loss is facilitated by the identification

364 365
Compendium of Paediatric Dentistry Abrasions, attrition, abfraction and erosion

Fig. 26.4. Erosive abrasions -

cup-shaped or pit-shaped cavities
with rounded edges on cusps,
Fig. 26.2. Uneven abrasions with sharp edges and shiny surfaces (left - mandibular deciduous edges of fillings above the level
fang, right - incisal edges of permanent maxillary anterior teeth. of the adjacent tooth surface.
W hen erosion and attrition occur simultaneously, concave lesions are the result of
Tooth erosion initially manifests itself in the loss of the enamel contour, the rounding of acids and flattening is the result of abrasion.
the recesses on the occlusal surface and an increase in the translucency of the incisive edges
of the teeth. At a later stage, shallow, wide depressions within the enamel (fissured at the
incisal edge) appear on smooth surfaces. They do not cover the enamel in the cervical region, Fig. 26.5. Erosive tooth wear in a child with early mixed
which is related to the buffering effect of the gingival crevice fluid. On the occlusal surface, dentition - enamel loss with dentin exposure in canines and
first deciduous molars, enamel loss and pitted depressions
nodules and furrows become rounded. Bowl-shaped or hollow cavities with rounded edges on the occlusal surfaces of second deciduous molars, slight
that are wider than they are deep appear. Gradually, dentin is exposed. The dentin is less enamel loss on the incisal margins of permanent incisors
mineralised than the enamel, which is why the cavities are increasingly visible. Exposure of (partial ly lost mamelons).

the pulp may occur. Tissue loss in the area of the fillings results in the edges of the fillings
being above the level of the adjacent tooth surface (Fig. 26.4). In the first three years oflife, Appropriate indices are used to assess the severity of non-carious tooth tissue loss,
erosive lesions most often occur on the palatal surfaces of the upper incisors and the edges of most commonly the tooth wear index according to Smith and Knight (TWI). Tooth da­
the lower incisors, in preschool age on the occlusal surfaces of molars, in the mixed dental mage on the buccal/labial, palatal/lingual, occlusal/ incisal edge, cervical region is grad­
period they appear on the nodules on the occlusal surfaces of the first molars, although they ed on a scale of O to 4 according to the following criteria:
are much less advanced corn-pared to changes on deciduous teeth. In adolescents, erosive
changes also occur on the palatal surfaces of the maxillary incisors (Fig. 26.3).

0 - without signs of enamel loss, without signs

of crown contour loss,

I - loss of enamel buccal, lingual, occlusal sur­

face characteristics (BLO), cervical area
Fig. 26.3. Co-occurrence of tooth attrition and erosion in an adolescent boy with bruxism and (C) minimal l oss of crown contour,
gastroesophageal reflux - lesions on the palatal surfaces of the maxillary incisors and canines
and the incisal margins of the incisors and canines of both arches, flattening of the occlusal
surface of the premolar teeth.

366 367
Compendium of Paediatric Dentistry Abrasions, attrition, abfraction and erosion

In the treatment of lesions of non-dental origin, early detection of non-advanced

tooth damage and identification of causative and additional factors that increase the risk
and severity of tooth tissue loss is important. This makes it possible to halt tooth tissue
2 - loss of enamel just exposing dentine < 1/, loss and treat it early and non-invasively.
of the BLO surface, C - dentin loss with a It is essential to explain to the patient and his parents the causes and consequences of
depth of < I 111111,
non-carious lesions and to provide recommendations to eliminate or minimise the effect
3 - loss of enamel with exposure to just of the causative factors diagnosed in the patient (e.g. avoidance of acidic foods, use
ex-posing dentine > ½ of the B LO surface, of low-abrasive toothpaste or soft toothbrush, treatment of parafunctions, orthodontic
Incisal area (I) - substantial dentine loss; treatment, removal of intra - and perioral jewellery, etc.), reduction of the sensitivity
C - defect up to 1-2 mm from the pulp,
without exposing pulp or secondary den­ of dental tissues to chemical and mechanical agents (use of agents containing fluorine
tin, and calcium-phosphate compounds). In cases of significant tissue loss, restorative treat­
ment (e.g. restoration with composite material, steel crowns) is indicated. In the case of
significant attrition of deciduous teeth, regular inspection of permanent first molars and
incisal teeth is mandatory (the presence of attrition discs on the cusps of permanent first
4 - complete enamel loss with exposure of pulp molars and incisal margins of anterior teeth is indicative of active bruxism). If causative
or secondary dentine ( B LO I), C - defect
more than 2 mm deep, or pulp exposure. systemic factors are present, collaboration with a paediatrician is essential.
Children with bruxism are treated with myotherapy, braces or relaxation splints
The BEWE index is also most commonly used to assess the severity of erosion, with (should be checked every three months due to ongoing growth processes) and relaxation
a code of O - no erosive tooth wear, 1 - initial loss of surface texture, 2 - distinct defect, techniques. For severe muscle spasticity, botulinum toxin administered intramuscularly
hard tissue loss < 50% of the surface area,3 - hard tissue loss 2: 50% of the sur-face area. is used.
Non-carious lesions due to mechanical and/or chemical factors can cause significant
References
weakening of the tooth, increased dentin sensitivity and, in advanced cases, even expo­
1 . Bartlett D, Dugmore C. Pathological or physiological erosion - is there a relationship to
sure of the tooth pulp. Deterioration of occlusal conditions and myarthropathy-like com­ age? Clin Oral I nvesting 2008 Mar; 12 Suppl I (Suppl I ):S27-3 l . doi: 1 0.1007/s00784-007-0177-
plications are also possible. It is therefore necessary to assess the dental complaints pre­ l . - 2 . Roberts WE et al. Pathophysiology of Demineralization, Part I: Attrition, Erosion, Abfrac­
tion and Noncarious Cervical Lesions. Curr Osteoporos Rep 2022; 20, 90-105 . - 3 . Nota A et al.
sent, feelings of numbness, muscle pain, temporomandibular joint pain and headaches.
Correlation between Bruxism and Gastroesophageal Reflux Disorder and Their Effects on Tooth
If bruxism is suspected, facial features (square face due to hypertrophy of the mas­ Wear. A Systematic Review. J Clin Med. 2022; 19: 11 (4): 1 1 07. doi: I 0.3390/jcm11041107. - 4.
seter and temporalis muscles), masticatory muscle tension (increased), masseter and Shellis RP, Addy M . The interactions between attrition, abrasion and erosion in tooth wear. Mono­
gr Oral Sci. 20 1 4;25 :32-45 . doi: I 0.1 1 5 9/000359936. - 5. Smith BG, Knight J K . A comparison of
temporalis muscle attachments and temporomandibular joint (pain), mandibular move­ patterns of tooth wear with aetiological factors. Br Dent J 1984; 157: 16- 1 9. - 6. Smith BG, Knight
ments, especially inversion (feeling of stiffness or restriction of mouth opening) should J K. An index for measuring the wear of teeth. Br Dent J 1984; 156:435-438 - 7. Smith BG, Robb
also be assessed. Temporomandibular joint pain rarely occurs in children (adaptability N D . The prevalence of toothwear in I 007 dental patients. J Oral Rehabii 1 996; 23:232-239.

of the developing masticatory motor system). It usually appears after a period of re­
placement of permanent teeth. In children, abnormal mandibular mobility and crackles
are more common symptoms. The primary additional test in the diagnosis of bruxism is
polysomnography (PSG).

368 3 69
 Oral mucosa] diseases i n children

Ulcers and erosions are changes characterized by interruption of the continuity of

Part VI the oral mucosa. An ulceration involves all layers of the epithelium and extends into the
connective tissue, whereas an erosion is a superficial lesion that does not extend beyond
Periodontal and gingival tissue diseases in children all layers of the epithelium. A distinction is made between ulcers:
acute, chronic (lasting more than 14 days) and recurrent (similar episodes of lesions
and adolescents
with periods of healing) (Fig. 27.1),
single and multiple,
local and systemic aetiology.
Chapter 27 Types of mucosa! ulceration/ulceration with examples of causative factors are shown
in Figure 27.1.
Oral mQcosal diseases in children

1
Ulcers, mucosal erosions
I
Dorota Olczak-Kowalczyk
l lrecurrent
I acute
I chronic 11 I
Oral mucosa! diseases in children and adolescents may be isolated or concomitant 1
single
1
multiple
1
single
l multiple l
single,
with other oral pathologies and/or systemic diseases and may be one of the symptoms of trauma viral and bacte- injury, necrotizing ulcerative multiple
a genetic syndrome or may be episodic, recurrent or chronic. They occur more frequently (e.g. mecha- rial infections, cancer (e.g. gingivitis, pemphigoid aphthous
in people with systemic diseases than in the generally healthy. They may represent the nical, thermal, erythema mul- cancer, lym- (rarely in children), recurrent aph-
chemical), tiforme, Ste- phoma), eosi- bullous epidermal se- thous ulcers
first clinically observable symptom of a general disease or may be an image of a neo­ drugs . vens-Johnson nophilic ulcer, paration, lichen planus,
plastic lesion. Although mild changes are most often observed in children, the diagnosis syndrome, tuberculosis, linear IgA bullous
allergic and drug syphilis, CMV dermatosis (LABO),
should also take into account conditions and changes that carry a high risk of developing reactions Melkersson-Rosenthal
cancer and in situ cancer. Precancerous lesions are chronic mucosa! diseases at risk of syndrome
malignant transformation. In children, these are most often lesions caused by human Fig. 27.1. Types of mucosal ulceration/ulceration and examples of causative factors.
papilloma virus i nfection (described below), much less frequently leucoplakia, lichen
planus and solar lip inflammation. Precancerous conditions are systemic diseases with
a significantly higher risk of developing cancer, including Plummer-Vinson syndrome, In children, the most common ulcerative and erosive lesions are mechanical, thermal,
pigmented parchment skin, congenital dyskeratosis, Fanconi anaemia, dystrophic forms electrical and chemical trauma, viral infections and aphthous and aphthous-like ulcers.
of vesicular epidermal detachment (described below), chronic pharmacological immu­ Injuries caused by trauma can be the result of accidental events ( iatrogenic and
nosuppression, HIV infection, chronic disease, graft versus host. non-atrogenic), the result of violence, intentional or unintentional self-harm ( e.g. in the
Oral mucosa! lesions are also classified as red, white and coloured lesions. case of emotional disorders, mental illness and chronic stress). Caused by mechanical
The most common lesions on the oral mucosa of children and adolescents in the general factors, they are usually located on the edge of the tongue, buccal mucosa, lip, less com­
population are ulcerations and erosions, lesions associated with viral infections, oral can­ monly on the hard palate and the vestibule of the mouth. Traumatic acute ulcerations are
didiasis, angular cheilitis, cheilitis, hyperkeratosis, geographic tongue, black hairy tongue, painful, soft, clearly demarcated by an erythematous seam, covered with fibrous plaque
cracked and coated tongue, exophytic lesions (e.g. retention cysts, fibrornas, granulomas).

3 71
370
Compendium of Paediatric Dentistry Oral mucosa! diseases in children

and, in the healing phase, with granulation tissue and epithelium. Causes may include chlorite in concentrations > 2% (shows alkalizing and oxidizing effect, pH = 10.8-12.9)
biting the lip, tongue or buccal mucosa, e.g. after local anaesthetic administration, trau­ - it is the cause of erosions covered with a white-yellow fibrous rash or ulcers, silver
ma caused by braces. Traumatic chronic ulcers result from the long-term persistence of a nitrate, formocresol, 37% orthophosphoric acid, H 202 in concentrations above 3% and
traumatic factor. They rarely cause pain, are surrounded by a hyperkeratotic rim, and are agents for teeth whitening - they cause chemical damage to the mucous membrane with
most commonly located on the lateral part of the tongue and buccal mucosa. a characteristic whitish appearance (given by the river membrane covering it, formed
In the youngest children, the sharp incisal edges of the mandibular anterior incisors from necrotic tissues and inflammable exudation).
may be the cause of Riga-Fede ulceration most often occurring on the tip or abdominal Erosions and ulcers of the oral mucosa are often accompanied by infections with
part of the tongue, rarely on its dorsal part and the mucous membrane of the lower lip viruses from the Herpesviridae family (Herpes simplex virus - HSV-1), varicella zos­
(Fig. 27.2). The occurrence of Riga-Fede ulcers is favoured by neurological disorders ter virus (VZV, H HV-3), Epstein-Barr virus (EBY, H SV4, HHV-4), cytomegalovirus
(e.g. cerebral palsy, pain insensitivity, Down syndrome). Treatment often requires re­ (CMV, H SV5, H H V-5), as well as RNA viruses: Enterovirus, i.e. Coxsackie viruses A
moval of th� causative teeth. and B. Viruses belonging to the family Herpesviridae are widespread in the human en­
vironment. Once the primary infection has passed, they produce a latent form, whose
reactivation and multiplication of the virus results in secondary infection.

Fig. 27.2. Riga-Fede ulceration on

the ventral part of the tongue.

T hermal burns (e.g. too hot food) are painful. They can manifest as redness, the
presence of vesicles turning into erosions and tissue necrosis. They are usually located Fig. 27.3. Primary herpetic stomatitis - erosions from ruptured vesicles, gingivitis on both the
vestibular/buccal and palatal/li ngual sides, tongue draped with erosions on the tip.
on the palate, lips and tip of the tongue.
Electrical damage manifests as redness, then after 3-4 days as painless foci of necro­
sis, white-grey or brown with a coagulated surface, surrounded by a narrow inflammato­ Bullous diseases, such as pemphigoid or pemphigus, are rare in childhood. Con­
ry limb, most often located on the lips, tongue and gums. genital epidermolysis bullosa (EB) occurs with a frequency of 2 per 1 00 000 people.
Chemicals (acids, bases, substances containing reactive metals) cause damage to the This is a group of mucocutaneous diseases that are genetically determined. Depending
mucous membrane with a type-dependent severity, concentration of the chemical and on the depth of formation of blisters provoked by injuries, ordinary EB - blisters in the
epidermis, connecting EB - blisters in the basement membrane, dystrophic EB - blisters
duration of its action, including: surface necrosis of the epithelium causing its exfoliation
below the basement membrane are distinguished. Blisters in the mouth rupture, develop­
(white lesion), erosions, ulcers, deep necrosis reaching the submucosa, and even bones.
ing into erosions/ulcerations surrounded by epithelial remnants of the bladder lid. In the
The acid results in coagulative necrosis, while the base results in liquefactive necrosis.
dystrophic form, the ulcers, as they heal, leave scars. This form is at risk of developing
Contact of the mucous membrane with alkali usually does not cause pain, while with
squamous cell carcinoma. Hypoplasia and hypomineralisation of the enamel and high
acid it causes severe, sharp pain. In the dental office, special care should be taken when
susceptibility to caries are also characteristic.
using medicinal products such as calcium hydroxide (pH of dental materials with cal­
cium hydroxide 9-13) - it causes redness and necrosis of the epithelium, sodium hypo-

372 373
Compendium of Paediatric Dentistry Oral mucosal diseases in children

a life-threatening condition. A process affecting 1 0-30% of the body surface is referred

Viral infections with erosion
and mouth ulceration to as the overlap syndrome between SJS and TEN. Blisters, vesicles, erosions, erythem­
HHV-1: atous and oedematous lesions appear on the skin and mucous membranes of the mouth
primary herpetic stomatitis - vesicles on the inflamed mucosa, cracking,
leave erosions with a tendency to melt, gingivitis, tongue covered with vesi­ and other regions of the body. Blistering on the redness of the lips causes bleeding and
cles and erosions on the edges; the duration of the d isease - I 0- 1 4 days; most the formation of crusted bloody scabs Damage to the skin and mucous membranes can
often i n the first five years of life (Fig. 27.3),
lead to severe complications, e.g. respiratory failure, dehydration, malnutrition, second­
recurrent (secondary) herpes - a feeling of tension, tingling, then a bubble
or a group of vesicles (usually on the border of red lips and skin), erosion and ary skin infections, and septicaemia.
scab; less often on the gums, hard palate, dorsal surface of the tongue; the Oval or round erosions or ulcers in the mouth with a clear border, surrounded by an
duration of the disease - 1 0- 1 4 days
inflammatory seam and covered with a fibrous coating, colloquially referred to as aph­
HHV-3:
chickenpox - erythema of the mucous membrane, loosely distributed vesi­ thae, are classified as:
cles transforming into erosions, most often on the palate and palatine arches; recurrent aphthous, including Mikulicz and Sutton, occurring in healthy people,
\
the duration of the disease - about 1 4 days,
most often on the mu-cous membrane covered with non-keratinizing epithelium
shingles - paraesthesia and pain, redness and asymmetrical vesicles on the
mucous membrane along the course of the trigeminal nerve (palate, cheeks, with an incompletely explained aetiology, which is characterized by recurrence and
tongue), less frequently the facial and lingual nerve cyclicity (Tab. 27.2),
HHV-4: aphthous-Iike lesions, including:
mononucleosis - pseudo membranes, ulcers on the tonsils, palatine arches, • accompanying systemic diseases, e.g. diseases of the gastrointestinal tract (ul­
soft palate and petechiae on the border of the soft and hard palate, bleeding
from the gums in thrombocytopenia, cerative colitis, Crohn's disease, coeliac disease), mucocutaneous diseases, col­
in immunodeficiency - hairy leucoplakia, mucosa[ hyperplasia associated lagenases (e.g. lupus erythematosus, vasculitis), immune deficiencies, especially
with lymphoproliferation, ulcers, petechiae and mucosa! bleeding those involving neutrophils, as a symptom of Behc;et's syndrome (recurrent aph­
HHV-5: thous ulcers of the mouth and genital PFAPA (Periodic Fever, Aphthous Stomati­
in immunodeficiency - unusual ulcers and foci of necrosis tis, Pharyngitis, Adenitis) (mainly in children under five years of age),
Coxsackie viruses type A (usually type 4): • being an adverse effect of drugs such as beta-blockers, non-steroidal anti-inflam­
herpangina - white papulovesicular lesion that turn into erosions or even
ulcers surrounded by a vivid red inflammatory limb on the posterior wall of matory drugs, sulphonamides, tetracyclines, anticancer cytostatics, immunosup­
the throat, tonsils and palatine arches, painful; disappear after about 7 days pressants (mycophenolate mofetil, sirolimus, tacrolimus), barbiturates.
Coxsackie viruses mainly type A (usually type 1 6):
disease of the hands, feet and mouth - papulovesicular lesions on the hands Tab. 27.2. Differential diagnosis of Mikulicz's aphtha and Sutton 's aphtha.
and feet (mainly on the dorsal surface near the nail plates, but also on the sur­
face of the hands and soles), vesicles that turn into erosi ons on the oral mu­ RAS minor (Mikulicz's aphthae) RAS major (Sutton's aphthae)
Parameters
cosa in different regions of the mouth, painful; disappear after about 7 days 80-85% · 1 0-15%
Diameter < 1 cm 2': I cm
Number 1 -5 1-10
Diseases more common in the developmental age group are erythema multiforme, usually the f ont part of the mouth:
r
more often the posterior part of
Stevens-Johnson syndrome and toxic epidermal necrolysis. Toxic epidermal necrolysis Frequent location lips and cheek, lip and abdominal the oral cavity - pharynx and soft
(TEN) and Stevens-Jonson syndrome (SJS) is a sudden, necrotic skin-mucosa! reaction surface of the tongue palate
up to 1 4 days, usually without a few weeks (or more),
(keratinocyte necrosis) usually triggered by medication, less frequently by infectious Healing
scars usually with a scar
agents. SJS affects less than I 0% and TEN more than 30% of the body surface and is

3 74 375
Compendium of Paediatric Dentistry Oral mucosa! diseases i n children

An algorithm for the diagnostic management of aphthous-type lesions and examples Chronic ulcers that persist for 2 weeks despite topical treatment and recurrent require
of the causes of aphthous lesions are shown in Figure 27.4. diagnosis and exclusion of systemic disease or neoplastic lesion.

Rccun-cnt ulcers
? associated symptoms ? local factors

Injury, . . .
White lesions
General symptoms

? localization on Aphlhous-like lesions

Morsicatio buccarum, labiorum, linguarum - the result of
the mucous chronic injuries in these areas, e.g. biting, chewing and sucking;
membrane of the
epithelium Inflammatory bowel disease, eoeliac disease symptoms: maceration and exfoliation of the epithelium, pete­
chiae, small erosions and furrows, and even hyperkeratosis; located
keralinized epithelium non-keratinized epithelium Cyclic ncutropenia on the mucous membrane of the cheeks in the projection of the bite
line are referred to as linea alba.
H IV

D
Ilchcct's syndrome
I lerpetifonn PFAPA team
aphlhous ulcers the MACJC team
Leukoedema - diffuse, white or greyish, opalescent mucous
membrane discoloration (similar to a veil), not removable, located
aphthous-like ulcers: HIV related to deficiencies of
mainly on the mucous membrane of the cheek (one-sided or bila­
cyclic nautropenia, .. idiopathic fc. folic acid. B 12. Zn
teral), less visible after stretching the mucosa.
Fig. 27.4. Diagnostic algorithm for recurrent u lcers and examples of causes of lesions.
Black hairy tongue - the effect of excessive keratosis and elon­
gation of the filamentous warts and the accumulation of black or
Treatment depends on the type of causative agent, the type and extent of the lesions on brown dye, e.g. from food products, hygiene agents, medicines
the mucosa. Local treatment of diseases manifested by the presence of erosions and mouth (antibiotics, e.g. erythromycin, iron preparations); usually without
ailments. It can cause a metallic taste, bad breath or a burning sen­
ulcers is symptomatic and depends on the severity of the lesions. It should take into account sation. It is also a symptom of Peutz-Jeghers syndrome, neurofibro­
the elimination of local irritants and pain, alleviate the severity of inflammation, prevent matosis type I and Addison's disease.
secondaty infections and accelerate healing. It is important to cany out hygienic procedures
that reduce the microbial load in the mouth (cleaning of teeth, tongue) and careful removal of Pseudomembranous candidiasis - white raids closely related
plaques to allow access of therapeutic agents to the lesion. Antiseptics, anti-inflanunatories, to the substrate, the removal of which leaves a vivid red, pain­
ful, sometimes bleeding surface; in infants called thrush; a causal
analgesics and accelerated healing agents can be used in the form of a gel, spray, swabbing,
factor - Candida spp. (mainly C. albicans); contributing factors:
brushing or mouthwash. Ozone therapy, agents containing natural ingredients (e.g. aloe vera, antibiotic therapy, treatment with glucocorticosteroids, hormonal
chamomile extract, and with panthenol, hyaluronic acid or polyvinylpyrrolidone, essential d isorders and immune deficiencies.
oils, chlorhexidine, acetylpyridine chloride, and in case of pain - analgesics and anti-inflam­
matory agents (e.g. benzamine hydrochloride) are recommended. Remedies for children
White sponge nevus - an autosomal dominant disease - thyroid
should be free of alcohol and choline salicylate. In acute conditions, topical application of thickening of the mucous membrane covered with white, opales­
corticosteroids is allowed. Due to the increased risk of superinfection and mucosa! atrophic cent, soft, corrugated epithelium with a sponge consistency located
symmetrically on the mucous membrane of the oral cavity covered
changes, topical glucocorticosteroid therapy should be short-term. ln viral inflammations, the with non-rooted epithelium, mainly on the cheeks; it does not cause
use of acyclovir within 72 hours of the first oral lesions is beneficial. discomfort, sometimes a feeling ofa foreign body.

376 377
Compendium of Paediatric Dentistry Oral mucosa! diseases in children

White lesions can be caused by a viral infection, such as: especially in febrile diseases, in dehydration and dry mouth, which cause the accumu­
HHV-4 causes hairy leucoplakia - excessive keratinisation and hypertrophy of the lation of food residues, exfoliated epithelium, leukocytes, bacteria and yeasts on the
filiform papillae of the tongue on its margins, less commonly on the ventral or dor­ surface of the tongue and the formation of a layer of white coating easy to remove (coa­
sal surface, ted tongue). In scarlet fever, the tongue is initially covered with a white coating, with
Human Papilloma Virus (HPV ) can cause: enlarged fungiform papillae visible (strawberry tongue); after the coating has flaked off,
• common warts - occur mainly in children, hard, whitish, sebaceous, limited exo­ it is vivid red with enlarged papillae (raspberry tongue).
phytic lesions with epithelial hyperkeratinisation and elongated apex, located on White, greyish-white or yellowish in colour are small, painless nodules appearing on
the lips, hard palate, gums and dorsal surface of the tongue, the gingival shafts and palate in newborns and infants (Fig. 27.6). These include:
condyloma acuminatum - small white or pink nodules, which may have a pe­ gingival cysts - small (diameter 1-3 mm), single or multiple nodules on the ridge of
duncle or broad base and a corrugated surface ("cauliflower flower") or resemble the gingival shaft, most often on both sides, in the region of the future appearance
a fibroma, often located on the tongue, lips, palate and floor of the mouth (the of milk molars, which arise from the remnants of the tooth moulding; most of them
presence in a patient of developmental age may be indicative of sexual abuse, as undergo spontaneous regression in the first 5 months of life; persisting longer, they
sexual contact is the main route of virus transmission), are referred to as so-called gingival pearls,
oral squamous papilloma - usually a single, small exophytic lesion with finger­ Bohn's nodules - nodules 2-3 mm in diameter in the lateral parts of the palate,
-shaped protrusions, pointed or on a wide base, pink or whitish in colour; often usually at the border of the soft and hard palate and on the buccal/ labial side of the
located on the soft palate, tongue, tongue nodule and lower lip (Fig. 27.5), gingival shaft, originate from salivary gland structures,
• focal epithelial hyperplasia (Heck's disease) - numerous, non-painful, flat, soft, - Epstein's pearls - hard nodules in the midline of the palate that develop from rem­
white or pink papules, often arranged in clusters, located mostly on the mucosa nants of epithelium from the foetal period in the palatal suture line.
of the lower lip and cheeks and less commonly on the tongue; occurs mainly in
children and young adults,
measles virus (Morbilli virus, MeV) is responsible for the presence of white spots
surrounded by a red inflammatory rim, the so-called Koplik spots on the mucous
membrane of the cheeks at the height of the molars.
Fig. 27.6. G i ngival
cysts in infants, right,
gingival pearl.

Red lesions
Haemorrhages, petechiae - m inor blood extravasations,
Fig. 27.5. Squamous papillo­
sometimes merging or larger ecchymosis, can occur on the
ma on the dorsal surface of the
lip, tongue, hard palate, gums; the effect of damage to the
tongue (left) and common wart
at the corner of the mouth (right). walls of the capillaries or small arteries usually as a result
of trauma or increase in blood pressure (e.g. cough, intense
crying); one of the symptoms of acquired and congenital hae­
The cause of white lesions may also be exposure of the mucous membrane to che­ morrhagic defects: shallow, plasma, vascular; petechiae at
the border of the soft and hard palate occur i n rubella ( Forch­
micals, including prophylactic agents (e.g. chlorhexidine, Listerine, toothpastes with heimer spots) and mononucleosis, petechiae or bruises in this
sodium lauryl sulphate may cause epithelial exfoliation, and hygienic negligence, area may be the result of sexual violence (fellatio).

378 379
Compendium of Paediatric Dentistry Oral mucosa! diseases in children

Haemangiomas/vascular malformations are benign tu­

mours that appear in the first weeks after birth as a small,
flat, red or pink spot, grow rapidly in the first six months of
life and become elevated, with a lumpy and uneven surface, Atrophic glossitis - smooth, red dorsal surface of the tongue,
bright crimson or light scarlet in colour; in the second year partially or completely free of filamentous warts, most often
of life it slowly fades and diminishes in size (approx. 40% of caused by deficiencies of iron, zinc, vitamins : E, B 12, 82,
haemangiomas disappear). PP, folic acid; may cause pain, burning and numbness of the
tongue and taste disorders.

Erythematous candidiasis is characterized by the presence

of vivid red, sometimes burning erythematous lesions, usual­ In the local treatment of oral candidiasis, agents containing chlorhexidine (exclu­
ly accompanied by inflammation of the angles of the lips; ding persons with xerostomia, mucositis and nystatin), plant extracts (e.g. thymol, euca­
the occurrence is facilitated by antibiotic therapy, vitamin
B 12 and folic acid deficiencies. Chronic form occurs in peo­ lyptol and bioflavonoids), sodium acid carbonate solution (baking soda) and antifungal
ple using prosthetic restorations and mobile orthodontic ap­ antibiotics (nystatin, miconazole, natamycin) are used. Necessary treatment of general
pliances.
disease, compensation for iron and B vitamin deficiencies and a low-carbohydrate diet.
Angular cheilitis is manifested by erythema, maceration, the
presence of fissures, cracks in the skin and redness of the lips
Brownish lesions
in the combination of the upper and lower lips; it can be the
cause of pain; associated with Candida spp. and S. aureus in­
fection. Contributing factors: systemic diseases (e.g. immune Brown-black changes in the colour of the oral mucosa are most often found on the
deficiencies, iron deficiency anaemia, diabetes, allergies),
malnutrition (especially B vitamin deficiencies) and local gums, tongue, mucous membrane of the cheek and hard palate. They result from the ac­
factors, e.g. habitual lip licking or finger sucking. cumulation of pigment in excessive quantities or in the wrong location. They may have
an exogenous or endogenous etiology (increased melatonin production or melanocyte
Geographic tongue, erythema migrans; benign migra­ count). Changes in the colour of exogenous origin arise as a result of accidental implan­
tory glossitis - on the dorsal surface of the tongue, there are tation of a foreign body in the mucous membrane, e.g. bismuth, iron, lead, silver (e.g.
changes in the shape, location and size of pale grey spots de­
void of filamentous warts in the centre and excessive kera­ amalgam tattoo), graphite (e.g. wounded with a graphite pencil). Brown-black coloration
tosis on the periphery ; it can cause hypersensitivity to acute, of endogenous mucosa occurs in people with adrenal insufficiency, Addison's disease,
acidic and salty foods; etiology unknown; often in patients liver disease with cholestasis, using drugs such as minocycline, doxycycline, phenytoin,
with systemic diseases, including heart defects, atopy, aller­
gy, endocrine disorders; it does not require treatment. ketoconazole, cyclophosphamide, as well as in genetic syndromes such as Mccune-Al­
bright syndrome, neurofibromatosis type 1, Peutz-Jeghers syndrome.
T he melanotic nevus is a brown, blue-grey or black flat or lumpy spot, most often
located on the hard palate, followed by the mucous membrane of the cheek or gum (Fig.
Median rhomboid glossitis - atrophy of the warts in the
midline of the dorsal surface of the tongue in front of the sur­ 27.7). It can be a congenital or acquired lesion and can occur at any period of life.
rounding warts; oval or round l esion, well delimited, smooth, Oral mucosa pigment changes require differential diagnosis to rule out malignancy.
shiny ; may cause pain or itching; etiology unknown; contri­
buting factors: Candida spp. infection and immunosuppres­
sive conditions, e.g. diabetes mellitus, treatment with inhaled
glucocorticosteroids.

380 381
Compendium of Paediatric Dentistry O ral mucosa! diseases i n children

Peripheral ossifying fibroma - an abnormal nodule on the gum,

Fig. 27.7. Pigmented sort or hard, the colour of the surrounding mucosa or red, with
lesions in a patient with a smooth or i rregular surface; rarely in the period or deciduous
adrenal insufficiency teeth, most often in adolescence; comes from cel ls of the peri­
(le ft ) and a melano­ odontal or periosteal ligament; occurs almost exclusively on the
tic nevus in an overall gums ( mainly in the anterior section ofthe jaw); often recurs after
healthy child (right). surgical treatment.

Exophytic lesions /soft tissue nodules protrude above the surface of the oral mu­ Peripheral giant cell granuloma - a soft or flexi ble nodule with
cosa. In children, they tend to be benign lesions. The most common are mucocells, fi­ or without pedicle, purple-red or blue-red, usually with a smooth
bromas and granulomas. Due to their similar clinical picture, fibromas and granulomas or irregular surface, often with an ulcer, about 2 cm in diameter;
may surround the tooth, move adjacent teeth, and resorb the un­
can be diffibult to distinguish. The diagnosis is made on the basis of histopathological derlying bone; origi nates from cells of the dentate or periosteal
examination. The most commonly observed include rhabdomyosarcoma and lymphomas. I igament, located on the gum and alveolar process; effect of local
(from the col lection of E. Kra­ irritation or trauma; peak morbidity during the period of mixed
Characteristics of the most common benign exophytic mucosa! lesions in children:
suska-Slawi1iska, IP CZD) dentition; rarely recurs after surgical treatment.

Mucous retention cysts, mucoceles - a soft, bubbling, bl ue-grey

exaggeration with a diameter of< I cm, well delimited from the
environment, covered with a tightened mucous membrane, filled Congenital epulis - pink, smooth or lobular, pinnate growth
with a transparent, yellow-brown mucous fluid, usually painless; ranging in size from a few millimetres to > 7 cm on the gums in
it occurs mai nly on the lower lip, less often the upper lip, the mu­ newborns, more often in the anterior section of the jaw than the
cous membrane of the cheeks, palate, abdominal surface of the mandible, usually single; etiology unknown, more often in girls;
tongue and the bottom of the mouth; in children, a more common may undergo spontaneous inversion; does not recur after surgical
non-ductal cyst (intersection of the duct) than ductal (obstruction treatment.
of the duct).

Localized juvenile spongiotic gingival hyperplasia - usually a

single, painless, bright red exaggeration with a papi llary or gra­
I rritation fibroma - an exophytic, firm and asymptomatic nod­
nular surface on the anterior gum in children (mean age 1 2 years),
ule with smooth surface, colour surrounding the mucosa, consis­
often over the root of the tooth; bleeding when touched; rarely re­
tency from hard to soft; located on the mucous membrane of the
curs after surgical treatment.
cheek, lip, tongue, on the border of the soft and hard palate; it is
formed in response to chron ic irritation or as a side symptom of
antiepi leptic drugs. Developmental anatomical anomalies
The most common developmental anatomical anoma l ies are c left upper lip, alveolar
Pyogenic granuloma - a nodule up to 2 cm in size, with or
process and palate, frenulurn defects (absence of frenulum, lateral accessory frenulum,
without a peduncle, bright red with a smooth surface or with
an ulcer, usually rapidly enlargi ng; often in adolescents and in congenital hypertrophy of lip frenulum) and pl icated tongue.
pregnant women (so-called pregnancy tumour); vascular change The cleft lip and palate are the lack of anatomical continuity of these tissues, their
in response to chronic i rritation, trauma, hormonal factors; most
often occurs on the gums in the anterior section of the jaw, can underdevelopment and deformity, accompanied by malocclusion, hypodontia (usua l l y
occur anywhere; often relapses after surgical treatment. lateral incisor teeth ), increased number of teeth in the cleft region, anomalies regarding
the shape and size of the teeth, delayed and ectopic eruption, and rotation of teeth i n the

382 383
Compendium of Paediatric Dentistry Oral mucosa! diseases in children

cleft region. The cleft lip and palate cause functional disorders of the masticatory organ, 20. Morris LG et al. Squamous cell carcinoma of the oral tongue in the paediatric age group:
including breathing, sucking, swallowing, pronunciation, chewing, tongue position, fa­ a matched-pair analysis of survival. Arch Otolaryng Head Neck Surg 20 I 0; 136(7): 697-70 I .
- 2 1 . Olczak-Kowalczyk D et al. Oral mucosa lesions and gingival bleeding can indicate the
cial expression, hearing. It occurs as an isolated defect or as one of the symptoms of progression of liver disease in children and adolescents aged two to 18 years. Acta Paediatrica
genetic syndromes, such as in Treacher Collins syndrome and Pierre Robin syndrome . 2018.107(5): 8 86-892. - 22. O lczak-Kowalczyk D, G6rska R. Mucosa! diseases in children and
adolescents - Part X In: Wsp6kzesna stomatologia wieku rozwojowego; ed. Olczak-Kowalczyk
The etiology is not explained. Caring for a patient with a cleft requires many years of
D, Szczepa11ska J, Kaczmarek U. Wyd. Med Tour Press lnt, Otwock 2017; 623-665 - 23. Pinto
multi-specialist treatment. A et al. Pediatric Soft Tissue Oral Lesions. Dent Clin N Am 2014;58 :43 7-453 - 24. Reis H LB
Plicated tongue - a developmental defect of the superficial muscle of the tongue et al. Oral H PV Related Diseases: a Review and an Update. I n : Saxena, SK, editor. Trends in
I nfectious Diseases [ I nternet] . London: lntechOpen; 20 1 4 [cited 2022 Apr 23]. Available from:
manifested around the age of 4, manifested by numerous furrows and fissures on the https://www.intechopen.com/chapters/46324 doi: I 0.5772/57574. - 25. Rossmann JA. Reac­
dorsal and lateral surfaces of the tongue (a language similar to a leaf or the surface of tive Lesions of the Gingiva: Diagnosis and Treatment Options. The Open Pathology J, 201 1 ;
the brain). It can cause bad breath. It often co-exists w ith a geographical l anguage. It is 5 :23-32. - 26. Sreeja C et al. Oral pigmentation: A review. J Phann Bioallied Sci. 2015;7(Suppl
2): S403-408. doi: I 0.4103/0975-7406.163471. - 27. Scul ly C, Hodgson T. Recurrent oral ulcer­
observed ir11 healthy children, as well as in Down syndrome, M e lkersson-Rosenthal syn­ ation: aphthous-like ulcers in periodic syndromes. Oral Surg Oral Med Oral Pathol Oral Radio!
drome, chronic granulomatous disease and psoriasis. Endod. 2008; I 06(6):845-852. - 28. Scully C, Felix D H . Oral medicine - update for the general
practitioner. Red and pigmented lesions. Brit Dent .J 2005; 199( I 0): 639-645 . - 29. Tannure PN et
al. Prevalence of dental anomalies in non-syndromic individuals with cleft lip and palate: A sys­
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tematic review and met analysis. Cleft Palate Craniofac 20 1 2;49: 1 94-200.
I . Akpan A et al. Oral candidiasis. Postgrad Med J 2002;78 :455-459 - 2. Aki KF. Black tongue.
J Pediatr Child H ealth2009; 45( 1-2): 73-74. - 3 . Bilinska M, Osmola K. Cleft lip and palate -risk
factors, prenatal diagnosis and health consequences. Ginekol Pol 2015;86( 1 1) ; doi: I 0.17772/
gp/60371. - 4. Bardellini E et al. Non-specific oral and cutaneous manifestations of Coronavirus
Disease 2019 in children. M ed Oral Patol Oral Cir Bucal. 2021 ;26(5):e549-e553; doi: I 0.4317/
medoral.2446 1 . - 5. Cecconi D et al. Mucoceles of the oral cavity: A large case series (1994-2008)
and a literature review. Med Oral Pathol Oral Cir Bucal, 201 0; I 5(4):55 1 -556. - 6. Conceicao JG
et al. Oral mucoceles: A clinical, histopathological and immunohistochemical study. Acta Histo­
chemica 2014; 16: 40-47. - 7. Danser M M et al. Tongue coating and tongue brushing: a literature
review. lnt J Dent Hygiene 2003; I : 1 51-158. - 8. Durlik M . Tumours in renal transplant recipients
- the role of viral infections and immunosuppressive treatment. Post N M ed 2009; I 0: 827-33 . - 9.
Erthal A et al. Oral mucosa I diseases in children - casuistics from the Department of Dermatology
- University of Sao Paulo - Brazil. An Bras Dermatol. 20 1 6;9 l (6): 849-85 1 .
I 0. Furlanetto D LC et al. Differences in methods of measuring the prevalence of oral mucosa!
lesions in children and adolescents. I nternational Journal of Paediatric Dentistry 2006; 16:31-39. -
11. Gorska R. Diagnosis and treatment of oral mucosa I diseases. Med Tour Press l nt, Otwock 20 1 1.
- 12. Hong CHL et al. World Workshop on Oral Medicine V i l : Relative frequency of oral mucosa I
lesions in children, a scoping review. Oral Dis 20 l 9;25(51 ): 193-203. - 1 3 . Handley TP et al. Dys­
keratosis congenita. Oral Oncol 2006; 42, 4: 3 31-336. - 14. Hofer A et al. Collision of squamous-cell
carcinoma with melanoma in situ in a child with xeroderma pigmentosum. Dermatol 200 1 ; 203 :66-
69. - 1 5 . Krasuska-Slawinska et al. Benign tumours and oral lesions at risk of malignant transforma­
tion in children. Part one - clinical picture. New Stoma toI 20 I 0; 2:74-77 - 16. Kumaraswamy K L,
Vidhya M. Human papilloma virus and oral infections: an update. J Can Res Ther 201 1 ;7: 1 20-127.
- 17. Legeret C, Furlano R. Oral ulcers in children- a cli nical narrative Overview. Italian .J Pediatrics
202 1 ; 47: 144. doi.org/ I 0.1186/s13052-021-0 I 097-2. - I 8. Majorana A, et al. Oral mucosa I lesions
in children from O to 12 years old: ten years' experience. Oral Surg Oral Med Oral Pathol Oral Ra­
dio! Endod. 20 1 0 I I 0( l ): e l 3-8. doi: I 0.1016/j.tripleo.2010.02.025. - 1 9. Mohiuddin K, Priya NS,
Ravindra S, Mu1thy S. Peripheral ossifying fibroma. J Indian Soc Periodontol. 20 1 3 ; 1 7( 4):507-509.

3 84 385
 Gingival and periodontal diseases in developmental age

clinical examination is a regular part of the patient's dental examination. Diagnosis of

Chapter 28 periodontal disease requires a dental and general medical history, clinical and radio­
graphic assessment, often additional tests (blood count, microbiological tests).
Gingival and periodontal diseases in developmental age
Periodontal specificities in developmental age
Dorota Olczak-Kowalczyk The morphology of the periodontium depends on the developmental stage of the
dentition (the development of the periodontium is related to the eruption of teeth), the
type of dentition (different anatomy of deciduous and permanent teeth) and the occlu­
Periodontal tissue disease is a common health problem in children. Bleeding gums, sal-occlusal conditions during the different developmental stages of the dental arch (e.g.
indicative of inflammation, already occur in the youngest children. The incidence of gin­ spacing of the deciduous dentition, tooth replacement).
givitis increases with age. They are more frequently observed in those with permanent Periodontal features in the deciduous dentition:
dentition th�n in children with deciduous or mixed dentition with predominantly decidu­ - soft, flaccid, extensible gingiva (rich vascularisation, smaller number and less dif­
ous teeth (Fig. 28.1). In the general population of children and adolescents, periodontitis ferentiated collagen fibres that form a poorly ordered arrangement, low degree of
is very rare. epithelial keratinisation, thick, rounded free gingiva, gingival sulcus deeper than in
adults ( l .4-2.1 mm), interdental papillae low, rounded (low positioning of proximal
■ gingival bleeding ■ pocket depth � 4 mm
% surfaces), thicker j unctional epithelium, narrower attached gingiva (1-6 mm wide),
loss of connective tissue attachment
- cement, mainly primary, cell-free, covers the root of the tooth with a very thin layer,

_ _ _ _ _ _ _g--
"'

-------
0
"' r--' - periodontal ligament wider and better vascularized, contains fewer collagen fibres,
M O'l

which at the time of tooth eruption are arranged along its long axis (the final arrange­
ment is obtained after contact with the opposing tooth is achieved by the tooth),
bone is characterised by poor calcification , better vascularisation, fewer and thicker
bone beams and larger marrow cavities, a thin compact lamina, a flatter alveolar
- ■
3 years 5 years 7 years 12 years 15 years 18 years ridge,
during the dental period, the reaction of the gum tissue to the presence of dental
Fig. 28. 1 . Prevalence of gingivitis and periodontitis in children in Poland. biofilm is poor (lower permeability of gum tissues to bacterial antigens, including
thicker junctional epithelium, delayed vascular reaction, lower number of leuko­
Gingivitis is a reversible process. Untreated, persistent chronic gingivitis is a risk cytes, lgM and IgG).
factor for periodontitis. Early recognition and treatment of inflammation and elimination During the period of replacement of deciduous to permanent teeth, the following are
of causative factors should therefore be considered a prerequisite for the prevention of characteristic:
periodontitis in adolescence and adulthood. Severe gingivitis persisting despite topical different levels of the gingival margin (Fig. 28.2),
treatment and periodontitis in childhood indicates the presence of a systemic disease or - increasing width of the attached gingiva (takes shape between the ages of 6 and 1 2),
immunodeficiency. Therefore, monitoring the gingival and periodontal status of children - presence of deciduous teeth subject to exfoliation (increased mobility, root resorp-
and adolescents is part of general disease diagnosis and general medical care of the tion, deepening of the gingival sulcus - displacement of the epithelial attachment
patient. The assessment of the condition of the periodontal tissues during the routine under the resorbing surface),

386 387
Compendium of Paediatric Dentistry Gingival and periodontal diseases i n developmental age

deep gingival sulcus with erupting permanent teeth (depth in the area of the erup­ -cement joint (CEJ), the depth of the gingival sulcus in the area of completely erupted
ting permanent tooth can reach 2-8 mm), teeth within 0.5-3 mm, in adolescents the distance between the upper edge of the inter­
greater permeability of the junctional epithelium (presumably in children the junc­ dental septum and CEJ within 0.4-1.9 mm. The gingival condition is assessed at all ages
tional epithelium is derived from reduced enamel epithelium), using the gingival index (Gl) or bleeding index (described in Chapter 4). The presence
- greater physiological mobility of the erupting tooth compared to the mature tooth, of gingivitis is evidenced by bleeding on probing with gingival pocket depths :S 3 mm,
- on X-ray, greater than 2 mm distance between the upper edge of the interdental sep- no loss of connective tissue attachment, no bone loss on X-ray. The main symptoms of
tum and the enamel-cement junction (CEJ) in the area: periodontitis are loss of attachment and alveolar bone with the formation of periodontal
• deciduous tooth close to exfoliation, pockets. An assessment of the periodontium in patients aged 7 to 18 years and preventive
• a deciduous tooth adjacent to an exfoliating tooth, and therapeutic needs can be made using a modified index of the baseline periodontal
• erupting permanent tooth. examination (BPE) (Tab. 28.1 ). The assessment is carried out at six points around teeth
The formation of the periodontium does not take place until the development of the 1 6, 11, 26, 36, 31 , 46. In children under 1 2 years of age, only gingival bleeding is as­
teeth is completely completed, and the occlusal-occlusal conditions are stabilised. sessed (risk of false results when assessing the depth of gingival sulcus around perma­
nent erupting and newly erupted teeth). In the area of incisor teeth and first molars, the
risk decreases progressively until the age of 12, and in the area of second permanent
molars until the age of 1 7.

Tab. 28.1. The Simplified Basic Periodontal Examination - assessment criteria, scope of preven­
tive and therapeutic activities.

Code Clinical findings Treatment needs

Fig. 28.2. Comparison of gum morphology i n the period of deciduous teeth (on the left - thick,
0 healthy periodontal tissues -
rounded margi nal gum, short, rounded interdental papillae), mixed (in the middle - different
levels of the gingival margin, gingivitis around erupting teeth) and fixed (on the right - bleeding during probe exami-
I oral hygiene instruction and prevention,
triangular, high interdental papillae nation
instruction and prevention, scaling above and below
calculus or local factors favou-
During the period of mixed dentition, immune system functions reach adult-like 2 gumline, in selected places, removal of factors con-
ring plaque retention
ducive to dental plaque retention,
levels. The condition of periodontal tissues is also influenced by sex hormones (oestrogen
full periodontal examination (clinical and radiolo-
in girls and testosterone in boys). The earliest age at which physiological puberty can shallow pockets gical), as in code 2; after 3 months, more intensive
3
begin was considered to be year 8 for girls and year 9 for boys. (depth 4-5 mm) treatment with root cement smoothing may be indi-
cated,
Deep pockets
Diagnosis of periodontal disease and treatment management 4 as in code 3 and referral to a periodontist or chit-
(depth 2: 6 mm)
dren 's dentist
The assessment of the periodontal condition requires a general medical and dental * Furcation
history, a clinical examination and, if necessary, additional tests (radiology, microbiolo­
gy, blood count with smear). In the clinical examination of the periodontal condition, the Treatment should always include hygienic instruction (brushing and cleaning of
who 621 probe is used in pediatric dentistry (pressure force up to 20-25 g). The features approximate surfaces), anti-smoking education, elimination of local factors conducive
of a healthy periodontium in developmental age are considered to be a distance of se­ to the occurrence of periodontal disease, professional cleaning of teeth and indica­
veral millimetres between the gingival margin of the free gingiva and the enamel- tion of appropriate local anti-inflammatory and antimicrobial agents for use at home.

388 389
Compendium of Paediatric Dentistry Gingival and periodontal diseases in developmental age

Depending on your needs, treatment of general disease, antibiotic therapy, surgical, cilitate the accumulation of bacterial biofilm, e.g. The local occurrence of gingivitis due
periodontal, conservative and orthodontic treatment, as we] 1 as restoration of function to biofilm is aggravated by factors that make it difficult to clean the teeth and/or facili­
and aesthetics, may be required. tate the accumulation of biofilm, e.g. reduced saliva secretion (weakened self-cleaning
mechanism), crowded teeth, use of fixed orthodontic appliances, mouth-breathing, tooth
PERIODONTAL H EALTH, OTHER CONDITIONS AF­ shape abnormalities, enamel malformation, abnormal (overhanging) fillings, carious le­
GINGIVAL DISEASES AND PERIODONTITIS FECTING THE PERIODON­ sions, as well as the replacement of deciduous teeth with permanent teeth (Fig. 28.4).
CONDITIONS T IU M DISEASES
Gingivitis related to mouth-breathing affects the labial side of the gingiva in the anterior
aspect of the maxilla and mandible (Fig. 28.5). Stimulated saliva in mouth-breathers
I. Periodontal and gingival health: I . Necrotic periodontal diseases: I. systemic diseases or conditions affecting
a. clinical gingival health on an intact a. necrotizing gingivitis, the periodontal supporting tissu..-:s of the is thought to have higher levels of free sialic acid, which Favors a greater load on the
pcriodontium, b. nccrotising periodontitis, periodontium
b. clinical gingival health on a reduced c. nccrot ising stomatitis mouth by bacteria.
periodontium: 2 Other periodontal conditions:
- patient wi�1 stable pcriodontitis, .
2. Pcrioclontitis as a manifestation of systemic a. Periodontal abscesses,
- patient without pcriodontitis b. endodonlic-pcriodontal lesions
diseases
The classification of these conditions should be
based on the primary systemic disease, accor­ 3. Mucogingival deformations and conditions
2. Gingivitis: dental biofilm-induced: ding to the ICD code - International Statistical around teeth:
a. associated with dental biofllm alone, Classification of Diseases. a. gingival phenotype,
b. modified by systemic or local risk factors, !=============== b. gingival/son tissue recession,
c. drug-influenced gingival enlargement 3. Pcriodontitis: c. lack of gingiva,
a. Stages - based on severity .iml complexity of d. decreased vestibular depth,
management: e. aberrant frenulum/musele position,
stage I - initial periodontitis, r. gingival excess,
3. Gingival diseases: non-dental biofilm-in­
duced:
stage II - moderate periodontitis,
stage Ill - severe periodontitis
g. abnormal colour,
h. exposed root surface
Fig. 28.4. Gingivitis caused by dental
a genetic/developmental disorders,
.
with potential for additional tooth loss, biofi lm associated with xerostomia.
b. specific infections, stage IV - Severe periodontitis 4. Traumatic occlusal forces
c. inflammatory and immunological with potential for loss of the clentilion a. primary occlusal trauma,
conditions, b. extent and distribution: localized; gener­ b. secondary occlusal trauma,
d. reactive processes, alised, molars - incisor distribution c. orthodontic forces
e. neoplasms, c. grades: evidence or risk or rapid progression, Fig. 28.5. Gingivitis related to mouth
f. endocrine diseases, nutrition and metabolic anticipated treatment response
- grade A - slow rate of progression,
S. Tooth and prosthesis related factors
a. localized tooth-related factors,
breathing - characteristic redness of the
diseases,
g. traumatic lesions, - grade 13 - average rate of progression, b. localized dental prostheses-related gingiva, enlargement of the gingival
h. gingival pigmentation - grade C - rapid rate of progression !actors
papil lae and rolling of the gingiva in the
anterior sections of both dental arches
Fig. 28.3. Classification of periodontal diseases (20 1 7). and no inflammation in the lateral sec­
tions of the dental arches.
Gum disease
Systemic risk factors for gingivitis are nicotine (smoking cigarettes, e-cigarettes, wa­
Gingival diseases in children and adolescents are most often dental plaque-induced
ter pipes, etc.) and drug addiction, hyperglycaemia (decompensated diabetes, Fig. 28.6),
gingival diseases modified or not by local and/or general factors, less often it is gingival
malnutrition, medications (e.g. immune-suppressing drugs, causing reduced salivation),
enlargement caused by medication or diseases not caused by dental biofilm.
sex hormones (changes accompanying puberty, occurring during the menstrual cycle or
The clinical signs of gingivitis are redness, swelling and bleeding spontaneously or
pregnancy, oral contraceptives), blood diseases, e.g. leukaemia (mainly acute myeloid leu­
provoked (e.g. during tooth brushing). Accompanying symptoms can be taste disorders,
kaemia), neutropenia (Fig. 28.7, 28.8). A characteristic symptom of gingival inflammation
pain, halitosis and the presence of dental deposits. Bacteria associated with gingivitis in
caused by a dental biofilm modified by systemic factors is the presence of inflammatory
children include. A ctinomyces spp., Capnocytophaga spp. , Leptotrichia spp. and Sele­
lesions with relatively little plaque and the failure to resolve the inflammation after plaque
nomonas spp.
removal. When exposed to nicotine, the occurrence of clinical symptoms depends on the
Locally, the occurrence of gingivitis and exacerbation of the inflammation caused by
duration and severity of the addiction. They can therefore only occur in adulthood.
dental biofilm are favoured by factors that make it difficult to clean the teeth and/or fa-

390 39 1
Compendium of Paediatric Dentistry Gingival and periodontal diseases in developmental age

Fig. 28.6. Gingivitis in a patient with decompensated type I

local increase in angiogenic factors such as vascular endothelial growth factor,
diabetes mel litus (potential causes of gingivitis in childhood changes in the composition of the bacterial biofilm (creation of a niche for perio­
diabetes mellitus - decreased salivary secretion, impaired neu­ pathogens).
trophil function, stimulation of immune cells to release inflam­
matory cytokines, impaired collagen metabolism, increased Characteristic features of gingivitis associated with sex hormones are swollen inter­
collagenase activity, in long-term diabetes mellitus - vascular dental papillae, spontaneous bleeding and a tendency to granulation and fibrosis.
changes of the gingival stroma).
Nutritional disorders negatively affect mucosal integrity, immune mechanisms, salivary
gland function, saliva and gingival fluid composition. Gingivitis is promoted by obesity, pro­
tein-energy malnutrition, deficiencies of vitamins B, C, D and calcium, magnesium and zinc.

Gingival enlargements (gingival hyperplasia or hypertrophy)

Localised gingival enlargements are discussed in Chapter 27. Gingival enlargements
can result from:
Fig. 28.7. Condition of the gums in a patient with leukaemia - proliferation, inflammation, local factors causing chronic gingivitis due to dental biofilm (e.g. in braces wearers,
bleeding (potential causes: infiltration with aleukaemic cells and resulting haematological mouth-breathers, plasmocytic gingivitis),
disorders: thrombocytopenia, neutropenia); possibl e discoloration of the gums
systemic factors causing non-inflammatory lesions (gingival diseases not caused by
- from redness to a dark purple colour.
dental biofilm), including hormonal factors (angiogenesis), cancer (leukaemia, lym­
phoma), drugs, vitamin C deficiency, granulomatous diseases (e.g. Crohn 's disease,
Wegener's granulomatosis, sarcoidosis) or genetic factors, e.g. neurofibromatosis,
hyalinosis, hereditary gingival fibromatosis (HGF) (Fig. 28.9, 28.1 0).

Fig. 28.8. Gingivitis in a girl with congenital neutropenia; the cause of gingivitis is neutropenia
(absolute number of neutrophils below 1500/µI) primary (genetically determined) or secondary
(caused by environmental factors, e.g. drugs, viral infections, cancer, chemical exposure,
malnutrition, autoimmunity) and disorders of neutrophil function.

Increased levels of sex hormones can cause: Fig. 28.9. Gingival enlargement in a boy Fig. 28. 1 0. Hereditary gingival fibromatosis
with chronic granulomatous disease. (HGF) during the period of deciduous teeth.
expansion of vessels and increase of their permeability and reduction of gingival
keratinization, which results in decrease of the effectiveness of the epithelial barrier,
Plasma cell gingivitis (PCG) is the result of spilled and massive infiltration of sub­
reduced efficiency of phagocytosis and neutrophil-dependent bactericidal mecha­
epithelial connective tissue by plasma cells in response to antigens, often found in che­
msms,
wing gums, toothpastes, food products (e.g. flavourings and spices: chili, pepper, cloves,
effects on pro-inflammatory mediators, such as prostaglandin E2,
cardamom, cinnamon). It manifests as diffuse redness and enlargement of the gingiva
via endotoxin-stimulated monocytes,
with a sharp border along the mucogingivalj unction with a tendency to bleed (Fig. 28.1 1 ).
influx of leukocytes into the inflamed gingiva and formation of granulation tissue,

392 393
Compendium of Paediatric Dentistry Gingival and periodontal diseases in developmental age

Fig. 28. 1 1 . Plasma cell gingivitis con­

firmed by histopathological examination
in a 1 2-year-old female patient - red­
ness, gingival enlargement, s l i ght sur­
face granulation. Fig. 28. 1 3 . Examples of gingival diseases not caused by dental biofi l m , in order from right:
Stevens-Johnson syndrome , dystrophic epidermolysis bul losa, brown gingival pigmentation
in a patient w ith adrenal insufficiency.
Drug-influenced gingival overgrowth may be caused by taking immunosuppressive
Periodontal symptoms of systemic diseases and developmental and acquired

,
drugs (cyclosporine A, tacrolimus, sirolimus), antiepileptic drugs (phenytoin, pheno­
barbital, vigabatrin, ethotoin, mefentoin, lamotrigine, ethosuximide, topiramate, primi­ diseases
done), calcium channel blockers (nifedipine, felodipine, diltiazem, verapamil, amlo-
Periodontal abscesses in developmental age can result from mechanical trauma (e.g.
dipine, nitrendipine).
hard food, dental floss or orthodontic separators), morphological anomalies on the tooth
The first symptoms of drug-induced gingival overgrowth (enlargement of the inter­
surface (e.g. enamel pearls), damage to the root (fractures, perforations, external resorp­
dental papillae) appear approximately three months after the start of treatment. T he pro­
tion). Root damage can also be the cause of endodontic-periodontal lesions.
liferation then extends to the marginal gingiva and can result in complete coverage of the
Mucogingival deformities, including gingival recessions, are more common in
tooth crowns (Fig. 28. 1 2). It occurs more frequently in children and adolescents than in
adults. Predisposing factors for recession are a thin gingival phenotype (< 1 mm), poor
adult patients. It results from the proliferation of gingival fibroblasts and their stimula­
oral hygiene, the presence of tooth tissue defects in the gingival area, and malocclusion.
tion to form a connective tissue matrix, and probably from reduced collagen catabolism.
In children, gingival recessions may resolve spontaneously, so observation is indicated
in stable conditions. If possible, surgical treatment should be carried out after tooth de­
velopment is complete.

Periodontal diseases
Fig. 28. 1 2. Gingival overgrowth i n The current classification of periodontal conditions distinguishes periodontitis (pre­
a patient with nephrotic syndrome
treated with cyclosporine A.
viously differentiated between aggressive and chronic periodontitis), necrotising peri­
odontal disease and periodontitis as a symptom of systemic disease.
Periodontal necrotic diseases are associated with infection with anaerobic
T he causes of gingival diseases not caused by dental biofilm in children and ado­
Gram-negative bacteria (spirochetes and spindles). Symptoms inclu.de pain, fever, ade­
lescents are also specific bacterial, viral (e.g. primary herpes gingivitis) and fungal (e.g.
nopathy, excessive salivation, ulceration or necrosis of interdental papillae covered with
candidiasis) infections, allergies, autoimmunity, mucocutaneous diseases, metabolic and
whitish-grey plaque, a tendency to spontaneous gingival bleeding, pseudo membrane
hormonal disorders, gum pigment changes (e.g. amalgam tattoo), traumatic damage (e.g.
formation and halitosis (Fig. 28.14). They can lead to bone sequestration. They occur
mechanical, chemical, thermal) (Fig. 28.13).
in people with immune deficiencies. They are characterised by rapid progression of the
disease process.

394 395
Compendium of Paediatric Dentistry Gingival and periodontal diseases in developmental age

hypoplasia of the root cementum and abnormal bonding of the tooth root to bone
(odonto-hypophosphatasia affects only the teeth and periodontium).
Changes in the periodontal tissues accompanying general disease often become ap­
parent soon after the eruption of deciduous teeth. In neutropenia or neutrophil dysfunc­
tion are observed even in children aged 2-3 years. They can be localised - with pro­
gressive periodontal destruction and little gingival inflammatory reaction in the affected
Fig. 28. 1 4. Necrotizing gingiv itis in a girl a fter a liver transplant (erythema, swelling of the
gums, necrosis of the gingival papillae, bleeding). areas, or generalised - with progressive periodontal destruction around most teeth and
clinically visible gingivitis (Fig. 28. 1 5, 28.16). Characteristic changes in severe neutro­
Periodontitis rarely occurs in childhood, but the onset of the disease can occur in penia are painful ulcers of the oral mucosa (so-called agranulocytic ulcers), which heal
childhood. In children, so-called "localised aggressive periodontitis" now classified as with leaving a scar.
stage III periotlontitis grade C has been described. It can already appear in deciduous
teeth. It occurs in the family. It is characterised by very rapid alveolar bone loss usually
localised (molar and incisal area) or generalised. In children and adolescents, periodon­
titis most often occurs in the course of general diseases. Periodontal destructions can be: Fig. 28.15. Gingivitis in area of per­
inflammatory: manent and deciduous teeth, peri­
• severe congenital neutropenia (blood neutrophil count 0-600hd), odontal inflammatory destruction
around deciduous teeth in a girl with
• cyclic neutropenia (reduction in neutrophil count below 200/µl every 2-4 weeks, severe neutropenia.
lasting 3-6 days),
• Chediak-Higashi syndrome (moderate to severe neutropenia),
• glycogenosis type lb (glycogen storage disorder - glucose-6-phosphate translo­
case deficiency, causing hyperlactatemia and hypoglycaemia; moderate, severe
neutropenia, neutrophil and platelet dysfunction, anaemia),
• Down syndrome (impaired function of T and B lymphocytes, NK cells, chemo­
taxis of neutrophils and monocytes and oxidative metabolism; type V I collagen
Fig. 28. 1 6. Gingivitis and periodontal destruction in permanent dentition
disorders, excessive gingival innervation, impaired fibroblast migration), in a boy with agranulocytosis.
• leukocyte adhesion deficiency syndrome types I, II, I I I (impaired adhesion to
vessel walls and neutrophil chemotaxis, in type III - impaired platelet function), Papillon-Lefevre syndrome - rapid progression of periodontal destruction occur­
• Papillon-Lefevre syndrome (impaired neutrophil function - chemotaxis and ring in a short time after the removal of deciduous and permanent teeth, loss of teeth in
phagocytosis); the order of their eruption; gingivitis and foetus ex ore may occur.
non-inflammatory: Histiocytosis X - gingivitis with a tendency to ulceration and granulation, progres­
• histiocytosis X (growth and accumulation of Langerhans cells), sive destruction of the alveolar process bone, which resembles advanced periodontal
• Ehlers-Danlos syndrome (type III or type I collagen disorders), disease and leads to tooth loss; bone resorption causes a characteristic radiological image
• hypophosphatasia (deficiency in the amount and activity of alkal ine phosphatase of "teeth floating in the air" (Fig. 28.17).
leading to abnormal mineralisation of bone and tooth tissue, including aplasia or

396 397
Compendium of Paediatric Dentistry Gingival and periodontal diseases in developmental age

I 0. Lang N P et al. Gingivitis as a risk factor in periodontal disease. J Clin Periodontol 2009;
36 (Suppl. 1 0): 3-8. doi : 1 0. I J I l /j. 1 600-05 I X.2009.0 1 4 1 5 .x. - 1 1 . Mathieu M et al. Necrotizing
Periodontal Diseases in Children: A Literature Review and Adjustment of Treatment, J Trop Ped
20 1 6 ; 62(4): 3 3 1 -337. - 1 2. Matosek- Rutkowska A et al. Manifestation of Langerhans cell histio­
Fig. 28. 1 7. 1-1 istiocytosis X cytosis in the oral cavity. Posti,py 1-1 ig i Med Dosw 202 1 ;75( I ):933-938. https://doi .org/ 1 0.2478/
- periodontal destruction ahem-202 1 -0006 - 1 3 . Oh T.J et al. Periodontal diseases in the child and adolescent. J Clin Peri­
around deciduous teeth. odontol 2002; 29: 400-4 1 0. - 1 4. Olczak-Kowalczyk D. Monitoring the oral health status of the
�olish population 20 1 6-2020. Carious disease and periodontal tissue status of the Polish popula­
tion. Summary of research results from 20 1 6-20 1 9 Department of Editing and Publishing WUM,
Ehlers-Danlos syndrome - bleeding gums, then the rapid progression of periodontal 202 l l SBN-978-83-763 7-448-2. - 1 5 . Olczak-Kowalczyk D. Monitoring the oral health status of
destruction (periodontal changes may occur in the deciduous teeth), traumatic damage the Polish population 20 1 6-2020. Determi nants of oral health status and traumatic damage to
teeth in children and adolescents in Poland in 2020. WUM Editorial and Publishing D epartment,
to the mucous membrane.

'
202 1 . - 1 6. Olczak-Kowalczyk D et al. Cigarette smoking as an oral health risk behavior in ado­
Hypophosphatasia - premature loss of deciduous teeth with roots without resorp­ lescents: a cross-sectional study among Polish youths. Anthropol Rev 2020; 83( 1 ): 5 3-64. - 1 7.
tion features and the presence of granulomatous lesions in the area of lost teeth (often the Olczak-Kowalczyk D et al. Candida spp. and gingivitis in chi ldren with nephrotic syndrome or
type 1 diabetes. BMC Oral Health 20 1 5; 1 5, 57. doi.org/ l 0. 1 1 86/s l2903-0 1 5-0042-6. - 1 8. Pari A
first visible symptom of the disease). et al. G i ngival Diseases in Childhood. Journal of Clinical and Diagnostic Research. 20 1 4; 8 ( 1 0):
Periodontitis in developmental age is usually indicative of the presence of a systemic ZE0 1 -ZE0. - J 9. Piekoszewska-Zii,tek P, Olczak-Kowalczyk D, Panczyk-Tomaszewska M et al.
Developmental Abnormalities of Teeth in Children With Nephrotic Syndrome. lnt Dent J 2022;
medical problem. During the deciduous period, symptoms of systemic disease include
doi : 1 0. 1 0 1 6/j . i dentj .202 1 . 1 1 .0 1 4.
loosening of teeth, premature tooth loss, increased gingivitis and gingival proliferation. 20. Spodzieja K, Olczak-Kowalczyk D. Premature Loss of Deciduous Teeth as a Symptom of
Premature loss of deciduous teeth is seen in Papillon-Lefevre syndrome, mucocuta­ Systemic Disease: A N arrative Literature Review. lnt. J. Environ. Res. Public H ealth 2022, 1 9(6),
3 3 86; doi .org/1 0.3390/ijerph I 90633 86.
neous dyskeratosis, Coffin-Lowry syndrome, congenital adrenal hyperplasia, Langer­
hans cell histiocytosis, cherubism, hypophosphatasia, acatalasia, Chediak-Higashi syn­
drome, cyclic neutropenia, erythromelalgia, Down syndrome, Hajdu-Cheney syndrome,
short bowel syndrome, leukocyte adhesion deficiency type 1 and Wiedemann-Steiner
syndrome.

References
I . American Academy of Pediatric Dentistry. Classification of periodontal diseases in infants,
children, adolescents, and individuals with special health care needs. The Reference Manual of
Pediatric Dentistry. Chicago, Ill. A merican Academy of Pediatric Dentistry; 202 1 :435-49. - 2 .
American Academy o f Periodontal and European Federation o f Periodontology. J Periodontal
20 l 8 ;89(Supp I ):S l -S8. John Wiley and Sons. Available at: https://aap.onlinelibrary.wiley.com/
doi/full/ 1 0. 1 002/JPER. 1 8-0 1 5 7. - 3 . Beaumont J et al. Gingival overgrowth Part I : aetiology and
clinical diagnosis. Br Dent J 20 1 7; 222:85-9 1 - 4. Cerehugh V, Tugnai A. Diagnosis and manage­
ment of periodontal diseases in chi ldren and adolescents Periodontology 2000, 200 I ;26: 1 46- 1 68 .
- 5 . G6rska R . Periodontal diseases. PZWL, Warsaw 20 1 7, I S B N : 978-83-200-5646-4. - 6. Giincli
GN et al. Effects of endogenous sex hormones on the periodontium - Review of literature. Aust
Dent J 2005 ;50:(3): 1 3 8- 1 45 . - 7. Halai 1-1, Somani C, Donos N et al. Clinical manifestations o f
chi ldren with COV I D- 1 9 : A systematic review. C l i n Oral Invest 24, 1 939- 1 95 1 (2020). https://doi.
org/ 1 0. 1 007/s00784-0 1 9-03055-z. - 8. Joshi C, Shukla P. Plasma cel l gingivitis. J Indian Soc Peri­
odontol 20 1 5 ; 1 9(2):22 1 -223 . - 9. Janam P, Nayar BR, Mohan R, Suchitra A. Plasma cell gingivi­
tis associated with che i l itis: A diagnostic di lemma! J Indian Soc Periodontal. 20 1 2 ; 1 6( I ) : 1 1 5- 1 1 9.

398 399
 Dental abscesses - pharmacological and surgical treatment

on the other hand, usually gives signs and/or symptoms, including pain and swelling. An
Part VII
acute (symptomatic) process may develop without prior chronic inflammation or may be
the result of an exacerbation of a previously chronic, asymptomatic lesion.
Odontogenic infections in the childchood Odontogenic infections pass through three key stages: stage I ( 1-3 days) - soft and
gentle swelling, stage II (2-5 days) - hard, red and very painful swelling, stage III (5-7
days) - the formation of an abscess.
Chapter 29 The main symptoms are pain, swelling and erythema. If the primary source of in­
fection is not eliminated, the inflammatory process can progress and lead to serious
complications (both local and systemic). Odontogenic infections in children are a com­
Dental abscesses - pharmacological and surgical treatment mon cause of seeking medical help. Although severe clinical cases are relatively rare,
life-threatening complications have been described in children. The therapeutic approach
Anna Turska-Szybka
depends on various factors, including the source and severity of the infection. The prima­
ry source of infection must be eliminated. It has been shown that rapid tooth extraction is
beneficial in most cases. W hile most children presenting with an odontogenic infection
In most cases, the stages of infection of odontogenic origin can be summarised as fol­
can be prescribed an oral antibiotic and the necessary interventions can be carried out at a
lows: stage of initiation of odontogenic infection by caries and subsequent pulp necrosis
later stage, patients suffering from severe infections, including severe swelling, cellulitis
extending to the apical region of the tooth or periodontal disease, penetration of the infec­
or abscess formation require immediate treatment (surgical incision and drainage under
tion into the bone marrow with subsequent production of purulent secretion. The pus then
local or general anaesthesia to remove accumulated pus). Antibiotic therapy is not a sub­
follows the path of least resistance, puncturing the cortical bone where the alveolar bone
stitute for surgical debridement or drainage and should be used as an adjunctive therapy.
is weakest and appears as a facial swelling, followed by the spread of purulent discharge
Maintaining airway patency during abscess drainage is a sine qua non condition. Starting
along the fascia] planes with the resulting possible sequelae, which can be fatal. The loca­
antimicrobial treatment soon after diagnosis and before surgery shortens the period of
tion of the affected tooth makes it possible to predict the route of spread of the infection
infection and minimises associated risks, such as bacteraemia.
and which fascia! spaces will eventually become infected. Infections usually start from the
Signs and symptoms vary greatly depending on the stage or degree of infection.
primary fascia! spaces and may then extend to secondary spaces and extra-dental areas.
A patient with an acute abscess presents with mild to severe pain and swelling. Trismus
The terms dental abscess, periodontal abscess, and odontogenic abscess are often
may occur. Systemic symptoms such as fever, lymph node enlargement, malaise, headache
used synonymously to describe abscesses formed in the tissues around the tooth. T he
and nausea may also occur. As the acute reaction to infection can develop very quickly, the
cause may be a dental infection (acute periapical abscess) or a periodontal infection
infected tooth may not show radiographic signs of periapical lesions. W hen a periapical
(periodontal abscess and periapical inflammation). Odontogenic infection of an
lesion (foci of translucency near the root apex) is visualised radiographically, the abscess
endodontic origin, develops only in the root canals of teeth without vital pulp. This
is usually the result of an exacerbation of a previous chronic asymptomatic condition. In
may be due to necrosis of the tooth pulp following caries or trauma, or removal of pulp
most cases, the tooth is very sensitive to percussion. CNS (central nervous system) symp­
tissue during previous root canal treatment. Once infected in the root canal, bacteria can
toms may also occur, e.g. reduced level of consciousness, headache or abnormal ocular
enter the periapical tissues through the apical and lateral foramen or root perforation
symptoms such as proptosis (exophthalmos), pupil dilation (mydriasis), diplopia (double
and cause a chronic or acute inflammatory response. The chronic reaction is usually
vision). The affected spaces may have accompanied oro-facial swelling due to abscess
asymptomatic and almost always leads to bone resorption around the root apex, which
or cellulitis, which usually varies in warmth, with a shiny surface or discharge from the
is the typical radiological feature of apical periodontitis. Acute periapical inflammation,

400 401
Compendium of Paediatric Dentistry Dental abscesses - pharmacological and surgical treatment

maxillary sinus. Patients will look ill and may quickly develop dysphagia and respiratory Treatment of periodontal abscesses should be based on three principles: early
distress. In severe cases, skin necrosis can occur. Without any intervention, fascia! infec­ diagnosis, removal of the cause of infection, local drainage and debridement.
tions can progress to necrotising fasciitis, mediastinitis, sepsis and ultimately death. The majority of odontogenic infections in deciduous or young permanent teeth are
The spread of infections to the fascia I spaces of the head and neck is conditioned by managed locally with pulp disease treatment, extraction to remove the source of infection
the position of the apex of the tooth affected by the infection in relation to the cortical or incision of the abscess and drainage. In some cases, drainage can be obtained through
buccal or lingual lamina, the thickness of the bone lying above it and the ratio of the the root canal, but if swelling is present, an incision should also be made for drainage
apex to the muscle attachment. If the infection affects the sublingual and submandibular whenever possible, as this procedure has been shown to produce faster improvement
spaces bilaterally, a condition known as Ludwig's angina is diagnosed. The swelling than drainage by opening the root canal only. However, if the abscess is more extensive
caused by Ludwig's angina can cause breathing difficulties and potentially fatal airway (involving adjacent areas, the vestibule bottom or other facial regions, or affecting
obstruction. Another example of abscess complications is infection of the middle part of the patient's general appearance) and the infection presents with systemic symptoms
the face, whicl\can be very dangerous and lead to cavernous sinus thrombosis. It is also a (e.g. raised temperature, facial cellulitis, difficulty breathing or swallowing, fatigue,
life-threatening infection, in which a thrombus formed in the cavernous sinus is released nausea), topical treatment should be supplemented with antibiotic therapy to limit the
and leads to the spread of infection. expansion of the infectious process. If topical treatment is not carried out correctly and
Other described complications of dental infections include: brain abscess, sepsis in a only antibiotics are prescribed, the virulence process decreases. Consequently, once the
patient with multiple myeloma, deep neck infection, mediastinitis, necrotising fasciitis, medication is discontinued, the disease is exacerbated again. Pain medication may be
orbital abscess and cervical spinal arthritis with epidural abscess. These conditions can be prescribed to control pain.
life-threatening and may require immediate hospitalisation with intravenous antibiotics, Selected cases in which antibiotics are indicated for acute periodontal abscesses
incision and drainage, and referral and consultation with an oral and maxillofacial include: abscesses associated with poor systemic condition including fever, malaise and
surgeon. lymphadenopathy; disseminated infections resulting in cellulitis, progressive extensive
It has been suggested that certain patient-related factors may contribute to the increased oedema and/or trismus and abscesses in patients in severe clinical condition who are at
morbidity and mortality associated with acute odontogenic abscesses, such as. diabetes increased risk of secondary (focal) infection following bacteraemia (Tab. 29. 1 ). There­
mellitus, HIV, measles, chronic malaria, tuberculosis, hyper- and hypothyroidism, fore, in complicated cases, it is highly recommended to start empirical antibiotic ther­
liver disease, renal failure, heart failure, blood disease, anaemia, sickle cell anaemia, apy in addition to rapid and aggressive surgical drainage. If necessary, it can be adjust­
radiation, corticosteroid therapy, cytotoxic drugs, excessive antibiotics, malnutrition, ed according to the results of antibiotic susceptibility tests. The combination of early
allergic reactions. diagnosis, initiation of empirical antibiotic therapy and rapid surgical intervention
Reasons for hospitalisation of a child or adolescent with odontogenic cellulitis: can be considered a decisive triad in the effective treatment of acute periodontal
general disorders and/or reduced immunity of the patient (diabetes mellitus, malnu­ abscess complications.
trition, HIV, etc.),
Tab. 29.1. Indications for antibiotic therapy (according to AAPD).
rapidly progressive cellulitis,
inflammation of the connective tissue extending into the deep spaces of the face, Indications for antibiotic therapy No indication of antibiotic therapy
fever above 38° C, shortness of breath and/or dysphagia and/or severe trismus limi­ I . Fever within the last 24 hours - indicates I . Pain - analgesics, anti-inflammatory
a systemic response to infection. drugs are indicated.
ting mouth opening to less than 10 mm,
2. Systemi c symptoms: malaise, fatigue, weak- 2. Swel l i ng - indicated anti-inflammatory
- the patient or his/her family are unable to comply with the prescribed treatment, ness, dizziness, rapid breathing and local drugs.
failure of initial treatment. lymphadenopathy - indicate impending sepsis.

402 403
Compendium of Paediatric Dentistry Dental abscesses - pharmacological and surgical treatment

3. Redness, heat - indicated anti-inflam-

necessary to achieve optimal antimicrobial activity, due to the extension of the spectrum
3. Trismus - indicates involvement of the
perimandibular spaces and may extend into matory drugs. of action against penicillin-resistant strains. However, a higher incidence of gastrointes­
secondary spaces, which may be potentially tinal side effects and diarrhoea was reported in association with clindamycin treatment
dangerous. Trismus also complicates intraoral
procedures, which must wait until the trismus
(Tab. 29.2).
subsides. Tab. 29.2. Antibiotics commonly used in paediatric dentistry. Selection and dosage for patients
4. As prophylaxis in patients with systemic dis- 4. Pus - resolves a fter purulent drainage. with and without penicillin hypersensitivity.
eases, e.g. rheumatic heart disease, endocardi-
tis, heart or orthopaedic prosthesis. Dosage in children Dosage in
Clinical
5. In immunocompromised patients - A I DS, 5. Localized abscess (e.g. socket absces- situation
Antibiotic and adolescents up to adolescents
cancer, autoimmune diseases, corticosteroid ses, periodontal abscesses) - disappears 14 years > 14 years
therapy, patients with immunocompromising after incision and drainage. First choice.
50 mg/kg b.w. (40 mg to 90 750 mg to 3 g of
diseases, e.g. cyclic neutropenia, pancytopenia, No allergy to
mg/kg b.w.).; amoxicillin per
uncontrolled diabetes. penicillins, pos- Amoxicillin
2-3 divided doses; day, in 2-3 divided
6. After transplantation, solid organ transplants 6. Sinus duct drainage (removal of the sibility of o ral
not exceed 100 mg/kg/day doses
(heart, kidney, bone marrow, l iver, bones). foci of infection causes the drainage administration
to subside and the sinus duct may heal Clindamycin 8-25 mg per kg b.w. per
itself or it may be necessary to surgical- day, in 3-4 divided doses;
ly excise it). in children weighing < 10 600-1800 mg per
ln case of allergy
kg - 37.5 mg of the drug day, in 3-4 divided
The most commonly used antibiotics are �-lactam antibiotics (penicillins, penicillins to penicillins
(2.5 ml of syrup) 3x/day; doses
with a �-lactamase inhibitor, cephalosporins - usually 2nd generation, bactams, penems), Azithromycin 1 5 mg/kg b.w.
Clarithromycin 15 mg/kg b.w.
clindamycin (an antibiotic of the lincosamide group) and metronidazole. In clinical prac­
tice, the choice of antibiotics is either empirical or based on the results of microbial In children and adolescents, it is necessary to decide on the form and method of
susceptibility testing. For diseases with a known microbiological cause, for which a administration of the drug (in young children, usually by parenteral route) and to de­
plausible microbiota has been established in the literature, empirical therapy can be used. termine the optimal dose per kilogram of body weight. In order to achieve an optimal
This is especially the case for acute dental abscesses, as the results of antibiotic suscepti­ concentration of the antibiotic in the blood, it is important to determine the frequency of
bility testing of anaerobic bacteria by culture can be too time-consuming (approximately administration of the drug. An analysis of side effects, including allergies, should also be
7-1 4 days). It is therefore better to choose an antibiotic whose spectrum of action covers carried out, as well as the possibility of interaction with other drugs. The ideal duration
the most commonly detected bacteria. Most species of bacteria that cause infections, of antibiotic therapy is one that will prevent clinical and microbiological recurrence and
including abscesses, are sensitive to penicillins. This makes these drugs the first choice is between 5 and 10 days. Treatment should be continued 3 to 4 days after the resolution
for the treatment of tooth infections when the patient's allergy to penicillins is excluded. of clinical symptoms. If there is no response to the antibiotic, a change of drug should be
Penicillin V or amoxicillin are commonly prescribed. As the use of antibiotics is limited made no sooner than 24-48 hours after the first dose.
to severe and complicated abscess infections, the use of amoxicillin, a semisynthetic
penicillin with a broader antimicrobial spectrum than penicillin V, seems reasonable. In References
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20 1 6 Mar 31. PM I D: 28855834; PM C I D : PMC5562470. - 2. Alsheneifi T, Hughes CV. Reasons
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gery and oral pathology. The Reference Manual of Pediatric Dentistry. Chicago, Ill.: Amer Acad Chapter 30
Pediatr Dent; 202 1 :450-60. - 4. American Academy of Pediatric Dentistry. Useful Medications
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S, K aur A, Ghanghas P. A review of complications of odontogenic infections. Natl J Maxillofac
Surg 20 1 5 ;6: 136-43. - 6. Bertossi D, Barone A, l urlaro A, Marconcini S, De Santis D, F inotti M , Extractions of deciduous teeth - indications,
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contraindications, technique, complications
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Science and Research (lJSR) (20 1 9) . https://www. ijsr.net/archive/v8i l /A RT20194158.pdf. - 8. Anna Turska-Szybka
Dar-Odeh N , Fadel HT, Abu-Hammad S, Abdeljawad R, Abu-Hammad OA. Antibiotic Prescrib­
ing for Orn-Facial I nfections in the Paediatric Outpatient: A Review. Antibiotics (Basel). 20 1 8
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Dar-Odeh N , Fadel HT, Abu-Hammad S, Abdeljawad R, Abu-Hammad OA. Antibiotic Prescrib­ Exodontia, or tooth extraction, is the painless removal of an entire tooth or tooth root,
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with minimal trauma to the surrounding tissues so that the bone heals without disruption.
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1 0 . Flyn n T. Principles of management of odontogenic infections. In Miloro M , Ghali G E, The removal of deciduous teeth is a relatively important part of paediatric dentistry, often
Larsen P, Waite P (eds) Peterson s principles of oral and maxillofacial surgery. 3"' ed. Beij ing: associated with a complication of caries treatment, trauma and for orthodontic reasons.
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edraurban.pl/ssl/book-sample-file/chirurgia-stomatologiczna/pdf/chirurgia_stornatologiczna.pdf. tive restoration of the tooth is difficult or impossible, and all the consequences resulting
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e.g. teeth in extrusion, if they cannot be intruded orthodontically, or when a tooth in ex­
464-470. trusion causes a mucous membrane to bite in an opposite arch.
Retained deciduous teeth - which are preserved after reaching the age of eruption.
Teeth retained in the jaw and causing discomfort to the patient or identified acciden­
tally and initiating pathological changes within the bone.
Pathology-related teeth - involved in cyst formation and associated with other pa­
thologies such as tumours, osteomyelitis, or cancers.
Injury - teeth that have been broken as a result of an acute injury and cannot be
preserved.

406 407
Compendium of Paediatric Dentistry Extractions of deciduous teeth - indications, contraindications, technique, complications

A tooth in a fracture fissure when it is an obstacle to the repositioning and proper Temporary general contraindications to tooth extraction in children:
fusion of broken bone fragments, as well as when it hinders healing and poses a risk of I . neurological disorders such as stroke and epilepsy,
infection in the fracture area; horizontal and vertical fractures of the tooth root when 2. pulmonary disorders such as bronchial asthma, tuberculosis, pulmonary effusion,
there is no possibility of treatment. 3. cardiovascular disorders such as hypertension, cardiomyopathy, valvular disorders,
Congenital tooth (erupted before birth) or neonatal tooth (erupted usually within a rheumatic heart disease, ischaemic heart disease and chronic heart failure,
month after birth) - consider removal if the tooth is mobile and likely to aspire or is a source 4. liver disorders such as acute l iver infections and cirrhosis,
of mechanical i1Titation, causing ulceration on the abdominal surface of the tongue or wart, 5. renal disorders such as glomerulonephritis, uraemia and chronic renal failure,
interfering with breastfeeding. A congenital or neonatal tooth may be a supernumerary tooth. 6. metabolic disorders such as diabetes, thyrotoxicosis, Addison's disease, myxoedema
Supernumerary teeth - can be incorrectly positioned or retained; they cause maloc­ and long-term corticosteroid therapy,
clusion, pain, periodontal disorders, pathologies, and sometimes also disrupt aesthetics. 7. haematological disorders such as severe anaemia, leukopenia, thrombocytopenia,
Exfoliation,- a tooth to be removed due to its mobility and root/root resorption; the pancytopenia, haemophi lia, leukaemia, agranulocytosis, patients taking anticoagu­
tooth has survived. lants and bleeding and blood clotting disorders,
Broken roots of deciduous teeth - the presence of the root apex should not be taken 8. immunocompromised patients,
as an indication for its removal. When the fragment of remaining root is small and stuck 9. acute systemic infections: rheumatic fever,
deep in the alveolus or when attempts to remove it have been unsuccessful, it can be left 10. irradiated bone - tooth removal should be avoided; if extraction is necessary, it
for observation. It is often resorbed or spontaneously excreted. should be carried out before radiotherapy. Osteoradionecrosis usually develops after
tooth extraction in an irradiated patient.
General medical reasons
Radiotherapy of the head and neck area - tooth extraction showing symptoms of Local contraindications:
pulp and/or periodontal disease in patients undergoing radiotherapy of the head and neck l. Acute periodontitis, mainly Acute Necrotizing Ulcerative Gingivitis (ANU, should
is indicated due to metabolic changes and weakened perfusion of tissues under radiation be treated as an absolute contraindication to tooth extraction. In other acute oral
therapy, which limits the effectiveness of drugs in a given area (e.g. anti-inflammatory infections, tooth extraction is contraindicated until the infection is eliminated. In the
drugs or antibiotics). Extractions after radiotherapy are at risk of osteoradionecrosis. case of odontogenic abscesses, tooth extraction may be indicated ( often at the same
Bisphosphonate therapy: these drugs cause metabolic changes in the bone and re­ time as antibiotic therapy) when there is a risk of infection spreading.
duce its perfusion. These factors increase the risk of osteonecrosis as a result of proce­ 2. Stomatitis and acute inflammation of the oral mucosa, e.g. viral infections ( e.g.
dures involving interference with bone structure and its exposure to bacteria present in herpesviruses, acute herpes stomatitis).
the oral cavity. Teeth with marginal or periapical periodontal lesions should be removed 3. Tooth embedded in a tumour, malignant hyperplasia, or haemangioma, or in its
prior to bisphosphonate therapy. vicinity - the extraction of such a tooth must be treated as an absolute contraindica­
Balancing extraction is the removal of a tooth from the opposite side of the same tion.
dental arch, in order to minimize the midline shift. Compensating extraction - from 4. Tooth in the area of the irradiated jawbone - the irradiated jaw is highly avascular;
the opposite quadrant to the forced one is aimed at minimizing occlusive interference extraction of the tooth in the irradiated area should be carried out with extreme cau­
by enabling the preservation of occlusive relationships during tooth removal. Serial ex­ tion due to the higher risk of infection and osteoradionecrosis.
tractions - during the mixed dentition period, several deciduous teeth are removed in 5. Tooth with acute infection, acute pericoronitis inflammation of the partially re­
order to avoid malocclusion in permanent dentition as the child grows. tained tooth and/or tooth abscess - extraction after the inflammation has subsided.

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Compendium of Paediatric Dentistry Extractions of deciduous teeth - indications, contraindications, technique, complications

If the tooth is associated with acute in fectious pathology, there is a risk of infection Mandibular molars
spreading leading even to bacteraemia. In this situation, the tooth must be extracted Deciduous molars have roots with a smaller diameter and more divergent than perma­
under appropriate antibiotic prophylaxis. In addition to antibiotics, local means for nent molars. Root fracture in deciduous molars is not uncommon due to these features,
drainage or decomposition should be used, which relieves pain and discomfort of the as well as potential root weakness caused by the eruption of their pennanent successors.
patient. Before extraction, the root ratio of the deciduous tooth to the developing permanent
Considering the chronology of tooth eruption, there are differences between age tooth should be assessed. To prevent unintentional extraction, displacement or trauma
groups in terms of the type of teeth extracted. I n young children (aged 3 to 5 years), to the permanent tooth, pressure in the furcation area should be avoided, and the tooth
incisor teeth are most commonly extracted, according to the caries pattern (ECC) and may need to be cut to protect the developing permanent tooth. Extractions of molars are
following dental trauma. In older children, lateral teeth are more frequently extracted carried out using slow, continuous palatal/lingual and buccal pressure to allow expansion
due to the chronology of eruption and exfoliation and the frequent occurrence of caries of the alveolar bone to accommodate the divergent roots and reduce the risk of root frac­
of these teeth i� school-age children. ture. During the extraction of mandibular molars, attention should be paid to the support
Prior to extraction, a radiograph of the periapical region should be taken to assess of the mandible to protect the temporomandibular joints from trauma.
the position, presence or absence of a permanent tooth attachment and informed consent
should be obtained. The length of unresorbed roots after extraction of a deciduous tooth Management of unerupted and impacted teeth
may come as a surprise to the parent (carer). The use of a pre-extraction radiograph and/ There is a wide clinical spectrum of eruptive disorders of deciduous teeth. These
or the use of a mixed dentition typodont are good methods to show root length before can be syndromic or non-syndromic and include ankylosis, secondary retention, tooth
extraction (Fig. 30.1 ). retention or primary non-eruption. Clinically, it can be difficult to distinguish between
individual disorders.

Supernumerary teeth
Supernumerary teeth are 10 times more common in the maxilla than in the mandible,
about 90% in the maxilla with a strong predilection for the anterior region. The most
common site is the midline of the maxilla (mesiodens). Early diagnosis and timely treat­
Fig. 30. 1 . Typodont of mixed denti­
tion to show the length of the roots ment are important in preventing and avoiding these complications. As only 25% of all
of the deciduous dentition. mesiodens spontaneously erupt, surgical treatment is often necessary. A mesiodens that
is conical in shape and not inverted is more likely to erupt than a mesiodens that is tubu­
Extraction of erupted teeth lar in shape and inverted. The surgical procedure depends on the size, shape and number
of supernumerary teeth and the development of the patient's dentition. Removal of de­
Front teeth of the maxilla and mandible ciduous mesiodens is not usually recommended, as surgical intervention may disrupt or
Most incisors and canines have single, conical roots. In most cases, anterior tooth damage the developing permanent teeth. The deciduous mesiodens are usually left until
extraction is performed in a rotating motion. However, cases of accessory roots in deci­ the eruption of the permanent dentition. Extraction of unerupted deciduous mesiodens
duous canines have been reported. Radiographic examination before extraction is help­ is recommended during the period of mixed dentition to allow the normal eruptive force
ful in identifying differences in root anatomy. Care should be taken not to exert force on of the permanent incisor to enter the oral cavity. In 75% of cases, extraction of the me­
adjacent teeth, which can easily be displaced due to the anatomy of the root. siodens during the mixed dentition period results in spontaneous eruption. If adjacent

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Compendium of Paediatric Dentistry Extractions of deciduous teeth - indications, contraindications, technique, complications

teeth do not erupt within 6-12 months, surgical tooth exposure and orthodontic treatment giving indications - it is recommended to remove the dressing after 1 0 min, to eat
may be necessary to facilitate eruption. lukewarm, semi-liquid food after approx. 2 hours.
Management prior to deciduous tooth extraction:
- a thorough interview with the patient's parent (legal guardian) regarding past medical Curette / dental elevator
history and comorbidities, After the administration oflocal anaesthesia, a sterile curette or dental elevator can be
parental (legal guardian) consent to perform the procedure, used to cut off the gingival attachment (Fig. 30.2). This first stage of the procedure can
thorough clinical examination of the dentition and oral mucosa, determine the child's behaviour during the rest of the procedure, as a very anxious child
behavioural assessment - special attention should be paid to the assessment of the will react negatively to even light pressure with the curette.
social, emotional and psychological condition of the patient-child before extraction
(AAPD, 2015),
- taking an RVG, pantornogram (as indicated).
Technique of deciduous tooth extraction:
infiltrative anaesthesia,
preparation of the correct instruments (dental elevators, forceps - the appropriate
type adapted to the crown of the tooth) and sterile swabs; the instruments should be
Fig. 30.2. Preparation of the tooth with a dental elevator or curette - cutting the gingival
placed behind the dental chair, out of the child's sight,
attachment (gingival separation).
- gentle detachment of the circular fibre with the capping device in order not to damage
the permanent tooth root (Fig. 30.2), luxation with a straight dental elevator (Fig. 30.3),
Luxation - luxation of the tooth
gripping the alveolar process of the maxilla or the alveolar patt of the mandible with
Luxation is the most important step to facilitate extraction and prevent fracture ofthe root
the dentist's hand to stabilise the child's head, exposing the surgical field and, to some
of a deciduous molar. The interproximal contacts of the molars are wide, flat and without cer­
extent, securing the pharynx and airway,
vical stenosis. The tip of the luxation instrument should be narrow (Fig. 30.3). Dental elevators
placing the forceps on the crown of the tooth - the beaks of the forceps must be firmly
are used relatively infrequently and, when using them to prepare a tooth, gentle movements
tightened around the neck of the tooth so that the tooth does not fall out of the forceps
should be made with little force. This step may not be necessary for incisors and canines with
during removal (Fig. 30.4, 30.5, 30.6),
conical, single roots, but may be helpful in some cases. The upper incisors can be luxated using
luxations of the deciduous tooth - extraction movements should be more careful (as
straight forceps with labial and palatal movements. During luxation, care should be taken not to
opposed to permanent teeth); during the extraction of the anterior teeth, it is permis­
include adjacent teeth, causing them to become mobile. If the adjacent tooth is movable before
sible to perform rotational movements, and during the extraction of the lateral teeth
extraction, inform the parent (caregiver) of the possibility of unintentional extraction.
- gentle and slow movements in the palatine and buccal axis of increasing amplitude;
during the extraction of the deciduous teeth, a smaller balancing force should be used
and the anatomy of their roots in relation to the permanent tooth buds should be taken
into account,
inspection of the alveolus to ensure that the tooth has been extracted in its entirety,
securing the post-extraction wound with a sterile gauze pad, checking haemostasis
after 5 min (Fig. 30.7), Fig. 30.3. Luxation of the deciduous molar with straight dental elevator.

41 2
413
Compendium of Paediatric Dentistry Extractions of deciduous teeth - i ndications, contraindications, technique, complication s

The sensation of pressure during luxation and extraction ("taking out the tooth") teeth of the jaw - the maxilla canines - the back teeth of the mandibula - the front
should be explained to the child. This sensation can be demonstrated by pressing on the teeth of the mandibula- the mandibula canines.
child's arm. If a previously cooperative child starts to cry, showing pain during the luxa­
tion, additional local anaesthesia is indicated. Complications after extraction:
l . General complications - postoperative pain, haemorrhage.
Application of forceps to the crown of a tooth
2. Problems with the removed tooth - root fracture, root displacement, stuck tooth in the
throat, aspiration to the respiratory tract. In the event of a fracture of the root of the
deciduous tooth, it is necessary to consider its further extraction - during removal,
a fragment may be pressed in and damage the permanent tooth bud, while leaving
it may cause infection or delay the eruption of the permanent tooth. If the root frag­
ment can be easily removed, the treatment should be continued. However, when a
fragment of the remaining root is small and deep in the socket or when attempts to
Fig. 30.4. Applying forceps Fig. 30.5. The correct position of the beaks of remove it have been unsuccessful, it can be left for observation - it is often resorbed
to the crown of the tooth (photo M UW). forceps below the enamel-cement line. or spontaneously expelled. In patients with systemic diseases in which foci of in­
fection should be excluded, the fractured fragment of the deciduous tooth root
should always be removed, as it may cause a tooth-derived infection. The pro­
cedure should be carried out very gently, taking care not to damage the permanent
tooth socket.
3. Damage to adj acent teeth - fracture or displacement of the adjacent tooth, luxation of
the adjacent tooth, extraction of the wrong tooth.
4. Soft tissue injury - abrasion, stab wound, tearing of the mucosal flap.
Fig. 30.6. Forceps positioning and alveolar Fig. 30.7. The use of a sterile gauze pad
5. Bone structure injury - fracture of the alveolar process, fracture of the maxillary
grip to control the force applied. (photo MUW).
tuberositi.
6. Damage to adjacent structures - nerve damage, blood vessel damage, damage to the
Multiple extractions - guidance:
temporomandibular joint.
1 The maxillary teeth are extracted first. Intraosseous anaesthesia works faster in the
7. Fistula.
maxilla, leading to an early start to the procedure. If the mandibular teeth are ex­
8. Fracture of the mandible.
tracted first, debris such as fractured crowns, bone fragments and fragments of filling
9. Delayed healing, infection, wound dehiscence, dry socket, osteitis.
material may fall into the alveoli in the mandible during extraction of the maxillary
teeth.
T he most important indications for care after the procedure to be given to the
2. Extractions should be started from the lateral teeth, as this allows the effective use of
patient:
dental elevators for luxation.
avoid mouthwash, hot food and drinks and intense activity for the first 24 hours,
3. Canines are the most difficult to extract teeth, so they should be removed last.
care should be taken not to remove the blood clot from the alveolus,
4. If the teeth of the maxilla and mandible of one side are to be removed during one visit,
if the alveolus is bleeding, apply pressure for about 10 minutes,
the recommended order of extraction is: the lateral teeth of the maxilla - the front

414 415
Compendium of Paediatric Dentistry Extractions of deciduous teeth - indications, contraindications, technique, complications

painkillers if necessary, 20. Olczak-Kowalczyk D. Preparation for denta l treatment. [in:] Olczak-Kowalczyk D, Wag­
ner L (eds). Introduction to paediatric dentistry. Oficyna Wydawnicza Warszawskiego Uniwer­
apply cold compresses to reduce swelling,
sytetu Medycznego. Warsaw 20 1 2; 1 8-3 1 . - 2 1 . Parkins G. Padiatric Ora-facial Fascia! Space
follow a well-balanced, soft diet for several days until you can chew carefully with lnfections . .l West Afr Coll Surg. 20 1 8 Oct-Dec;8( 4):x-xiv. - 22. Peterson L. Principles of uncom­
your remaining teeth, pl icated tooth extractions. [In:] Peterson L ed: Dental and maxillofacial surgery. Czelej 200 I : 1 43-
93 - 23. Schlabe J, Kabban M, Chapireau D, Fan K. Paediatric dento-facial infections - a potential
brush your teeth carefully, taking care not to dislodge the blood clots that prevent pulpoctomy for identifying children at risk of neglect? Br Dent .I . 20 1 8 Oct 26;225(8):757-76 l .
bleeding and help protect against infection, doi: I 0. 1 03 8/sj .bdj .20 I 8.862.
for young people - avoid smoking,
if the pain or swelling worsens or the temperature rises, contact your dentist.

References
I . American Academy of Pediatric Dentistry. Management considerations for paediatric oral
surgery and oral �athology. The Reference Manual of Pediatric Dentistry. Chicago, 1 1 1 . : American
Academy of Pediatric Dentistry; 202 1 :450-60. - 2. American Academy of Pediatric Dentistry:
guideline on paediatric oral surgery. AAPD reference manual, revised 20 I 0, 20 1 4; 36, 6: 276-83. -
3. American Association of Oral and Maxillofacial Surgeons: Parameters of care: clinical practice
guidelines for oral and maxillo facial surgery. J Oral Maxillofacial Surg 20 1 2; v. 5.0, supplement.
- 4. Ara(1j o MG, S ilva CO, Misawa M, Sukekava F. Alveolar socket healing: what can we learn?
Periodontol 2000. 2015;68( I ): 1 22-34. - 5. Cameroon AC et al. Paediatric dentistry. Issue 2. Elsevier
Urban&Partner, Wrocfaw 20 1 6. -6. Cobourne MT et al. A guideline for the extraction of first perma­
nent molars in children. Fae Dent Surg 20 1 4 - 7. Dym H, Weiss A. Exodontia: tips and techniques
for better outcomes. Dent Clin North Am. 2012;56( I ):245-66. - 8. Extraction of primary teeth - bal­
ance and compensation file:///C:/Users/G RAM/Downloads/extractp%20( I ).pdf.February 202 1 . - 9.
Guideline on Use of Local Anesthesia for Pediatric Dental Patients, Amer Acad Pediatr Dent 20 1 5 .
1 0. https://books.google. pl/books?id=hqagDwAAQBAJ&pg=PA5&dq=Tooth+ Extraction
+ H u bertus + van+ Waes+ Book+ Editor(s): PD+Dr. +med. +dent. + Klaus+ W. +N euhaus+ M M A +
M A S , Prof. +em. + Dr. + med. + dent. + Adrian+ Lussi+ dipl. + Chem . lng. + ETHZ&lr =&hl= pl&­
source=gbs_selected_pages&cad=2#v=onepage&q&f=false. - 1 1 . van Waes H . Tooth Extraction
First published: 05 July 20 1 9 https://doi.org/ 1 0. 1 002/978 l l 1 9372684.ch4.3. - 1 1 . van Waes H .
Tooth Extraction First published: 05 July 20 1 9 https://doi.org/ 1 0. 1 002/978 l l l 9372684.ch4.3. -
1 2 Jabkcka A i wsp. Fundamentals of clinical pharmacology - allergies, drug interactions and se­
lected problems in dentistry. I ssue I . Czelej . Lublin 2005 . - 1 3 . Jain A. Principles and Techniques
of Exodontia. DOI: 1 0. 1 007/978-98 1 - 1 5- 1 346-6_ 1 3 !n book: Oral and Maxillofacial Surgery for
the Clinician file:///C:/Users/G RAM/Downloads/Principles_and_Techniques_of_Exodontia%20
(2).pdf. - 1 4 . .lohri A, Piecuch J F. Should teeth be extracted immediately in the presence of acute
infection? Oral M axillofac Surg Clin North Am.201 1 Nov;23(4):507- 1 1 . - 1 5 . Koga DH, Salva­
joli JV, Alves FA. Dental extractions and radiotherapy in head and neck oncology: review of the
literature. Oral Dis. 2008 Jan; 1 4( I ):40-4. - 1 6. Lim ST. M anagement of the infected, abscessed
primary tooth - a report. Singapore Dent J. 2004 Dec;26( I ):49-54. P M I D: I 5736842. - 1 7. Lodi
G, Figini L, Sardella A, Carrassi A, Del Fabbro M, Furness S. Antibiotics to prevent complications
following tooth extractions. Cochrane Database Syst Rev. 20 1 2; 1 1 :CD0038 I I . - 1 8. Nayyar J,
Clarke M, O 'Sullivan M, Stassen LF. Fractured root tips during dental extractions and retained
root fragments. A clinical dilemma? Br Dent J. 20 1 5 ;2 1 8(5):285-90. - 1 9. Olczak-Kowalczyk D,
Kaczmarek U, Szczepa11ska J. Contemporary dentistry of the developmental age. Med Tour Press,
Warsaw, 20 1 6.

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 Specifics of the management of patients with intellectual and physical disabilities

Part VIII The five main types are: spastic, ataxic, athetoid (dyskinetic), hypotonic, and mixed
cerebral palsy. Children affected by spasticity may experience unilateral or bilateral in­
volvement of the upper or lower limbs or the four limbs and trunk.
Patient with a general medical problem at the dental office In addition to motor impairments, people with CP sometimes have epilepsy, reflux
disease, intellectual disability, behavioural, visual and hearing impairments. Characte­
ristics that a paediatric dentist may observe are poor oral hygiene, increased gum dis­
Chapter 3 1 ease and sometimes overgrowth, a tendency to bruxism, malocclusion, tongue thrusting,
mouth breathing, increased incidence of caries, trauma, increased vomiting reflex, dro­
oling (sialorrhea), erosions. The diagnosis of CP does not determine the child's fitness.
Specifics of the management of patients with This group can range from children who function independently to those who require
intellectual and physical disabilities constant care from others.
Down syndrome (DS) - is a genetic syndrome caused by an aberration in the 21 pair
Grazyna Marczuk-Kolada
of chromosomes. This means that instead of two chromosomes, there are three. It can
occur in a small percentage in a translocated form (chromosome 21 or a fragment of it
is attached to another chromosome) or in a mosaic form (an extra chromosome is found
Disability - as defined by the World Health Organisation - means a limitation or lack
in part of the cells and the normal number of chromosomes is present in the others). I n
of ability to perform an activity in the manner or to the extent considered n01mal for a
the translocation form, the symptoms of the disease are not affected, while i n the mosaic
human being, resulting from damage to or impairment of a bodily function. I n the case of
form the symptoms may be slightly milder. In DS, a flat facial profile with underdevelop­
developmental age people, we relate the range of activities and how they are performed
ment of the central part of the face, oblique positioning of the eyelid crevices, a diagonal
to the peer group. Disabilities can be congenital and acquired. Depending on its severity,
wrinkle (corner of the eye covered by a skin fold), small, low-set ears, excess skin on
it is described as mild, moderate and severe.
the nape of the neck, smaH, wide hands with a single flexion furrow are observed. De­
Disability varies widely. The term is used to refer to physical, sensory, cognitive,
fects and disorders from different systems can coexist with Down syndrome. The most
mental retardation, mental illness, and various types of chronic diseases. The societal
common include heart defects, coeliac disease, hypothyroidism, type 1 diabetes, skeletal
relevance and context of disability issues is provided by the International Classification
disorders, ophthalmic disorders and hearing loss. Characteristic features observed in the
of Functioning, Disability and Health (ICF). ICF was established in 2001 by the World
oral cavity of ehildren with DS include central facial hypoplasia, a large, fissured tongue,
Health Assembly.
a narrow high-arched palate, delayed eruption of teeth, hypodontia, microdontic and
Disability can be divided into many broad categories. The paediatric dentist most
sometimes hypoplastic enamel, and drooling.
often encounters disabilities belonging to the following groups:
Visual impairments range from total blindness to reduced vision of size, color, dis­
- reduced mobility found in people with congenital or acquired musculoskeletal
tance, shape. The oral health status of children with visual impairment does not differ
dysfunctions, such as childhood cerebral palsy,
from the average peer. Children with this disability may have a tactile oversensitivity.
- reduced intellectual capacity, which includes Down's syndrome,
Hearing loss is an impairment that is mostly acquired with age; however, some chil­
- sensory disabilities, resulting from damage to the sensory organs, including blind and
dren are born with partial or complete hearing loss. It can occur alone or in combination
partially sighted people, deaf and hard of hearing people.
with other disorders. There is little data on the oral health of children with hearing loss,
Cerebral palsy (CP) - is a group of non-progressive neuromuscular disorders caused
but it is suggested that oral lesions do not differ significantly from the peer group.
by early brain damage. Damaging factors can be prenatal, perinatal and postnatal.

418 41 9
Compendium of Paediatric Dentistry Specifics of the management of patients with intellectual and physical disabilities

Children with developmental disorders, including conditions affecting behaviour sary to inform the patient about switching on devices and inserting instruments into the
and cognition, often have limitations in performing activities of daily living. They may oral cavity. Patients with hearing impairment are mostly able to lip-read. Both the den­
have special health care needs and for this reason are more likely to have unmet dental tist and the assistant should clearly move their lips when speaking. The mask should
needs than normally developing children. It is widely believed that they have a higher be removed. In the case of prosthetic children, it may be suggested, after discussing
risk of developing dental diseases. Reasons for this include frequent use of high-sugar relevant issues related to the examination and treatment plan, that the hearing aid is re­
medicines, dependence on the caregiver for regular oral hygiene, reduced removal of moved or switched off and switched on again after the procedure is completed (sounds
food from the mouth, impaired salivary function, preference for carbohydrate-rich foods, coming from the scaler, turbine or vibrations transmitted from the contra-angle can be
a liquid or pureed diet and food aversion. The side effects of chronic medication in these very unpleasant to hear).
patients should also be taken into account. If, after using communication techniques, the patient's behaviour is unsatisfactory,
As a rule, treatment planning for children with motor, intellectual, visual and audi­ a method of protective stabilisation of the child can be used with the consent of the
tory disabilities do not differ from the general principles. In contrast, the way in which parent (guardian). If non-pharmacological behavioural techniques are ineffective, the
this plan is implemented must take into account the problems arising from the degree of physician may order sedation or general anaesthesia to safely and effectively carry out
disability. the treatment plan (how patients qualify according to ASA Chapter 3).
Planning preventive and therapeutic treatment requires the dentist to familiarize The timing of the first visit is very important. The American Academy of Pediatrics
himself with the history of the patient's disease, which should be updated at each (AAP) recommends that paediatricians encourage parents of children with developmen­
subsequent visit, noting changes in health, newly diagnosed diseases, allergies, drug tal disabilities to seek dental care before the age of one ("first visit before first birthday").
changes, medical interventions related to the underlying disease or injury. In order to Early contact with the dentist allows for correct educational and preventive measures.
make a diagnosis, accurate, comprehensive information should be obtained about the Treatment interventions for patients with disabilities use methods that are widely
child's main ailments and conditions and the entire dental, medical and social histo­ known by clinicians. However, it is recommended to use groove and gap sealants in
ry. The history should also take into account the developmental stage, the cognitive a wider range. Due to the more difficult conditions in the oral cavity of children with
abilities of the patient, in order to be able to anticipate cooperation with the patient. disabilities (tongue crowding, vomiting reflex, salivation), the use of glass-ionomer ce­
The physician should become familiar with these issues in the initial examination ments for this purpose is proposed more frequently. It is also recommended to use more
in order to modify traditional patient care accordingly. The caries risk assessment, frequent interim therapeutic restorations (ITR) using glass-ionomer cements, which in
physical examination and additional tests are carried out according to general prin­ these cases can be used as a prophylactic and therapeutic method.
ciples (Chapter 14), modifying them accordingly. In caring for patients with disabilities, educational measures for both patients and
In a certain percentage, children with the listed disabilities can be treated in a den­ parents (carers) are very important. They should focus on oral hygiene and diet. Parent
tal office setting. Practice staff must take into account that preventive and therapeutic (caregiver) education is crucial to ensure proper implementation of hygiene interven­
procedures for patients with disabilities are more time-consuming and often require tions and adequate nutrition. The dentist should develop an individualised oral hygiene
a greater commitment. Behavioural methods of shaping the child's behaviour should programme taking into account the patient's disability (choice of appropriate brush,
be used extensively (Chapter. 2). The "tell-show-do" method is particularly recom­ toothpaste, brushing method). Dietary recommendations should encourage an anti-ca­
mended. In the case of patients with visual disabilities, attention should be paid to the ries diet according to general principles (Chapter 17). If the use of a diet rich in carbohy­
appearance and format of written materials available for use by patients. The size of drates or high-calorie dietary supplements is necessary for medical reasons, the dentist
the letters (minimum 14 pt), the type of font (should not be stylised) and the type of should take this fact into account in the preventive plan by changing the frequency and
paper (non-reflective) are important. Handle the operating lamp with care. It is neces- increasing the number of treatments.

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Compendium of Paediatric Dentistry

References Chapter 32
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six months of life? Child Neural 20 1 9; 2 8.57: 29-33. - 2. Norwood KW Jr, Slayton RL. Oral
Health Care for Children With Developmental Disabilities. Pediatrics 20 1 3 ; 1 3 1 ,3: 6 1 4-6 1 9. - 3 .
Dieguez-Perez M, d e Nova-Garcfa MJ, Mourelle-Martfnez R , Bartolome-Villar B . Oral health in
Oral diseases and general health
children with physical (Cerebral Palsy) and intellectual (Down Syndrome) disabilities: system­
atic review I. J Clin Exp Dent. 20 1 6; 8(3): e337-43. - 4. Bensi C, Costacurta M, Docimo R. Oral Grazyna Marczuk-Kolada, Dorota Olczak-Kowalczyk
health in children with cerebral palsy: A systematic review and meta-analysis. Spee Care Dentist
2020;40:40 1 -4 1 1 . - 5. American Academy of Pediatric Dentistry. M anagement of dental patients
with special health care needs. The Reference M anual of Pediatric Dentistry. Chicago, 111.: Amer
Acad Pediatr Dent; 202 1 :287-94. - 6. Wei bury RR, Duggal MS, Hosey MT. Paediatric dentistry. Oral health is one component of general health. The oral cavity harbours one of
2005; Oxford 3,d Ed: 3 85-4 1 1 .
the most diverse and abundant groups of microorganisms in the human body. They are
located in various places, such as the teeth, tongue, gingival pocket, palate, mucous
membrane and saliva. This ecological system is very complex and attracts a variety of
micro-organisms, including bacteria, fungi and viruses. The oral microbiome is formed
within minutes after birth and its main component is bacteria. The microorganisms in
the microbiome enter into a dynamic balance with the host's immune system. Due to
various causes, e.g. the use of systemic antibiotics, hygienic neglect, endodontic infec­
tions, periodontal disease, weakened defence mechanisms, mucosa[ lesions, nutritional
changes, dysbiosis occurs and a pathogen-rich ecosystem is formed. The increased im­
mune-inflammatory response to this pathogenic colonisation causes damage primarily to
the periodontium and mucosa, which become "permeable" to these pathogens. Advances
in medical science, especially regarding genomic research in microbiology, have meant
that it is now known that oral pathobionts can enter blood vessels to circulate throughout
the body, causing many systemic diseases in remote locations. It has been proven that
systemic inflammation caused by periodontitis is linked to the risk of cardiovascular
disease (coronary heart disease, myocardial infarction, stroke, vascular atherosclerosis),
diabetes, rheumatoid arthritis, neurodegenerative diseases (Alzheimer's disease), osteo­
porosis and other diseases such as glomerulonephritis, pneumonia, iritis and retinitis,
as well as anaemia. Periodontal pathobionts are also responsible for premature births
and low birth weight of newborns. In addition, they have been linked to pancreatic can­
cer, colorectal cancer, among others. Porphyromonas gingivalis, Actinomyces actinomy
cetemcomitans, Prevotella intermedia, Tanarella forsythia, Fusobacterium nucleatum
were considered the most pathogenic.
Changes in the oral cavity, especially bacterial, also increase the risk of general infec­
tious complications (e.g. sepsis, periodic fever syndromes, bacterial endocarditis, organ
abscesses, osteomyelitis, cerebral artery thrombosis).

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Oral bacteria can affect other organs and systems directly - as a result of bacteria Dental treatment
entering the bloodstream or aspiration into the respiratory tract or gastrointestinal tract,
or indirectly - through inflammatory-immune reactions. Non-immunocompetent patients require team treatment and collaboration between
Bacteraemia occurs as a result of dental procedures causing bleeding (provoked bac­ the dentist and the general medical practitioner providing general medical care. An oral
teraemia) or spontaneously, e.g. during chewing or hygienic procedures (spontaneous health assessment is also required prior to planned immunosuppressive or anti-cancer
bacteraemia) with an increase in the "permeability" of tissues, e.g. in the presence of in­ treatment before long-term surgical procedures and sanatorium treatment.
fectious lesions in the oral cavity, especially in the case of periapical dental inflammation The assessment of the oral condition requires a subject and physical examination
or periodontitis, as well as in the weakening of the physical barrier of the mucosa (e.g. according to the principles (Chapter 4). It is advisable to take a panoramic radiograph
caused by mechanical trauma) or immune (immunodeficiency). or, when this is not possible, a series of intraoral radiographs, limiting their number to
Immune reactions and inflammatory processes play an important role in the indirect teeth with fistulae, devoid of living pulp, covered by crowns, with periodontal lesions
effects of bacteria. It has been proven that lipopolysaccharide (LPS) is a building com­ or suspected lesions in the periapical tissues. Treatment management should include
ponent of Gram-negative bacteria. During infection, LPS becomes the agent that triggers endodontic treatment for pulp and periapical tissue disease, while inflammatory lesions
the body's inflammatory response. The TLR4 receptor activated by LPS activates two in the periodontium should be eliminated by non-surgical and surgical treatment. If the
signalling pathways leading to the production of inflammatory response mediators, such methods used fail, we qualify the tooth for extraction.
as: interleukins- l a, l L-1 �, l L-6, l L-8, tumour necrosis factor TNF-a. Cytokines affect The emphasis should be on disease prevention by implementing good oral care habits
all phases of the immune response. They affect activation, proliferation, differentiation and routine dental check-ups.
of B and T lymphocytes, NK cells, monocytes, macrophages and granulocytes, as well
as the liver, stimulating the release of acute phase proteins, coagulating factors, which General principles of antibiotic prophylaxis before procedures at risk
of bacteraemia
leads to damage to the target organ. Studies on the impact of periopathogens on general
health have identified adhesins, exotoxins, extrinsic proteolytic enzymes called gingi­
The phenomenon of bacteraemia involves the release of bacteria and their toxins
pains as important bacterial factors. Proteolytic enzymes are involved in processes such
into the blood. Bacteraemia can occur as spontaneous or provoked. Spontaneous oc­
as degradation of antibacterial peptides, antibodies, complement system components or
curs during chewing or routinely performed hygiene procedures such as tooth brushing,
inflammatory mediators such as cytokines. Gingipains, in addition to the local action in
flossing, irrigators, interdental brushing. Provoked bacteraemia occurs during invasive
the gum pockets, are transported by exocrine vesicles released from the surface of the
dental procedures accompanied by bleeding. For some conditions, antibiotic prophylaxis
bacteria to further areas of the affected tissue. This thus increases their extent and the
is used to reduce or eliminate transient, provoked bacteraemia.
extent of the inflammation.
There is now a trend towards reducing the indications for antibiotic prophylaxis. This
Bacterial LPS are also present in root canals and inflamed periapical tissues of teeth
is because the widespread use of antibiotics causes bacterial resistance and can cause
with dental pulp diseases. They activate endothelial cells and macrophages to produce
adverse reactions associated with their use.
inflammatory mediators. "Endodontic" bacteria also produce enzymes (e.g. collagena­
I t is now recommended that an antibiotic be administered before all dental proce­
ses, hyaluronidases, proteases) with the ability to damage host cells.
dures that involve periodontal, periapical or oral mucosal surgery. It is suggested to
Despite great advances in research, there is a need to clarify the mechanisms of oral
refrain from antibiotic prophylaxis during injection of anaesthetics through uninfected
bacterial transmission to distant organs and the exact role of oral pathobionts in the
tissues, wearing orthodontic appliances, moving prosthetic restorations, exfoliation of
pathogenesis of many diseases.
deciduous teeth, bleeding as a result of lip or oral mucosa inj ury.

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Compendium of Paediatric Dentistry Oral diseases and general health

These are the following: Tab. 32. J . Principles of antibiotic use before dental procedures.
people with a high risk of infectious endocarditis (IE) - with an artificial valve
Clinical situation Antibiotic Adults Children
or artificial material used for repairing the valve, previous bacterial endocarditis,
May take medica-
after heart transplantation, also in the case of a cyanotic congenital heart defect Amoxicill in 2g 50 mg/kg b.w.
tion by mouth
without surgical correction or with the presence of residual defects, palliative joints Do not take Ampici l l in or Cepha- 2 g i.m. or i.v. * 50 mg/kg, i .m. or i.v.
or conducts, congenital heart defect after complete correction, with the presence of medication orally zolin or Ceftriaxone I g i.m. or i.v. 50 mg/kg, i.m. or i.v.
artificial material placed as a result of cardiac surgery or percutaneous surgery up to Cephalexin (or other
2g 50 mg/kg b.w.
first - or second-ge-
6 months after the surgery, with a residual defect at the place of implantation of the Allergy to penicillin neration cephalospo-
artificial material or device during cardiac surgery or percutaneous surgery, or ampicil lin, takes rin),
500 mg 1 5 mg/kg b.w.
medication orally Azithromycin or
conditions with impaired defence mechanisms such as human immunodeficiency < 45 kg - 2.2 mg/kg b.w.
Clarithromycin, or
virus (HIV,) infection, Immoral or T-cell deficiencies (e.g. severe complex 1 00 mg > 45 kg - I 00 mg
Doxycycl ine
immunodeficiency - SCIDS), neutropenia, cancer chemotherapy, bone marrow Allergy to penici l l in
or vascular organ transplantation, head and neck radiotherapy, haemodialysis, or ampicillin, does Cefazolin or Cef-
1 g i.m. or i.v. 50 mg/kg i.m. or i.v.
not take medication triaxone
autoimmune diseases (e.g. juvenile arthritis, systemic lupus erythematosus), orally
sickle cell anaemia, asplenia or splenectomy, chronic immunosuppressive therapy * i.m. - i ntramuscular; i.v. - i ntravenous.
(e.g. glucocorticosteroids), poorly control led diabetes mellitus, especially type
1 , bisphosphonate therapy. When secondary immunodeficiencies in the course of In case of a risk of impaired wound healing, after consultation with the attending physi­
other diseases are suspected, consultation with the patient's general practitioner is cian, prolongation of antibiotic therapy should be considered, often until the wound heals.
necessary,
patients with valves used to treat hydrocephalus (in the case of valves with access to References .
the cardiovascular system). I . American Dental Association. Oral health topics: Antibiotic stewardship. American Den­
tal Association website. September 29, 2020. Accessed July 20, 202 1 . https://www.ada.org/en/
Contrary to previous recommendations, it is suggested that patients with joint pros­ member-center/oral-health-topics/antibiotic-stewardship. - 2. American Academy of Pediatric
theses should not use prophylactic antibiotics before dental procedures. For patients with Dentistry. Antibiotic prophylaxis for dental patients at risk for infection. The Reference Manual
of Pediatric Dentistry. Chicago, Ill.: Amer Acad Pediatr Dent; 202 1 :465-70. - 3. Cullinan MP et
a history of joint replacement surgery complications who are undergoing dental pro­
al. Periodontal disease and systemic health: current status. Austr Dent J 2009; 54: ( 1 suppl), 62-
cedures involving gingival manipulation or mucosa] incisions, prophylactic antibiotics 69. - 4. Daly CD. Antibiotic prophylaxis for dental procedures. Aust Prescr 201 7;40: 1 84- 1 88. - 5 .
should be considered only after consultation with the patient and orthopaedic surgeon. If van der Meulen TA e t a l . The microbiome - systemic diseases connection. Oral Diseases; 20 1 6:
22, 7 1 9-734. - 6. Hillsmann M i wsp. Endodontic treatment and general health- interaction and
necessary, it is appropriate for an orthopaedic specialist to order an appropriate antibiotic therapeutic implications (I). Endodoncja.pl 201 2; 1 : 36-43. - 7. Kitamoto S et al. The Bacterial
regimen and write a prescription. Connection between the Oral Cavity and the Gut Diseases. J Dent Res; 2020:99(9) 1 02 1 - 1 029.
When there is a need for numerous tooth extractions or other treatments over several - 8. Kumar PS. From focal sepsis to periodontal medicine: a century of exploring the role of the
oral microbiome in systemic disease. J Physiol; 20 1 7: 595.2, 465-476. - 9. Olczak-Kowalczyk D
visits, there should be an interval of several days (4-9 days) between treatments or an et al. Bacteria and Candida yeasts in inflammations of the oral mucosa in children with secondary
antibiotic from a different group should be given before each visit. The pattern of anti­ immunodeficiency. J Oral Pathol Med 20 1 2; 4 1 :568-76.
1 0. Park DJ et al. Leaky Gum: The Revisited Origin of Systemic Diseases. Cells 2022; 1 1 :
biotic use prior to dental procedures (single dose 30 to 60 minutes before the procedure) 2- 1 7. - 1 1 . Roberts DJ et al. Duration, prevalence and intensity of bacteraemia after dental ex­
is shown in Table 3 2.1 . tractions in children. Heart 2006; 92: 1 274-77. - 1 2. Somma F et al. Oral inflammatory process
and general health Part I : The focal infection and the oral inflammatory lesion. Eur Rev Med

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Pharmacol Sci 2010; 1 4: 1 085-95. - 13. Somma F et al. Oral inflammatory process and general Index
health Part 2: How does the periapical inflammatory process compromise general health? Eur Rev
Med Pharmacol Sci 20 11; 15: 35-5 1 . - 14. Zheng D et al. Interaction between microbiota and
immunity in health and disease. Cell Research; 2020: 30:492-506.
A - Dentinogenesis i111pe1fecla 1 18
- dysplasia 1 17
Abscess Developmental enamel defects 103
- periapical 272 - Amelogenesis impe,fecta I 09
- submucosal 272, 273 - classification I 09
- subperiosteal 272 - fluorosis I 08, 256
Anaesthesia Diagnostic radiology 58
- complications 3 6 - ALADA principle 58
- general 37 - types 60
- inferior alveolar nerve 35 Direct pulp capping 282
- intraligamentary 37 - condition of the pulp 55
- intraosseous 36 - dental 43
- intrapapil lary 35 - dental history 44
- local 34 - extraoral 46
- surface 3 3 - intraoral 46
- periradicular tissues 57
B - saliva 6 1
Discolouration of teeth 111
Behaviour rating scale 12 Diseases of the pulp
- classification 266
C - treatment 279

Communication E
- non-verbai 23
- verbal 24 Examination
- dental history 44
D - extraoral 46
- intraoral 46
Dental anxiety 16
Dental biofi l m 151 F
Dental caries
- CAM BRA 185 Fissures sealing 200, 235
- early childhood 178 Fluorescence 54
- ICDAS classification 172 Fluoride
- Manji scale 173 - dosage 250
- risk assessment 183 - safety 256
- types 167 Frankl 's behaviour rating scale 12
Dental pulp diseases
- classification 266 H
- revascu larisation 305
Developmental abnormalities of dentin 1 1 6 Health education 227
- defects I I 7

428 429
I R

I mpregnation 20 I Rem i nera I ization 1 98, 229

Index
- approximal plaque 48 s
- Basic Periodontal Examination 3 89
- D MF/dmf 1 60 Sedation 3 8
- frequency of caries 1 60 - Nitrous oxide 3 9
- gingival 50 Staining dental deposits 49
- intensity 1 60 Sugar substitutes 237
- oral hygiene 47
- plaque 48 T
- PU FA 1 6 1
- specific (SaC) 1 60 Tooth abnormalities
I ndirect Pulp Caj:tping 294 - agenesis 84
- hypodontia 86
M - macrodontia 89
- microdontia 88
Microbiological tests 61 - morphology 91
- rhizomegaly 91
0 - rhizomicria 90
- taurodontism 98
Oral hygiene 230 Tooth development
- amelogenesis 68
p - cementogenesis 72
- dentinogenesis 67
Pathological resorption 309 - tooth pulp 69
Periodontal diseases Tooth eruption
- classification 390 - disorders 1 42
Prevention of caries Transillumination 63
- in the prenatal period 226 Traumatic dental injuries
- in the post-eruptive period229 - Andreasen 's classification 3 1 6
- in the postnatal period 226 - E l l is cassification 3 1 8
Pulpectomy 289
Pulpotomy 283

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