CRASH COURSE IN

PEDIATRIC DENTISTRY

WWW.DENTISCOPE.ORG

DONE BY : SIMA HABRAWI

EDIT BY : HAIF ALQAHTANI DENTISCOPE 2020
Crash Course in Pediatric Dentistry

Table of Contents
Basics of child phycological development ............................................................................... 5
Behavior management .......................................................................................................... 6
Behavior rating scales.....................................................................................................................6
Behavior modification ....................................................................................................................7
Behavior management ...................................................................................................................7
Early childhood caries - ECC.................................................................................................... 9
Caries in Permanent teeth.................................................................................................... 11
Diet analysis [ 24 hours diet chart ] ............................................................................................... 11
Restoring caries in young permanent teeth .......................................................................... 13
ICDAS ........................................................................................................................................... 13
Caries risk in pediatric patients ..................................................................................................... 13
Restorative materials for primary teeth ............................................................................... 15
Stainless steel crowns [ SCC] ......................................................................................................... 16
Amalgam ..................................................................................................................................... 17
Resin composite ........................................................................................................................... 17
GIC............................................................................................................................................... 17
RMGIC ......................................................................................................................................... 17
Compomers .................................................................................................................................17
Fissure sealants ............................................................................................................................ 17
PRR .............................................................................................................................................. 17
Pulp therapy in primary teeth .............................................................................................. 19
Indirect pulp capping .................................................................................................................... 20
Direct pulp capping ...................................................................................................................... 20
Pulpotomy ................................................................................................................................... 20
Pulpectomy .................................................................................................................................. 21
Fluoride modalities in pediatrics .......................................................................................... 23
Fluoride varnish ........................................................................................................................... 23
APF gel ......................................................................................................................................... 24
Silver diamine fluoride [ SDF] ........................................................................................................ 24
Titanium tetrafluoride .................................................................................................................. 25

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Fluoride supplements ................................................................................................................... 25

Fluoride toxicity ........................................................................................................................... 26
Dental fluorosis ............................................................................................................................ 26
Fluoride calculations .................................................................................................................... 26
Fluoride toxicity calculcations ....................................................................................................... 27
Inhalation sedation.............................................................................................................. 28
Conscious sedation ....................................................................................................................... 28
Nitrous oxide ............................................................................................................................... 28
Slow induction ..................................................................................................................................................... 29
Rapid induction ................................................................................................................................................... 29
Early to ideal sedation ......................................................................................................................................... 29
Over sedation ...................................................................................................................................................... 29

Dental trauma in Primary teeth ........................................................................................... 31

Management of any dental trauma follows WASH protocol .......................................................... 31
Clinical examination of any trauma follows MP3 protocol ............................................................. 31
Trauma in primaty teeth ............................................................................................................... 32
Dental trauma to young permanent teeth ............................................................................ 34
Ellis classification of permanent teeth fractures ............................................................................ 34
Trauma in young permnanet teeth ............................................................................................... 34
Management of avulsion in primary teeth ........................................................................... 37
Management of avulsion .............................................................................................................. 38
FARAH protocol............................................................................................................................ 38
Splinting....................................................................................................................................... 38
De coronation .............................................................................................................................. 39
Auto transplantation .................................................................................................................... 39
Apexogenesis & apexification .............................................................................................. 40
Regenerative endodontics ............................................................................................................ 41
Pediatric facial injuries......................................................................................................... 42
Management of facial fractures .................................................................................................... 43
Management of medically compromised children ................................................................ 44
Congenital heart disease .............................................................................................................. 44
Asthma ........................................................................................................................................ 45

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Cystic fibrosis : respiratory disease ............................................................................................... 45

Renal disease ............................................................................................................................... 45
Liver disease ................................................................................................................................ 45
Diabetes ...................................................................................................................................... 46
Platelet disorders ......................................................................................................................... 46
Coagulopathies ............................................................................................................................ 46
Thalassemia .................................................................................................................................46
Leukemia ..................................................................................................................................... 46
Immunodeficiency........................................................................................................................ 47
Organ transplants......................................................................................................................... 48
Cerberal palsy .............................................................................................................................. 48
Visually impaired.......................................................................................................................... 48
Hearing impairment: .................................................................................................................... 48
Down syndrome ........................................................................................................................... 49
Pediatric oral medicine & oral pathology ............................................................................. 49
Odontogenic infections ................................................................................................................ 49
Primary Herpetic Gingivostomatitis .............................................................................................. 50
Herpangia .................................................................................................................................... 50
Acute pseudomembranous candidosis .......................................................................................... 50
Recurrent apthous ulcers .............................................................................................................. 50
Erythema multiforme ................................................................................................................... 51
Stevens Johnson syndrome........................................................................................................... 51
Eruption cyst or haematoma......................................................................................................... 51
Phenytoin enlargement ................................................................................................................ 51
Cyclic neutropenia ........................................................................................................................ 51
Epstein’s pearls ............................................................................................................................ 51
Bohn’s nodules............................................................................................................................. 52
Anomalies in pediatric dentistry ........................................................................................... 53
Developing dentition in pediatric pts .................................................................................... 57
Dentition stage............................................................................................................................. 57
Molars the relationship ................................................................................................................ 58
• Early mesial shift ......................................................................................................................................... 58

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• Late mesial shift .......................................................................................................................................... 58

Incisal liability .............................................................................................................................. 58

Leeway space of Nance................................................................................................................. 58
Ugly duckling stage [ Broadbent phenomenon] ............................................................................. 59
Interceptive orthodontic procedure in pediatrics .................................................................. 60
Interceptive procedures ............................................................................................................... 60
Habit breaking appliances ............................................................................................................ 60
Mouth breathing ................................................................................................................................................. 61
Lip bumper .......................................................................................................................................................... 61

Anterior crossbite......................................................................................................................... 62
Management of premature loss of primary teeth in mixed dentition ............................................. 63
Space maintainers for unilateral space loss ........................................................................................................ 63
Space maintainers for Bilateral space loss [ mandible ] ..................................................................................... 64
Space maintainers for Bilateral space loss [ maxilla] .......................................................................................... 64

References........................................................................................................................... 65
Disclaimer ......................................................................................................................... 66

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Basics of child phycological development

Stages of physcosexual development [ freud]: Stages of physcosocial development [ Erikson]:

1- Oral : First year of life – child is completely • Trust vs mistrust [ oral stage – kid has
dependent on the mother separation anxiety ]
2- Anal: 1-3 years old – toilet training is done • Autonomy vs doubt [ anal stage – child
in this stage should think that what the dentist is
3- Phallic : 3-6 years old – sexual identity doing is their own choice]
develops • Initiative vs guilt [ phallic stage]
Kids at this stage have mutilation anxiety [ • Industry vs inferiority [ latency stage]
they are afraid of being injured ] Ortho tx starts at this stage
4- Latency: 6-12 years old – care free years • Identity vs role confusion [ genital
5- Genital :12- 18 years old stage]

Object concept:

2-3 months – child will only observe at an object

3-6 months – child will grab the object
6-11 months – child will look for a hidden object

Before the age of 7 you explain things to the child using [ immediate sensation] → tell the child that
they need to brush their teeth so they looks white and nice and they have a very nice smell that
everyone will like.

After the age of 7 you explain things to the child using [ abstract reasoning] → you need to brush your
teeth to prevent plaque and caries

Q: how is classic conditioning related to dentistry?

The child comes the first visit and sees you wearing a lab coat , you give them an injection [ sth painful ] ,
the next visit when they see a lab coat they start crying.

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Behavior management
The first objective of behavior management is establishing communication

• Positive reinforcement = providing the child with a pleasant stimulus [ high five, praise tap on
the back etc ]
• Negative reinforcement = remove a negative stimulus after the child behaves properly [ex: if
they don’t like your assistant, you tell them I can ask this person to leave but you have to open
wide!
• Omission: removal of pleasant stimulus [ ex: taking away their fav toy ]
• Punishment: giving un pleasant stimulus [ ex: mildest form is voice control, withdrawal of fun
activities ]

Positive reinforcement types :

1- Direct : gifts and rewards [ most effective]

2- Vicarious : watching someone else getting a reward
3- Self administered : child feels proud of being good

Q: how do you establish effective communication with the child? Before the child gets in you already
know their name, what they like what is their nickname, fav superhero etc.. get down the their level [
your eye level should be the same and the child’s eye level ] and talk to them.

Behavior rating scales

Frankl scale :

• Definitely positive : very cooperative

• Positive : accepts tx but is sometimes cautious
• Negative : reluctant to accept tx
• Definitely negative : refuses tx

Wright’s scale :

• Cooperative : most children

• Potentially cooperative :
• Lacking cooperative ability / pre cooperative [very young or special needs patients]
- Objective fear : caused by direct physical stimulation [ ex: you gave the child an injection that was
painful ]
- Subjective fear: feelings and attitudes suggested by others [ex: the child’s friend will tell them that
they went to the dentist and the dentist hurted them a lot]

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Q: what can you do to positively affect a child’s behavior in the clinic?

1- Gather data about the child before they enter [ their fav toy, nick name etc..]
2- Structure your treatment [ explain to the child before each stage of the treatment or show them
on a model]
3- Distract the child during the procedure [ make then hold the suction or watch cartoons etc ]
4- Be flexible [ accommodate each child’s needs]
5- Wear colorful colors and scrubs [ avoid wearing a lab coat ]
6- Make sure the clinic’s environment is friendly and pleasant
7- Make appointments short [ because kids have short attention span ] + make them in the
morning when they will be well rested and more cooperative

Behavior modification
1- Desensitization: Tell show do [ tell them what you will do , show them on a model and then do
it on them] – make sure your communication with the child is very simple and link it to things
they know [ syringe = special water , LA = sleeping medicine for the tooth , rubber dam = rain
coat for your teeth etc..]
2- Modeling : the child watches other kids or videos of kids getting treatment and behaving
properly → the child will later behave the same way
When the child watches a video of other kids getting tx this is called vicarious modelling
3- Contingency management: presentation or withdrawal of reinforces [ positive reinforcement =
giving gifts, praise, high fives etc]

Behavior management
1- Voice control : loud voice to gain child’s attention then go back to your normal tone.
2- Physical restraint [ aversive conditioning]: you need to brief the parents before + get consent
A. Mouth props :
• At the time of injection
• When children become fatigued
• Stubborn or defiant children
• Mentally / physically handicapped children
• Very young children
B. Parent / assistant : parents sits in the dental chair with the child in their lap, the parents
places one hand over the forehead and the other over the child’s hands
C. Body wrappings : papose boards, Vac pac
D. Hand over mouth [ HOME] : firmly place your hand over the child’s mouth until the verbal
outburst stops - Done to :
• Gain child’s attention
• Stop verbal outburst + Establish communication
indications Contraindications
Normal children who become Very young children
momentarily defiant or hysterical Immature and frightened children
Child is mature to understand simple Physical / mental / emotional handicap
verbal commands

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3- Pharmacological management:
• LA : Maximum allowed dose of LA = 4.4 mg / kg [ one carpule for every 10 kgs ]
• Oral sedation: desired effect is seen in 30 -60 mins
Adv: no injections, you give it orally and the child starts to get sleepy then you work on
them
Disadv: child is still not fully cooperative because they are sleepy and cranky + you can’t
titrate the dose
• Intramuscular sedation: desired effect is seen in 20 mins – injection sites:
A. Upper outer quadrant of gluteal region
B. Anterior aspect of the thigh
C. Middle of the posterior lateral aspect of the deltoid
• Intravenous sedation:
pt is still conscious
benzo diazepine – desired effect is seen in 20-25 seconds
once you see dropping of the eye lids → pt is well sedated

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Early childhood caries - ECC

ECC = nursing bottle caries , baby bottle tooth decay

A. Seen in infants and preschool children [ below the age of 6

]
B. Demineralization at the necks of the upper incisors –
mandibular incisors are not affected
C. Decay pattern:
Maxilla: incisors , canines, first molars
Mandible: canines , first molars
D. Lesion progresses to grind the necks of the teeth in
advanced cases only a root stump is left

Q: why does ECC follow this specific pattern?

1- Chronology of primary tooth eruption

2- Duration of the deleterious habit [ bottle feeding]
3- Muscular pattern of infant sucking

Early colonization of MS is the most imp risk factor for developing ECC – MS transmission can be through
the mother or from peers [ other kids]

MS Colonization of pre dentate children is mostly associated with maternal factors [ high level of MS in
the mother, poor OH and active caries ]

Q: how is nocturnal bottle feeding / breastfeeding related to ECC?

When child laid to rest, the bottle or breast nipple rests against the palate and tongue covers the lower
incisors [ that’s why they are not affected] - As the child becomes sleepy, saliva flow and swallow reflex
are reduced → Sugar remains stagnant around the neck of the teeth

Q: what practices increase the chance of developing ECC?

1- Prolonged night time bottle feeding

2- On demand breast feeding after the age of 1
3- Frequent snacking with sugary foods
4- Frequent sipping of sugary drinks throughout the day

Q: why should you treat ECC ?

1- Relieve pain
2- Prevent infection
3- Improve child’s self esteem
4- Retain teeth → maintain proper nutrition, occlusion and speech

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Q: how would you manage a case of ECC?

1- Identify the cause and stop the habit

2- Give parental instruction on proper oral hygiene measures + diet counselling
3- Decide if the case can be managed in clinic [ with regular LA or nitrous sedation ] or the child
needs GA
If the case is treated in the clinic : full assesment of all affected teeth to know which teeth can
be restored, which need pulp therapy and which need extractions

Q: what instructions would you give the parents to a child with ECC?

1- STOP NIGHT TIME BOTTLE FEEDING / stop breast feeding at will after the first tooth erupts
2- Feed the child while being held + burp the infant after feeding
3- Clean the teeth after each feeding [ wipe the teeth with a wet gauze]
4- regularly lift the upper lip to check for signs of demineralization of the upper Anteriors
E. OH should start with the eruption of the first tooth – wipe the teeth with gauze and for ages 2-
6 brush with low fluoride tooth past [ 400-500 ppm] – parental supervision until the child can
properly spit
F. Children are encouraged to drink from a cup as they become 1 year old
G. Avoid frequent snacking and have regular meals instead
H. First dental visit should be combined with immunization dates [ at or before 6 months]

Prevention of ECC ideally begins pre natally:

1- give the mother information about diet and OH

2- treat the mother’s own oral diseases and lower MS count by mouthrinses and restorative care
3- educate the mother on modes of transmission of MS [ don’t lick spoons or pacifiers etc..]

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Caries in Permanent teeth

• Primary dentition = from 4-6 months till 6 years
• Mixed dentition = 6- 12 years old
• Permanent dentition = when all primary teeth are replaced with their permanent successors

Caries in mixed or permanent dentition have the same predisposing factors [ diet high in refined
carbohydrates , poor OH, decreased salivary flow etc..]

Diet analysis [ 24 hours diet chart ] = should be filled for 7 days [ must include a
weekend – because the child will eat different types of food when they are not at school]

Q: what salivary parameters should you measure when you are determining caries risk?

1- Consistency : thin or viscous [ thin watery is better – but not too thin because it means it’s
protective contents are also diluted ]
2- PH and bicarbonate content [ bi carbonate content neutralizes acids in the mouth]
3- Ca/ Po4 /fluoride content [ to determine the ability of remineralization]
4- Immunoglobins content [ ability to resist caries]
5- Flow rate

Q: if the child has high MS count , how can you lower it? Treat gross caries + prescribe antibacterial
mouth wash if the child is above 6 yo.

most to least susceptible teeth : first molar → upper molar → second molars → premolars → upper
centrals & canines → lower centrals and canines

NOTE: when caries level is low most of the caries occur on the occlusal surfaces [ pits and fissure caries ]
as caries level increase the proximal and smooth surfaces get affected as well.

Fluoride protects against smooth and proximal surface caries but not against pits and fissures [ that’s
why even in fluoridated areas you’ll still see Pits and fissure caries that need to be prevented by fissure
sealants]

If the child has caries on their primary dentition they will mostly develop caries in their permanent
dentition as well. [ because the oral environment is not changed – this is why it is important to treat
caries in the primary dentition + improve OH and diet to prevent caries in the permanent dentition]

Caries on the distal of E → will increase the risk of developing caries on the mesial surface of the 6 by
15 times [ even if the lesion is arrested you need to restore it because the hole will accumulate food
and plaque → bacterial colonization and caries on the mesial surface of the 6.

If you detect caries on one arch → examine the opposing arch & if you detect on one side → examine
the contralateral side

Hidden [ occult caries ] = the surface is intact and well mineralized but actually the lesion is huge inside
the tooth because caries progress underneath – this is mostly seen in well fluoridated areas .

• Best management of hidden occult caries is early detection using radiographs

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NOTE: worldwide there was a decrease in caries prevalence because of water fluoridation but then
caries prevalence increased again because many countries stopped water fluoridation and investing in
other programs + the diet changed and became more cariogenic [ processed foods, high sugar foods etc]

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Restoring caries in young permanent teeth

ICDAS = you must clean the tooth surface first before you determine the score [ otherwise caries will
be underscored] – detect surface discontinuity with a perio probe not a sharp explorer because it can
induce cavitation.
• 0 = sound tooth
• 1= opacity when drying the tooth
• 2= opacity without drying the
tooth
• 3= microcavities – loss of surface
integrity
• 4= underlying shadow
• 5- 6= cavitation

Caries risk in pediatric patients

Low Moderate High
- Optimal fluoride exposures - Suboptimal systemic - Suboptimal topical fluoride exposure
both systemic and topical fluoride exposure with - Frequent between meal snacking (3 or
- Consumption of simple optimal topical exposure more)
sugars limiting to mealtime - Between meal snacking (1- - Low level caregiver socioeconomic
- High caregiver 2) status.
socioeconomic status - Midlevel caregiver - No usual source of dental care
(financially stable) socioeconomic status - Active caries present in the mother
- Regular dental visits - Irregular use of dental - Children with special health care needs
services Conditions decreasing saliva flow
(medications, radiotherapy)
Examine the tooth surface :

• If you suspect caries → take BW [ enamel caries do PRR , dentine caries drill and fill ]
• If you are sure there are no caries → seal with fissure sealant

If the first permanent molar has deep caries and signs of pulpitis:

A. Crowding present → do ortho consult → extract the tooth [ usually all 4 first molars are
extracted to allow the 7 and 8 to drift mesially and fill the space]
B. No crowding →
• Acute pulpitis → pulpotomy [ CaOH2 or MTA]
• Chronic pulpitis → apexification or pulpectomy

Before extracting the first molars you need to verify that the child as 3rd molars [ radiographical
evidence of 3rd molars is usually seen at 9 year and 6 months ]

• If you are using composite ideally use etch and rinse adhesive systems [ it will result in the
strongest bond but it results in a higher chance of post op sensitivity and needs a cooperative
child]

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• Self etch adhesives will save time and are perfect for uncooperative child and results in less
post op sensitivity but they result in a weaker bond.
• Self etch adhesives are very hydrophilic, If you are using self etch adhesives → apply a layer of
flowable composite over it to make it more hydrophobic
• Diamond burs leave more uncut collagen fiber → better bond strength
• When you are bonding to enamel → make sure the cavity is dry
• When you are bonding to dentine → the cavity should not be very dry and slightly humid to
erect the collagen fibers and get better bonding

To ensure max bond strength :

1- Use etch and rinse adhesive systems when you can – if you use self etch cover it with a layer of
flowable composite
2- Use diamond burs to leave more uncut collagen
3- Make sure if the cavity is in dentine that it is not too dry [ to erect the collagen fibers]

Stainless steel crowns for permanent teeth:

1- Hypoplasia / hypomineralization
2- Large carious lesions and lesions requiring pulp therapy
3- Special needs patients
If stainless steel crown is placed on a perm tooth you need to adjust the crown margins and
this is temporary until the child reaches 18 and can get a PFM or a porcelain crown.

Hypoplastic anterior teeth can be treated by:

1- Microabrasion
2- Small saucer like preparations over the discolored areas and then fill them with composite

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Restorative materials for primary teeth

Q: why do you need to restore primary teeth ?

1- Restore function [ mastication, speech , occlusion, esthetics]

2- Relive pain and prevent spread of infection
3- Maintain occlusal height and arch length [ by restoring proximal caries]
4- Prevent the need for extractions and loss of space
5- By restoring primary teeth + reinforcing OH → you change the oral environment → less chance
of caries in the perm dentition
6- Prevent possible damage to perm teeth [ ex: untreated infection in primary teeth can lead to
turner’s tooth in perm teeth ]

Q: how is restoring primary teeth different from restoring permanent teeth?

1- Primary teeth have limited life span

2- Variable levels of cooperation by the child
3- Primary teeth have different morphology

Q: how is the morphology of primary teeth different from permanent?

• Greatest convexity is at the cervical 3rd

• Different MD width and crown height
• Enamel and dentine are thinner [ high chance of pulp
exposure ]
• Larger pulp with more prominent pulp horns [ high
chance of pulp exposure ]
• Pulp is closer to the mesial surface
• Contact areas are broad and flat
• Roots are longer , more slender and more flared
• Enamel rods at the cervical region are directed occlusally

Q: how are materials used to restore primary teeth different from perm teeth ?

1- Materials used can have less longevity [ less wear resistance, less durability and less ability to
withstand masticatory forces]
2- Have adequate strength even if placed in less bulk
3- Materials must have quick setting reaction
4- Able to work in moisture and less technique sensitive
5- Have good adhesive properties since less cavity prep is required

NOTE:

If after caries excavation you are not sure of the prognosis of the tooth → place GIC

A. Pain goes away → remove a little bit of the GIC and place composite
B. Pain is still there → consider pulpotomy / pulpectomy then composite or SCC

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Stainless steel crowns [ SCC]

Indications :

- After pulpotomies / pulpectomies

- Multisurface caries / fractured teeth
- Developmental defects [ amelogenesis / dentinogenesis imperfecta]
- Wear and loss of occlusal height
- Young kids with high caries risk being treated under GA
• Full coronal coverage but poor esthetics – this can be fixed by placing a labial veneer with
composite [ the veneer usually debonds + it’s very expensive to place]

Procedure : https://www.youtube.com/watch?v=sBYXJjgXKZQ

1- Check occlusion before you start

2- Select crown size [ proper MD width, height and SLIGHT resistance to seating]
Bring 3 crown sizes before you start [ the actual size you think will fit , one size bigger and one
size smaller]
3- Adequate LA [ block or STA ( single tooth anesthesia )]
4- Occlusal reduction [ 1 – 1.5 mm] following cusp anatomy
Occlusal reduction should be done before caries removal or pulpotomy [ or you can do
pulpotomy – restore the tooth and then do occlusal reduction]
You can check occlusal reduction by comparing the tooth to the adjacent marginal ridge [ it
should be 1.5 mm lower than the marginal ridge of the adjacent tooth ] or you ask the child to
bite on AlUWAX [ if you have enough reduction you will not see any perforations in the wax]
5- Caries removal / pulpotomy
6- Restore tooth after pulpotomy
7- Interproximal reduction [ just open the contact] + bevel all line angles
No buccal reduction Is made because you want the bulge of the cervical region buccaly to aid in
retention of the crown
8- Try the selected crown by placing it on the LINGUAL side then rotating it towards BUCCAL
9- Using an explorer make a scratch line on the gingival margin – remove the crown and using
scissors or acrylic bur cut 1 mm below the scratch line then reinsert the crown
10- Check for any gingival blanching [ blanching means you need to trim a little bit more from the
margins]
11- With crimping pliers crimp the margins to fit into the undercuts of the prep → after this the
crown should snap into position under firm pressure – seat the crown again and check all the
margins [ any open margins → crimp again ]
Crown should have proper occlusion – same marginal level as adjacent – margins should be 1
mm below gingival margin
12- finish the cervical margin with finishing stones and polish
13- cement the crown using RMGIC – place a cotton roll and ask the child to bite down – remove
excess + the marking on the buccal side

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TIPS:

• if you are placing crowns on the first and second primary molars → do more interproximal
reduction + fit the crown on the second molar first
• if the 6 did not erupt yet make sure you do enough distal reduction of the primary second molar
[ if you place an over sized crown on E → ectopic eruption or impaction of the 6]
• most common size for D = 4 or 5 most common size for E = 4

in class II → the width of the isthmus is ½ the occlusal table width + you round the axiopulpal line angle

Restorative materials in pedo :

Amalgam – rarely used [ sometimes used if moisture control is very difficult]

Resin composite [ highest esthetics + good micromechanical retention by acid etching –
technique sensitive and requires good moisture control + cooperative child]

GIC [ bonds chemically to the tooth structure - can be placed if moisture control is not excellent –
poor esthetics – releases fluoride + gets recharged with fluoride every time the child brushes, poor
wear resistance ]

RMGIC [ resin + GIC → chemical bonding + light curing , stronger than GIC and better esthetics ]
Compomers [ used if you want a material that is stronger / more esthetic than GIC but less
technique sensitive than composite]

THE GOLD STANDARD MATERIAL IN PEDO IS PACKABLE COMPOSITE – USED IN ALL CASES

Fissure sealants: for deep fissures – you etch and then apply [ no bonding]
PRR if there are carious areas on the occlusal surface you drill those areas slightly place flowable
or packable composite and fissure sealants on the rest of the fissures

PRR TYPES:
Type A – caries are confined to the enamel
Type B – caries are small but extend to the dentine
Type C - caries are deeper into the dentine

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Restoring primary anterior teeth :

Single discolored tooth due to trauma but the tooth is vital → treat by a labial composite veneers

Full coronal coverage for anterior teeth is indicated when:

1- Multisurface caries / Caries involving incisal edge

2- Extensive cervical decalcification
3- After pulpotomy / pulpectomy
4- Very poor oral hygiene - high risk caries
5- If you are doing treatment under GA

Composite strip crowns [ cellulose crown former]:

1- Incisal reduction + remove caries

2- Proximal reduction
3- Trail fitting of the cellulose crown – make a hole on the palatal surface
4- Etch the tooth – wash and dry then apply bonding
5- Fill the crown with composite resin - remove excess from the palatal hole and cure
6- Remove the crown former - usually no need for finishing but make sure you remove any excess
cervically

Anterior SCC : not esthetic but a labial composite veneer can be added

Esthetic primary anterior crowns [ zirconia crowns ]

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Pulp therapy in primary teeth

In primary teeth the initial signs of pulpal inflammation are seen in between the roots because Pulp
chamber floor is very thin and porous + most accessory canals open into the furcation area [at a
later stage the PA region will have a radiolucency as well]

Q: when can you only treat by a restoration ?

1- Caries confined to the enamel or slightly into dentine

2- No symptoms or pain [ or signs of reversible pulpitis ]
3- No signs of iireversible pulpitis
4- PDL + PA region are sound radiographically

Q: why is the pulp easily affected in primary teeth ?

Primary teeth have thin enamel + large pulp chambers + wide DT → inflammation easily reaches the
pulp

PULP THERAPY
INDICATIONS CONTRAINDICATIONS
Bleeding disorders and coagulopathies • Congenital heart disease [ risk of
[ hemophilia and von willbrand disease] infective endocarditis]
In such cases you want to avoid extraction • Immunocompromised pt [ cancer pts
because you don’t want bleeding and long term corticosteroid users ]
• Poorly controlled diabetics [ poor healing
potential ]
• Special needs / dis abilites
In such cases you want to extract and not do
pulp therapy because you don’t want to leave a
source of infection

• If the tooth is close to it’s shedding time → extract don’t do pulp therapy
• Pulpotomies and pulpectomies are better done on young primary teeth that will stay for a long
time
• If the child has on and off pain that is not annoying them very much → do indirect pulp capping
[ remove caries and keep affected dentine → apply CaOH2 then GIC ]
• You can’t really depend on history of pain in children to determine pulp status because children
don’t really know how to describe the pain
• If the tooth is mobile → indicates pulp necrosis + PA involvement

After pulp therapy posterior teeth should be restored with SCC and Anteriors with strip crowns
[celluloid crowns]

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PULP THERAPY :

Indirect pulp capping

• There should not be any signs of pulpitis
• Remove caries → keep affected dentine [ make sure DEJ is free of caries ] → place CaOH2 then
ZOE followed by GIC [ if you want excellent coronal seal → place composite over the GIC]

Direct pulp capping [ NOT DONE IN PEDO ]

• Unsuccessful in pedo
• Pulp is already inflamed so if you place pulp capping material → internal root resorption

Pulpotomy : removal of the coronal pulp tissue

Indications Contraindications
1- Pulp is reversibly and minimally 1- Spontaneous, unprovoked pain
inflamed [Signs of irreversible pulpitis /
2- Destruction of marginal ridge in first necrosis]
primary molar 2- Intra-oral swelling
3- Radiographic evidence: 3- Mobility
A. Caries extends >2/3 depth 4- On coronal pulp removal:
through dentine A. No haemorrhage - necrotic
B. No sign of pathological root pulp
resorption B. Hyperaemia - irreversible
4- Minimal hemorrhage on pulpotomy pulpitis
5- Tooth is restorable 5- Tooth close to the date of
exfoliation
6- Non restorable tooth

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Pulpotomy procedure :

1- Adequate LA
2- Use large size round bur to remove all caries and overhangs
3- Spoon excavator to remove all soft caries
4- Use low speed round bur to open and de roof the pulp chamber
5- If the pulp is inflamed it will start bleeding → with spoon excavator or large round bur remove
the pulp from the pulp chamber Do We Still Need Formocresol in Pediatric
6- Control hemorrhage by applying a cotton soaked with CHX or saline Dentistry?
7- Place ferric sulfate [ formacresol] or MTA https://www.cda-adc.ca/jcda/vol-71/issue-
8- SCC / anterior strip crown 10/749.pdf
• if you place Ferric sulfate in a cotton pellet for 1 min then remove the cotton and place ZOE or IRM
• if after removing the coronal part of the pulp chamber, radicular pulp still bleeds → you need to do
pulpectomy
Insert a small file inside the canals and remove the pulp tissue → enlarge to 2 sizes larger using files
→ irrigate with saline / CHX→ dry canals and place Metapex [ CaOH2 + iodoform] → place ZOE then
GIC then composite and next session prepare for SCC

Q: what medications can be used for pulpotomy ?

1- Formocresol – contains formaldehyde ( carcinogen ) – bactericidal

2- Ferric sulphate – excellent hemostatic agent but no bactericidal effect
3- Calcium hydroxide [ not used in primary teeth because it causes internal resorption - used
only for Cvek partial pulpotomy in permanent teeth ]
4- Glutardehyde
5- Electrosurgery
6- MTA

Q: how can you know that the pulpotomy worked?

1- No radiographic evidence of internal resorption

2- No breakdown of periradicular tissues
3- No symptoms like pain or swelling

Material from inside to outside : MTA → ZOE → GIC → composite → SCC

Pulpectomy : removal of the coronal pulp tissue + radicular pulp tissue

Indications Contraindications
1. Evidence of pulpal necrosis 1. Non restorable teeth
2. Hyperaemic pulp / irreversibly inflamed 2. internal root resorption
3. Evidence of furcation / periapical involvement 3. Mechanical or carious perforations of the
on radiographs floor of the pulp chamber
4. Spontaneous (unstimulated) pain 4. bone loss
5. Presence of dental or follicular cyst

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Q: what medications can be used in pulpectomy?

1- calcium Hydroxide (Vitapex - CaOH + iodoform)

2- Zinc Oxide Eugenol ( non - reinforced) – paste consistency in the chamber and thin consistency
in the canals but takes time to mix and place
3- Iodoform paste (e.g. Kri paste)

If pulpectomy fails → you need to extract the tooth

Long term success after pulp therapy depends on coronal seal

Most failure in pulp therapy is due to inappropriate case selection [ diagnosis]

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Fluoride modalities in pediatrics

Q: what are the protective mechanisms of fluoride?

1- Fluoride changes HA crystals to fluoro apetite crystals which are more acid resistant and less
soluble
2- Fluoride binds to proteins in plaque and stays there to be released when the PH drops below 5.5
3- Fluoride inhibits bacterial enolase → inhibits acid production

Fluoride acts in 2 ways:

A. Pre eruptive : fluoride gets incorporated into the enamel while the → makes enamel stronger +
alters the grooves and makes them less plaque retentive
B. Post eruptive

NOTE: the percentage of fluoride in the water depends on the climate of the place [ cold countries →
fluoride in water = 1 ppm , hot countries fluoride in water = 0.7 ppm ]

Fluoride varnish / mouthwashes are contraindicated in children below 6 because they will swallow
most of it.

• Ages 2- 6 years old → low fluoride containing toothpaste [ 400- 600 ppm] – smear or pea
amount - Children above 6 and at high caries risk → use toothpaste with 1000 ppm
• If the child is at high risk you tell them to spit and not rinse after brushing.
• children should be monitored until the age of 6-8

Fluoride varnish: DURAPHAT [ 5% sodium fluoride ] – 2.26 % fluoride ion

• wipe the teeth with gauze to dry them → apply varnish onto tooth surface [ you can use
absorbing dental floss and insert fluoride interproximally]
• the varnish will form a sticky coat on the teeth that dissolves slowly over several days [
maximum absorption of fluoride into the tooth surface and minimal risk of fluoride ingestion]
• fluoride varnish also increases the fluoride content of saliva
CAUTION: instruct the child to not eat or drink for 1 hour and do not brush their teeth same day
of the application
Fluoride varnish tubes are no longer used because the fluoride used to settle in the lower end of
the tube and there would not be equal concentration of fluoride all over the tube.
Even if you are using fluoride packs make sure you mix it well before application

Prophylaxis does not increase the effect of fluoride – applying it over plaque is more beneficial [ Fl is
released when PH drops below critical point ]

Q: do you need to do prophylaxis before placement of fluoride varnish / APF gel? If there is a lot of
calculus / plaque with gingival inflammation → do prophylaxis and apply fluoride in the NEXT session [
because there will be bleeding when you do prophylaxis]

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But if plaque is minimal keep it and apply fluoride [ fluoride will adhere to the proteins in the plaque and
release when the PH drops below 5.5]

APF gel : 1.23% acidulated phosphate fluoride gel

• CAUTION: APF gel contains hydrofluoric acid to increase enamel porosity then fill it with fluoride
to change HA into FA crystals – but it cannot be applied if the child has open carious lesions [
the acid will easily reach the pulp]
If there are enamel or dentine lesions you can still use APF , you only can’t use it if there is
frank cavitation [ in this case use sodium fluoride varnish]
• recommended at ages 6- 18 , every 3 – 6 months for an application time of
4 minutes
• APF has 3 types :
1 minute foam
1 minute gel
4 min gel [ the only one that is effective]

application: APF gel is applied in foam trays [ both upper and lower arches are together ]

1- Load 3rd of the tray with the gel and insert both upper and lower trays into the mouth at the
same time
2- Ask the child to grind or chew to change the thixotropic gel into a solution allowing it to go
interproximally
Application time = 4 minutes
Patient should be sitting up right with head tipped forward and has high saliva ejector in their
mouth
3- Ask the child to spit for 1 minute after application
Child should not eat / drink for 30 mins

Silver diamine fluoride [ SDF] : applied on active carious lesions to arrest them.
• Active component is SILVER [ anti bacterial and anti fungal – when applied will stabilize all cariogenic
bacteria in the cavity – the lesion is then mineralized by fluoride]
• Ammonia is added to stabilize silver

Drawback of SDF: when applied it changes the carious lesions black.

SDF/ KI [ Riva star] : SDF alone will cause the lesion to turn black but if it is coated by potassium iodide
the lesion does not change color [ remains brown ]

Indications of SDF:

1- Caries control in all ages

2- Extreme caries risk [ xerostomia / ECC]
3- Tx Behavioral / medical compromised pt [ hospitalized pts , eldery , uncooperative children ]
4- If you can’t treat all lesions in one session

SDF can also be applied for : Acute pulpitis / as cavity liner / indirect pulp capping

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Application of SDF :

1- Dry the tooth surface

2- Apply 1 drop / kg of body weight per visit
3- Apply for 1 minute then rinse
4- You can cover SDF with GIC or composite

Titanium tetrafluoride
• Excellent for caries and tooth erosion – results in glazed like layer
• Higher and more rapid uptake of fluoride because each titanium ion hold 4 fluoride ions that quickly
remineralize any demineralized spot

Sorbitol in toothpaste = laxative

Nitrate containing toothpastes [ used to reduce hypersensitivity] = can cause methemoglobinemia

Fluoride supplements:
Indicated only in high risk children whom dental disease will cause a risk to their general health [
children at risk of infective endocarditis]

They are only effective if they are given over a long time – the aim is to make the child caries free to a
point where you don’t need to do any Tx. [ because each procedure would require prophylactic ABX]

Q: what would you consider before prescribing fluoride supplements ?

1- Age
2- Caries risk
3- Other sources of fluoride [ specially content of fluoride in drinking water]

Age Fluoride in water

<0.3 mg/ L 0.3 – 0.5 mg / L
6m – 4 years 0. 25 mg 0
4 - 8 years 0.5 mg 0.25 mg
8+ 1 mg 0.5 mg

Q: how much fluoride supplements should an 8 YO child take who drinks Fluoridate water that
has less than 0.3 mg/ L fluoride ? 1 mg of fluoride

Probable toxic dose = minimal dose that can cause toxic signs and symptoms = 5mg / kg of body weight
per day

GIT symptoms can occur at 3-5 mg / kg of body weight

Certain lethal dose = 32- 60 mg / kg of body weight

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Fluoride toxicity:
Symptoms : nausea, vomiting, diarrhea, abdominal cramps convulsions , cardiac and respiratory arrest

Management:

1- Know the type , amount, concentration and time of fluoride ingestion + child’s weight
2- Minimise further absorption by giving calcium products [ milk,yougurt , calcium gluconate, or anti
acids containing calcium carbonate ]
3- DO NOT INDUCE VOMITING
4- Monitor vital signs and seek medical help ASAP

Dental fluorosis:
Increased fluoride concentration within the microenvironment of the ameloblasts during the period of
enamel formation.

A daily dose higher than 0.05mg of F per 1 kg body weight per day for children with developing teeth
can lead to risk of fluorosis.

• 1 year old weight 5 Kg= the max dose 0.25mg F ion per day.
• 2 year old weight 10Kg= the max dose 0.5mg F ion per day.
• 4 year old weight 15 Kg= the max dose 0.75mg F ion per day.

Management :

• Mild fluorosis → Surface remineralisation – CPP-ACP (Tooth Mousse)

• If enamel surface is defective → microabrasion: Dilute hydrochloric acid / 35% Phosphoric acid and
pumice paste, followed by remineralisation with topical F or artificial saliva
• Severely discolored enamel / mottling and loss of portions of enamel → Composite resin buildup or
Veneers [ Composite / porcelain]

Fluoride calculations: Molecular weight of sodium fluoride

= 2.2
To find the percentage of fluoride divide the percentage of the
gel by the molecular weight . Molecular weight of stannous
fluoride = 4.1
What is the percentage of fluoride in 1 ml of 1.23 % NAF gel ?

1.23/ 2.2 = 0.56 %

What is the percentage of fluoride in 1 ml of 0.6 % SnF2 gel?

0.6 / 4.1 = 0.15 %

Then if you want to get the amount of Fluoride in ml → multiply the fluoride % by 10.

0.56 % fluoride = 5.6 mg F/ ml

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0.15 % fluoride = 1.5 mg F/ ml

Then if you want to get the amount in PPM → multiply the mg/ ml by 1000

5.6 mgf/ ml = 5600 ppm 1.5 mgf/ ml = 1500 ppm

APF gel [ the % of APF gel = the % of fluoride ] – Ex: 1.23 % AP gel has 1.23 % fluoride → 12.3 mgF/ ml
and 12300 ppm

You first find % then mgF / ml then ppm

Fluoride toxicity calculcations

A 2 year-old child weighing 10kg swallows one tube of toothpaste (90g of a 0.76% MFP toothpaste):

Fluoride dosage ingested: 90mg/10kg= 9mg/kg [ PTD = 5 mg / kg ]

3 year old ingested 25 NaF tablets - each tablet has a concentration of 1mg F ion and the child’s
weight is 14kg:

• Since the child swallowed 25 tablets each containing 1mgF → total swallowed = 25 mg F
• PTD = 5 mg / kg → 5 X 14 = 70 mg F [ this is the dose that would kill the child]

Teeth will be affected by fluoride toxicity : [ helps you know which teeth will be at risk of fluorosis
depending on the child’s age ]

A daily dose higher

than 0.05mg of F per 1
kg body weight per day
for children with
developing teeth
[during calcification]
can lead to risk of
fluorosis

If the crown is fully

formed → no risk of
fluorosis

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Inhalation sedation
Conscious sedation
• A state of depression of the central nervous system
• Reduces anxiety
• Patient is still able to independently maintain an open mouth, adequate function of protective
reflexes (e.g laryngeal reflex) & respond to verbal commands

Nitrous oxide
• The only agent that meets conscious sedation requirements
• Low solubility in blood which causes it to have a very rapid onset & recovery time
• Produces euphoria and depresses the CNS

Nitrous oxide sedation

Indication Contraindication
1. Patients who are mild to moderately anxious 1- Inability to communicate or very young
[Fear of needles/ needle phobic] children
2. Child with some special needs or medically 2- Child fears the mask
compromised 3- Mouth breathing
3. When profound LA cannot be obtained 4- Cold / rhinitis
4. Patients with a gag reflex or persistent 5- Chronic obstructive airway disease
fainting 6- Otitis media
5. Prolonged or unpleasant treatment 7- Muscular depression activity
8- Psychiatric disease

NOTE: ASTHMA IS NOT A CONTRAINDICATION FOR USING NITROUS SEDATION

ASA I Normal healthy patients

ASA II Patient with mild Systemic disease

ASA III Patients with severe systemic disease that is limiting but not incapacitating.
ASA IV Patient with incapacitating disease that is a constant threat to life.
ASA V Patient not expected to live more than 24 hours

ONLY INDIVIDUALS IN GROUP ASA I AND ASA II ARE SUITED TO RECEIVE CONSCIOUS SEDATON

Nitrous oxide causes slight depression in cardiac output but the peripheral resistance is increased this
is why the BP is not affected

Nitrous oxide suppresses gag reflex but increases risk of nausea

Technique of administration:

1. Select the correct nasal hood size [ the mask should fit snuggle around the nose ]
2. Patient assessment and baseline monitoring should be carried out.

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3. Introduce 100% oxygen for 1 –2 minutes

4. The level of N2O is increased in 5 –10 % increments until signs of sedation are observed
(minimum O concentration = 23%)
5. The end point will vary, usually between 30 –40% of nitrous oxide
6. Dental treatment can usually commence within 5 minutes of induction
7. If patient appears over sedated N2O may be decreased by 5 –10 % the patient will be less
sedated in 30 to 60 seconds.
Lack of response to any command indicates that treatment should be terminated and
100% oxygen delivered.
8. Once treatment has been completed N2O flow is terminated and 100% oxygen is given for
3 –5 minutes to decrease the possibility of diffusion hypoxia.

Slow induction Rapid induction

- for inexperienced operators and older - for younger children
patients - risk adverse effects is greatly increased
- Begin with 100% O then increase NO - Patient is introduced to 40% NO and after 2-
concentration by 10% every minute until 3mins of careful monitoring, the dose is
desired effect is reached. titrated accordingly

Signs and symptoms of No2 sedation [ relative analgesia]:

1- Floating sensation / heavy feeling

2- Feeling of warmth
3- Tingling in extremities + numbness of lips
4- Voices, sounds seem distant
5- Relaxation of skeletal muscle + eyes take on distant gaze

Early to ideal sedation Over sedation

Light headed Sleepiness **
Warmth Visual disturbances [ “ doctor the room is
Tingling sensations + numbness of the lips spinning”]
Euphoria Sweating
Laughing / crying **
Nausea **

Q:When nitrous oxide sedation of a child , the child starts to laugh hysterically what should you do?
Lower the sedation by 5% and monitor the child [ laughing Is a sign of over sedation]

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Advantages of nitrous sedation Disadvantages of nitrous sedation

1- Non invasive 1. Depends largely on psychological
2- Drug level may be altered or discontinued [ reassurance
titration] 2. Mask close to the operation site
3- Rapidly onset and recovery 3. Nasal seal may be broken during patient
4- Minimal impairment of any reflex – cough movement
reflex 4. N2O pollution [ the one at highest risk
5- Some analgesia [ by changing the patient’s during No2 sedation is the dentist]
mood their pain threshold become higher]
**Patient must respond favorably to tell-show-do for placing nasal hood and breathing through nose +
nitrous sedation works best when combined with non pharmacological behavior management

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Dental trauma in Primary teeth

Management of any dental trauma follows WASH protocol

Remember to ask 4 main questions
1- Where did it happen ?
2- where is the tooth?
W 3- Was there a state of unconsciousness after the trauma?
4- Was there previous trauma to the same area?
NOTE: if there was a state of unconsciousness you are not allowed to touch the child before
doing a neurological exam
A Articulation – check if there is any disturbance in biting
S Sensitivity – might be due to exposed dentine or pulp
How did it happen? [ medico legal aspect ]
H NOTE: in coherent stories of how the trauma happened indicate a planned trauma or abuse →
you need to report

Tetanus shot decision depends on vaccine history and wound condition

No need Advisable
Child took 3 doses or more Child took less than 3 doses
Vaccine was less than 5 Years ago Vaccine was more than 5 Years ago
Wound minor and clean Wound is big and soiled

Clinical examination of any trauma follows MP3 protocol

M Mobility – tested in vertical and horizontal directions + compared to a sound tooth
Percussion – done on a normal tooth first + done horizontally and vertically
Sharp sound → normal
P Dull sound → might indicate PA pathology
Pain on vertical percussion → PA problem
Pain on horizontal percussion → PDL problem
Pulp testing – done on normal tooth first , not very reliable [ many false +ve and false -ve]
Ex : false +ve if the tooth has liquefactive necrosis the pulp is necrotic but the canal is filled with
P
fluid that can transmit the electrical current and the child feels pain in the PA region
Or false -ve if the child does not feel anything but the pulp is vital [ pulp is in state of shock]
P Peri apical / panoramic radiograph

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TRAUMA IN PRIMATY TEETH

TRAUMA CONDITION Signs / symptoms Management
CONCUSSION TTP only
SUBLUXATION - Slight mobility but no displacement Basic protocol
- Bleeding from gingival crevice
LUXATION - Tooth appear to be separated from it’s Depending on degree of looseness either
[ EXTRUSION] socket reposition or extract
- Bleeding from gingival crevice + basic protocol
- Looseness
LATERAL - Alveolar bone fracture - Spontaneous repositioning
LUXATION - Tooth is inclined palately [ firm ] or - Repositioning
inclined labially [loose] - Extraction
- Bleeding from gingival crevice + basic protocol
INTRUSION - Tooth is firm - Spontaneous repositioning
- Infra occlusion - Extraction
- Alveolar bone fracture + basic protocol
- Bleeding from gingival crevice
AVULSION Tooth is completely out of the socket - DO NOT REIMPLANT
NOTE: if the tooth is not found in the vicinity - Just wait for the permanent tooth to
of the accident, do a chest X-ray To verify it is erupt
not inhaled inside the air way
ENAMEL Crack in the enamel without tooth structure -
Fluoride application
INFARCTION loss or just chipped enamel -
Widen the crack with a small round bur
ENAMEL and it with GIC
FRCATURE - Smoothen the rough edge or place
composite
ENAMEL DENTIN 1- LA → Clean the area with saline / CHX → Disinfect with NaOCl
FRACTURE 2- Place GIC then build up with composite
WITHOUT PULP 3- F/U = radiograph after 6-8 week and after 1 year
ENAMEL DENTIN - Pulp capping :
FRACTURE WITH 1. LA → Clean the area with saline / CHX → Disinfect with NaOCl
PULP 2. Place capping material CaOH2 or MTA
3. Place GIC then build up with composite
F/U = radiograph after one week , then 6-8 week and after 1 year
- Partial pulpotomy
- Extraction
CROWN ROOT Bleeding horizontal line on the crown - Extraction
FRACTURE - Zirconia pedo crowns
WITHOUT PULP - GIC and composite [ you remove the
fragment and place GIC apically and
then composite
CROWN ROOT - Extraction
FRACTURE WITH - Pulpotomy + GIC & composite
PULP - Pulpotomy + zirconia pedo crown

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ROOT FRACTURE - Extraction

- If there is a small root fragment left
leave it → will be pushed out by the
erupting perm
ALV BONE Group of teeth inclined palatally - Clean the area → LA → reposition
FRACTURE You will just see PDL widening on the xray fragment using 2 fingers [ one palatal
No damage to perm tooth because the tooth and one buccal ] until you hear a click →
moves away place splint for 4 weeks
- don’t attempt to move after you hear
the click you might damage the perm
tooth bud
- F/U after 1 week , 3-4 weeks, 6-8 weeks

** basic protocol = Careful observation & watchful follow up + NSAIDs + Good OH + Inform
parents about future possibilities [ tooth might change color or become necrotic]

Primary teeth have an aprismatic layer covering the enamel → this will make etching harder [ the layer
must be removed by gently by moving the bur over the surface to expose the prismatic enamel that can
be etched] – in primary teeth you need to etch longer [for 20 seconds]

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Dental trauma to young permanent teeth

If a primary tooth is subjected to trauma and breaks it is because it is weakened by caries and not
because of the trauma

If a sound tooth is subjected to traumas wither intrusion or avulsion

Most to least affected : upper centrals → lower centrals → upper laterals → lower laterals

Ellis classification of permanent teeth fractures

• Class 0 = crown infarction
• Class 1 = only enamel
• Class 2 = enamel + dentine
• Class 3 = enamel + dentine + pulp
• Class 4 = entire crown
• Class5 = root fracture
Anderson classification:
Uncomplicated crown fracture → Ellis 1 and 2
Complicated crown fracture → Ellis 3 and 4 [ involves pulp or root or both]

Q: why can’t we apply Ellis classification to primary teeth ? when primary teeth are subjected to
trauma they will not fracture and they will be displaced into the bone [ because the jaw bone is weaker
than teeth in children ]

The main aim of treating trauma of young permanent teeth is :

A. Save the pulp

B. Save the space

TRAUMA IN YOUNG PERMNANET TEETH

CONDITION Signs / symptoms Management
INFRACTION Incomplete crack in the enamel Etch → bond and seal
without loss of tooth structure or make small cavity and fill with
composite according to the size of the
damage
+ basic protocol
ENAMEL FRACTURE Fracture confined to the enamel with Smoothen or do composite filling
ELLIS 1 loss of tooth structure according to size of the damage.
+ basic protocol

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ENAMEL + DENTINE Fracture confined to the enamel + Glass ionomer indirect pulp cap then build
FRACTURE dentine [ without the pulp] with loss up with composite or do FRAGMENT
ELLIS 2 of tooth structure restoration [Exact original shape/ shade +
Fragment acts as a mega filler for
composite resin] – hold the fractured
fragment using soft wax piece
ENAMEL + Fracture of the enamel + dentine [ Pulp capping or pulpotomy
DENTINE+ PULP with the pulp] and loss of tooth
FRACTURE structure
ELLIS 3
CROWN-ROOT Fracture of the enamel + dentine + extraction of loose fragment and
FRACTURE cementum [ without the pulp] and restoration of the crown remaining or
WITHOUT loss of tooth structure fragment restoration using GIC adhesive
EXPOSING THE cement
PULP
CROWN-ROOT Fracture of the enamel + dentine + 1. Fragment removal then pulpotomy
FRACTURE cementum [ with the pulp] and loss 2. Extraction (of the whole tooth).
WITH EXPOSING of tooth structure 3.Orthodontic extrusion.
THE PULP 4. Surgical extrusion.
5. Coronectomy
ROOT Fracture of the dentine + cementum Reposition in the socket + splint [fracture
FRACTURE [ with the pulp] line will not disappear on the xray]
Apical root fracture have best prognosis
because they are closest to blood supply
and furthest away from the oral cavity +
bacteria
CONCUSSION TTP Relief the contact with the opposing
splinting is not needed it is only to relief
the child

SUBLUXATION Slight mobility but no displacement Relief the contact with the opposing
Bleeding from gingival crevice splinting is necessary
F/U because the tooth might need RCT, or
apexification or bleaching [ an abscess
might form or it changes color]
EXTRUSION Tooth is displaced coronally – longer
than adjacent teeth
Loose tooth
No response to EPT Reposition the tooth
Widening of PDL Relief the contact
LATERAL Alveolar bone fracture Splint for 4 weeks
LUXATION Tooth is firm – locked inside bone F/U because the tooth might need RCT, or
Crown displaced palately and root apexification or bleaching
labially
No response to EPT
Bleeding from gingival crevice
Widening of PDL

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INTRUSION The worst prognosis. Re-eruption is expected within 3 months

Alveolar bone fracture for incompletely formed roots.
Tooth is firm – locked inside bone Monitor pulp condition
In cases of total intrusion → Needs Ortho-assisted re-eruption is indicated in
periapical radiography to distinguish fully formed roots or if the tooth did not
from avulsion. erupt in 3 months, but it might fail should
ankylosis occur.
Surgical repositioning may produce a
faster result.

NOTES:

- Sometimes the trauma causes the fragment to get a brighter shade than the rest of the tooth. Still
you can use the fragment and then do full labial composite resin veneer to mask both the color
difference and the fracture line.
- In case of a big trauma and you want a quick solution to maintain pulp vitality and prevent space
loss → use celluloid crowns filled with CaoH2
• Open apex has better prognosis than closed apex +maxillary teeth have better prognosis than
mandibular teeth [ because of rich blood supply]
• CAUTION: NOT ALL DISCOLORED TEETH HAVE NECROTIC PULPS - TRAUMA CAN CAUSE
BLEEDING AND DISCOLORATION
• Dystrophic pulp calcification can be left untreated if it is asymptomatic
• during splinting period there will be an initial transient breakdown of tissues prior to tissue
repair.

Pulp capping procedure : Pulpotomy procedure:

6- LA → Clean the area with saline / 1- LA → Clean the area with saline / CHX → Disinfect
CHX → Disinfect with NaOCl with NaOCl
7- Place capping material CaOH2 or 2- Perform pulpotomy to a depth of 2 mm
MTA 3- Control bleeding by saline cotton pellet
8- Place GIC then build up with 4- Place CaOH2 or MTA
composite 5- Place GIC then build up with composite
F/U = radiograph after 6-8 week F/U = radiograph after 6-8 week and after 1 year
and after 1 year

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Management of avulsion in primary teeth

Avulsion = total separation of the tooth from the socket

CAUTION: if the parent tells you that they couldn’t find the tooth , take a radiograph it might
be a case of total intrusion – if not take chest x ray the child might have inhaled the tooth.

Q: a distressed parent calls you and tells you “ my child’s tooth is knocked out” what
should I do ?

1- Hold the tooth by the crown [ the white part] and avoid
touching the root. IF THE TOOTH IS PRIMARY – DO NOT
2- If the tooth is clean, try to put it back. PUT IT BACK!
3- If the tooth is dirty, don’t wash it.
4- Put the tooth in milk, contact lenses solution or under the THERE IS A HIGH CHANCE IT WILL
child’s tongue. - Don’t wrap it in cotton or tissue. GET ANKYLOSED AND PREVENT THE
5- Visit dental facility ASAP. ERUPTION OF THE PERMANENT
TOOTH

If the PDL cells are assumed to be alive → replant the tooth then do endo
If the PDL cells are assumed to be necrotic → endo then replant

The PDL cells are assumed to be alive and the tooth can be replanted [ without being stored in any
solution ] if it is done within 30 mins of the accident

Solution How long the PDL cells will stay viable

Hanks balanced salt solution 24 hours
Milk 6 hours
Saliva 2 hours
Saline 1 hour
Nothing 30 mins

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Management of avulsion
Immediate replantation Debride the mouth and congratulate the parents for a well done job +
[Tooth replanted onsite of FARAH
injury by parents or by an
adult in the vicinity]
Debride the tooth gently [ remove visible dirt using saline]
Early replantation Debride the socket gently.
[Tooth brought to your clinic Re-insert the tooth gently.
with “assumed” vital PDL- If the bone is sound, you may hear or feel a click that it’s in the exact
kept in the correct solution] right position.
Splint + FARAH
Gently remove necrotic PDL.
Rinse tooth with 2% NaFl solution to help minimize possible ankylosis.
Late replantation Extirpate pulp tissue. Then fill root canal with Ledermix paste. Gently
[ dry tooth] debride the socket.
Gently insert the tooth back.
Splint + FARAH

FARAH protocol
F Fix (splint) the tooth.
A Attend for any tooth fragment (chest X-ray)
R Repair (suture) damaged soft tissue
A Antibiotic and NSAID’ s
H Home care instructions.

Splinting
A. Rigid = does not allow physiological movement [ composite with ortho wire] – high chance of
ankylosis
indicted when there is bone fracture [ mostly avulsion and lateral luxation cases ]
B. Non rigid = allows physiological movement [ composite with nylon thread or wired orthodontic
bands] – minimizes chance of ankylosis

Q: How long should the splint stay for ? minimum 2 weeks and then evaluate if a 3rd week is needed
– in case of alveolar bone damage → 4 weeks

Q: is RCT needed after the replantation of a young perm tooth ?

• If the apex is closed → Start treatment within 2 weeks, fill the canal with Ledermix for 3
month, Followed by CaOH for another 3 months then proceed with RCT

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• If the apex is open [ more than 2 mm ] and the tooth is replanted immediately or early → no
need for RCT unless there is evidence of infection. In case of infection → do Apexification [
Fill the canal with Ledermix for 3 month, Followed by repeated CaOH canal medication
every 3 month , Untill apical calcification is evident by x-ray]

One of the complication after replantation is external replacement resorption : but at least the
replanted tooth will maintain the proper bone height and the proper position of the adjacent teeth until
the child can get an implant

To prevent external resorption → place multiple dressings of CaOH2

Ankylosis can occur after replantation [ since the jaw is growing the area of the ankylosed tooth will not
grow and cause a deformity ]

To minimize ankylosis :

1- Extra alveolar time should be kept to minimal and storage media should be appropriate
2- Handling [ rinse with 2% NaF ]
3- Splinting [ with non rigid splints ]

Q: how can ankylosis be managed? By de coronation

De coronation
1- Crown is cut
2- intentional trauma to the periapical region to establish a healthy blood clot which will
develop into healthy bone suitable to support an implant.
[ insert a bur all the way to the apex and leave a thin shell of the root → this shell will later
be replaced through external resorption to form bone that is suitable for implant
placement]

Auto transplantation = using supernumerary or impacted teeth to replace an avulsed tooth

Latest advancements:

1- using stem cells from deciduous teeth to grow tooth germs

2- Emdogain: enamel matrix derivative → may mediate cementum formation.
3- Alendronate → inhibits odontoclastic activity and prevents external resorption

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Apexogenesis & apexification

• stem cells are there waiting for signals from growing permanent teeth to turn into
odontoclasts to start the process of physiologic shedding

complicated crown fracture in young permanent teeth [ open apex] :

A. tooth is vital → you can so pulp capping OR pulpotomy OR apexogenesis

B. tooth is non vital → you can do apexification OR pulp revascularization

Apexogenesis Apexification
Indication: VITAL young perm tooth with open apex Indication: non vital young perm
tooth with open apex
Aim: preserve vital non inflamed pulp tissue to continue root Aim: create an apical hard tissue
formation and closure of the apex barrier that will allow root canal
Maintain proper C:R ratio [ because the root will continue to filling to be placed
grow ] Maintain the tooth in the arch for
function + aesthetics
Procedure: Procedure:
1- Local anaesthesia 1- Remove pulp tissue
2- Rubber dam isolation 2- Place CaOH2 to create apical
3- amputation of coronal pulp tissue with a high speed hard tissue barrier
diamond bur with constant water cooling + Pulp is 3- RCT can be completed after
washed with saline until hemorrhage stops - this is to the barrier is formed
minimize irritation to the pulp
Removal of 2 mm of pulpal tissue to a level of vital Root will not elongate more and will
uncontaminated tissue stay at that stage of growth
4- Non-setting CaOH / MTA is placed over the pulp
directly and is then covered with a setting CaOH.
Calcified barrier will form underneath the CaOH2 + Very poor prognosis because the root
stem cells in the pulp will be stimulated to form is short + dentine walls are very thin
odontoblasts to continue root formation & close the → tooth fractures cervically
apex
5- GIC base is placed over the dressings and the tooth is
restored with composite resin.
The technique may be performed at any level of the root
canal
F/U: every 3 -6 months with pulp vitality tests
+ Radiographs to check for hard tissue barrier formation and
continued root development

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Regenerative endodontics
Indication : non- vital young perm tooth with open apex

Procedure:

1- Irrigation with 2.5% NaoCl + treatment with triple antibiotic paste

2- ca(OH)2 medication in the coronal third of the root canals for 3 weeks
3- induction of apical bleeding + coronal sealing with white MTA

this process may lead to completed root formation

Decoronation Regenerative endodontics
Apex is traumatized to form a blood clot that will turn Apex is traumatized to form a blood clot that will act
into bone and allow the placement of an implant → as a scaffold for un differentiated mesenchymal cells
tooth is completely destroyed to enter the pulp and differentiate into odontoblasts
to continue root formation → tooth is preserved

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Pediatric facial injuries

Crumple zones = areas in the facial skeleton that absorb the traumatic energy and dissipate it away
from vital structures

Ex: Orbital bones are designed To absorb the impact and break away from the eye ball [ broken specules
go to sinus direction and not to orbital cavity] + The condyle is designed to break and prevent energy
from going into the middle ear

The major crumple zone in the skull = the nasal cavity

• Most traumas in children are sustained by the nose followed by the mandible
• The overall frequency of facial fractures in children is much lower than that in adults
• It is lowest in infants and increases progressively with age
• Two peaks are observed in children’s facial fractures 6-7 years and 12-14 years

NOTE: if you see malunion of facial fractures → suspect child abuse

Q: how is the skull and facial skeleton different in children ?

1- Cranium /Face ratio. 8:1 at birth - 2.5: 1 for adults.

2- Extent of para nasal sinuses is different
3- Type of bone and soft tissue.
4- Dental development [ developing dentition]

Clinical picture of maxillary Clinical picture of mandibular Children have:

fractures fractures
1- Facial swelling 1- Facial swelling • less facial fractures [ cranium
2- Occlusal disturbance 2- Occlusal disturbance takes all of the impact]
3- Peri orbital 3- Chin asymmetry • More susceptibility to green
emphysema 4- Sublingual ecchymosis stick fractures
4- Peri orbital ecchymosis 5- Trismus • More susceptibility to cranial
5- Diplopia injury
6- CSF epistaxis
7- Mid facial mobility + GREENSTICK FRACTURE: the ends of
paresthesia the bone are still connected and
there’s only a crack on one side of the
NOTE: if you see CSF epistaxis [ clear fluid coming out of the nose ] bone [ most common fracture in
→ indicates fracture of the base of the skull [ DO NOT TOUCH THE children]
PT AND CALL A NEUROLOGIST]

Q: why are radiographs in children not very accurate in cases of trauma [ limitations of radiographs in
pedo ] ?

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1- Incompletely calcified bone with underdeveloped cortical plates.

2- Numerous tooth buds undergoing development may mask injured areas.
3- Small nasal sinuses.
4- Green stick fractures are hard to recognize due to lack of bone displacement.
5- Questionable child cooperation.

Q: what can you do is you suspect a fracture and you can’t take a CBCT or radiograph? Ask the child to
break a tongue depressor with their open – if they can’t → suspect a fracture

Q: how can you detect orbital floor fractures clinically ? Ask the child to look up →
one eye will stay dropped because part of the eye muscle s is “trapped” inside the
orbital fracture.

Q: most of facial fractures in children are treated by? conservative tx

Management of facial fractures

1- Conservative Tx [ most commonly used ]
2- Closed reduction – you bring the teeth into occlusion and fix them using ivy loops or IMF
3- Intermaxillary fixation [ IMF] – done for 3 weeks during this time the child eats soft food that
goes through a straw behind the last molar tooth
4- Osteosynthesis [ open reduction] – access surgically
then bring both ends of the fractures together and fix
them with surgical plates [ lateral removed so they
don’t disturb growth ]

If the fracture is between 2 teeth → ivy loop

IMF = ivy loop on the lower + ivy loop on the upper and then
tie them together by another wire

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Management of medically compromised children

Congenital heart disease

Clinical appearance:

A. Cyanosis of the mucosa

B. Shortness of breath
C. Clubbing of the fingers

Dental management: those pts have risk of developing infective endocarditis → treatment should only
be done on stable pts after consultation with a cardiologist

If the child has an unstable cardiac condition → you cannot do anything until the condition is stable

Q: which cardiac conditions need ABX prophylaxis ? **

1- Prosthetic cardiac valve or prosthetic material used in valve repair

2- Previous endocarditis
3- Congenital heart disease in the categories below:
• Unrepaired cyanotic congenital heart disease including shunts
• Completely repaired defects in the first 6 months
• Repaired with residual defects [ ex: heart murmur ]
4- Cardiac transplantation recipients with cardiac valvular disease

NOTE: if surgery to repair congenital heart defect was done more than 6 months ago no need for ABX

Q: which dental procedures need ABX prophylaxis? All procedures that involve manipulation of the
gingival tissues / periapical region of teeth or perforation of the mucosa

ABX is NOT needed in :

1- Placing ortho appliances / brackets or prosthetic devices

2- Injections in non infected tissues
3- Bleeding from trauma to the lips or mucosa
4- Shedding of deciduous teeth
5- Radiographs

ABX prophylaxis in pediatrics [ single dose 30 -60 mins before the procedure]
Route Medication Dose
Oral Amoxicillin 50 mg / kg
Unable to take oral medication Ampicillin 50 mg / kg [ IV or IM]
Allergic to penicillin Azithromycin 15 mg/kg
Allergic to penicillin and cannot Clindamycin 20 mg / kg [ IV or IM]
take oral medication

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ABX for infections in pediatrics [ abscess, odontogenic

infections]
Medication Dose
Augmentin 312 mg in 5 ml OR
Pediatric dosage for paracetamol =
157 mg in 5 ml [ for very
young children] 15 mg / kg
Amoxicillin 25 mg / kg
**Both can be combined with metronidazole
7 – 7.5 mg /kg

Asthma
Dental management :
if the child has an asthmatic attack of wheezing and coughing → give 2-3 puffs of Ventolin
you need to check if the child in under steroid medication [ given in severe cases of asthma]
because long term steroid therapy can cause adrenal crisis and the child might collapse
NO CONTRAINDICATION FOR NITROUS OXIDE SEDATION

Cystic fibrosis : respiratory disease

CAUTION: those children are treated with tetracyclines and have teeth stains
Management: Use of general anesthesia must be discussed with respiratory pediatrician Long
appointments should be avoided

Renal disease
End-stage renal failure → progressive hypertension, fluid retention and build-up of metabolites
Dental implications :
1. Growth retardation
2. Pale and Bleeding tendency
3. Children on dialysis are under anticoagulants [ heparin → risk of bleeding]
4. Caries rate is low due to ammonia release
5. Uraemic stomatitis
6. Tooth calcifying during renal failure will exhibit hypoplasia

Liver disease
Clinical appearance = jaundice
Dental implications:
A. Intrinsic blue-green stain of primary teeth
B. Coagulation disorder (vitamin K-dependent)
C. Liver transplant recipients are immunocompromised
D. Altered drug metoblism **

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Diabetes Type l or insulin dependent is the most common in children

Dental implications :
Impaired defense against infection
delayed healing
Antibiotic prophylaxis are recommended for invasive dental procedures
Morning dental appointments [ after insulin injection and regular meal ] + always keep glucose
source ready
If they are being treated under GA [ dextrose and insulin infusion ]

If the pt is on steroids → stress from dental procedure can cause adrenal crisis , you need to put the
child under IV steroids before the procedure and then taper the steroids after the procedure is done.

Platelet disorders
Clinical signs : petechiae [ pinpoint bleeding ] , purpura
[ larger subcutaneous bleeding]
Thrombocytopenia :
Dental implication: failure of the blood clot to form [ it
is preferable to have platelet levels >50X 106/L before
extraction]

Coagulopathies
• haemophilia A (deficiency of factor 8)
• haemophilia B (deficiency of factor 9 )
• von willebrand’s disease (abnormality of factor 8 molecule complex)

Dental implications:

o Extraction and periodontal therapy requires factor replacement with consultation with
haematologist
o Endodontic therapy can be safely carried out without factor replacement
o Use rubber dam to minimize chance of ST injury

Thalassemia avoid treatment if hemoglobin is less than 100 g/L

Leukemia Acute lymphoblastic leukemia (ALL) : is the most common in children

Oral Complications:
• Erosive or ulcerative lesions
• Oral infection & Candidiasis
• Gingival bleeding
• Gingival hypertrophy -direct invasion of tissue by an infiltrate of leukemic cells
• Spontaneous dental abscess formation
• Loss of teeth: necrosis of the PDL

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NOTE: if you notice that the child has gingivitis and abscess formation without any local cause → test
for leukemia

Management:

1- No active dental treatment should be carried out untill the child is in remission ( remove
abnormal cells from the blood and bone marrow)
2- Dental pain treated conservatively by the use of antibiotics and analgesics
3- Swabbing the mouth with chlorhexidine mouthwash and use of antifungal agents + LA
preparations at mealtime [ to reduce pain from the ulcers ]

Once leukaemia is in remission dental treatment done with the following adjustment:

1- Haematological information required for invasive procedures

2- Prophylactic antibiotic to prevent postoperative infection
3- Children who are immunosuppressed need active antifungal treatment
4- Long term preventative care

Immunodeficiency
Qualitative defects in neutrophils
– Leukocyte adhesion defect
– Chediak-Higashi syndrome
Quantitative defects in neutrophils
- Neutropenia
- Cyclic neutropenia
Phagocytic disorders
- Agammaglobulinaemia
Defect in microbial killing
- Chronic granulomatous disease
Primary immunodeficiencies

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– Involving T cells, B cells, complement or combined defects and acquired disorders (e.g.
HIV,chemotherapy and radiotherapy)
Management :
Dental implications:
1- Prophylactic antibiotic therapy
1- Candidiasis 2- Extraction of pulpally involved
2- Severe gingivitis/prepubertal periodontitis teeth **
3- Gingivostomatitis 3- Acyclovir for recurrent HSV
4- Recurrent aphthous ulceration 4- Antifungals
5- Recurrent herpes simplex infection 5- Chlorhexidine 0.2% mouthwashes
6- Premature exfoliation of primary teeth **

Organ transplants : those children are mostly on cyclosporine immunosuppressants →

Management :

1. Eliminate infection [ teeth with large caries, tooth soon to be exfoliated should be
extracted ]
2. Perfect OH
3. ABX prophylaxis before invasive procedures
4. Gingivectomy if needed

gingival overgrowth

Cerberal palsy:
• Cognitive ability of a child with cerebral palsy should be determined because many
patients have no intellectual impairment
• Reflex limb extension patterns may be triggered when the limbs are in extension or
when the head is unsupported → transfer of the child to the dental chair should be
done with care
• Gag, cough, bit and swallowing reflexes may be impaired or abnormal → Mouth props
may be used but these kids are at risk for aspiration [ all used instruments should be
tied with floss to avoid being swallowed by the child]

Visually impaired
• Allow the child to touch the instruments and smell the materials + you need to explain to
them before you do the procedure [ do not surprise them because they can have a startle
reflex and push you]
• Use safety glasses as they are light sensitive

Hearing impairment:
• Those children can lip read so face the child and speak slowly and clearly
• Try to learn basic sign language

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• Maintain visual contact

• Deaf children are sensitive to vibration so introduce high speed hand drills with care
• Hearing aid volume need to be adjusted [ lower the volume of the hearing aid device so
they are not annoyed by the sounds in the dental clinic]

Down syndrome
• Determine the need for endocarditis prophylaxis [ because some might have cardiac
anomalies]
• Down syndrome children are susceptible to periodontal disease → emphasize on:
daily tooth brushing with fluoride tooth paste 500ppm
0.12% chlorhexidine mouth wash in older children

Pediatric oral medicine & oral pathology

Presentation of pathology in children is often different from adult

Odontogenic infections
Acute Chronic
1. sick and upset child 1. Sinus tract
2. Raised temperature 2. Mobile tooth
3. Anxious and distressed parents 3. Halitosis [ because of the puss]
4. Red and swollen face [Facial cellulitis] 4. Discolored tooth [ because of the
posterior spread of maxillary canine fossa necrotic pulp]
infection may lead to cavernous sinus
thrombosis
Mandibular infection may compromise the
airway
If infection has perforated the cortical plate child
may not be in pain

Management of odontogenic infections in children :

• Removal of the cause + Local drainage and debridement If the child does not respond to oral
• Maintenance of fluids ABX [ persistent fever, raised tongue
• Use of antibiotics ( penicillin or Amoxicillin + metronidazole and difficulty breathing / swallowing ]
or augmentin +/- metronidazole ] → transfer the child to the hospital to
• 0.2% chlorhexidine gluconate mouth wash get parental ABX
• Pain control with paracetamol

ABX for infections in pediatrics [ abscess, odontogenic infections]

Medication Dose

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Augmentin 312 mg in 5 ml OR
157 mg in 5 ml [ for very young children]

Amoxicillin 25 mg / kg
**Both can be combined with metronidazole
7 – 7.5 mg /kg
Paracetamol = 15 mg / kg

Primary Herpetic Gingivostomatitis

• Most common cause of severe oral ulceration in children
• Mostly caused by HSV l [ Usually occurs after 6 months of age]
• Fever , malaise then appearance of Vesicles and ulcers → Self-limiting ulcers heal
spontaneously with in 10 to 14 days

Management:

1- Oral fluids + Analgesics

2- Mouthwash 0.2% chlorhexidine gluconate
3- Antiviral oral suspension for severe cases - Administration of aciclovir in the first 72 hrs of
infection before the vesicle formation may resolve the infection

Herpangia
• Caused by Coxsackie group A virus
• fever and malaise before the appearance of the vesicles → Self-limiting ulcers heal
spontaneously with in 10 to 14 days
Most common viral infections in
Management: symptomatic care children = herpangia and primary
herpetic gingiva stomatitis
1- Oral fluids + Analgesics
2- Mouthwash 0.2% chlorhexidine gluconate Most common fungal infection in
children = Acute pseudomembranous
Acute pseudomembranous candidosis candidosis
Thrush in infants [ White plaques which on removal reveal an
erythematous base ]

Management : Antifungal medication Nystatin or amphotericin B for at least 4 weeks

Recurrent apthous ulcers

• Minor aphthae : crops of shallow ulcers [ Yellow pseudomembranous slough with
erythematous border ] measuring up to 5mm on the non-keratinized mucosa - Heals with in 10
– 14 days

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• Major aphthae: on keratinized mucosa - Last longer and heal with scarring
Management: Symptomatic care + mouthwash + Topical steroids

Erythema multiforme
• Self limiting with mucosal involvement limited to the oral cavity
• target lesions occur on the limbs.
• This lesion has concentric colour with erthematous halo and central blister.

Management :

Debridement with 0.2% chlorhexidine gluconate + Adequate fluid replacement + Pain control

Stevens Johnson syndrome

• Acute febrile illness + generalized exanthema +oral lesions and purulent conjunctivitis
• Vesiculobullous eruption over the body
• Severe involvement of multiple mucous membranes: oral, vulva, penis and conjunctiva.

Management : Debridement with 0.2% chlorhexidine gluconate +Adequate fluid replacement and + Pain
control

Eruption cyst or haematoma

Follicular enlargement appearing just before tooth eruption [ Lesion tend to be blue-black ] – the
erupting tooth will eventually rupture it

Management : No treatment unless infected

Phenytoin enlargement
Enlargement of the inter dental papilla + delayed eruption due to bulk of fibrous tissue

Management : Maintenance of oral hygiene + 0.2% chlorhexidine gluconate mouth wash +

Gingivectomy

Cyclic neutropenia
Episodic decrease in the number of neutophils every 3 to 4 wks - Peripheral neutrophil count drops to
zero during this period the child is susceptible to infection.

Recurrent oral ulceration, gingival and periodontal involvement resulting in mobile of teeth.

Management: Early preventive involvement + Dental care though all stages of cycle + 0.2%
chlorhexidine gluconate mouth wash

Epstein’s pearls Small nodules present on midline of the hard palate

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Bohn’s nodules Remnants of dental lamina occur on the labial or buccal aspect of the maxillary
alveolar ridge

Management: No treatment

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Anomalies in pediatric dentistry

Hypodontia : less number of teeth – usually associated with microdontia / is part of a syndrome
Most commonly affected teeth = lateral incisors + mand 2nd premolars
I. Andontia : no teeth
J. Oligodontia : few missing teeth
Hypodontia Is seen in: Cleft palate can cause failure of the
A. Rubella [ german measles ] tooth bud to develop → hypodontia
B. Down syndrome
C. Ectodermal dysplasia Or splits the tooth bud into two →
D. Cleft palate [ most commonly missing tooth with CP hyperdontia
= lateral incisor ]

Management of hypodontia: pedodontist + orthodontist + prosthodontist

A. Crowded arch → teeth are reshaped and adjusted to look like normal teeth
B. Spaced arch → ortho tx + artificial teeth to act as space maintainers until the age of 20 [ so the
pt can get fixed prostho]
• Hyperdontia : super numerary teeth – associated with (Cleido Cranial Dysostosis, Gardner
Syndrome) – might occur on both sides of a cleft palate
Mesiodense = extra tooth between the central incisors [ most common]
Paramolar = extra tooth in molar region either buccally or lingually
Distomolar = extra tooth behind the last molar
Hyperdontia can be complex [ island of enamel , dentine and cementum mixed together as a
disorganized mass] or can be compound [organized into tooth structures]

Management of hyperdontia: extraction of the extra teeth to prevent :

1- Ectopic / disturbed eruption.

2- cystic degeneration.

Fusion
• Union between dentin and-or enamel of two separately developed
teeth
• One tooth missing - Radiographically, roots appear separate

Gemination
• Incomplete division of single tooth bud + Notching of the incisal edge.
• Normal teeth count - One root radiographically.

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Microdontia
• smaller teeth than normal
• mostly lateral incisors and 3rd molars – can be associated with Ectodermal dysplasia & pituitary
dwarfism
- Management: Build up when available space is convenient, consider extraction and orthodontic
treatment.

Sanjad Sakati Syndrome Dwarfism + Mental retardation. + Microdontia. + High arched palate. +
Micrognathia.
Macrodontia: larger than normal tooth
- Management: crown reduction to 1 mm is acceptable. Consider extraction and prosthesis, implants
and or orthodontic treatment.

Dense evaginatus An enamel covered tubercle projecting from the occlusal

surface of a premolar, canine or molar tooth.

- Management: Composite build-up to support the tubercle – Gradual enamel

reduction

Dense invaginatus [ dense in dente] : A developmental invagination of the

cingulum pit with only a thin hard tissue barrier between the oral cavity and the pulp

- Management: Fissure seal as early as possible

Talon cusp A horn like projection of the cingulum of the maxillary incisor
teeth.

- Management: If occlusal interference present - gradual reduction of enamel

or elective pulpotomy or RCT
If it is not disturbing the pt → leave it

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- Enamel hypo plasia = defective quantity of enamel

- Enamel hypocalcification = defective quality of enamel
Turner’s hypoplasia: Localised infection or trauma to a deciduous tooth affects enamel formation
of the underlying permanent tooth.

Amelogenesis imperfecta :
• normal size and shape.
• normal dentine and pulp. abnormal enamel
hypoplastic/ hypominiralised or both

Dentinogenesis imperfecta : teeth have

normal contour at eruption, but present with a
distinctive amber-like hue

enamel is normal, but it is weakly attached to the

dentine and is rapidly lost → teeth show marked
attrition

• Type 1 – DI with osteogenesis imperfecta.

• Type 2 – DI “stand alone" with no systemic
involvement.
• Type 3 – Brandywine type with large pulp chambers.

Regional odontodysplasia : Poorly mineralized enamel & Dentin - large pulp chambers with pulp
stones present.

Taurodontism (Bull-like tooth) : molar with elongated crown & apically placed furcation of the
roots, resulting in an enlarged rectangular coronal pulp chamber.

Associated with : Ectodermal dysplasia, Klinefelter's syndrome , Down's syndrome

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Dilaceration : Sharp bend or angulation of the root - results from trauma during
tooth development

Concrescence : two or more teeth united by cementum

Hypocementosis: reported in some conditions including cleidocranial dysostosis and

hypophosphatasia

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Developing dentition in pediatric pts

Q: what are self correcting anomalies in children ? anomalies that get corrected with time and by the
eruption of the permanent teeth [ Ex: large perm teeth , crowded lower anteriors , spacing between
upper incisors]

At 2 years the primary dentition is complete [ 20 teeth] and the primary dentition continues till the age
of 6 .

Primary teeth will undergo attrition leading to edge to edge occlusion.

Q: Edge to edge bite in children is normally seen at ? 5.5 years

AGE NOTES
DENTITION
STAGE
0 – 6 MONTH Gum pads No teeth just gum pads
The gum pads contact posteriorly resulting in anterior open
bite that is occupied by the tongue
6 – 36 MONTH Eruption of primary The first primary tooth to erupt is the lower incisor
teeth Anterior teeth erupt in an upright position → less overjet
There is deep bite
6 M – 6 YEARS Primary dentition A. Spaced dentition = less risk
of crowding later on

B. Closed dentition = more risk

of crowding later on [ but
the increase in the
intercanine width in the
maxilla and the mandible +
jaw growth gives space and prevents crowding]

Primate spaces = physiological

spaces [ present in both spaced
and closed primary dentitions]
Located mesial to the upper
primary canine and distal to the
lower primary canine.
6-9 Early mixed When the first perm molar erupts , they erupt in an end to
dentition end occlusion then they will move mesially closing the
lower primate space → resulting in class 1 relationship [
early mesial shift]
9-12 Late mixed Eruption of the perm premolars and canines
dentition

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Molars the relationship

In the permenant molars the relationship is cusp to fossa and you use
Angle’s classification.

But in primary molar teeth the relationship is based on a line drawn distal
to the primary second molars

• Mesial step = lower primary second molar is mesial to upper

primary second molar
• Distal step = lower primary second molar is distal to upper primary
second molar
• Flush terminal plane = staright line between upper and lower second primary molars

If the child has mixed dentition you need to classify the primary molar relationship and the perm molar
relationship

Q: how does the end to end occlusion of the perm first molars change into class 1 relationship ?

Either by early mesial shift ( age 6-9 ) [ when the lower perm molars erupt and move mesially utilizing
the lower primate space and resulting in class I occlusion ] or by using the late mesial shift ( age 9-12) [
even if there is not enough primate space, the molar relationship will still change to class I because
primary molars and canines have a larger MD width than perm premolars and canines [ leeway space]
→ the perm molars use this leeway space and result in class I occlusion]

• Early mesial shift = the molars utilize the primate spaces

to result in class I occlusion
• Late mesial shift = the premolars erupt and the molars
utilize leeway space

Incisal liability the MD of the primary incisors is smaller than the MD of the perm incisors [ tooth
size difference is 6-7 mm]

Q: how does the incisal liability get adjusted ?

1- Interdental spacing will give 2-3 mm

2- Intercanine arch growth will give 3-4 mm
3- Incisor labiality [ labial inclincation of the upper incisors] will give 1-2 mm

Leeway space of Nance the MD width of the primary molars and canine is larger than the
MD width of the perm premolars and canines

• Leeway space in the maxilla = 0.9 mm in one side and 1.8 mm in both sides
• Leeway space in the mandible = 1.7 mm in one side and 3.4 mm in both sides

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As you go from the primary dentition to the perm dentition the arch length is reduced [ because of the
mesial movement of the perm molars – the late mesial shift ]

Ugly duckling stage [ Broadbent phenomenon] – from 9- 11 years :

Flaring of the upper perm central and lateral incisors – it is a transient malocclusion that will be
corrected by the eruption of the perm canines .

Q: what causes the ugly duckling stage / flaring in the perm incisors? because when
the perm canines erupt they will apply pressure on the roots of the upper perm centrals
causing the flaring. But as the canine continues to erupt down the diastema closes

Ortho tx is only done if after the eruption of the canine there was residual diastema.

• If the molars are already in class I relationship but there is anterior crowding → hold the molars
using a retainer [ nance or lingual arch ] and use the leeway space to adjust the incisor
crowding.

Serial extraction: sequential extractions of primary teeth to allow the proper alignment of the perm
teeth

ADV: no force is used to align the teeth + no problems with retention

DISADV: you need proper diagnosis + pt follow and compliance

1- The primary canines are extracted to provide space and allow the eruption of the permanent
lateral incisors
2- The primary first molars are extracted to accelerate the eruption of the 1st perm premolars to
erupt before the perm canines if possible
3- Extraction of the first perm premolars to allow the perm canines to move distally and fill the
space of the 1st perm premolars

Final outcome after serial extractions:

1- Aligned incisors
2- Missing first premolar
3- Canine occupying space of 1st premolar
4- Spacing in the posterior segment

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Interceptive orthodontic procedure in pediatrics

Interceptive procedures you see a problem during mixed dentition and you interfere at this
stage to prevent it from becoming malocclusion in the perm dentition

Tongue thrusting and thumb sucking will lead to → upper anterior proclination , anterior open bite and
posterior crossbite.

• The pressure from the tongue on the palate will cause the anterior teeth proclination + the
tongue does not allow the posterior teeth to contact → supra eruption of the post molars →
anterior open bite
• The thumb also pushes the tongue down → allowing un apposed contraction of the buccinator
msucles → maxilla constricts → posterior crossbite

If the thumb sucking habit is stopped → normal muscles will correct mal occlusion and the anterior open
bite should close in 6 month

Habit breaking appliances used for tongue

thrusting and thumb sucking [ usually used around the age of
8- 9 years]

Has a fence to prevent the thumb from entering the mouth and
to prevent tongue thrusting

The fence should not contact the lower incisors

If the child cannot tolerate a removable appliance → do fixed nance appliance and then solder the fence
over the wire

Hayley’s reminder appliance Blue grass appliance

Nance appliance + Teflon ring →

prevents thumb sucking

The child plays with the ring then

eventually stops the habit

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Mouth breathing
Causes of anatomical mouth breathing :

1- Deviated nasal septum

2- Allergic rhinitis, nasal polyps
3- Enlarged adenoids or tonsils
4- Short upper lip preventing lip seal
5- Obstruction in the bronchial tree

Habitual mouth breathing is not associated

with any anatomical defects – as a dentist you
can only fix habitual mouth breathing – using
In Habitual mouth breathing – the lips are
Oral screen [ acrylic plate placed on the buccal
flaccid [ low lip competence ] ➔ a ring can be
vestibule , the plate has perforations to allow
attached to the oral screen so the child pulls
breathing and you gradually close those
the ring and the screen up and down to
perforations with composite so the child stops
stretch the lips and increase lip tonicity and
mouth breathing and breathes through the
competence
nose.

Lip bumper can be used to correct lower

anterior crowding and distalize the molars +
correct lower anterior retroclination caused by
lower lip biting

The acrylic will push the lower lip forward →

prevent the child from biting on the lower lip

The force of the orbicularis oris will be

transmitted through the acrylic button then
through the wires to the molars causing
distillation providing space to correct lower
crowding.

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Anterior crossbite [ tx options]

• Tongue blade therapy
• Lower inclined plane (catalan’s appliance)
• Removable Hawley’s appliance [ simplest way to correct anterior
cross bite]
• Fixed appliances

Hawley’s appliance = acrylic plate + Z spring [ to move the teeth buccaly ]

+ posterior bite plane [to open the bite and bring the teeth to an edge to
edge contact ]

catalan’s appliance = acrylic plate fixed on the lower arch and

inclined at 45° [ child wear’s it for 10 -14 days only].

During biting the upper anterior teeth will slide against the lower
45° incline and move labially correcting the crossbite

Q: what happens if you give catlan’s appliance for more than 10

days? It will cause supra eruption of the posterior teeth and
anterior open bite

Tongue blade therapy = used when you see that the tooth is erupting in a
crossbite relationship – you ask the child to bite down on a tongue blade to give a
labial push while the tooth is erupting .

Tonugue blade therapy is done for a few hours daily for 2-3 weeks

Fixed appliance= helix appliance or acrylic plate with midline screw to cause
maxillary expansion

Tongue thrusting , mouth breathing ,

thumb sucking all cause posterior
crossbite

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Management of premature loss of primary teeth in mixed dentition

1- Space supervision : done when the primary teeth are removed and you don’t know wether the
perm tooth is erupting or not → take an OPG + PA radiographs
+ upper and lower casts for space analysis It takes 6-8 months for a tooth to
2- Space maintainer : indicated if the tooth need more than 6 move 1 mm in bone.
months to erupt [ there is bone covering the tooth + the root
is not fully formed ]
If more than 2/3 of the root is formed → the tooth is in active eruption [ no need for space
maintainer]
3- Space regainer : used if there is space deficiency

No bone covering the tooth + there is enough space or the tooth is in active eruption → just do space
supervision

Space maintainers for unilateral space loss

A. Band and loop / crown and loop

B. Distal shoe space maintainer: used if the 6 is not erupted

Acts as an eruption guiding appliance to guide the eruption of

the perm first molar + a space maintainer for the perm
premolar

The distal extension will guide the eruption of the perm molar
in an upright position , once the 6 is erupted → remove the
distal shoe and replace it with a band and loop space
maintainer

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Space maintainers for Bilateral space loss [ mandible ]

• lower lingual holding arch : the wire should contact the incisors

Space maintainers for Bilateral space loss [ maxilla]

A. Transpalatal Arch (Bar) : used for space loss [ as a space regainer] , both molars are moved
together – can be used if the child can’t tolerate nance acrylic button
B. Nance Appliance: has an acrylic button to prevent the molar from moving forward [ more
effective but the acrylic can
be annoying to the child]

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References

▪ McDonald, R. E., Avery, D. R., & Dean, J. A. (2011). McDonald and Avery's dentistry for
the child and adolescent. Maryland Heights, Mo: Mosby/Elsevier.
▪ World Health Assembly. Resolution. 60.17. New York, NY, USA: United Nations; 2006.
Oral health: action plan for promotion and integrated disease prevention.
▪ United States Environmental Protection Agency. Report to Congress. section 112 (n) (16)
Washington, DC, USA: Clean Air Act; 2000. Fluoride.
▪ Warren JJ, Levy SM. Current and future role of fluoride in nutrition. Dental Clinics of
North America. 2003;47(2):225–243.
▪ Hellwig E, Lennon AM. Systemic versus topical fluoride. Caries Research.
2004;38(3):258–262.
▪ Limeback H. A re-examination of the pre-eruptive and post-eruptive mechanism of the
anti-caries effects of fluoride: is there any anti-caries benefit from swallowing fluoride?
Community Dentistry and Oral Epidemiology. 1999;27(1):62–71.
▪ Ismail AI, Hasson H. Fluoride supplements, dental caries and fluorosis: a systematic
review.Journal of the American Dental Association. 2008;139(11):1457–1468.
▪ Choi AC, Sun G, Zhang Y, Grandjean P. Developmental fluoride neurotoxicity:a
systematic review and meta-analysis. Environmental Health Perspectives.
2012;120(10):1362–1368.

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