Faculty of Oral

and Dental
Medicine

Periodontics
OMP 512

Fifth year –Spring 2023

 OMP 512 (Periodontics)

Intended learning outcomes of course (ILOs):

a- Knowledge and understanding:

a1- Describe the features of the normal periodontium and their clinical relevance.
a2- Classify periodontal diseases according to the World Workshop 2017
classification scheme of periodontal and peri-implant diseases and conditions.
a3- Recognize spectrum of periodontal health as well as different diseases affecting the
periodontium.
a4- Recognize the role of dental biofilm in etiology of periodontal disease.
a5- Describe the role of tooth and prosthesis related factors and systemic conditions
affecting the periodontal supporting tissues.
a6- Describe the periodontal pathogenesis.
a7-Recognize various treatment options for chemical and mechanical plaque control.
a8- State indications, contraindications and types of periodontal surgeries.
a9- Recognize the proper flap design that improve your treatment outcome.
a10- Identify different regenerative materials used for treatment of periodontal defects.
a11- State types of periodontal plastic and esthetic surgeries.
a12- Explain healing of the periodontium after surgical and non-surgical periodontal therapy.

b- Intellectual skills:
b1- Formulate a diagnosis for the periodontal disease.
b2- Assess prognosis of periodontal disease.
b3- Design a treatment plan for periodontal disease.
b4- Illustrate the difference between various periodontal diseases.
b5- Select the appropriate regenerative material that suits different periodontal defects.

QA/CS/EN/22F/23S
 Contents

1. Treatment plan for periodontal diseases

2. Prognosis of periodontal disease and periodontal

risk assessment

3. Non-surgical periodontal therapy

4. Surgical periodontal therapy

5. Periodontal regeneration and reconstructive

Surgery

6. Periodontal plastic and esthetic surgery

8. References
 Treatment plan for periodontal disease

Treatment Plan

for

Periodontal Diseases

Student’s Learning Outcomes (SLOs):

By the end of this topic, you should be able to:

1. Design the master treatment plan.

2. Perform a treatment plan using phases of periodontal
therapy.
3. Explain the sequence of therapeutic procedures.
 Treatment plan for periodontal disease

The Master Plan for Total Treatment

 After the diagnosis and prognosis have been established, the treatment is
planned.

 The plan should encompass short- and long-term goals.

 The short-term goals are the elimination of all infectious and inflammatory
processes that cause periodontal and other oral problems that may hinder
the patient’s general health. Basically, the short-term goals are to bring the
oral cavity to a state of health.

 The long-term goals are the reconstruction of a healthy dentition that

fulfills all functional and esthetic requirements

The sequence in which dental therapy is performed may vary to

some extent in response to the requirements of the case. However, the
preferred sequence, which covers the vast majority of cases is as follows:

Phases of dental/periodontal therapy (integrated

together):

Emergency phase (preliminary phase)

Treatment of emergencies

 Pulpal/Periapical (e.g. acute pulpitis, acute periodontal abscess)

 Periodontal (e.g. periodontal abscess)
 Other
Extraction of hopeless teeth and provisional replacement if needed (may be
postponed to a more convenient time).
 Treatment plan for periodontal disease

Etiotropic phase (phase I therapy)

Plaque control and patient education

 Diet control (in patients with rampant caries)

 Scaling and root planing (SRP) and oral hygiene education/motivation.
 Correction of restorative and prosthetic irritational factors (e.g.
overhanging margins, unstable partial denture).
 Exacavation of caries and tooth restoration (temporary or final,
depending on whether a definitive prognosis for the tooth has been
arrived at and on the location of caries). If after excavation of caries,
the gingival seat of the cavity is situated subgingivally, periodontal
therapy (SRP + surgical crown lengthening) must be done in order to
be able to place the final restoration.
 Antimicrobial therapy (local or systemic whenever indicated).
 Occlusal adjustment in case of chronic trauma from occlusion.
 Minor orthodontic movement.
 Provisional splinting and prosthesis.
Evaluation of response to etiotropic phase: If after 3-4 weeks, still PPD >
5mm persists, consider open flap debridement + use of bone graft/
membrane.

Surgical phase (phase II therapy)

 Periodontal surgery (open flap debridement + use of bone graft/

membrane, surgical crown lengthening …. etc) including placement
of implants
Restorative phase (phase III therapy)

 Final restorations
 Treatment plan for periodontal disease

 Endodontic therapy
Maintenance phase (phase IV therapy)

Periodic check up:

 Presence of plaque and calculus
 Periodontal condition
 Occlusion
 Other pathologic changes
Immediately after completion of phase I therapy, the patient should be placed
on the maintenance phase (phase IV) to preserve the results obtained and
prevent any further deterioration. While the patient is on the maintenance
phase, he/she enters into the surgical and reparative phases of treatment
(Phases III and IV).

Preferred sequence of dental/periodontal therapy

Emergency phase

Etiotropic phase

Maintenance phase

Surgical phase Restorative phase

Note that: In any case you must write the treatment plan following the
above four phases.

For further reading refer to the following reference (article):

 Treatment plan for periodontal disease

Ower P: Minimally-Invasive Non-Surgical Periodontal Therapy. Dent Update

2013; 40: 289–295.

Formative Assessment Question:

1) Correct the UNDERLINED word(s) in the following statement:

Treatment of the periodontal abscess starts during the surgical phase.

2) Case :

A 56-year-old woman came to the dental clinic complaining of bad

appearance due to elongation of the upper anterior teeth. Medical history
revealed that she’s systemically free. Clinical examination showed
generalized deposits of plaque and calculus as well as generalized deepening
of the periodontal probing depth and loss of clinical attachment. The upper
anterior teeth also showed gingival recession. Radiographic examination
revealed generalized bone loss with a horizontal pattern allover. The lower
posterior quadrants only showed infrabony defects in the premolars and
molars.

Formulate the main outline of the treatment plan using treatment phases.
 Periodontal Risk Assessment

Periodontal Risk Assessment

Student’s Learning Outcomes (SLOs):

By the end of this topic, you should be able to:

Assess prognosis of periodontal disease.

Evaluate patient’s risk for recurrence of
periodontitis by using the functional diagram.
Demonstrate parameters used to construct the
functional diagram.
Measure the patient’s individual periodontal risk
assessment.
 Periodontal Risk Assessment

Formative Assessment Question:

Case:

A 40-year-old man came to the dental clinic suffering

from bleeding gums. After Phase1 therapy was performed, the
patient was scheduled for recall appointment during the
maintenance phase. Upon clinical examination, the following
parameters were recorded, 17% bleeding on probing, 3 sites with
probing depth≥5mm, 3 missing teeth, the ratio of BL/Age was
0.2. The patient had no systemic condition and he was a non-
smoker.
Categorize the patient periodontal risk assessment
and clarify the reason for your answer.
What is the recommended recall period?
 ORIGINAL ARTICLE

Periodontal Risk Assessment (PRA) for

Patients in Supportive Periodontal Therapy
(SPT)
Niklaus P. Langa/Maurizio S. Tonettib

Summary: The subject risk assessment may estimate the risk for susceptibility for progression of peri-
odontal disease. It consists of an assessment of the level of infection (full mouth bleeding scores), the
prevalence of residual periodontal pockets, tooth loss, an estimation of the loss of periodontal support
in relation to the patient’s age, an evaluation of the systemic conditions of the patient and finally, an
evaluation of environmental and behavioral factors such as smoking. All these factors should be con-
templated and evaluated together. A functional diagram may help the clinician in determining the risk for
disease progression on the subject level. This may be useful in customizing the frequency and content
of SPT visits.
Key words: periodontitis, maintenance, recurrent periodontitis, risk assessment, risk evaluation, peri-
odontal infection, reinfection, bleeding on probing, residual pockets, bone loss, smoking

Oral Health Prev Dent 2003; 1: 7–16. Submitted for publication: 21.06.02; accepted for publication: 14.11.02.

linical diagnosis during supportive periodontal gression of periodontal breakdown of a previously

C therapy (SPT) has to be based on the health sta-
tus obtained following successful active periodontal
treated periodontal site.
From a clinical point of view the stability of peri-
treatment. This, in turn, means that new baseline odontal conditions reflects a dynamic equilibrium
parameters will have to be established once the between bacterial challenge and an effective host
treatment goals of active periodontal therapy are response. Whenever changes occur in either of
reached and periodontal health is restored (Claffey, these aspects, homeostasis is disturbed. Hence, it
1991). Under optimal circumstances, SPT would be is evident that the diagnostic process must be
able to maintain stable clinical attachment levels based on a continuous monitoring of the multilevel
for many years. Hence, it is apt to determine the risk profile. The time intervals between diagnostic
clinical parameters which may serve as early indi- assessments should be chosen based on the over-
cators for a new onset or recurrence of the peri- all risk profile and the expected benefit for the pa-
odontal disease process, i.e. reinfection and pro- tient. It should be understood that, so far, the use
of individual risk profiles to determine the content
and frequency of preventive services has been
demonstrated to be very cost-effective (Axelsson
a University of Berne, School of Dental Medicine, Berne, Switzerland. and Lindhe, 1981a,b; Axelsson et al, 1991).
b University College London, Eastman Dental Institute, London, UK. By virtue of their previous disease experience, all
patients under a periodontal maintenance program
represent a population with a moderate to high risk
for recurrent periodontal infection. As opposed to
Reprint requests: Prof. Dr. Niklaus P. Lang, Department of Periodon- the general population without such a history, peri-
tology and Fixed Prosthodontics, University of Berne, School of Dental
Medicine, Freiburgstrasse 7, CH-3010 Berne, Switzerland. odontal patients need to participate in a well-orga-
E-mail: [email protected] nized recall system which should provide both a

Vol 1, No 1, 2003 7
Lang/Tonetti

Fig 1 Functional diagram to evaluate the

patient’s risk for recurrence of periodonti-
tis. Each vector represents one risk factor
or indicator with an area of relatively low
risk, an area of moderate risk and an area
of high risk for disease progression. All fac-
tors have to be evaluated together and
hence, the area of relatively low risk is
found within the center circle of the poly-
gon, while the area of high risk is found
outside the periphery of the second ring in
bold. Between the two rings in bold, there
is the area of moderate risk.

continuous risk assessment and adequate support- 1. Percentage of bleeding on probing,

ive care. Without this, the patients are likely to ex- 2. Prevalence of residual pockets greater than
perience progressive loss of periodontal attach- 4 mm (≥ 5 mm),
ment (Axelsson and Lindhe, 1981a; Kerr, 1981; 3. Loss of teeth from a total of 28 teeth,
Becker et al, 1984; Cortellini et al, 1994, 1996). 4. Loss of periodontal support in relation to the pa-
The assessment of the risk level for disease pro- tient’s age,
gression in each individual patient would enable the 5. Systemic and genetic conditions, and
practitioner to determine the frequency and extent 6. Environmental factors, such as cigarette smoking.
of professional support necessary to maintain the
attachment levels obtained following active therapy. Each parameter has its own scale for minor,
The determination of such risk levels would thus moderate and high-risk profiles. A comprehensive
prevent both undertreatment, and excessive over- evaluation of the functional diagram will provide an
treatment, during SPT (Brägger et al, 1992). individualized total risk profile and determine the
frequency and complexity of SPT visits. Modifica-
tions may be made to the functional diagram if ad-
SUBJECT RISK ASSESSMENT ditional factors become important according to new
evidence.
The patient’s risk assessment for recurrence of pe-
riodontitis may be evaluated on the basis of a num-
ber of clinical conditions whereby no single para- Compliance with the recall system
meter displays a more paramount role. The entire
spectrum of risk factors and risk indicators ought Several investigations have indicated that only a
to be evaluated simultaneously. For this purpose, a minority of periodontal patients complies with the
functional diagram has been constructed (Fig 1) in- prescribed supportive periodontal care (Wilson et
cluding the following aspects: al, 1984; Mendoza et al, 1991; Checchi et al,

8 Oral Health & Preventive Dentistry

 Lang/Tonetti

1994; Demetriou et al, 1995). Furthermore, it has 1. Percentage of sites with bleeding on probing
been established that treated periodontal patients (BOP)
who comply with regular periodontal maintenance
appointments have a better prognosis than pa- Bleeding on gentle probing represents an objective
tients who do not comply (Axelsson and Lindhe, inflammatory parameter which has been incorpo-
1981a; Kerr, 1981; Becker et al, 1984; Cortellini rated into index systems for the evaluation of peri-
et al, 1994, 1996). Non- or poorly compliant pa- odontal conditions (Löe and Silness, 1963; Mühle-
tients should be considered to be at higher risk for mann and Son, 1971) and is also used as a param-
periodontal disease progression. A report that in- eter by itself.
vestigated the personality differences of patients Although there is no established acceptable lev-
participating in a regular recall program as com- el of prevalence of bleeding on probing in the den-
pared to patients who did not, revealed that pa- tition above which a higher risk for disease recur-
tients who did not take part in a maintenance pro- rence has been established, a BOP prevalence of
gram following periodontal therapy had higher inci- 25% has been the cut-off point between patients
dences of stressful life events and less stable per- who maintained periodontal stability for 4 years
sonal relationships in their lives (Becker et al, and patients with recurrent disease in the same
1988). time frame in a prospective study in a private prac-
tice (Joss et al, 1994). Further evidence of BOP per-
centages between 20 and 30% determining a high-
ORAL HYGIENE er risk for disease progression originates from
studies of Claffey et al (1990) and Badersten et al
Since bacterial plaque is by far the most important (1990).
etiologic agent for the occurrence of periodontal In assessing the patient’s risk for disease pro-
diseases (for review, see Kornman and Löe, 1993), gression, BOP percentages reflect a summary of
it is evident that the full mouth assessment of the the patient’s ability to perform proper plaque con-
bacterial load must have a pivotal impact in the de- trol, the patient’s host response to the bacterial
termination of the risk for disease recurrence. It challenge and the patient’s compliance, especially
has to be realized, however, that regular interfer- when only few residual pockets remain after active
ence with the microbial ecosystem during periodon- periodontal therapy. The percentage of BOP, there-
tal maintenance will eventually obscure such obvi- fore, is used as the first risk factor in the functional
ous associations. In patients treated with various diagram of risk assessment (Fig 1). The scale runs
surgical and non-surgical modalities, it has been in a quadratic mode with 4, 9, 16, 25, 36 and
clearly established that plaque-infected dentitions > 49% being the critical values on the vector.
will yield recurrence of periodontal disease in mul- Individuals with low mean BOP percentages
tiple locations, while dentitions under plaque con- (< 10% of the surfaces) may be regarded as pa-
trol and regular supportive care maintain periodon- tients with a low risk for recurrent disease (Lang et
tal stability for many years (Rosling et al, 1976; Ax- al, 1990), while patients with mean BOP percentag-
elsson and Lindhe, 1981a,b). Studies to date have es > 25% should be considered to be at high risk
not identified the level of plaque infection compati- for periodontal breakdown.
ble with maintenance of periodontal health. Howev-
er, in a clinical set-up, a percentage of tooth surfac-
es covered by visible plaque of 20–40% might be 2. Prevalence of residual pockets ≥ 5 mm (resid-
tolerable in most patients. It is important to realize ual pocket greater than 4 mm)
that the full mouth plaque score has to be related
to the host response of the patient, i.e. compared The enumeration of the residual pockets with prob-
to inflammatory parameters. ing depths greater than 4 mm represents – to a cer-
tain extent – the degree of success of periodontal
treatment rendered. Although this figure per se does
not make much sense, when considered as a sole
parameter, the evaluation in conjunction with other
parameters such as bleeding on probing and/or
suppuration will reflect existing ecological niches

Vol 1, No 1, 2003 9
Lang/Tonetti

from and in which reinfection might occur. It is, there- 4. Loss of periodontal support in relation to the
fore, conceivable that periodontal stability in a den- patient’s age
tition would be reflected in a minimal number of re-
sidual pockets. Presence of high frequencies of The extent and prevalence of periodontal attach-
deep residual pockets and deepening of pockets ment loss (i.e. previous disease experience and
during supportive periodontal care has, in fact, been susceptibility), as evaluated by the height of the al-
associated with high risk for disease progression veolar bone on radiographs, may represent the
(Badersten et al, 1990; Claffey et al, 1990). most obvious indicator of subject risk when related
In assessing the patient’s risk for disease pro- to the patient’s age. In light of the present under-
gression, the number of residual pockets with a standing of periodontal disease progression, and
probing depth of ≥ 5 mm is assessed as the sec- the evidence that both onset and rate of progres-
ond risk indicator for recurrent disease in the func- sion of periodontitis might vary among individuals
tional diagram of risk assessment (Fig 1). The and during different time frames (Van der Velden,
scale runs in a linear mode with 2, 4, 6, 8, 10 and 1991), it has to be realized that previous attach-
≥ 12% being the critical values on the vector. ment loss in relation to the patient’s age does not
Individuals with up to 4 residual pockets may be rule out the possibility of rapidly progressing le-
regarded as patients with a relatively low risk, while sions. Therefore, the actual risk for further disease
patients with more than 8 residual pockets as indi- progression in a given individual may occasionally
viduals with high risk for recurrent disease. be underestimated. Hopefully, the rate of progres-
sion of disease has been positively affected by the
treatment rendered and, hence, previous attach-
3. Loss of teeth from a total of 28 teeth ment loss in relation to patient’s age may be a
more accurate indicator during SPT than before ac-
Although the reason for tooth loss may not be tive periodontal treatment. Given the hypothesis
known, the number of remaining teeth in a denti- that a dentition may be functional for the most like-
tion reflects the functionality of the dentition. Man- ly life expectancy of the subject in the presence of
dibular stability and individual optimal function may a reduced height of periodontal support (i.e. 25–
be assured even with a shortened dental arch of 50% of the root length), the risk assessment in
premolar to premolar occlusion, i.e. 20 teeth. The treated periodontal patients may represent a reli-
shortened dental arch does not seem to predis- able prognostic indicator for the stability of the
pose the individual to mandibular dysfunction (Wit- overall treatment goal of keeping a functional den-
ter et al, 1990, 1994). However, if more than 8 tition for a lifetime (Papapanou et al, 1988).
teeth from a total of 28 teeth are lost, oral function The estimation of the loss of alveolar bone is
is usually impaired (Käyser, 1981, 1994, 1996). performed in the posterior region on either periapi-
Since tooth loss also represents a true end point cal radiographs, in which the worst site affected is
outcome variable reflecting the patient’s history of grossly estimated in per cent of the root length or
oral diseases and trauma, it is logical to incorpo- on bitewing radiographs in which the worst site af-
rate this risk indicator as the third parameter in the fected is estimated in millimeter. On bitewing radio-
functional diagram of risk assessment (Fig 1). The graphs, one millimeter is considered to be equal to
number of teeth lost from the dentition without the 10% bone loss. The percentage is then divided by
third molars (28 teeth) is counted, irrespective of the patient’s age. This results in a factor. As an ex-
their replacement. The scale runs also in a linear ample, a 40-year-old patient with 20% of bone loss
mode with 2, 4, 6, 8, 10 and ≥ 12 being the critical at the worst affected posterior site would score
values on the vector. BL/Age = 0.5. Another 40-year-old patient with 50%
Individuals with up to 4 teeth lost may be regarded bone loss at the worst affected posterior site would
as patients in a low risk category, while patients with score BL/Age = 1.25.
more than 8 teeth lost may be considered as being In assessing the patient’s risk for disease pro-
in a high-risk category. Rationale for this stems from gression, the extent of alveolar bone loss in rela-
the significance of further tooth loss in terms of pres- tion to the patient’s age is estimated as the fourth
ervation of the function of the dentition. risk indicator for recurrent disease in the functional
diagram of risk assessment (Fig 1).

10 Oral Health & Preventive Dentistry

 Lang/Tonetti

The scale runs in increments of 0.25 of the fac- tients showed significantly higher BOP percentages
tor BL/Age, with 0.5 being the critical value to dis- and a higher proportion of patients which yielded
criminate between low and moderate risk and 1.0 higher BOP % during a one-year recall period than
being the value for moderate and high risk. This, in the IL-1 genotype negative control patients (Lang et
turn, means that a patient who has lost a higher al, 2000). Also, the latter group had double as
percentage of posterior alveolar bone than his/her many patients with improved BOP % during the
own age is at high risk regarding this vector in a same maintenance period indicating that IL-1 gen-
multi-factorial assessment of risk. otype positive subjects, indeed, represent a group
It may be argued that the incorporation of only of hyper-reactive subjects even if they are regularly
the worst site with bone loss in the posterior seg- maintained by normally effective SPT (Lang et al,
ment may overestimate an individual’s rate of pe- 2000). In a prospective study over 5 years on Aus-
riodontal destruction when only an isolated ad- tralian white and blue collar workers at a university
vanced bony lesion is present due to local etiolog- campus, the IL-1 genotype positive age group
ic factors, while an underestimation of the rate of above 50 years showed significantly deeper prob-
destruction may exist in a case of generalized ad- ing depths than their IL-1 genotype negative coun-
vanced disease. Nevertheless, in patients suc- terparts, especially when they were non-smokers
cessfully treated for periodontitis it has recently (Cullinan et al, 2001).
been demonstrated that the worst site with bone In assessing the patient’s risk for disease pro-
loss in the posterior segment may, indeed, repre- gression, systemic factors, if known, are only con-
sent the past history of destruction of the entire sidered as the fifth risk indicator for recurrent dis-
dentition (Persson et al, 2003). ease in the functional diagram of risk assessment
(Fig 1). In this case, the area of high risk is marked
for this vector. If not known or absent, systemic fac-
5. Systemic and genetic aspects tors are not taken into account for the overall eval-
uation of risk.
The most substantiated evidence for modification Research on the association and/or modifying
of disease susceptibility and/or progression of pe- influence in susceptibility and progression of peri-
riodontal disease arises from studies on Type I odontitis of physical or psychological stress is
and Type II (insulin-dependent and non-insulin-de- sparse (Cohen-Cole et al, 1981; Green et al, 1986;
pendent) diabetes mellitus populations (Gusberti Freeman and Goss, 1993). The hormonal changes
et al, 1983; Emrich et al, 1991; Genco and Löe, associated with this condition, however, are well
1993). documented (Selye, 1950).
It has to be realized that the impact of diabetes
on periodontal diseases has been documented in
patients with untreated periodontal disease, while, 6. Cigarette smoking
as of today, no clear evidence is available for treat-
ed patients. It is reasonable, however, to assume Consumption of tobacco, predominantly in the
that the influence of the systemic conditions may form of smoking rather than snuffing or chewing,
also affect recurrence of disease. affects the susceptibility and the treatment out-
In recent years, genetic markers have become come of patients with chronic periodontitis. Clas-
available to determine various genotypes of pa- sical explanations for these observations have in-
tients regarding their susceptibility to periodontal cluded the association between smoking habits
diseases. and poor oral hygiene as well as unawareness of
Research on the Interleukin-1 (IL-1) polymor- general health issues (Pindborg, 1949; Riv-
phisms has indicated that IL-1 genotype positive era-Hidalgo, 1986). More recent evidence, howev-
patients show more advanced periodontitis lesions er, has established that smoking per se repre-
than IL-1 genotype negative patients of the same sents not only a risk marker, but also probably a
age group (Kornman et al, 1997). Also, there is a true risk factor for periodontitis (Ismail et al,
trend to higher tooth loss in the IL-1 genotype pos- 1983; Bergström, 1989; Bergström et al, 1991;
itive subjects (McGuire and Nunn, 1999). In a ret- Haber et al, 1993). In a young population (19–30
rospective analysis of over 300 well maintained pe- years of age), 51–56% of periodontitis was asso-
riodontal patients, the IL-1 genotype positive pa- ciated with cigarette smoking (Haber et al, 1993).

Vol 1, No 1, 2003 11
Lang/Tonetti

Fig 2 Functional diagram of a low-risk

maintenance patient. BOP is 15%, 4 resi-
dual pockets ≥5 mm are diagnosed, 2
teeth had been lost, the bone factor in re-
lation to the age is 0.25, no systemic fac-
tor is known and the patient is a non-
smoker.

The association of smoking and periodontitis has must be considered as the sixth risk factor for re-
been shown to be dose-dependent (Haber et al, current disease in the functional diagram of risk as-
1993). It has also been shown that smoking will sessment (Fig 1). While non-smokers (NS) and
affect the treatment outcome after scaling and former smokers (FS; more than 5 years since ces-
root planing (Preber and Bergström, 1985), modi- sation) have a relatively low risk for recurrence of
fied Widman flap surgery (Preber and Bergström, periodontitis, the heavy smokers (HS; as defined by
1990), and regenerative periodontal therapy smoking more than one pack per day) are definitely
(Tonetti et al, 1995). Furthermore, a high propor- at high risk. Occasional smokers (OS; < 10 ciga-
tion of so-called refractory patients have been rettes a day) and moderate smokers (MS; 10–19
identified as consisting of smokers (Bergström cigarettes a day) may be considered at moderate
and Blomlöf, 1992). The impact of cigarette risk for disease progression.
smoking on the long-term effects of periodontal
therapy in a population undergoing supportive pe-
riodontal care has been recently reported. Smok- CALCULATING THE PATIENT’S INDIVIDUAL PE-
ers displayed less favorable healing responses RIODONTAL RISK ASSESSMENT (PRA)
both at reevaluation and during a 6-year period of
SPT (Baumert-Ah et al, 1994). In spite of the pau- Based on the six parameters specified above, a
city of evidence relating cigarette smoking to im- multi-functional diagram is constructed for the PRA.
paired outcomes during supportive periodontal In this diagram, the vectors have been formed on
care, it seems reasonable to incorporate heavy the basis of the scientific evidence available. It is
smokers (≥ 20 cigarettes/day) in a higher risk obvious that ongoing validation may result in slight
group during maintenance. modifications.
In assessing the patient’s risk for disease pro-
gression, environmental factors such as smoking

12 Oral Health & Preventive Dentistry

 Lang/Tonetti

Fig 3 Functional diagram of a medi-

um-risk maintenance patient. BOP is 9%, 6
residual pockets ≥5 mm are diagnosed, 4
teeth had been lost, the bone factor in re-
lation to the age is 0.75,the patient is a
Type I diabetic, but a non-smoker.

Fig 4 Functional diagram of a high-risk

maintenance patient. BOP is 32%, 10 re-
sidual pockets ≥5 mm are diagnosed, 10
teeth had been lost, the bone factor in re-
lation to the age is 1.25, no systemic
factor is known and the patient is an occa-
sional smoker.

Vol 1, No 1, 2003 13
Lang/Tonetti

Fig 5 Functional diagram of another

high-risk maintenance patient. BOP is close
to 50%, more than 12 residual pockets
≥5 mm are diagnosed, but only 2 teeth had
been lost. The bone factor in relation to the
age is 0.5, no systemic factor is known and
the patient is a non-smoker. Additional pe-
riodontal therapy may change this patient’s
risk into the moderate or even low-risk cat-
egory, since BOP and residual pockets
would be affected.

A low PRA patient has all parameters within the ACKNOWLEDGEMENTS

low-risk categories or – at the most – one parame-
ter in the moderate-risk category (Fig 2). This project has been supported by the Swiss National
A moderate PRA patient has at least two para- Foundation for Scientific Research (SNF); Grant Nr. 3200-
0377763.93/1, and by the Clinical Research Foundation (CRF)
meters in the moderate category, but at most one for the Promotion of Oral Health, University of Berne, Switzer-
parameter in the high-risk category (Fig 3). land.
A high PRA patient has at least two parameters
in the high-risk category (Fig 4).
In a high-risk patient who yields high BOP per- REFERENCES
centages and high numbers of residual pockets
(Fig 5), the patient’s risk for disease progression 1. Axelsson P, Lindhe J (1981a). Effect of controlled oral hygiene
procedures on caries and periodontal disease in adults. Re-
may be reduced into the moderate category if fur- sults after 6 years. J Clin Periodontol 1981;8:239-248.
ther periodontal therapy is provided. These two pa- 2. Axelsson P, Lindhe J (1981b). The significance of mainte-
rameters (BOP and residual pockets) are easily af- nance care in the treatment of periodontal disease. J Clin
fected by therapy, while other parameters, such as Periodontol 1981;8:281-294.
numbers of missing teeth or systemic and genetic 3. Axelsson P, Lindhe J, Nyström B. On the prevention of caries
and periodontal disease. Results of a 15-year longitudinal
factors are either irreversible and cannot be re- study in adults. J Clin Periodontol 1991;18:182-189.
duced or may only be affected with great additional 4. Badersten A, Nilvéus R, Egelberg J. Scores of plaque, bleed-
efforts (smoking cessation). The factor determining ing suppuration and probing depth to predict probing attach-
the percentage of experienced alveolar bone loss in ment loss. J Clin Periodontol 1990;17:102-107.
relation to the patient’s age may be reduced only 5. Baumert-Ah M, Johnson G, Kaldahl W, Patil K, Kalkwarf K.
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16 Oral Health & Preventive Dentistry
 Non-surgical Periodontal Therapy

Non-surgical Periodontal
Therapy
Phase I therapy
Cause-related therapy

Student’s Learning Outcomes (SLOs):

By the end of this topic, you should be able to:
1. Differentiate between regeneration, repair, and recognize how to get
predictable amount of regeneration.
2. Recognize various options for chemical and mechanical plaque control.
3. Describe non-surgical therapy in terms of its objectives, indications,
and healing following the treatment.
4. Define perioceutics and identify the rationale of perioceutics in
periodontal therapy.
5. Describe different types of perioceutics.
 Non-surgical Periodontal Therapy

Goal of phase I therapy

Removal of pathogenic biofilms, toxins and calculus, and the
reestablishment of a biologically acceptable root surface.

Rationale for phase I therapy:

The objective of phase I therapy is to alter or eliminate the microbial
etiology and factors that contribute to gingival and periodontal diseases
therefore

• halting the progression of disease and

• returning the dentition to a state of health and comfort.

Sequence of procedures:
1. Plaque biofilm control instruction.
2. Removal of supragingival and subgingival plaque biofilm and calculus.
3. Recontouring defective restorations and crowns.
4. Management of carious lesions.
5. Tissue reevaluation.

Healing after periodontal therapy:

The process consists of the removal of degenerated tissue debris and the
replacement of tissues destroyed by disease.
Modes of periodontal healing:
Regeneration: occurs through growth from the same type of tissue that has been
destroyed or from its precursor. In the periodontium, gingival epithelium is replaced
by epithelium, and the underlying connective tissue and periodontal ligament are
derived from connective tissue. Bone and cementum are replaced by connective
tissue, which is the precursor of both.
Repair: Repair simply restores the continuity of the diseased marginal gingiva and
reestablishes a normal gingival sulcus at the same level on the root as the base of the
preexisting periodontal pocket. This process, called healing by scar, arrests bone
destruction but does not result in gain of gingival attachment or bone height.
 Non-surgical Periodontal Therapy

The downgrowth of epithelial cells (E) results in a long junctional epithelium (JE).
The proliferation of connective tissue (CT) may result in connective tissue adhesion
± root resorption. With the predominance of bone cells (B), there is root resorption
and/or ankylosis. With the ingress of periodontal ligament (PDL) and
perivascular cells from the bone, a regenerated periodontium develops.

To get predictable amount of regeneration we have to:

1. Control infection: through the removal of local irritants by either

closed or opened debridement, chemical adjunctive therapy either
systemically or locally at a site, and oral self care.
2. Control apical migration of epithelial attachment: by the use of
guided tissue materials with or without bone fillers.
3. Maximizerecruitment of the periodontal tissues, namely PDL
and bone cells to repopulate the destroyed periodontal tissues by
the use of biologic enhance modifiers.
4. And finally to render the root surface more biocompatible for PDL
and bone cell colonization (Gamal et al J. Clinc. Periodontology
2002: 29; 763- 770).
 Non-surgical Periodontal Therapy

Non-surgical approaches

Early studies observed that bone filling was possible with radicular
scraping and planing treatment, followed by strict hygiene. These
techniques are based on the principal that a biocompatible radicular
surface and a strict hygiene control favor the development of the innate
regenerative capacity of the periodontal tissue. Conservative therapy or
non surgical therapy is defined as “Plaque removal, plaque control,
Supra- and sub- gingival scaling, root planing, and the adjunctive use
of chemical agents”.

 Scaling, root planing and subgingival curettage:

Mechanical scaling and root planning remains the principal

means of root surface decontamination.

Areas of plaque accumulation in a deep periodontal

lesion.

Scaling:
 Refer to the removal of calculus, bacteria and their products from
the crown and root surfaces or lying free in the pocket.
 Non-surgical Periodontal Therapy

Root planing:
 Refer to the removal of calculus, bacteria and their products, and
contaminated cementum and dentine from the root surface
(Bacterial endotoxin contamination from plaque, calculus,
diseased cementum and pocket epithelium, which initiate a host
inflammatory response and prevent PDL attachment), rendering
the root surface more biocompatible for periodontal ligament
fibroblasts adhesion, and smooth enough to prevent plaque retention
and subsequent re-infection.
 Incomplete calculus removal forming calculus veneer or the organic
smear layer may be compatible with resolution of periodontal
inflammation, but may also act as a physical barrier, which prevent
new attachment and regeneration of a functional attachment
apparatus.

Curettage:
 Refers to scraping of the inner surface of the gingival wall of the
periodontal pocket to clean out, separate and remove diseased soft
tissue.
 Epithelial tissue possesses the fastest growing and moving cells,
being faster to arrive at, and colonize the wound than other internal
tissues. it was proposed to increase by curettage the distance that the
epithelial cells needed to travel, allowing the slower connective
tissue to reach the radicular surface first.
 Currently, the need for curettage is questionable since it was proven
that when doing proper scaling and root planning, the major source
of bacteria disappears, and the pocket pathologic changes resolve
with no need to eliminate the inflamed granulation tissue by
curettage.
 The granulation tissue is slowly resorbed and the bacteria present in
the inflamed granulation tissue are destroyed by the defense
mechanisms of the host.

Objectives of non surgical therapy:

 Non-surgical Periodontal Therapy

1- Biofilm physical disruption:

Since bacterial biofilm is protected to a great extent from both
intrinsic and extrinsic chemotherapeutic agents, physical disruption
remains central to any periodontal therapy (to expose bacteria to the
host mediators and chemotherapeutic agents).

2. Endotoxin removal:
Removing calculus and superficial cementum may also eliminate
bacterial toxins incorporated into root surface.

Indications of non-surgical therapy:

1- Pocket reduction:
 Shallow and moderately deep pockets could be completely
debrided by scaling and root planing, complete debridement for
deep pockets could not be achieved for two reasons:
a. Scaling and root planing are extremely difficult for deep pockets
without direct vision, since the root surface exhibit a wide variety of
irregularities and grooves.

b. Heavy instruments (scalers, hoe) could not be used for sub-gingival

curettage, as it does not get to the bottom of the pocket.

o The amount of pocket reduction induced by non-surgical

approach depends on:
o The original depth of the pocket
o The amount of the edematous fluid in the tissue.
o The amount of the fibrous connective tissue.
o The thoroughness of root preparation.

 Pocket reduction following scaling and root planing occur through

a combination of:

A- Tissue shrinkage:
due to reduction in gingival inflammation (hyperemia and
edema).
 Non-surgical Periodontal Therapy

B- New attachment by long junctional epithelium. (Why)

Pocket epithelium migrates rapidly( mitotic activity of the epithelium

in wounds may reach 20 time that of normal tissue) since it possesses 3
factors important for rapid migration:
1- CT for nutrition.
2- Substratum (fibrin strands) as contact guidance.
3- In addition, gingival epithelial cells and PDL cells affected by
bacterial and host challenges secrete fibronectin and laminine which
enhance proliferation of epithelial cells

On the other hand the CT of the periodontal ligament (PL) is slower

in his rate of growth because of the:
1- Slow angiogenises of the periodontal ligament (limited surface area)
and avascular root.
2- Limited surface area of the periodontal ligament structure with its
associated limited cell number.

These resulted in epithelium that proliferate apically on the root surface

before the other supporting tissues reach the area, with only longer
junctional epithelium will form. Such epithelial proliferation eventually
covers the granulation tissue, which failed to attach to the root. This form
of healing is classified as a repair and not regeneration because the
original form and architecture of the tissue have not been restored.
 Non-surgical Periodontal Therapy

Schematic drawings illustrating: (A) the inflamed soft tissue region and
bone resorption associated with periodontitis (note the loss of both
epithelial attachment and connective tissue attachment to the root surface);
(B) periodontal repair, as evidenced by formation of a long junctional
epithelium; and (C) periodontal regeneration, as shown by new epithelial
and connective tissue attachment to the root.

Light micrograph illustrating formation of a long junctional epithelium

(LJE) ending at the coronal-most end of regenerated cementum (C). D,
dentin. (Paraffin section stained with hematoxylin and eosin.)
 Non-surgical Periodontal Therapy

2. Re-adaptation of the gingival connective tissue to the root surface

decreasing retractability of the soft tissue from the tooth surface.

Probe penetration in healthy and diseased sites.

3. Pre-surgical preparation of tissue: (deep pockets);

 Render the tissue easier to handle during surgery.
 Decrease bleeding and increase visibility during surgery.
 Decrease postoperative pain, and infection.
 Some degree of pocket reduction which my render surgical outcome
unnecessary.

4. Treatment of compromised situations:

A- Patients psychologically unwilling to accept surgical

manipulation of their tissue.
B- Systemic and medical problems may render the patient not be able
to undergo more extensive surgery (Ex, Leukemia, hemophilia,
heart failure, uncontrolled diabetes….).
C- When scaling and root planning was intended as a pre-surgical
preparation but after that the patient and or the therapist decide to
discontinue treatment because of the dramatic improvement of the
periodontal condition.
 Non-surgical Periodontal Therapy

5. Maintenance of the treated patients:

Repeated scaling and root planing and soft tissue curettage is necessary
to prevent recurrence of disease in a previously treated areas.

Healing following non surgical therapy:

Healing usualy occur by long junctional epethelium;
 Junctional epithelium is an epithelial structure that mediates
adhesion of the gingiva to the tooth, due to its unique location at
the hard soft tissue interface it play a role in progression of
periodontal disease.
 Long junctional epithelium is a term applied to the junctional
epithelium after treatment; it is a form of repair not regeneration,
since regeneration is the restoration of the damaged tissue by the
same type of tissue to its original form.
 Actually this type of long junctional epithelial healing is an
unfavorable type of healing, as we know junctional epithelium
is a non keratinized, has wide intercellular spaces, and has great
sparesty of desmosomes, all factors that render it more
permeable to bacteria and bacterial products to enter from the
gingival sulcus into the connective tissue with subsequent
reinfection.
 However junctional epithelial attachment has also a protective
role through: subepethelial basement membrane restricting
penetration of harmful substances into CT., high turnover rate,
and non keratinized structure facilitate flow of leukocyte and
serum derived substances through it.

Perioceutics

Perioceutics are pharmacotherapeutic agents specifically developed to

produce beneficial changes in the microflora and host response as
adjunctive therapy in the management of susceptible patients who develop
periodontal disease. Perioceutics are either systemically or locally.

Rationale of perioceutics in periodontal therapy:

 Non-surgical Periodontal Therapy

- Periodontal pathogens present within the microbial biofilms initiate the

periodontal disease by producing harmful by-products andenzymes that
break down extracellular matricessuch as collagen, as well as host cell
membranes.

- This results in a Host immune- inflammatory response in the

periodontal tissues characterizedby the production of (Inflammatory
cytokines), (Arachinoid acid metabolites)and enzymes including the
matrixmetalloproteinases (MMPs).

- Beside a family of chemicals that actively promote resolution

(Proresolving molecules)and tissue repair(Growth factors), the levelof
the inflammatory mediators and enzymes in theperiodontal tissues is
usually balanced by the (Anti inflammatory cytokines), (Tissue
inhibitors of MMPs), and (soluble receptors of cytokines)which
ultimately functionsto protect the host.

- Perioceutics are indicated for susceptible patients at increased risk and

for whom conventional therapeutic approaches are not effective alone.

Perioceutics are classified into:

A) Antimicrobial therapy aims to reduce the bacterial challenge and its

harmful products or modify bacteria in plaque biofilm

B) Host Modulating therapy aims to reduce tissue destruction and

stabilize or even regenerate the periodontium by modifying or
downregulating destructive aspects of host response, and upregulating
protective or regenerative responses

A) Antimicrobial therapy

Chemical control of dental plaque

Antimicrobial, antibacterial, chemotherapeutic, or chemical agents are all
terms used to describe agents employed to control plaque, gingivitis and
 Non-surgical Periodontal Therapy

periodontitis. Antimicrobial therapy is defined by the AAP as the use of

specific agents for the control or destruction of microorganisms, either
systemically or at specific site. Now it is generally accepted that the
formation of dental plaque at the interface of the tooth and gingiva is one
of the main causes of gingival inflammation, which may lead to
periodontitis. Therefore, anti-microbial agents have been developed in
order to achieve a greater level of oral hygiene and improved oral health
for plaque control.

Factors that limit anti-microbial chemotherapeutic agents effect:

The ideal chemotherputic agent should have three important

characteristics;

The first is its ability to kill and prevent re-growth of bacteria,

The second is to reach the site of infection in an effective concentration.
The third is the ability to maintain active drug level in the plaque
environment for long time at concentration exceeding the minimum
inhibitory concentration producing sustained antimicrobial effect against
plaque.
However some factors may limit the effect of antimicrobial chemotherapy
in the oral environment:

1- Transient effect:
* Due to the fact that plaque formation is a continuos process and re-growth
of new plaque will occur as soon as the antimicrobial agent is eliminated
(3-4 H after cleaning).

* Salivary flow, drinking, eating all results in rapid topical agent clearance.

2- Mouthwashes do not penetrate the periodontal pocket, it should be

delivered and retained in the pocket.

3- Some bactericidal agents could be of no value due to the limited contact

time with bacteria, or coating of bacteria by some extraneous materials
as sugar, carbohydrates, and proteins within bacterial biofilm.
 Non-surgical Periodontal Therapy

4- Biofilm phenomena in the plaque protecting the pathogens;

Biofilm is a barrier, meaning that when bacteria produce substances they
are retained within the gel like mass (Inter-microbial matrix derived from
saliva and GCF) thus increasing the concentration, which in turn used for
metabolic interactions among bacteria. Also biofilm protects bacteria from
harmful substances such as anti-bacterial agents.

5-Some bacteria may produce neutralizing factors that may negate

chemotheraputic effect.
1- Drug binding to tissues.
2- Effectiveness of the host defenses.
3- Pathogens in periodontal tissues , root surface and extra dental sites not
affected by therapy.

Indications of adjunctive therapy:

Antibiotics and chemotheraputics have been prescribed for:
1- Patients who do not respond to conventional mechanical therapy.
2- Acute periodontal infections associated with systemic
manifestations.
3- Prophylaxis in medically compromised patients.
4- As an adjunct to surgical and non surgical periodontal therapy.

Agents acting as adjunctive therapies:

The agents used for chemical plaque control fall into 5 categories:
1- Antiseptics, that inhibit microorganisms (in general) and are broad
spectrum.
2- Antibiotics, that inhibit or kill a specific group of bacteria.
3- Enzymes, that break up the gel like matrix that hold bacterial biofilm
together.
4- Non-enzymatic agents that alter metabolic activity of plaque bacteria.
5- Agents that interfere with attachment of bacteria to pellicle or to one
anther.

Methods of delivery for adjunctive therapies:

 Non-surgical Periodontal Therapy

Methods of delivery include: Tooth brush, Intrdental aid, mouth-rinses,

irrigation both supra-gingival and sub-gingivally, controlled- release
devices and systemic administration.

1. Tooth brushing:
Toothbrush is the most commonly used method of delivery of dentifrices.
Dentifirices appears to have a limited value as an antimicrobial delivery,
in spite of its great value as a mechanical way of plaque control as :
Incorporation of antimicrobial into dentifrices presents a problem of
compatibility with the dentifrice components.
Tooth brushing reach only 2-3 mm below the gingival margin.

2. Interdental aid:
Application of antimicrobials with interdental brushes is anther delivery
method recommended for localized periodontal pockets and or furcation
defects. This method has a limited efficacy.

3. Mouth rinses:
Like dentifrices the major limitation of rinses , is that the agent penetrates
subgingivally for only few mm.

4. Irrigation:
It has been reported to penetrate periodontal pocket well, however the
concentration of the chemical agent used decline rapidly because blood and
GCF levels can deactivate the agent.

Chemotherapeutic agents in dentifrices, irregation and mouth washes;

The ideal chemotrherapeutic agent used in dentifrice and mouthwashes
should have the following criteria’s:
- Non toxic
- Non allergic.
- Non irritating.
- Clinically causing significant reduction in plaque and gingivitis.
- Substantive.
- Has selective and specific effect on pathogenic microbiota.
- Pleasant tasting.
- Economic.
 Non-surgical Periodontal Therapy

- Easy to use.

Chlorhexidine (CHX) (in mouth wash 0.012% )

Is a cationic bisbiguanide that is a substantive broad-spectrum antibacterial

agent.
Its mechanism of action is related to its positive charge and affinity for the
salivary pellicle, and the negatively charged bacterial cell surface. At high
concentration chlorhexidine will cause bacteriolysis and precipitation of
the cytoplasm. At low concentration it interfere with membrane function.

CHX advantages:
 Due to its substantivity to oral mucosa, hydroxylapatite and salivary
glycoprotein (pellicle) it is the most effective antimicrobial currently
available for control of subgingival plaque and gingivitis.
(Substantivity, is defined as the ability of an agent to be retained in
the oral cavity for a long period of time wit subsequent slow and
sustained release of the active ingredients at effective level).
 Sustained release of chlohexidine in active form has been
demonstrated 8-12 h. following application. Approximately 30% is
retained in the oral cavity after rinsing.

CHX Side effects include,

 Brown staining of teeth , tongue, and composite restorations. It is
advised to use H2O2 in controlling the stain.
 Formation of supra-gingival calculus.
 Unpleasant taste.
 Reversible oral desquamation in young children.

5. Local delivery antimicrobials (LDA):

Local delivery is to deliver high concentration of an antimicrobial directly
to the site of the periodontal infection, giving higher concentration and
lower side effects than those of the systemic administration do.

The medication used as a local delivery should meet five criteria:

1- Inhibit or kill putative pathogens.
2- Reach the site.
 Non-surgical Periodontal Therapy

3- Have adequate concentration.

4- Retained for extended period of time.
5- Do no harm.

The 5 FDA approved LDA include;

a. Tetracycline fiber( Actisite)

- A polymer Ethylene Venyl Acetate (EVA) in 25% tetracycline HCL.

- The fiber is flexible can be folded in the pocket.
- Release TTC for 14 days.
-Provide 150 times bactericidal effect than that of the systemic use.

b. Doxcycycline polymer ( Atridox)

- Biodegradable polymer ( polylactic acid) saturated with 10% doxycycline

hyclate.
- Its liquid form packed within the pocket by a syringe and start to set when
it contact moisture.
Since the system is biodegradable it does not have to be removed.

c. Chlorhexidine chips ( perio chip)

- Small biodegradable film ( 4x5mm) of gelatin into which incorporated

2.5 mg of chlorhexidine gluconate.
- It delivers chlorhexidine to the site at a concentration above 125ng/ml for
at least 7 days.
- Removal appointment is unnecessary.

d. Minocycline ointment ( periocline)

- Inert ointment containing 2% minocycline HCL applied with a syring into

the pocket
- Most studies have applied the material once a week for four weeks.

e. Metronidazole gel ( Elyzol)

 Non-surgical Periodontal Therapy

- Is a gel containing 25% metronidazole inserted by a syringe intro the

pocket.
- Most researches have applied the gel multiple times.

6. Systemic antibiotic adminestration:

Advantages
Systemic antibiotic therapy has certain advantages over topical
admenestration:
A) systemic admenestration via serum can reach microorganisms at the
base of the deep pocket ,in furcation areas, and within gingival
epithelium and conective tissue.
B) Affecting periodontal pathogens colonizing oral mucosa, and other
extra dental sites.
C) Posibility of reducing periodontal pathogens from the entire mouth
may reduce the risk for future recolonization of periodontal pocket.
D) Low finantial coast for the patient.

Disadvantages:
A) inability to achieve high gingival cevicular fluid concentration.
B) Adverse drug reaction.
C) Creation of multiple antibiotic resistant microorganisms.
D) Uncertain compliance.
 Non-surgical Periodontal Therapy

Formative Assessment Questions:

Choose the BEST answer from the alternatives a, b, c and d:

1. Non-surgical therapy is indicated for pre-surgical preparation of the deep
pockets with the aim of…..
a) rendering the tissues easier to handle during surgery.
b) root biomodification.
c) recruitment of PDL cells to the root surface.
d) obtaining new attachment.
2. Curettage refers to………
a) scraping of the inner surface of the gingival wall of the pocket.
b) removal of contaminated cementum from the root surface.
c) removal of calculus below the gingival margin.
d) removal of endotoxin from the root surface.

3. Non-surgical therapy is indicated for pre-surgical preparation of the deep

pockets with the aim of…..
e) rendering the tissues easier to handle during surgery.
f) root biomodification.
g) recruitment of PDL cells to the root surface.
h) obtaining new attachment.
 Surgical
Periodontal
Therapy
 Student’s Learning Outcomes (SLOs):

By the end of this topic, you should be able to:

State objectives, contraindications, and purpose of

surgical periodontal therapy.
Classify periodontal surgeries.
Recognize definition, indications, contraindications,
and techniques of different types of periodontal surgeries.
Justify the use of different periodontal surgical
techniques.

Surgical Periodontal Therapy

Surgical periodontal therapy includes the intentional incision of gingival tissues
with the purpose of:
1. Controlling periodontal disease.
2. Correcting morphological defects that: favor plaque accumulation, pocket
recurrence and periodontal disease, impair esthetics or prevent placement of proper
prosthetic appliances.
3. Placing dental implants as well as improving the environment for implants
placement and function (soft and hard tissue augmentation as well as treatment of
periimplantitis).
The OBJECTIVES of surgical phase of periodontal therapy are:

▪ To eliminate pathological changes in the pocket wall.

▪ To create an environment conductive to control of dental plaque via
⮚ Eliminating periodontal pockets
⮚ Correcting morphologic abnormalities of gingiva and alveolar bone that interfere
 with plaque control to allow easier oral hygiene measures.
⮚

⮚ Creating an easy to clean embrasure space.

▪ To promote periodontal regeneration.
▪ To improve prognosis of teeth and their replacements: Create environment suitable
for prosthodontic treatment e.g., crown lengthening procedure.
▪ To improve esthetics e.g., covering denuded root to treat gingival recession.
▪ To solve mucogingival problems e.g. widen the zone of attached gingiva.
Contraindications for periodontal surgery:
1. Uncooperative patients. Since post-operative plaque control is essential for the
success of periodontal treatment.
2. Poorly controlled diabetic, acute leukemia, agranulocytosis and lymphoma
patients.
3. Myocardial infarction patients should not be subjected to periodontal surgery
within 6 months following hospitalization.
4. Periodontal surgical procedures are classified into:

I. Pocket reduction surgery II. Correction of anatomic morphologic

defects

1. Resective e.g. gingivectomy. 1. Plastic surgery techniques to widen attached

The gingivectomy technique was gingiva e.g. free soft tissue autograft.
widely performed in the past.
Improved understanding of healing
mechanisms and the development
of more sophisticated flap methods
have relegated the gingivectomy
to a lesser role in the current
repertoire of available
techniques.

2. Regenerative periodontal surgery 2. Esthetic surgery e.g. root coverage and

- flaps with bone grafts. recreation of interdental papillae.

- flaps with barrier membranes.

3. Preprosthetic techniques: crown lengthening

and ridge augmentation.

5. Placement of dental implants including

techniques for site development for implants

e.g. guided bone regeneration.

 Gingival Surgical Techniques

Gingival Curettage

It is defined as scraping of gingival wall of periodontal pocket to remove diseased

soft tissue. Curettage removes the chronically inflamed granulation tissue that
forms the wall of periodontal pocket. This tissue contains bacterial colonies.This
inflamed granulation tissue is lined by epithelium, and deep strands of epithelium
penetrate into the tissue. The presence of this epithelium is construed as a barrier
to the attachment of new fibers in the area.

Currently, the need for curettage is questionable

When the root is thoroughly planed, the major source of bacteria disappears, and
the pathologic changes in the tissues adjacent to the pocket resolve with no need
to eliminate the inflamed granulation tissue by curettage. The existing
granulation tissue is slowly resorbed and the bacteria present in the tissue without
replenishment of their numbers from the plaque in the pocket are destroyed by
the defense mechanisms of the host. It has been shown that scaling and root
surface debridement (RSD) with additional curettage do not improve the
condition of the periodontal tissues beyond the improvement resulting from
scaling and root surface debridement (RSD) alone.

Gingivectomy

Definition: Excision of the gingiva. By removing the pocket wall, gingivectomy

provides visibility and accessibility to the tooth surface. Gingivectomy creates a
favorable environment for the restoration of physiologic gingival contour.

Grant et al. (1979) defined gingivectomy as the excision of the soft tissue wall
of a pathologic periodontal pocket. It is the procedure that aims at pocket
elimination together with recontouring of the diseased gingiva to restore the
physiologic form.
Gingivectomy may be performed by scalpels, electrodes or Laser. The
surgical method by scalpels and periodontal knives is still the most recommended
technique. Other types of gingivectomy include: Laser gingivectomy and
gingivectomy by electrosurgery. chemosurgery by chemicals is not used
nowadays.

Indications of gingivectomy: Contraindications of gingivectomy:

1. Elimination of gingival 1. Esthetic considerations,

enlargement. particularly in anterior maxilla.
2. Elimination of suprabony 2. Intrabony pockets.
pocket. 3. Pockets extending beyond the
3. Elimination of suprabony mucogingival junction (when

periodontal abscess. bottom of pocket is apical to MGJ).

4. Crown lengthening procedure.

5. Class III furcation
involvement.

Steps of surgical gingivectomy:

Step 1. The pockets on each surface are explored with a periodontal probe and
marked with a pocket marker. Each pocket is marked in several areas to outline its
course on each surface.

Step 2. Periodontal knives (e.g., Kirkland knives) are used for incisions on the
facial and lingual surfaces. Orban periodontal knives are used for interdental
incisions. Bard-Parker blades #12 and #15, as well as scissors, are used as auxiliary
instruments. The incision is started apical to the points marking the course of the
pockets and is directed coronally to a point between the base of the pocket and the
crest of the bone. Either interrupted or continuous incisions may be used. The
incision should be beveled at approximately 45 degrees to the tooth surface and
recreate the normal festooned pattern of the gingiva.

Step 3. Remove the excised pocket wall.

Step 4. Carefully curette the granulation tissue and remove any remaining calculus

Step 5. Cover the area with a surgical pack

Limiting factors for gingivectomy:

Current periodontal surgery must consider the
(1) conservation of keratinized gingiva,
(2) minimal gingival tissue loss to maintain esthetics,
(3) adequate access to the osseous defects for definitive defect correction, and
(4) minimal postsurgical discomfort and bleeding by attempting surgical
procedures that will allow primary closure. The gingivectomy surgical technique
has limited use in current surgical therapy because it does not satisfy these
considerations
in periodontal therapy. The clinician must carefully evaluate each case as to the
proper application of this surgical procedure.

Gingivoplasty

Definition: Reshaping of the gingiva to create physiologic gingival contours.

Gingival and periodontal disease often produces deformities in the gingiva that is
conducive for plaque accumulation and food debris, which prolongs and aggravates
the disease process. Such deformities include (1) gingival clefts and craters, (2)
craterlike
interdental papillae caused by acute necrotizing ulcerative gingivitis, and (3) gingival
enlargements.

Gingivoplasty is done by periodontal knives and scalpels to

- taper the gingival margin,

- create a scalloped gingival margin,
- thin the attached gingiva,
- create vertical interdental grooves,
- shape the interdental papilla to provide sluiceways for the passage of food

Periodontal Flaps
Definition: Section of the gingiva and/or alveolar mucosa surgically elevated from
the underlying tissues to provide access and visibility to the alveolar bone and the
root surface.

Classification of periodontal flaps:

Periodontal flaps can be classified based on the following:

1. Bone exposure after flap reflection.

2. Placement of the flap at the end of surgery.
3. Management of the papilla.
1. Based on bone exposure after flap reflection, flaps are classified into:

Full-thickness Flap Partial-thickness or Split-thickness

Flap
● Mucoperiosteal flap. ● Mucosal flap.
● Reflection is done by blunt ● Reflection is done by sharp
dissection by dissection by scalpel to be able
mucoperioosteal elevator. to separate the mucosa from
the periosteum.
● Reflects all soft tissue ● Leaves periosteum on bone.
including periosteum.
● Expose alveolar bone. ● Alveolar bone is not exposed.
● Examples: Modified Widman flap ● Example: lateral displaced flap.
and conventional flap.

2. Based on the placement of the flap at the end of the surgical

procedure, flaps are classified into
Located at the position it had before surgery

Undisplaced flaps i.e. the flap is returned and sutured in

(unpositioned) its original position it had before surgery.

Which can be located

Dispalced flaps - Lateral to its original position it had

(positioned) before surgery e.g. laterally positioned flap.
- Coronal to its original position e.g. coronally
positioned flap
- Apical to its original position e.g. apically
positioned flap.

3. Based on the management of the interdental papilla, flaps are

classified into
 A. Conventional flap
In the conventional flap, the interdental papilla is split apical to the contact
area of the two adjacent teeth into a facial half and a palatal or lingual half
to allow reflection of buccal and lingual flaps.

The conventional flap is used when interdental spaces are narrow, thus
excluding the possibility of preservation of papilla and when the flap is to
be displaced. Examples of conventional flaps include the modified Widman
flap and the apically displaced flap.

B. Papilla preservation flap

The papilla preservation flap incorporates the entire interdental gingiva in one
flap by means of crevicular interdental incisions to sever the connective tissue
attachment and a horizontal incision at the base of the papilla, leaving the papilla
connected to one of the flaps.

Incisions for periodontal flaps

Periodontal flaps use horizontal and vertical incisions. Horizontal incisions are
directed along the gingival margin in a mesial or distal direction.

1. Internal bevel incision: It is done by #15 or #11 scalpel.

It starts one mm away from the gingival margin and is directed to the crest of
alveolar bone (directed apically). It is the incision from which the flap is
reflected

Objectives of the internal bevel incision:

a) It removes the pocket lining.

b) It relatively conserves the outer surface of the gingiva which, if apically
positioned, becomes attached gingiva.
c) It produces a thin flap margin for proper flap adaptation at the
end of the surgery.
Internal bevel incision is called:

Reverse bevel incision because its bevel is in a reverse direction from that of
the gingivectomy incision i.e. it is directed apically while the gingivectomy
incision is directed coronally. It is also called primary incision because it is the
initial incision in the periodontal flap.

2. Crevicular incision (Second

incision)

● It is done by #15 or #12 scalpel.

● It starts at the bottom of pocket and is directed to the bone crest.
● The crevicular incision with the internal bevel incision forms a
triangular wedge of tissue (V-shaped wedge) ending at crest of bone.
This wedge of tissue contains the portion of the gingiva left around the
teeth which contains the epithelium of the pocket lining and the
adjacent granulation tissue. It will be discarded after the interdental
incision is performed.
After doing the crevicular incision, a mucoperiosteal elevator is inserted
into the internal bevel incision and the flap is reflected.

3. Interdental incision

● It is done by Orban knife.

● It is also called the third incision.
● It is done after the flap is elevated.
It is done
- At the facial and lingual surfaces to separate the collar of the gingiva left
around the teeth, which contains the pocket epithelium.

- Interdentally with the Orban knife placed just coronal to the

crest of bone to separate the interdental tissues from bone to free
the gingiva completely from around the teeth.
 Technique for Access and Pocket Depth
Reduction/Elimination

The three different categories of flap techniques used in periodontal flap

surgery are (1) the modified Widman flap, (2) the undisplaced flap, and the
(3) apically displaced flap.

The modified Widman flap has been described for exposing the root surfaces
for meticulous instrumentation and for removal of the pocket lining, however,
it is not intended to eliminate or reduce pocket depth.

The undisplaced (unrepositioned) flap improves accessibility for

instrumentation, but it also removes the pocket wall, thereby reducing or
eliminating the pocket. This is essentially an excisional procedure of the
gingiva.

The apically displaced flap provides accessibility and eliminates the pocket,
but it does the latter by apically positioning the soft tissue wall of the
pocket.Therefore it preserves or increases the width of the attached gingiva by
transforming the previously unattached keratinized pocket wall into attached
tissue.

I. Modified Widman Flap

Ramfjord and Nissle (1974), described the modified Widman flap that is also
known as open flap curettage. It differs from the original Widman flap
described by Widman in 1918 in that there is no apical displacement of the
flap and no osseous recontouring.

Technique of the modified Widman flap:

Step 1: The initial incision is an internal bevel incision to the alveolar crest starting
0.5 to 1 mm away from the gingival margin. Scalloping follows the gingival margin.
Care should be taken to insert the blade in such a way that the papilla is left with a
thickness similar to that of the remaining facial flap.

Step 2: The gingiva is reflected with a periosteal elevator

Step 3: A crevicular incision is made from the bottom of the pocket to the bone,
circumscribing the triangular wedge of tissue containing the pocket lining.

Step 4: After the flap is reflected, a third incision is made in the interdental spaces
coronal to the bone with a curette or an interproximal knife and the gingival collar is
removed

Step 5: Tissue tags and granulation tissue are removed with a curette. The root
surfaces are checked, then scaled. Residual periodontal fibers attached to the tooth
surface should not be disturbed.

Step 6: Bone architecture is not corrected, except if it prevents good tissue adaptation
to the necks of the teeth. Every effort is made to adapt the facial and lingual
interproximal tissue adjacent to each other in such a way that no interproximal bone
remains exposed at the time of suturing .

Step 7: Continuous, independent sling sutures are placed in both the facial and palatal
and covered with a periodontal surgical pack.

II. Undisplaced Flap

It differs from the modified Widman flap in that the soft tissue pocket wall is
removed with the initial incision; thus it may be considered an “internal bevel
gingivectomy.” It surgically removes the pocket wall. To perform this technique
without creating a mucogingival problem, the clinician should determine that
enough attached gingiva will remain after removal of the pocket wall.

Technique of the undisplaced flap

 Step 1: The pockets are measured with the periodontal probe, and a bleeding point
is produced on the outer surface of the gingiva to mark the pocket bottom.

Step 2: The initial, or internal bevel, incision is made after scalloping the bleeding
marks on the gingiva. The incision is usually carried to a point apical to the alveolar
crest, depending on the thickness of the tissue.

Step 3: The second, or crevicular, incision is made from the bottom of the pocket to
the bone to detach the connective tissue from the bone.

Step 4: The flap is reflected with a periosteal elevator (blunt dissection) from the
internal bevel incision. Usually there is no need for vertical incisions because the
flap is not displaced apically.

Step 5: The third, or interdental, incision is made with an interdental knife,

separating the connective tissue from the bone.

Step 6: The triangular wedge of tissue created by the three incisions is removed with
a curette.

Step 7: The area is debrided, removing all tissue tags and granulation tissue using
sharp curettes.

Step 9: A continuous sling suture is used to secure the facial and the lingual or
palatal flaps.

III. Apically Displaced Flap

the apically displaced flap technique can be used for (1) pocket eradication and/or (2)
widening the zone of attached gingiva. Depending on the purpose, it can be a
fullthickness (mucoperiosteal) or a split-thickness (mucosal) flap.

Step 1: An internal bevel incision is made. To preserve as much of the keratinized

and attached gingiva as possible, it should be no more than about 1 mm from the crest
of the gingiva and directed to the crest of the bone.

Step 2: Crevicular incisions are made, followed by initial elevation of the flap; then
interdental incisions are performed, and the wedge of tissue that contains the pocket
wall is removed.
Step 3: Vertical incisions are made extending beyond the mucogingival junction. If
the objective is a full-thickness flap, it is elevated by blunt dissection with a periosteal
elevator. If a split-thickness flap is required, it is elevated using sharp dissection with
a Bard-Parker knife to split it, leaving a layer of connective tissue, including the
periosteum, on the bone.

Step 4: After removal of all granulation tissue, scaling and root planing, and osseous
surgery if needed, the flap is displaced apically.

Step 5: If a full-thickness flap was performed, a sling suture around the tooth prevents
the flap from sliding to a position more apical than that desired, and the periodontal
dressing can avoid its movement in a coronal direction. A partialthickness flap is
sutured to the periosteum.

Flaps for reconstructive surgery:

In current reconstructive therapy, bone grafts, membranes, or a combination of these,
with or without other agents, are used for a successful outcome The flap design
should therefore be set up so that the maximum amount of gingival tissue and papilla
are retained to cover the material(s) placed in the pocket. Two flap designs are
available for reconstructive surgery: the papilla preservation flap and the
conventional flap with only crevicular incisions.

I. Papilla Preservation Flap (PPF)

Step 1: A crevicular incision is made around each tooth with no incisions across the
interdental papilla.

Step 2: The preserved papilla can be incorporated into the facial or lingual/palatal
flap, although it is most often integrated into the facial flap. In these cases, the lingual
or palatal incision consists of a semilunar incision across the interdental papilla in its
palatal or lingual aspect.

Step 3: An Orban knife is then introduced into this incision to sever half to two-thirds
the base of the interdental papilla. The papilla is then dissected from the lingual or
palatal aspect and elevated intact with the facial flap.

Step 4: The flap is reflected without thinning the tissue.

 II. Conventional Flap
Step 1: Using a #12 blade, incise the tissue at the bottom of the pocket and to the crest
of the bone, splitting the papilla below the contact point. Every effort should be made
to retain as much tissue as possible.

Step 2: Reflect the flap, maintaining it as thick as possible, not attempting to thin it
as is done for resective surgery. The maintenance of a thick flap is necessary to
prevent exposure of the graft or the membrane resulting from necrosis of the flap
margins.
 Minimally invasive techniques
Minimally invasive surgeries were originally proposed by Harrell and Rees 1995
with the objective of minimal wounds, minimal flap reflection and gentle handling
of the soft and hard tissues.

MIST is an effective surgical approach for the treatment of isolated deep intra-bony
defects with periodontal regeneration.

Minimally Invasive Surgical Technique (MIST) Cortellini & Tonetti 2007

The clinical rationale for the development of the MIST includes the following:

(1) reduction of surgical trauma,

(2) increase in flap/wound stability,

(3) improvement of primary closure of the wound,

(4) reduction of surgical chair time, and

(5) minimization of intra-operative and post-operative patient discomfort and

morbidity.

The background foundations for the MIST:

● The concept of minimally invasive surgery, Harrel and Rees 1995

● Papilla preservation technique, Cortellini et al. 1995, 1999.

● Microsurgical approach, Cortellini & Tonetti 2001, 2005

The defect-associated inter-dental papilla is accessed either with the papilla

preservation technique. The inter-dental incision is extended to the buccal and lingual
aspects of the two teeth adjacent to the defect. These incisions are intra-sulcular to
preserve all the height and width of the gingiva, and their mesio-distal extension was
kept at a minimum to allow the corono-apical elevation of a very small full-thickness
flap with the objective to expose just 1–2mm of the defect-associated residual bone
crest.
Modified Minimally Invasive Surgical Technique (M-MIST) Cortellini &
Tonetti 2009
An enhancement of the MIST, the modified minimally invasive surgical
technique, has been designed to further reduce the surgical invasiveness, with
three major objectives in mind:

(1) minimize the interdental tissue tendency to collapse,

(2) enhance the wound/soft tissue stability

(3) reduce patient morbidity.

The surgical approach consists of a limited inter-dental incision in which only a

buccal triangular flap is elevated, while the papilla is left in place, connected to
the root of the crest-associated tooth with its supracrestal fibres. The
palatal/lingual tissues are not involved in the surgery.

Crown lengthening:

Crown lengthening aims to increase the clinical crown length of a tooth or teeth
for either esthetic or restorative purposes or a combination of both. The surgical
procedure is designed to increase the extent of the supragingival tooth structure
by apically positioning the gingival margin,removing supporting bone, or both.

The procedure is based on two principles: biologic width (BW) establishment and
maintenance of adequate keratinized gingiva (KG) around the tooth.
Factors taken into consideration include excessive gingival display (known as a
gummy smile), altered passive eruption (in which the alveolar crest is £2 mm
from the cemento-enamel junction [CEJ]), lack of tooth structure, or access for
restorative purposes (requiring the removal of soft or hard tissue or a combination
of both) and the adjacent periodontium of neighboring teeth. Indications for
crown lengthening thus include teeth with subgingival caries or extensive caries
that shortens the tooth, fractures, and short clinical crowns caused by incomplete
exposure of the anatomic crowns.

Formative Assessment Question:

Case : 55 year old woman presented to the clinic with generalized

periodontitis. She was systemically healthy and a non-smoker. After scaling
and root surface debridement, most of the pockets showed reduction in
probing depth, however, a 7 mm pocket was still present at the mesial
aspect of the upper right lateral incisor. The radiograph showed the
presence of a narrow intrabony defect.

According to the above, mention the best flap technique to access the
infrabony defect in the upper left lateral incisor.
Mention the objectives of your choice of the surgical technique.
 Periodontal Regeneration
and
Reconstructive Surgery

Student’s Learning outcomes (SLO’s):

Define different forms of periodontal wound healing.
Describe the outcome of periodontal regenerative techniques clinically,
histologically and radiographically.
Classify reconstructive techniques for treatment of intrabony defects.
Explain rationale for the use of different regenerative techniques for treatment of
intrabony defects.
Formulate a treatment plan for an intrabony defect based on analysis of data of the
case and the use of evidence-based dentistry to reach a successful outcome.
Recognize future directions for periodontal regeneration.
Definition of regeneration and repair:

When the periodontium is damaged by inflammation or as a result of surgical

treatment, the defect heals either through periodontal regeneration or repair. In
periodontal regeneration, healing occurs through the reconstitution of a new
periodontium, which involves the formation of alveolar bone, functionally aligned
periodontal ligament, and new cementum. Alternatively, repair due to healing by
replacement with epithelial and/or connective tissue that matures into various
nonfunctional types of scar tissue, is termed new attachment.

Histologically, patterns of repair include long junctional epithelium, ankylosis,

and/or new attachment. Unfortunately, this approach cannot be used in human studies
as it would be unethical to extract the treated tooth, especially when it responded
positively to therapy to determine whether regeneration or new attachment has
occurred. Possible healing patterns for a periodontal wound shown in diagram below,
which are dependent on the four possible cell types that predominate that wound site.
The downgrowth of epithelial cells (E) results in a long junctional epithelium (JE).
The proliferation of connective tissue (CT) may result in connective tissue adhesion ± root
resorption. With the predominance of bone cells (B), there is root resorption and/or
ankylosis. With the ingress of periodontal ligament (PDL) and perivascular cells from the
bone, a regenerated periodontium develops.
 Clinical and radiographic methods for evaluation of periodontal reconstruction
include comparisons between pretreatment and post-treatment pocket probings and
determinations of clinical gingival findings. The probe can be used to determine
pocket depth, attachment level, and bone level (see diagram below). Clinical
determinations of attachment level are more useful than probing pocket depths
because the latter may change as a result of displacement of the gingival margin.
Radiographic evaluation of periodontal regeneration using standardized techniques
allows assessment of the bone tissue adjacent to the tooth.
Reconstructive surgical techniques:
Reconstructive techniques can be subdivided into three major therapeutic approaches:
I. Non–bone graft–associated
II. Graft-associated
III. Biological mediator–associated regeneration
In clinical practice, it is common for clinicians to combine these various approaches
(combined techniques). Selection of most appropriate technique for each case depends
on reviewing most recent literature in terms of:
Evidence-based dentistry: it aims to help practitioners provide their patients with
optimal care. This concept is based on integrating sound research evidence with
personal clinical expertise and patient values to determine the best course of
treatment. Decision trees: these are provided to show an overview of clinical
determinants that should be considered for the best-practice management of
intrabony defects.

All regenerative techniques require presurgical scaling, occlusal adjustment as needed,

and exposure of the defect with a full-thickness flap. The flap technique best suited for
grafting purposes are the conventional flap and the papilla preservation flap, these designs
provide maximum amount of gingival tissues and papillae to cover the regenerative
material(s) used. The use of antibiotics after the procedure is generally recommended.
After membrane placement, healing is allowed to proceed for 4 to 6 weeks without probing
the periodontal defect.

I. Non–Graft-Associated Reconstructive Procedures:

This includes:
A) Guided tissue regeneration (GTR) is the main procedure used in clinical practice.
B) Laser-assisted new attachment procedure (LANAP).

A) Guided Tissue Regeneration:

GTR is used for the prevention of epithelial migration along the cemental wall of the
pocket and maintaining space for clot stabilization. This method is based on the assumption
that periodontal ligament and perivascular cells have the potential for regeneration of the
attachment apparatus of the tooth.
 GTR consists of placing barriers of different types (membranes) to cover the bone
and periodontal ligament, thus temporarily separating them from the gingival epithelium
and connective tissue. Excluding the epithelium and the gingival connective tissue from
the root surface during the postsurgical healing phase not only prevents epithelial migration
into the wound but also favors repopulation of the area by cells from the periodontal
ligament and the bone. GTR is often performed with some type of bone graft as a
scaffolding agent, so it is a combined therapy. Today in clinical practice, most GTR
procedures use biodegradable membranes, while the nonresorbable membranes are used
for implant site development.

GTR is classified according their degradation characteristics, into two groups:

nonresorbable and resorbable (synthetic, collagen-based).

🞂 Ideal requirements of GTR include:

1. Biocompatibility to allow integration with the host tissues without eliciting
inflammatory responses.
2. Proper degradation profile to match those of new tissue formation.
 3. Adequate mechanical and physical properties to allow its placement in vivo
(clinically manageable).
4. Sufficient sustained strength to avoid the membrane collapse thus provides space for
the healing tissue and perform their barrier function.

Nonresorbable Membranes: e.g. expanded polytetrafluoroethylene (e-PTFE)

The major problem with using non-resorbable membranes is that the membrane
requires a second surgery for its removal (not before 6 weeks). Moreover, it might get
exposed to the oral environment during healing. Upon exposure, the membrane is
contaminated and colonized by oral microflora. Several studies have shown that
contamination of the surgical field can result in decreased formation of new attachment.
Much of our current understanding of GTR is based on studies using e-PTFE
membranes. The more recent d-PTFE has smaller pore size than e-PTFE allowing complete
block of bacteria thus can be left exposed in the oral cavity and is easier to remove in
second stage surgery. After membrane removal, the area should not be probed for 3 months.
Radiographic evidence of bone fill is usually present after 6 months and should continue
over the course of 1 year.
Evidence-based literature:
Clinical studies have shown that e-PTFE membranes used in GTR procedures are
more effective than surgical debridement in correcting intrabony defects. In intrabony and
furcation defects, there are gains in clinical attachment level (3 to 6 mm), improved bone
levels (2.4 to 4.8 mm), and probing depth reductions (3.5 to 6 mm). Studies have
demonstrated that these regenerative results can be maintained over the course of several
years.

Biodegradable (Resorbable) Membranes:

There are basically three types of bioresorbable membranes:
(1) polyglycoside synthetic polymers (i.e., polylactic acid, polylactate/polygalactate co-
polymers)
(2) collagen
Polyglycoside membranes degrade as the result of random nonenzymatic cleavage of the
polymer, producing polylactide and polyglycolide, which are converted to lactic acid and
pyruvate, respectively, and metabolized by the enzymes of the Krebs cycle. Collagen
membranes are degraded by collagenases and subsequently by gelatinases and peptidase.
Several features make these bioresorbable membranes easier to manage clinically: (1) they
are more tissue compatible than nonresorbable membranes; (2) the timing for resorption
can be regulated by the amount of cross-linkage in the synthetic polymer and collagen
membrane or the amount of heat-processed calcium sulfate chips in calcium sulfate barrier;
and (3) a second surgical procedure is not required to retrieve the nonresorbable membrane.
Evidence-based literature:
A recent GTR study compared the use of bioresorbable membranes
(polylactate/polygalactate copolymer) versus e-PTFE membranes, with surgical
debridement as a control. After 1 year, significant gains in clinical attachment level (CAL)
were observed in all three groups. There was no difference in CAL gain between the two
membrane groups, with both of them gaining 2 mm or more. In both membrane groups,
83% of the sites improved 4 mm or more, which was significantly better than the surgical
debridement control group. These findings indicate GTR procedures are equally effective
using resorbable and nonresorbable membranes. This finding has been confirmed by other
investigators.
The potential of using autogenous periosteum as a membrane and also to stimulate
periodontal regeneration has been explored in different studies with conflicting results.
B) Laser-Assisted New Attachment Procedure (LANAP):
The use of neodymium: yttrium-aluminum-garnet (Nd:YAG) to perform surgical LANAPs
has been reported for the management of chronic periodontitis by root surface and soft
tissue decontamination during closed or open flap debridement. This can potentially result
in new attachment and periodontal regeneration. So far, there’s still controversy regarding
their results with a need for randomized controlled trials (RCTs) followed by meta-analysis
to determine if LANAP is equivalent or superior to other conventional therapy.
C) Examples of other studied Non–Graft-Associated Procedures:
 1. Biomodification of Root Surface: Changes in the tooth surface wall of periodontal
pockets (e.g. degenerated remnants of Sharpey’s fibers, accumulation of bacteria and
their products, disintegration of cementum and dentin) interfere with new
attachment. Although these obstacles to new attachment can be eliminated by
thorough root surface debridement, the root surface of the pocket can be treated to
improve its chances of accepting the new attachment of gingival tissues. Several
substances have been proposed for this purpose, including citric acid, fibronectin,
and tetracycline.
2. Surgical Techniques: Surgical techniques have been recommended to eliminate the
pocket and junctional epithelium. The excisional new attachment procedure (ENAP)
consists of an internal bevel incision performed with a surgical knife, followed by
removal of the excised tissue without flap elevation. This approach has been
modified and is used in conjunction with the Nd:YAG laser in the previously
described LANAP procedure.
II. Graft-Associated Reconstructive Procedures:
Grafts are either categorized by their origins and function during healing.
Categorization by origin include: (1) autografts are bone obtained from the same
individual; (2) allografts are bone obtained from a different individual of the same species;
(3) xenografts are bone from a different species and (4) alloplasts which are inorganic
synthetic materials.
Bone graft materials are also evaluated based on their function by having osteogenic,
osteoinductive, or osteoconductive potential. Osteogenesis refers to the formation or
development of new bone by cells contained in the graft. Osteoinduction is a chemical
process by which molecules contained in the graft (e.g., bone morphogenetic proteins)
convert the neighboring cells into osteoblasts, which in turn form bone. Osteoconduction
is a physical effect by which the matrix of the graft forms a scaffold that favors outside
cells to penetrate the graft and form new bone.
Considerations that govern the selection of a material are as follows: biologic
acceptability, predictability, clinical feasibility, minimal operative hazards, minimal
postoperative sequelae, and patient acceptance. It is difficult to find a material with all
these characteristics, and to date, there is no ideal material or technique.
A) Autogenous Bone Grafts
 Sources of bone from intraoral sites include bone from healing extraction
wounds, bone from edentulous ridges, bone trephined from within the jaw without
damaging the roots, newly formed bone in wounds especially created for the purpose,
bone removed from tuberosity, and the ramus and bone removed during osteoplasty
and ostectomy.
E.g.: “Bone blend technique” uses an autoclaved plastic capsule and pestle. Bone is
removed from a predetermined site, triturated in the capsule to a workable, plastic-like
mass, and packed into bony defects.
The use of extraoral sites as a source of bone for grafting into periodontal osseous
defects has been reviewed, using bone from the tibia and the iliac crest (cancellous bone).
Some of the problems were postoperative infection, bone exfoliation, sequestration,
varying rates of healing, root resorption, and rapid recurrence of the defect. Other problems
were increased patient expense and difficulty in procuring the donor material. However,
because of numerous problems associated with its use, the technique is no longer in use.
B) Bone Allografts
Obtaining donor material for autograft purposes necessitates inflicting surgical
trauma on another part of the patient’s body (second surgical site). Both allografts and
xenografts are foreign to the patient and, therefore, have the potential to provoke an
immune response. Attempts have been made to suppress the antigenic potential of
allografts and xenografts by radiation, freezing, and chemical treatment. Bone allografts
are commercially available from tissue banks. Numerous steps are also taken to eliminate
viral infectivity.
Examples include freezed dried bone allograft (FDBA) which is considered an
osteoconductive material, whereas demineralized FDBA (DFDBA) is considered an
osteoinductive graft. Preparation of DFDBA exposes the components of bone matrix,
which are closely associated with collagen fibrils and have been termed bone
morphogenetic proteins (BMPs).
Evidence-based literature:
Multiple studies provided strong evidence that DFDBA in periodontal defects results in
significant probing depth reduction, attachment level gain, and osseous regeneration. The
combination of DFDBA and GTR has also proved to be very successful.
C) Xenografts
Bone products from other species have a long history of use in periodontal therapy.
Bovine-derived bone (Bio-Oss; Osteohealth) is widely used in combination with GTR for
periodontal regeneration. It is an osteoconductive, porous bone mineral matrix from bovine
cancellous or cortical bone.

Evidence-based literature:
Periodontally, Bio-Oss has been used as a graft material covered with a resorbable
membrane (Geistlich Bio-Gide®). The membrane prevents the migration of fibroblasts and
connective tissues into the pores and between the granules of the graft. Histologic studies
of this technique have shown significant osseous regeneration and cementum formation.
Other Xenografts include:
Pepgen (P-15) comprises anorganic bovine bone matrix (ABM) coupled with a
synthetic cell-binding polypeptide (P-15) that is an analog of a 15–amino acid
sequence of type I collagen. this combination seems to enhance the bone-
regenerative results of the matrix alone in periodontal defects.
D) Alloplasts
These are inorganic synthetic bone grafts, classified into: ceramics and polymers. They
include:

1. Calcium Phosphate Biomaterials. Calcium phosphate biomaterials have excellent

tissue compatibility and do not elicit any inflammation or foreign body response.
These materials are osteoconductive, therefore, they act as a scaffold for blood clots
to be retained to allow bone formation.
Two types of calcium phosphate ceramics have been used, as follows:
● Hydroxyapatite (HA) has a calcium-to-phosphate ratio of 1.67, similar to that
found in bone material. HA is generally non-bioresorbable.
● Tricalcium phosphate (TCP), with a calcium-to-phosphate ratio of 1.5, is
mineralogically B-whitlockite. TCP is at least partially bioresorbable.
Evidence-based literature:
 Several controlled studies were conducted on the use of hydroxylapatite (Periograf)
and Calcitite; clinical results were good, but histologically these materials appeared
to be encapsulated by collagen

2. Bioactive Glass. Bioactive glass consists of sodium and calcium salts, phosphates,
and silicon dioxide. When this material comes into contact with tissue fluids, the
surface of the particles becomes coated with hydroxy-carbonate apatite, incorporates
organic ground proteins such as chondroitin sulfate and glycosaminoglycans, and
attracts osteoblasts that rapidly form bone.

3. Coral-Derived Materials. Two different coralline materials have been used in

clinical periodontics: natural coral and coral-derived porous hydroxyapatite. Both
are biocompatible, but whereas natural coral is resorbed slowly (several months),
porous hydroxyapatite is not resorbed or takes years for resorption.
III. Biological mediator-associated regeneration (Tissue Engineering with Biologic
Mediators):
In wound healing, the natural healing process usually results in tissue scarring
or repair. Using tissue engineering, the wound healing process is manipulated so that
tissue regeneration occurs. This manipulation usually involves one or more of the
three key elements: the signaling molecules, scaffold or supporting matrices, and cells
(see diagram below).

Biologic mediators (signaling molecules) have very short biological half-lives

(minutes to a few hours). The carrier function to release these factors at different rate
such that the release can be sustained over one to several weeks.
The major roles for the supporting matrices are to:
1. Provide physical support for the healing area so that there is no collapse of the
surrounding tissue into the wound site. Examples of this would be bone allografts and
synthetic ceramics such as tricalcium phosphate.
2. Serve as a barrier to selectively restrict cellular migration. This is best exemplified
by principles of GTR and guided bone regeneration (GBR) where nonresorbable
polytetrafluoroethylene and resorbable polylactate, polyglycolic acid, and calcium
sulfate are used.
 3. Serve as a scaffold for cellular migration and proliferation. Examples include the
collagen matrix.
4. Potentially serve as a time-release mechanism for signaling molecules.
Early clinical examples involving tissue engineering principles include the use of
bone allografts and autologous platelet-rich plasma (PRP). Investigations indicated that
the success rates with these materials were inconsistent. With the development of
recombinant growth factors and morphogens, and the use of synthetic scaffolds, the level
of success has improved. Some of these biologic mediators are commercially available
such as recombinant human bone morphogenetic protein (rhBMP), enamel matrix
derivative (EMD) and platelet-derived growth factor (PDGF).
Tissue engineering is now clinically applicable with two commercially available
tissue engineering systems for periodontal regeneration which involve the use of enamel
matrix derivative (EMD) and platelet-derived growth factor-BB (PDGF-BB)-beta-
tricalcium phosphate (β-TCP).
Emdogain is a mixture of enamel matrix derivatives (EMDs) that can be used for
regeneration treatments. Emdogain has been shown to enhance proliferation and cell
differentiation of osteoblasts which can lead to improved bone regeneration.
Evidence-based literature:
There have been several studies comparing the use of EMD alone or in conjunction with
other regenerative approaches. When EMD treatment was compared to GTR using
bioresorbable membranes, the clinical results were comparable and stable over as much as
a 10-year period. In a study comparing EMD, GTR, EMD+GTR to open flap debridement,
all three resulted in superior result to open flap surgery with no additional improvement
when EMD was used in conjunction with GTR. Others have confirmed this finding.
Recombinant Human Platelet-Derived Growth Factor for Periodontal
Regeneration. PDGF is one of the earliest growth factors studied for its effect on wound
healing because it is a potent mitogenic and chemotactic factor for mesenchymal cells in
cell culture. rhPDGF in combination with a β-TCP carrier is now commercially available.
Evidence-based literature:
Preliminary studies using rhPDGF-TCP suggest it is easy to use, requires no barrier
membranes, and had results comparable or superior to other regenerative graft materials.
The potential for using rhPDGF for regeneration of furcation defects and implant site
preparation still needs to be evaluated. Additionally, there has been considerable clinical
interest in combining rhPDGF-BB with other bone replacement grafts, particularly bone
allografts and xenografts.
Bone Morphogenetic Proteins are a group of regulatory glycoproteins that are
members of the transforming growth factor β (TGF-β) superfamily that function as
differentiation factors. These proteins induce cellular differentiation of stem cells into
chondroblastic and osteogenic cells. Much of the research interest has focused on
BMP-2 (OP-2), BMP-3 (osteogenin), and BMP-7 (OP-1). The amount of BMPs have
been demonstrated to be present in FDBA and DFDBA, but the levels are so low that
it is not biologically active. In fact, the amount of BMP is so low that it takes
approximately 10 kg of bovine bone to yield only 2 μg of BMP. It is only through
recombinant DNA technology that BMP has been made available for clinical use.
Evidence-based literature:
Although early studies using crude preparations of BMP-2 and BMP-3 applied in surgically
induced furcation defects appeared to stimulate periodontal regeneration, recent study with
rhBMP-2 indicates that periodontal regeneration was associated with areas of ankyloses
which is a matter of concern.

Future Directions for Periodontal Regeneration:

Cell therapy has been recently employed in periodontal surgery. The most common
application involves a cell expansion strategy in an ex vivo environment followed by
transplantation back into the defect area. Reducing or eliminating gingival recession has
been the objective of most of these studies. It is suggested that a reasonable tissue-
engineering approach would be to augment appropriate cells in conjunction with current
commercial kits containing BMP-collagen or rhPDGF-BB-βTCP to further enhance
regeneration.
Gene therapy can be used for extended local delivery of signaling molecules. Gene
transfer can provide a sustained level of growth factors, but may be detrimental toward the
continuous progression associated with differentiation or wound healing as its need varies
according to stage of healing in process. The first successful evidence of periodontal tissue
engineering employing gene therapy was demonstrated with BMP-7 transduced fibroblasts
to stimulate repair of alveolar bone wounds and periodontal defects which resulted in
increased bone formation and differentiation into osteoblasts.

Clinical decision tree for the management of advanced periodontal defects:

Decision making depends on many factors:
1. Tooth importance in prosthetic rehabilitation: The critical question to be
addressed is if the involved dentition is strategically important. If not, the required
expense and strategic extraction may avoid potential technical difficulty,
postsurgical complications, and expenses.
2. Endodontic status: Once a tooth is deemed essential, it is important to assess its
endodontic status. If the tooth is endodontically healthy, regeneration may
proceed. If not, then treatment of the endodontic component must be performed
and resolution of the endodontic problem must be ascertained prior to the
regenerative procedure. Given the expense for endodontic treatment, periodontal
regenerative procedures, crown buildup, and the crown, strategic extraction and
possible replacement with a prosthesis or a dental implant should be seriously
considered.
3. Characteristics of the periodontal defect: such as the overall defect depth, width,
and walls, can influence clinical outcome in response to regenerative surgery.
Studies have consistently shown that the deeper defect is correlated with increased
clinical attachment level and probing depth. One is more likely to achieve improved
regenerative results in narrow and circumferential, three- or two-walled
configuration. Conversely, one- or zero-walled and wide defects are less amenable
to regenerative procedures.
4. Oral hygiene status and patient’s compliance for periodontal maintenance: poor
plaque control and poor postoperative recall compliance have indicated that much
of the therapeutic gain from periodontal surgery will deteriorate. Note that
smoking is one of the habits that adversely influence periodontal regeneration.
Platelet concentrates in periodontal regeneration:
One of the important action of platelets is their role in haemostasis and healing of wound.
Now they are gaining popularity in Dentistry in periodontal regeneration. Earlier fibrin
glue was introduced as sealant, later the platelet-rich plasma (PRP); first generation of
platelet concentrates was utilized in various fields of Dermatology from chronic ulcer
management to trichology and also in aesthetics. Choukroun et al. in Francein 2000’s
introduced the second generation of platelet concentrates (PRF)Platelet Rich Fibrin. PRF
have comparatively several advantages over traditionally prepared PRP.
Conclusion:
A variety of graft materials and regenerative strategies are now available, however,
they all have limitations. The clinician must carefully evaluate the case and decide which
treatment modality may offer the best clinical outcome. Accordingly, the use of decision
trees and reviewing most recent systematic reviews help greatly to reach a suitable
treatment option.
An example of a well conducted systematic review is that of Kao et al. published in
2015 with the title “Periodontal regeneration-Intrabony Defects: A Systematic Review
from the AAP Regeneration Workshop”.
The purpose of this systematic review is to update those consensus reports by
reviewing periodontal regeneration approaches developed for the correction of
intrabony defects with the focus on the following (focused questions):
1) What is the evidence for periodontal regeneration in intrabony defects related
to: a) patient-centered behavioral and systemic considerations; b) what is
achievable and maintainable; c) the influence of tooth mobility; d) surgical
considerations (flap design); e) surgical considerations (defect morphology,
including width, depth, and containment); and f) surgical complications, factors to
increase stability, and stability relapse management?
2) What is the evidence for the following regenerative procedures: a) updated
classic regenerative approach (demineralized freeze-dried bone allograft [DFDBA];
GTR, and GTR combined with graft materials); b) laser-assisted regeneration (LAR);
c) enamel matrix derivative (EMD) (EMD alone, EMD versus GTR, and EMD
combination); and d) recombinant human platelet-derived growth factor BB
(rhPDGF-BB)?
3) What is the optimal timing of regenerative treatment of intrabony defects in
relation to orthodontic and endodontic therapy?
The reviewers’ conclusions are the following:
1) The use of biologics (EMD and rhPDGF-BB + b-TCP) generally increase bone fill
and improve CAL and reduce PD compared with OFD procedures in the treatment
of intrabony defects. These improvements are comparable with those found with
DFDBA and GTR regenerative approaches.
2) Histologic evidence of regeneration has been demonstrated with laser therapy,
but there are no data that define the clinical effectiveness and predictability of this
approach.
3) Clinical outcomes will be most significantly influenced by patient behaviors,
surgical approach, and much less by tooth and site characteristics.
4) Long-term studies indicate that the clinical results achieved with regenerative
therapy are maintainable up to 10 years, even in severely compromised teeth.
Regenerative therapy is capable of improving tooth prognosis.
Formative Assessment Question:

Case: A 45-year-old man came to the dental clinic complaining of

bleeding gums. Medical history revealed a systemically free patient.
Clinical and radiographic examination revealed an infrabony defect
related to mesio-buccal aspect of 46 with GI = 2, PI =2, PD= 7mm
and CAL=3mm. Treatment plan was formulated and executed. Re-
evaluation after 1 month revealed reduction in PD to be 5 mm.

According to the above case, choose the best answer from the
alternatives a, b, c and d:

Bovine bone mineral acts mainly as………….

osteoconductive.
osteoinductive.
osteogenic.
osteoinductive and osteoconductive.

Alloplasts have an osteoinductive effect if they are combined

with………….
growth factors.
antibiotics.
anti-inflammatory agents.
antiviral drugs.
 Periodontal Plastic and
Esthetic Surgeries

Student’s Learning Outcomes (SLOs):

By the end of this topic, you should be able to:

1. Illustrate definition, objectives, and types of periodontal

plastic and esthetic surgeries.
2. Clarify steps of different periodontal plastic and esthetic
surgeries.
3. Design a decision tree for the management of gingival
recession and identify the most appropriate periodontal
esthetic surgical technique indicated in different cases with
justification.
 Periodontal Plastic and Esthetic Surgery
The term Mucogingival Surgery describes surgical procedures for the correction
of relationships between the gingiva and the oral mucous membrane with reference
to three specific problem areas: attached gingiva, shallow vestibule, and a frenum
interfering with the marginal gingiva.

The 1996 World Workshop in Clinical Periodontics renamed mucogingival surgery

as “Periodontal Plastic Surgery,” a term that includes:

1- Periodontal-prosthetic corrections

2. Esthetic surgical corrections

3. Coverage of denuded root surface

4. Reconstruction of interdental papillae

5. Esthetic surgical correction around implants

6. Surgical exposure of unerupted teeth for orthodontics

7- Crown lengthening

8- Ridge augmentation

Periodontal plastic surgery is defined as surgical procedures performed to correct

or eliminate anatomic, developmental, or traumatic deformities of the gingiva
and/or alveolar mucosa.

Objectives of periodontal plastic surgery:

1. To solve problems associated with attached gingiva

2. To solve problems associated with a shallow vestibule.

3. To solve problems associated with an aberrant frenum.

4. Esthetic surgical therapy.

5. Tissue engineering.
Periodontal plastic surgical techniques include

(1) Widening of attached gingiva.

(2) Deepening of shallow vestibule.

(3) Resection of aberrant frenum.

Abnormal or aberrant frenum is detected visually, by applying tension over it to

see the movement of papillary tip or blanching produced due to ischemia of the
region.

Frenum should be characterized as pathogenic when there is no enough zone of

attached gingiva along the midline, or the interdental papilla when the frenum is
extended.

Problems Associated with Attached Gingiva

The ultimate GOAL of mucogingival surgery is the creation or widening of the

attached gingiva around teeth and implants.

Width of attached gingiva is determined by subtracting the depth of sulcus or

pocket from the distance between the crest of the gingival margin and the
mucogingival junction.

Rationale for mucogingival surgery is based on that a minimal width of attached

gingiva is required to maintain optimal gingival health.

Techniques to Increase Attached Gingiva (widen the zone of attached gingiva)

• Gingival augmentation apical to the gingival recession.

A graft is placed on recipient bed apical to the recessed gingival margin.

No attempt is made to cover the denuded root surface.

• Gingival augmentation coronal to the gingival recession (root coverage).

A graft is placed to cover the denuded root surface.

Both the apical and the coronal widening of attached gingiva enhance oral
hygiene procedures, but only the latter can correct an esthetic problem.
Widening of attached gingiva (apical or coronal to the area of recession) can
be done by numerous techniques:

I. Gingival Augmentation Apical to Recession

Techniques for gingival augmentation apical to the area of recession include:

1. Free Gingival Autograft.

2. Free Connective Tissue Autograft.

3. Apically Positioned Flap.

Free Gingival Autograft (Free soft tissue autograft)

Free gingival grafts are used to create a widened zone of attached gingiva.

Surgical steps of the free gingival graft

Step 1: Prepare the recipient site.

The purpose of this step is to prepare a firm connective tissue bed to receive the
graft. This step can be done by 2 techniques.

A- The Classic Technique: The recipient site is prepared by incising at the

existing mucogingival junction with a #15 blade, blending the incision on both
ends with the existing mucogingival line.

B- Another technique (James and McFall, 1978)

- It consists of outlining recipient site with two vertical incisions from the incised
gingival margin into the alveolar mucosa.
- Extend incisions to approximately twice the desired width of attached gingiva,
allowing for 50% contraction of the graft during healing.
- The #15 blade is used to incise along the gingival margin to separate a flap
consisting of epithelium and underlying connective tissue.
- Extend flap to depth of vertical incisions.
- Suture the flap where the apical portion of the free graft will be located.
In both techniques the periosteum should be left covering bone.
Make an aluminum foil template of recipient site to be used as a pattern for graft.

Grafts can also be placed directly on bone in the recipient site. For this
technique, flap should be elevated by blunt dissection by mucoperiosteal elevator.

Step 2: Obtain the graft from the donor site.

Free gingival graft technique consists of transferring a piece of keratinized tissue to

the recipient site. The hard palate is the usual site from which the donor tissue is
obtained. The graft should consist of epithelium and underlying connective tissue.

Place the template over donor site, and make a shallow incision around the
template with a #15 blade. Insert blade to desired thickness at one edge of graft.
Elevate the edge and hold it with tissue forceps.

Continue to separate the graft with the blade, lifting it gently as separation
progresses.

Placing sutures at the margins of the graft:

- helps control it during separation and transfer.

- Facilitates placement and suturing of the graft to the recipient site.

Proper thickness of the graft is important for survival of the graft:

Ideal thickness of the graft is from 1.0 to 1.5 mm.

It should be thin enough to permit diffusion of fluid from the recipient site, which
is essential in the immediate post transplant period.

If the graft is too thin, graft necrosis and exposure of the recipient site may occur.

If the graft is too thick, its peripheral layer is jeopardized because of the excessive
tissue that separates it from new circulation and nutrients.

Thick grafts may also create a deeper wound at the donor site, with the possibility
of injuring major palatal arteries.

Since the submucosa in the posterior region of palate is thick and fatty, it should
be trimmed after the graft is separated so that it will not interfere with
vascularization of the graft.
Step 3: Transfer and immobilize graft.

Position the graft and adapt it firmly to the recipient site.

A space between the graft and the underlying tissue impairs vascularization
and jeopardizes the graft.

Suture the graft at lateral borders and to the periosteum to secure it in position.

The graft must be immobilized, since any movement interferes with healing.

Avoid excessive tension, which can distort the graft. Every precaution should
be taken to avoid any trauma to the graft.

Step 4: Protect the donor site.

Cover the donor site with a periodontal pack for one week, and repeat if necessary.
A retainer is used to cover the pack on the hard palate.
Postoperative care:

1. Systemic antibiotics for 10 days.

2. Chlorhexidine mouthrinse for 2 weeks.
3. Pain medication as needed.
4. Inactivity for 24 hours and ice applied to face for 24 hours.
5. Cold liquids for first three meals.
6. No mastication or tooth brushing at surgical site for 2 to 3 weeks.
7. Remove sutures at 2 to 4 weeks.
Free Connective Tissue Autograft

The connective tissue carries the genetic message for the overlying epithelium to
become keratinized. Therefore only connective tissue from beneath a keratinized
epithelium zone can be used as a graft.

The common site for obtaining free connective tissue autograft is the hard palate.
Advantages of free connective tissue autograft compared to the free gingival
autograft:

▪ Donor tissue is obtained from the undersurface of a palatal flap, which is

sutured back in primary closure; thus healing is by first intention.

▪ The patient has less discomfort postoperatively at the donor site.

▪ Improved esthetics can be achieved because of better color match of grafted

tissue to adjacent areas.

II. Gingival Augmentation Coronal to Recession

(Root Coverage)
Gingival recession is defined as the apical shift of the gingival margin with
respect to the cementoenamel junction (CEJ); it is associated with attachment loss
and with exposure of the root surface in the oral environment.

Predisposing factors for gingival recession.

1. Periodontal biotype and attached gingiva

A thin periodontal biotype, absence of attached gingiva, and reduced

thickness of the alveolar bone due to abnormal tooth position in the arch are
considered risk factors for the development of gingival recession.

The presence of attached gingiva is considered important for maintenance

of gingival health. About 2 mm of Keratinized tissue and about 1 mm of attached
gingiva are desirable around teeth to maintain periodontal health.

2. Tooth brushing

“Improper” tooth brushing method has been proposed as the most important
mechanical factor contributing to the development of gingival recession. Several
studies reported potential risk factors like duration of tooth brushing, brushing
force, frequency of changing the toothbrush, brush (bristle) hardness and
tooth‐brushing technique.
 3. Cervical restorative margins

Sites with minimal or no gingiva associated with intra‐sulcular

(subgingival) restorative margins are more laible to gingival recession and
inflammation.

4. Orthodontic treatment

There is a possibility of gingival recession initiation or progression of

recession during or after orthodontic treatment. This depends on the direction of
tooth movement and bucco‐lingual thickness of gingiva.

Incorrect tooth
brushing.
Aberrant frenal
Etiological factors of gingival

Mechanical attachment
Factors
Iatrogenic causes
recession

Habits

Inflammatory loss of supporting structures

periodontal (periodontitis) lead to apical
diseases migration of gingival crest

Classification of Gingival Recession

Sullivan and Atkins classified gingival recession into four anatomic categories:

(1) shallow-narrow,
(2) shallow-wide,
(3) deep-narrow,
 (4) deep-wide.
Miller’s classification of Gingival Recession

Class I. Marginal tissue recession does NOT extend to the mucogingival junction.
There is NO loss of bone or soft tissue in the interdental area. This type of
recession can be narrow or wide.

Class II. Marginal tissue recession extends to or beyond the mucogingival

junction. There is NO loss of bone or soft tissue in the interdental area. This type
of recession can be narrow or wide.

Class III. Marginal tissue recession extends to or beyond the mucogingival

junction. There is bone and soft tissue loss interdentally or malpositioning of the
tooth.

Class IV. Marginal tissue recession extends to or beyond the mucogingival

junction. There is severe bone and soft tissue loss interdentally or severe tooth
malposition.

A modern recession classification based on the interdental CAL

measurement has been proposed by Cairo et al. (2011)

• Recession Type 1 (RT1): Gingival recession with no loss of inter‐

proximal attachment. Interproximal CEJ is clinically not detectable at both mesial
and distal aspects of the tooth.

• Recession Type 2 (RT2): Gingival recession associated with loss of

interproximal attachment. The amount of interproximal attachment loss (measured
from the interproximal CEJ to the depth of the interproximal sulcus/pocket) is less
than or equal to the buccal attachment loss (measured from the buccal CEJ to the
apical end of the buccal sulcus/pocket).

• Recession Type 3 (RT3): Gingival recession associated with loss of

interproximal attachment. The amount of interproximal attachment loss (measured
from the interproximal CEJ to the apical end of the sulcus/pocket) is greater than
the buccal attachment loss (measured from the buccal CEJ to the apical end of the
buccal sulcus/pocket).
The Cairo classification is a treatment‐oriented classification to predict the
potential for root coverage through the assessment of interdental CAL:

- In Cairo RT1 (Miller Class I and II) 100% root coverage can be predicted.

- In Cairo RT2 (Miller class III) some randomized clinical trials indicate the limit
of interdental CAL loss within which full root coverage (100%) is predictable
applying different root coverage procedures.

- In the Cairo RT3 (over‐lapping the Miller class IV) full root coverage is NOT
achievable.

Techniques used for root coverage

1. Free Gingival Autograft.

2. Free Connective Tissue Autograft.

3. Subepithelial Connective Tissue Graft (Langer technique)

4. Pedicle Autografts:

▪ Laterally Positioned Pedicle Flap

▪ Coronally Positioned Flap;

▪ Semilunar Coronally Positioned Flap (Tarnow technique)

5. Guided Tissue Regeneration (GTR)

Free Gingival Autograft

Step 1: Root planing.

Root planing is performed by application of saturated citric acid for 5 minutes on

root surface.

Step 2: Prepare the recipient site.

 • Make a horizontal incision in IDP at right angle.

• Vertical incisions are made at proximal line angles of adjacent teeth and the
retracted tissue is excised.

• Maintain an intact periosteum in the apical area.

Steps 3 and 4. As discussed before.

Free gingival autograft results in predictable coverage of denuded root surface but
it presents Esthetic Color Discrepancies with adjacent gingiva because of the
Lighter color of the graft.

Free Connective Tissue Autograft

The difference between this technique and free gingival autograft is that donor
tissue is Connective Tissue.

Steps of the free connective tissue autograft:

1. Divergent vertical incisions are made at the line angles of tooth to be

covered, creating a partial-thickness flap to at least 5 mm apical to the
receded area.
2. Suture the apical mucosal border to the periosteum.
3. Scaling and root planing.
4. From the palate, obtain a connective tissue graft.
5. The donor site is sutured after the graft is removed.
6. Transfer the graft to the recipient site, and suture it to the periosteum with a
gut suture. Good stability of the graft must be attained with adequate sutures.
7. Cover the grafted site with dry aluminum foil and periodontal dressing.

Subepithelial Connective Tissue Graft (Langer technique)

This technique was described by Langer and Langer in 1985.

It is indicated for:

- Wide and multiple recession defects,

 - with Good Vestibular Depth and Gingival Thickness to allow a split-
thickness flap to be elevated.

The connective tissue is Sandwiched between the Split Thickness Flap elevated
adjacent to the denuded root surface (recipient site).

Sagittal views
A. Facial recession.
B. Split-thickness incision at
recipient site.
C. Flap reflection.
D. Connective tissue placed over
denuded root. The apical
portion of donor tissue is
placed between the portions
of the split thickness flap.
E. Recipient site flap is closed.

Pedicle Autografts
1. Laterally Positioned Pedicle Flap

2. Coronally Positioned Flap

3. Semilunar Coronally Positioned Flap (Tarnow technique)

Laterally Positioned Pedicle Flap

Indication: It is used to cover

- isolated, denuded root surface that have;

- adequate donor tissue laterally and

- adequate vestibular depth.

Steps:

Step 1: Prepare the recipient site.

Epithelium is removed around the denuded root surface. The exposed connective
tissue will be the recipient site for the laterally displaced flap.

The root surface will be scaled and root planed.

Step 2: Prepare the flap.

The periodontium of the donor site should have:

- a satisfactory width of attached gingiva,

- No or minimal loss of bone,

- No dehiscence or fenestration.

A full-thickness or partial-thickness flap may be used, but partial thickness is

preferred because it offers the advantages of

- Rapid healing at the donor site.

- Reduction of the risk of loss of facial bone height.

Step 3: Transfer the flap.

- Slide the flap laterally onto the adjacent root, making sure that it lies flat and
firm without excess tension on the base.

- Fix the flap to the adjacent gingiva and alveolar mucosa with interrupted
sutures.

- Make a suspensory suture around the involved tooth to prevent the flap
from slipping apically.

Step 4: Protect the flap and donor site.

 - Cover the operative field with aluminum foil and a periodontal dressing.

- Remove the dressing and sutures after 1 week.

Laterally Positioned Pedicle Flap

Coronally Displaced Flap

The purpose of coronally displaced flap procedure is to create a Split-

thickness Flap in area apical to the denuded root and position it coronally to
cover the root.

Two techniques are available for this purpose:

First Technique

Step 1.

Make two vertical incisions to delineate the flap.

Incisions should extend beyond mucogingival junction.

Make an internal bevel incision from the gingival margin to bottom of the pocket
to eliminate the diseased pocket wall.
Elevate a mucoperiosteal flap using careful sharp dissection.

Step 2. Scale and plane the root surface.

Step 3. Return the flap and suture it at a level coronal to the pretreatment position.

Cover the area with a periodontal dressing.

Remove the sutures and dressing after 1 week.

Variation to the First Technique of the Coronally Displaced Flap

(Double Step Procedure for coronally displaced flap)

▪ Results of coronally displaced flap technique are often unfavorable

because of insufficient keratinized gingiva apical to the recession.

▪ To overcome this problem and to increase the chances of success, gingival

augmentation with a free autogenous Graft can be performed before the
coronally positioned flap.

▪ This creates several millimeters of attached keratinized gingiva apical to the

denuded root.

▪ Two months after this surgery:

- A second-stage procedure is performed.

- Apply Citric acid with a pH 1.0 for root conditioning.

- Coronally position the flap that includes the free autogenous graft.

Significant degree of reduction in recession treated by this double-step

procedure was reported 2 years after treatment.

Semilunar Coronally Positioned Flap

to cover isolated denuded root surface
Step 1.
Semilunar incision is made following the curvature of receded gingival margin,
ending 2 to 3mm short of the tip of the papillae.

This location is very important since the flap derives its blood supply from the
papillary areas.

Step 2. Perform a split-thickness dissection coronally from the incision, and

connect it to an intrasulcular incision.

Step 3. The tissue will collapse coronally, covering the denuded root.

It is then held in its new position for few minutes with a moist gauze. Many cases
do not require either sutures or pack.

This technique is simple and provides 2 to 3 mm of root coverage.

This technique is indicated when:

- recession is not extensive (3 mm).

- facial gingival biotype is thick.

It is successful for treatment of recession in the maxillary teeth.

It is not recommended for the mandibular teeth.

Guided Tissue Regeneration Technique for Root Coverage

GTR should result in reconstruction of the attachment apparatus, along with

coverage of the denuded root surface.

Steps

1. A Full-thickness flap is reflected to MGJ, continuing as a partial-thickness flap

apical to MGJ.

2. A membrane is placed over denuded root surface and adjacent tissue. It is

trimmed and adapted to root surface and covers at least 2 mm of marginal
periosteum.
 3. A suture is passed through the portion of the membrane that will cover the bone.

Suture is knotted on the exterior and tied to bend the membrane, creating a space
between root and membrane. This space allows growth of tissues beneath
membrane.

4. The flap is then positioned coronally and sutured.

Four weeks later, a small envelope flap is performed, and membrane is carefully removed.

The flap is then again positioned coronally, to protect the growing tissue, and
sutured. One week later these sutures are removed.

Resorbable membranes were also used for root coverage. BUT, the inability to
create space between resorbable membrane and the denuded root, because of
resorbable membrane softness, may present a problem (even though not needing a
second surgery is an advantage).

Clinical studies comparing GTR with coronally displaced flap showed that GTR
technique is better when the recession is greater than 4.98 mm apicocoronally.

Crown lengthening procedure

Rationale:
1: To overcome problems with a "gummy" smile
Patients who have a high lip line and "short front teeth" expose a broad zone of
gingival tissue and often express concern about their "gummy smile".
The following factors must be considered before treatment of a gummy smile:
• Location of gingival margin in relation to cementoenamel junction and bone crest.
• Crown-root-alveolar bone relationships.
• Size and shape of the upper lip.
• Location of the lip during speech and during a broad, relaxed smile.
In the normal young adult the healthy gingival margin resides about 1 mm
coronal to the cementoenamel junction.
Some patients have clinical crowns shorter than the anatomical crown. If, in such a
patient, the periodontium is of the thin biotype, exposure of the anatomical crown
can be accomplished by a gingivectomy procedure.
If the periodontium is thick biotype and there is a bony ledge at the osseous crest,
an apically positioned flap procedure should be performed. This will allow for
osseous recontouring.
Patients who have short anatomical crowns in the anterior section of the
dentition: The clinical crowns can be made longer by surgically exposing root
structure and by locating the cervical margins of the restorations apical to the
cementoenamel junction.
2: To expose sound tooth structure:
Rationale:
• Subgingival location of carious lesions
• Subgingival location of fracture lines
• Inaccessibility of subgingival margins of failing restorations
• Inaccessibility of subgingivally prepared tooth structure for proper impressions

Surgical Crown Lengthening

Indications
1. Subgingival caries or fracture
2. Inadequate clinical crown length for retention
3. Unequal or unesthetic gingival heights.

Contraindications
1. Surgery would create an unesthetic outcome
2. Deep caries or fracture would require excessive bone removal on contiguous
teeth.
3. The tooth is a poor restorative risk
 Reduction of soft tissue alone is indicated if there is adequate attached
gingiva and more than 3 mm of tissue coronal to the bone crest. This may be
accomplished by either gingivectomy or flap technique without bone
recontouring.

Cases with inadequate attached gingiva and less than 3 mm of soft tissue
require a flap procedure and bone recontouring.

In the case of caries or tooth fracture, to ensure margin placement on sound

tooth structure and retention form, the surgery should provide at least 4 mm
from the apical extent of the caries or fracture to the bone crest.

Procedure for Crown Lengthening

1. Preoperative temporization.
2. Inverse-beveled incisions are used, especially palatally, for reduction of bulky
tissue.
3. Flaps are extended at least one tooth anterior and posterior to the affected area to
permit adequate osseous surgery to be performed.
4. Maximum preservation of keratinized gingiva is recommended (4-5 mm) if
intrasulcular marginal placement is critical.
5. The scalloping of the flap should anticipate the final underlying osseous contour.

6. The flap is reflected as a full-thickness flap if there is an adequate zone of

keratinized gingiva. The flap is reflected as a full-thickness flap to the
mucogingival junction and then split apically if a minimum zone of keratinized
gingiva is present and the flap margin will be positioned at or apical to the crest of
bone.

7. Proper degranulation is critical for

a. Reduced bleeding
b. Visual detection of
 Osseous topography
 Tooth structure
 Apical extent of Decay, Margins or Fracture
8. Osteoplasty and Ostectomy are performed. At least 4 mm of healthy tooth
structure coronal to the osseous crest are required.

9. Ostectomy and scalloping of the bone buccally and lingually are now performed
not only on the affected tooth but also onto the adjacent teeth for blending and
gradualization of osseous architecture.
10. Suturing: Flap position postsurgically is determined by the quantity of
keratinized gingiva present:
a. Wide zone (> 4-5 mm): flap positioned 1 mm coronal to the osseous crest
b. Normal zone (3 mm): flap positioned at the osseous crest
c. Narrow zone (< 3 mm): flap positioned below the crest of bone (partial-
thickness flap) or supragingival marginal placement.
Formative Assessment Question:

Case:

A thirty-year-old woman presented to the dental clinic with an

esthetic concern about her anterior tooth. Clinical examination revealed
a localized gingival recession that doesn’t extend to the mucogingival
junction affecting the labial surface of upper central incisor and no loss
of interdental tissues. Radiographic examination revealed no interdental
bone resorption. She had good oral hygiene and a thin gingival biotype.
You decided to perform a surgical procedure for root coverage.

Choose the best answer from the alternatives a, b, c and d:

1. This type of gingival recession fits Miller ……..
a) Class I.
b) Class II.
c) Class III.
d) Class IV.

2. Techniques for gingival augmentation apical to the area of

recession include :
a) Modified Widman Flap.
b) Conventional flap.
c) Papilla preservation flap.
d) Apically Positioned Flap.

3. The ideal thickness of the free soft tissue autograft is….

a) from 0.5 to 0.75 mm

b) from 1.0 to 1.5 mm
c) from 2 to 2.5 mm
d) from 3 to 3.5 mm

1)
 References

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Rose LF, Mealy B, Genco R and Cohen W: Periodontics, Medicine,

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Wolf HF, Rateitschack EM,Rateitschack KH and Hassell TM:

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