PERIODONTICS

REVISITED
Uploaded by http://dentalebooksfree.blogspot.com
Shalu Bathla MDS (Gold Medalist)
Reader
Department of Periodontology and Oral Implantology
MM College of Dental Sciences and Research
Mullana, Ambala, Haryana, India

Assisted by
Manish Bathla MD
Assistant Professor
Department of Psychiatry
MM Institute of Medical Sciences and Research
Mullana, Ambala, Haryana, India
Forewords

SG Damle
Thomas E Van Dyke

JAYPEE BROTHERS MEDICAL PUBLISHERS (P) LTD

New Delhi Panama City London

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25

Chronic Periodontitis
Shalu Bathla, Anish Manocha

1.
2.
3.
4.

Introduction
Classification
Clinical Features
Radiographic Features

INTRODUCTION
Chronic periodontitis is the most common form of
destructive periodontal disease in adults; it can occur over
a wide range of ages. It can occur in both the primary and
secondary dentition. It usually has slow to moderate rates
of progression, but may have periods of rapid progression.
Chronic periodontitis is initiated and sustained by
bacterial plaque, but host defense mechanism plays an
integral role in its pathogenesis. The progressive nature
of the disease can only be confirmed by repeated
examinations. It is reasonable to assume that the disease
will progress further if treatment is not provided.
Chronic Periodontitis is defined as an infectious disease
resulting in inflammation within the supporting tissues of
the teeth leading to progressive attachment and bone loss. It
is also characterized by pocket formation and/or gingival
recession. It is recognized as the most frequently
occurring form of periodontitis.
CLASSIFICATION
Chronic periodontitis can be further characterized by
extent and severity. Extent is the number of sites involved
and can be described as localized or generalized.
Localized if 30% of the sites are affected (Fig. 25.1)
Generalized if > 30% of the sites are affected (Fig. 25.2)

5. Progression of Periodontal Disease

6. Risk Factors or Susceptibility
7. Treatment

Severity can be described for the entire dentition or

for individual teeth and sites. As a general guide, severity
can be categorized on the basis of the amount of clinical
attachment loss (CAL) as follows:
Slight = 1 to 2 mm CAL
Moderate = 3 to 4 mm CAL
Severe 5 mm CAL.
CLINICAL FEATURES
1. Amount of destruction is consistent with the presence of
local factors: Characteristic clinical finding in patient
with chronic periodontitis include supragingival and
subgingival plaque accumulation that is frequently
associated with subgingival calculus formation
(Fig. 25.3).
2. Gingival inflammation: The gingiva ordinarily is
slightly to moderately swollen and exhibits
alterations in color ranging from pale red to magenta.
Loss of gingival stippling and changes in the surface
topography may include blunted or rolled gingival
margins and flattened or cratered papillae. Gingival
bleeding, either spontaneous or in response to
probing, is frequent, and inflammation related
exudates of crevicular fluid (Fig. 25.4).
3. Periodontal pocket formation: Pocket depths are variable,
and suppuration from the pocket can be found.

CHAPTER 25: Chronic Periodontitis 187

Fig. 25.1: OPG showing localized bone loss in localized chronic

periodontitis
Fig. 25.4: Gingival inflammation associated with chronic
periodontitis

Fig. 25.2: OPG showing generalized bone loss in generalized

chronic periodontitis

Fig. 25.5: Generalized loss of attachment

4. Loss of periodontal attachment: Chronic periodontitis

with slight to moderate loss of periodontal
supporting tissues may be localized or generalized
(Fig. 25.5).

PERIODONTICS REVISITED

Fig. 25.3: Increased amount of calculus and plaque associated with

chronic periodontitis

5. Loss of alveolar bone: Resorption of alveolar bone in

the form of both horizontal and vertical bone loss
can be seen. There is considerable variation in both
the form, pattern and rate of alveolar bone
resorption.
6. Mobility: Tooth mobility often appears in advanced
cases when bone loss has been considerable.
7. This type of periodontitis can be associated with local
predisposing factors (e.g. tooth-related or iatrogenic
factors).
8. May be modified by and/or associated with
systemic diseases (e.g. diabetes mellitus, HIV); can
be modified by factors other than systemic disease
such as cigarette smoking and emotional stress.
9. Slow to moderate rate of progression, but may have
periods of rapid progression also.

188 SECTION 4: Pathology of Gingival and Periodontal Diseases

RADIOGRAPHIC FEATURES
Radiographic examination is an essential part of
periodontal diagnosis and with certain limitations
provides evidence of the alveolar bone height, extent,
form of bone destruction, and the density of cancellous
trabeculation. Various bone loss patterns can be seen in
chronic periodontitis patient (Fig. 25.6) and is explained
in chapter 24 Bone defects. In a marginal periodontitis,
bone destruction is indicated first by the loss of the dense
margin, which delineates the alveolar process in health.
As bone density decreases the bone margins becomes
radiolucent and indistinct. With continuing bone
resorption the height of the alveolar bone is reduced.

i. Continuous disease model: In this model, loss of

attachment has commenced and proceed continuously
and slowly until tooth loss eventually results. Linear
correlation between age and loss of attachment,
supports this concept of gradual destruction (Fig. 25.7).
ii. Random burst disease model: In 1982, Goodson et al
challenged the continuous disease model and

Chronic periodontitis is diagnosed by:

Chronic inflammatory changes in the gingiva
Presence of periodontal pockets
Loss of clinical attachment and
Alveolar bone loss

PROGRESSION OF PERIODONTAL DISEASE

Fig. 25.7: Continuous disease model

PERIODONTICS REVISITED

Chronic periodontitis does not progress at an equal rate

in all affected sites throughout the mouth. Some involved
areas may remain static for long periods of time, whereas
others may progress more rapidly. More rapidly
progressive lesions occur most frequently in interproximal
areas and are usually associated with areas of greater
plaque accumulation and inaccessible areas to plaque
control measures (furcation areas, overhanging margins,
malposed teeth).
Following are the models that describe the rate of
disease progression:

Fig. 25.6: Radiograph of chronic periodontitis showng various pattern

of bone loss: 1. Vertical bone loss, 2. Furcation defect, 3. Horizontal
bone loss

Fig. 25.8: Random burst disease model

CHAPTER 25: Chronic Periodontitis 189

proposed that destruction occurs during periods of
exacerbation, interjected with intervals of remission.
Breakdown occurs in recurrent acute episodes/bursts
of activity over a short time span, interspersed with
periods of quiescence (Fig. 25.8).
iii. Stochastic disease model: In 1989 Manji and Nagelkerke
proposed Stochastic model for periodontal
breakdown that essentially combines both of the
above models. They suggested that, as well as an
underlying slow continuous breakdown (the
progression rate of which depends on host and sites),
some sites of some individuals are also undergoing
random bursts of activity as a result of a combination
of biological events.
RISK FACTORS OR SUSCEPTIBILITY

TREATMENT
The goals of periodontal therapy are to alter or eliminate
the microbial etiology and contributing risk factors for
periodontitis, thereby arresting the progression of the
disease and preserving the dentition in a state of health,
comfort, and function with appropriate esthetics; and to
prevent the recurrence of periodontitis. In addition,
regeneration of the periodontal attachment apparatus,
where indicated, may be attempted. Clinical judgement
is an integral part of the decision making process. Many
factors affect the decisions for the appropriate
therapy(ies) and the expected therapeutic results.
Patient-related factors include systemic health, age,
compliance, therapeutic preferences, and patients ability
to control plaque. Other factors include the clinicians
ability to remove subgingival deposits, restorative and
prosthetic demands, and the presence and treatment of
teeth with more advanced chronic periodontitis.
Treatment considerations for patients with slight to
moderate loss of periodontal support are described
below:

PERIODONTICS REVISITED

Prior History of Periodontitis: Although not a true risk

factor for disease but rather a disease predictor, a prior
history of periodontitis puts patients at a greater risk for
developing further loss of attachment and bone, given a
challenge from bacterial plaque accumulation. This
means that patient with pocket and attachment and bone
loss will continue to lose periodontal support if not
successfully treated.
Bacterial risk factors: Plaque accumulation on tooth and
gingival surfaces at the dentogingival junction is
considered the primary initiating agent in the etiology
of chronic periodontitis. Specific microorganisms have
been considered as potential periodontal pathogens but
it is clear that although pathogens are necessary, their
mere presence may not be enough for disease activity to
occur. Microbial plaque (biofilm) is a crucial factor in
inflammation of the periodontal tissues, but the
progression of gingivitis to periodontitis is largely
governed by host-based risk factors. Microbial biofilms
of particular compositions will initiate chronic
periodontitis in certain individuals whose host response
and cumulative risk factors predispose them to
periodontal destruction rather than to gingivitis.
Systemic Factors: The rate of progression of plaqueinduced chronic periodontitis is generally considered to be
slow. However, when chronic periodontitis occurs in a
patient who also suffers from a systemic disease that
influences the effectiveness of the host response, the rate of
periodontal destruction may be significantly increased.
Diabetes is a systemic condition that can increase the severity
and extent of periodontal disease in an affected patient.
Age: Although the prevalence of periodontal disease
increases with age it is unlikely that becoming older in

itself greatly increases susceptibility to periodontal

disease. It is more likely that the cumulative effects of
disease over a lifetime, i.e. deposits of plaque and
calculus, and the increased number of sites capable of
harboring such deposits, as well as attachment and bone
loss experience, explain the increased prevalence of
disease in older people.
Smoking: It is not only the risk of developing the
disease that is enhanced by smoking, but also the
response to periodontal therapy is impaired in smokers.
A further feature in smokers is that their signs and
symptoms of both gingivitis and chronic periodontitis,
mainly gingival redness and bleeding on probing, are
masked by the dampening of inflammation.
Stress: Stress and other psychosomatic conditions may
have direct anti-inflammatory and/or anti-immune effects
and/or behavior mediated effects on the bodys defenses.
Genetics: There is convincing evidence from twin
studies for a genetic predisposition to the periodontal
diseases. The twin studies have indicated that risk of
chronic periodontitis has a high inherited component. It
is likely that chronic periodontitis involves many genes,
the composition of which may vary across individuals and
races. Much attention has focused on polymorphisms
associated with the genes involved in cytokine
production. Such polymorphisms have been linked to
an increased risk for chronic periodontitis but these
findings have yet to be corroborated.

PERIODONTICS REVISITED

190 SECTION 4: Pathology of Gingival and Periodontal Diseases

1. Contributing systemic risk factors may affect
treatment and therapeutic outcomes for chronic
periodontitis. These may include diabetes, smoking,
certain periodontal bacteria, aging, gender, genetic
predisposition, systemic diseases and conditions
(immunosuppression), stress, nutrition, pregnancy,
HIV infection, substance abuse and medications.
Elimination, alteration, or control of risk factors which
may contribute to chronic periodontitis should be
attempted. Consultation with the patients physician
may be indicated.
2. Instruction, reinforcement and evaluation of the
patients plaque control should be performed.
3. Supragingival and subgingival scaling and root
planing should be performed to remove microbial
plaque and calculus. To accomplish this, the
following procedures may be considered:
Removal or reshaping of restorative overhangs
and over-contoured crowns
Correction of ill-fitting prosthetic appliances
Restoration of carious lesions
Odontoplasty
Tooth movement
Restoration of open contacts which have resulted
in food impaction
Treatment of occlusal trauma.
4. Antimicrobial agents or devices may be used as
adjuncts.
5. Evaluation of the initial therapys outcomes should
be performed after an appropriate interval for
resolution of inflammation and tissue repair. A
periodontal examination and re-evaluation may be
performed with the relevant clinical findings
documented in the patients record. These findings
may be compared to initial documentation to assist
in determining the outcome of initial therapy as well
as the need for and the type of further treatment.
6. For reasons of health, lack of effectiveness or noncompliance with plaque control, patient desires, or
therapists decision, appropriate treatment to control
the disease may be deferred or declined.
7. If the results of initial therapy res olve the periodontal
condition, periodontal maintenance should be
scheduled at appropriate intervals.
8. If the results of initial therapy do not resolve the
periodontal condition, periodontal surgery should be
considered to resolve the disease process and/or
correct anatomic defects.
9. Periodontal Surgery: A variety of surgical treatment
modalities may be appropriate in managing the
patient.

Gingival augmentation therapy.

Regenerative therapy: Bone replacement grafts,
Guided tissue regeneration and Combined
regenerative techniques.
Resective therapy: Flaps with or without osseous
surgery and Gingivectomy.
11. The desired outcome of nonsurgical and surgical
periodontal therapy in patients with chronic
periodontitis should result in: Significant reduction
of clinical signs of gingival inflammation; reduction
of probing depths; stabilization or gain of clinical
attachment and reduction of clinically detectable
plaque to a level compatible with gingival health.
12. Compromised therapy: In certain cases, because of
the severity and extent of disease and the age and
health of the patient, treatment that is not intended
to attain optimal results may be indicated. In these
cases, initial therapy may become the end point. This
should include timely periodontal maintenance.
BIBLIOGRAPHY
1. Chronic Periodontitis. In, Manson JD. Periodontics 4th ed
Wright 1980 Henry Kimpton Publishers; 97-117.
2. Kinane DF and Lindhe J. Chronic Periodontitis. In, Lindhe J,
Karring T, Lang NP. Clinical Periodontology and Implant
dentistry. 4th ed Blackwell Munksgaard 2003;209-15.
3. Nagy RJ, Novak MJ. Chronic periodontitis. In, Newman, Takei,
Carranza. Clinical Periodontology 9th ed WB Saunders 2003;398402.
4. Periodontitis. In, Grant DA, Stern IB, Listgarten MA.
Periodontics. 6th ed CV Mosby Company 1988;348-75.

MCQs
1. To be diagnosed as localized form of chronic
periodontitis, the number of sites involved should
be less than:
A. 10%
B. 20%
C. 30%
D. 40%
2. In chronic periodontontitis:
A. Amount of destruction is consistent with the
presence of local factors
B. Amount of destruction is inconsistent with the
presence of local factors
C. It depends upon age
D. None of the above
Answers
1. C

2. A