Chronic Periodontitis.


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)


Fig. 1: OPG showing localized bone loss in localized chronic periodontitis

Fig. 2: OPG showing generalized bone loss in generalized chronic periodontitis

Severity can be described for the entire dentition o for individual teeth and sites. As a general guide, severity can be categorized on the basis of the amount of clinicalattachment loss (CAL) as follows:
• Slight = 1 to 2 mm CAL
• Moderate = 3 to 4 mm CAL
• Severe ≥ 5 mm CAL.
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).

Fig. 3: Increased amount of calculus and plaque associated with chronic periodontitis
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).
Fig4: Gingival inflammation associated with chronic periodontitis

3. Periodontal pocket formation: Pocket depths are variable, and suppuration from the pocket can be found.
4. Loss of periodontal attachment: Chronic periodontitis with slight to moderate loss of periodontal supporting tissues may be localized or generalized (Fig. 5).
Fig. 5: Generalized loss of attachment

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.

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. 6) and is explained in chapter 24 Bone defects. In a marginal periodontitis,
bone destruction is indicated first by the loss of the densemargin, 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.

Fig. 6: Radiograph of chronic periodontitis showng various pattern of bone loss: 1. Vertical bone loss, 2. Furcation defect, 3. Horizontal bone loss

Chronic periodontitis is diagnosed by:
Chronic inflammatory changes in the gingiva Presence of periodontal pockets Loss of clinical attachment and Alveolar bone loss
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:
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. 7).

Fig. 7: Continuous disease model

ii. Random burst disease model: In 1982, Goodson et al challenged the continuous disease model and proposed tha 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. 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.

Fig. 8: Random burst disease model

Prior History of Periodontitis: Although not a true ris 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 body’s 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.
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 patient’s ability to control plaque. Other factors include the clinician’s 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
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 patient’s physician may be indicated.
2. Instruction, reinforcement and evaluation of the patient’s 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 therapy’s 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 patient’s 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 therapist’s 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.
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;398- 402.
4. Periodontitis. In, Grant DA, Stern IB, Listgarten MA. Periodontics. 6th ed CV Mosby Company 1988;348-75.
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
. 1C               2. A

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