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Aggressive Periodontitis: Need to Assess the Prevalence and to plan the Management Strategies in Indian Scenario

Vandana A. Pant and R. M. Mathur

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Adult periodontitis is defined as inflammation of the gingiva and the adjacent dental attachment apparatus. The disease is characterized by loss of clinical attachment due to destruction of the periodontal ligament and loss of the adjacent supporting bone. As discussed earlier, dental plaque bacteria play a key role in what is now understood to be the complex process by which the common types of oral diseases occur C’ dental caries and periodontal diseases. As with other infectious diseases, there is a balance between the host immune responses on one hand, and the microbial pathogenesis on the other hand. In health, host immune responses are sufficient to hold in check the pathogenic potential of both the normal resident microbial flora and exogenous microbial pathogens. Infectious diseases such as periodontal disease occur when this equilibrium is disturbed. Clinical features may include combinations of the following signs and symptoms: edema, erythema, gingival bleeding upon probing, and/or suppuration.

Adult periodontitis with slight to moderate destruction is characterized by a loss of up to 1/3 of the supporting periodontal tissues; a loss of over 1/3 of the periodontal supporting tissues is seen in advanced adult periodontitis. Radiographic evidence of bone loss is apparent in advanced adult periodontitis, and may be evident in adult periodontitis with slight to moderate destruction. Adult periodontitis with slight to moderate or advanced loss of periodontal supporting tissues may be localized, involving one area of a tooth’s attachment, or more generalized, involving several teeth or the entire dentition. A patient may simultaneously have areas of health and adult periodontitis with slight, moderate, and advanced destruction.

The therapeutic goals of periodontal therapy are to alter or eliminate the microbial etiology and contributing risk factors for periodontitis, thereby arresting the progression of 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 judgment is an integral part of the decision-making process.

Many factors affect the decisions for appropriate therapies 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 sub-gingival deposits, prosthetic demands, and the presence and treatment of teeth with more advanced adult periodontitis.

In general the treatment should include oral hygiene instruction, and reinforcement and evaluation of the patient’s plaque control; mechanical therapy, i.e., supra- and sub-gingival scaling and root planing to remove microbial plaque and calculus; and control of other local factors. If this initial therapy resolves the periodontal condition, supportive periodontal therapy should be scheduled at appropriate intervals; but if the periodontal condition is not resolved, periodontal surgery should be considered to correct anatomic defects, and/or to regenerate hard and soft tissues.

Early-onset periodontitis encompasses distinct types of periodontitis that affect young persons who, in most cases, otherwise appear healthy. The age of the disease onset, the rapid rate of the disease progression, manifestations of defects in host response, and composition of the associated subgingival microbial flora may distinguish early-onset periodontitis from adult periodontitis.

Early-onset periodontitis includes three forms: prepubertal periodontitis localized and generalized juvenile periodontitis, and rapidly progressive periodontitis. There is evidence that genetic factors influence susceptibility to the different forms of early onset periodontitis. However, it is unlikely that a specific gene will be identified as causing enhanced disease susceptibility. It is more likely that the genetic influences are as multifactorial as the diseases themselves, and a complex interplay between genetically determined host responses and environmental challenges may determine whether disease is present.

Pre-pubertal periodontitis is associated with attachment loss (gingival pocket formation and radiographic evidence of bone loss) around teeth of the deciduous and/or permanent dentition. It can occur between the time of tooth eruption and the beginning of puberty. As a consequence of this destruction, exfoliation of the deciduous teeth starts prior to the eruption of the permanent dentition. Pre-pubertal periodontitis may occur in either generalized or localized forms. The generalized form is most frequently associated with severe congenital defects of hematological origin and is usually accompanied by alterations in neutrophil chemotaxis function.

Some forms of pre-pubertal periodontitis can be considered to be complications of a severe systemic disorder, such as acrodynia, cementopathia, Ch’diak-Higashi syndrome, chronic neutropenia, histiocytosis X, HIV infection, hypophosphatasia, leukemia, Papillon-Lef’vre syndrome, and fibrous dysplasia. The localized form is usually not associated with a systemic disorder, and presently there is no evidence that localized prepubertal periodontitis will carry over to the permanent dentition. In most reported cases of generalized prepubertal periodontitis with congenital defects of hematologic origin, the disease could not be arrested unless all the teeth were extracted. There are very few reports concerning the treatment of localized prepubertal periodontitis in which aggressive treatment consisted of extraction of hopeless teeth, scaling and root planing, daily subgingival irrigation, and antibiotic coverage.

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