Immunological differences and similarities between chronic periodontitis and aggressive periodontitis

Chronic periodontitis is an inflammatory response in the periodontal tissues, which is elicited by the microorganisms present in dental plaque. The clinical manifestation of the disease is dependent upon the nature of this response, which, in turn, is determined by the patient s innate susceptibility. Chronic periodontitis in adults typically follows a cyclical course, with some forms remaining stable over many years and other forms progressing with subsequent tooth loss despite extensive treatment (44, 49). The initial immune response in chronic periodontitis occurs following colonization of the gingival sulcus by periodontopathic bacteria. The presence of the bacteria induces the production of cytokines and chemokines by the gingival epithelium. This results in the expression of adhesion molecules, increased permeability of gingival capillaries and chemotaxis of polymorphonuclear neutrophils through the junctional epithelium and into the gingival sulcus. The specific cytokines and chemokines produced by this initial response lead to a perivascular T-cell ⁄ macrophage dominated inflammatory infiltrate in the connective tissues. If this cell-mediated immune response does not control the bacterial challenge, progression to a B-cell ⁄ plasma-cell lesion occurs. The antibodies subsequently produced may be protective and control the infection, or may be nonprotective with resultant connective tissue destruction and bone loss (reviewed in 42,44). The effectiveness of this response varies among individuals and appears to be important in determining disease susceptibility. Currently, however, there is little evidence that aggressive periodontitis, either localized or generalized, follows the typical cyclical course of chronic periodontitis. Additionally, aggressive periodontitis appears to differ from chronic periodontitis in that clinically the gingival lesion is often absent, suggesting that the lesion of aggressive periodontitis may not follow the same sequence of initiation and progression as chronic periodontitis (from gingival T-cell lesion to progressive B-cell lesion). While further investigation of the nature of the immune response in both chronic periodontitis and aggressive periodontitis is clearly required, this review is not a comprehensive analysis of the immunopathology of these conditions but rather will cover only those elements where a direct comparison of similarities or differences is possible or where further work may highlight possible differences.