Abstract

Principal lines of evidence that immune reactions are central to the pathogenesis of periodontitis are reviewed. Necessary components of immunologic reactions are present in gingiva in the periodontal diseases. Differences between healthy and periodontitis patients with respect to some measures of immune function further indicate that immune reactions do occur in the gingiva during periodontitis. They are probably responsible for at least some of the destruction of connective tissue and bone that occurs. Classical antibody-mediated hypersensitivity reactions probably do not provide the reasons. Mechanisms are more likely to be found in the pro-inflammatory and tissue-degrading effects of cytokines released in host-protective, antigen-specific and polyclonal responses to oral bacterial constituents or products. Some evidence suggests that limitation of clinical destruction in localized early onset periodontitis (JP) may in part be a function of a protective antibody response which develops after an initial rapidly progressive infection. A relatively deficient immune responsiveness may allow progression to more severe and generalized disease (RPP). Suggestions are made for studies needed to confirm suspected pathogenetic mechanisms, approach resultant targeted therapies, and test hypotheses for contrasting roles of immune reactions in different clinical expressions of periodontitis.