Modulation of immune responses to periodontal bacteria.

There is little doubt that the interaction between the host immune mechanisms and putative periodontal bacteria is fundamental in the clinical manifestations of the different forms of adult chronic inflammatory periodontal disease. Recent work regarding the function of polymorphonuclear neutrophils indicates that, in addition to their established protective and destructive roles, these cells may have a regulatory function in periodontal disease. Equally, emerging evidence suggests that T-cell responses in adult periodontal disease are antigen specific. Further, the migration and retention of specific T cells in the periodontal tissues appears to be related not to the expression of adhesion molecules but rather to the presence of a specific antigen. T-cell subsets are now characterized on the basis of their cytokine profiles. Type 1 T cells produce interleukin-2 and interferon-gamma, whereas type 2 T cells produce interleukin-4 and interleukin-10. A hypothesis based on this characterization of T cells is presented. According to this hypothesis, susceptible subjects have a type 2 response, whereas nonsusceptible subjects respond predominantly with type 1 T cells. The possible role of interleukin-12 in controlling this response is highlighted, thus demonstrating the marriage of innate and adaptive immune responses in adult periodontal disease.