Possible mechanisms involved in the immunoregulation of chronic inflammatory periodontal disease.
It is generally agreed that immunological mechanisms are involved in the pathogenesis of periodontal disease; however, regulation of these mechanisms has hitherto received scant attention. Regulatory networks exist at both a cellular and a molecular level. At the cellular level, the existence of helper (T4-positive) and suppressor (T8-positive) T lymphocytes, the expression of Class II major histocompatibility complex antigens, and the heterogeneity of macrophage subpopulations are central to an understanding of the regulatory mechanisms involved. It is only recently that studies of these separate components, in both humans and experimental animals, have begun to provide a basis for understanding the complex interactions occurring in periodontal disease. Studies using the human experimental gingivitis model have shown an immunoregulatory picture consistent with a controlled immunological reaction with an essentially normal T4:T8 ratio of 2.0. In contrast, studies utilizing cells extracted from adult periodontitis lesions have shown a reduced T4:T8 ratio (approximately 1.0) and an inability to respond in, or to stimulate, an autologous mixed lymphocyte reaction. Animal studies using athymic nude rats have supported the concept of a central role for T-cell control in periodontal disease and the possibility of an imbalance in this control with disease progression. These results are reviewed and areas of future research explored.
Seymour
G J
GJ
D000818:Animals; D000907:Antibodies, Bacterial / Q000096:biosynthesis; D001402:B-Lymphocytes / Q000276:immunology; D001419:Bacteria / Q000276:immunology; D002908:Chronic Disease; D006801:Humans; D007375:Interleukin-1 / Q000276:immunology; D010518:Periodontitis / Q000276:immunology*; D013601:T-Lymphocytes / Q000276:immunology
D000907:Antibodies, Bacterial; D007375:Interleukin-1