Periodontics into the 21st century.
In recent years advances in clinical techniques and procedures such as guided tissue regeneration and implants, have dominated periodontics. However, as we move towards the 21st century, emphasis is swinging 'back to basics' with the recognition that patient susceptibility to periodontal disease determines the ultimate outcome not only of the disease process but also of the treatment undertaken. In this context attention is returning to the host response and with the advent of clonal and molecular biological techniques, new insights are being gained into the nature of host susceptibility. Previous studies have suggested that a T-cell/macrophage immunoregulatory imbalance may exist locally in the periodontitis lesion and that this imbalance may be antigen specific. More recently, T-cell subsets have been dichotomized on the basis of their cytokine profiles. In general, Th1 cells produce IL-2 and IFN-gamma while Th2 cells produce IL-4, IL-5 and IL-6. The major function of Th1 cells is to mediate delayed type hypersensitivity. In contrast the major function of Th2 cells is to provide B-cell help. A model for periodontal disease has now been developed based on this functional dichotomy which provides a framework for the study of cytokine profiles in periodontal disease. Early studies in this context have demonstrated higher proportions of IL-4 and IL-13 producing cells in periodontitis tissues together with possible variations in IL-10 production. Clonal studies have shown that the selection of a particular cytokine profile is not antigen dependent and that differences may be due to the host susceptibility although this remains to be determined.
Seymour
G J
GJ
Department of Dentistry, University of Queensland.
Gemmell
E
E
Westerman
B
B
Cullinan
M
M
D000293:Adolescent; D000328:Adult; D001315:Australia / Q000453:epidemiology; D016207:Cytokines / Q000096:biosynthesis / Q000276:immunology; D004198:Disease Susceptibility; D006801:Humans; D008875:Middle Aged; D010518:Periodontitis / Q000453:epidemiology / Q000209:etiology / Q000276:immunology* / Q000382:microbiology; D015995:Prevalence; D012307:Risk Factors; D012907:Smoking / Q000009:adverse effects; D006377:T-Lymphocytes, Helper-Inducer / Q000276:immunology / Q000378:metabolism
D016207:Cytokines