Cellular immunity and hypersensitivity as components of periodontal destruction.
BACKGROUND
Cellular immunity has been implicated in periodontal destruction for over 25 years. Studies in the 1970s used lymphocyte transformation and lymphokine assays to establish a role for cell-mediated mechanisms in periodontal disease. Immunohistological studies subsequently showed that the formation of gingivitis followed a similar pattern to the formation of a delayed type hypersensitivity reaction. Further functional studies suggested that a T cell/macrophage immunoregulatory imbalance may exist locally in the periodontitis lesion and that this imbalance may be antigen specific. RECENT EVIDENCE: More recently, T cell subsets have been dichotomised on the basis of their cytokine profiles. In general, ThI 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.


OBJECTIVE
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 a higher proportion of IL-4 producing cells in periodontitis tissues suggesting a role for Th2 cells in the progressive lesion. 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.


CONCLUSIONS
These emerging data clearly establish a role for cell-mediated mechanisms in the control of periodontal destruction and raise the possibility that in the future cytokine therapy for the treatment of periodontal disease in susceptible subjects may become a viable option.
Seymour
G J
GJ
Department of Dentistry, University of Queensland, Brisbane, Australia.
Gemmell
E
E
Kjeldsen
M
M
Yamazaki
K
K
Nakajima
T
T
Hara
K
K
D000818:Animals; D000942:Antigens, Bacterial / Q000276:immunology; D016207:Cytokines / Q000096:biosynthesis / Q000276:immunology*; D018450:Disease Progression; D004198:Disease Susceptibility; D000939:Epitopes; D006801:Humans; D006968:Hypersensitivity, Delayed / Q000150:complications*; D007111:Immunity, Cellular; D010510:Periodontal Diseases / Q000209:etiology / Q000276:immunology* / Q000382:microbiology; D010518:Periodontitis / Q000276:immunology; D010519:Periodontium / Q000276:immunology; D016176:T-Lymphocyte Subsets / Q000276:immunology* / Q000378:metabolism; D018417:Th1 Cells / Q000276:immunology; D018418:Th2 Cells / Q000276:immunology
D000942:Antigens, Bacterial; D016207:Cytokines; D000939:Epitopes