title: Cellular immunity and hypersensitivity as components of periodontal destruction.
abstract: 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.
authors.affiliation: Department of Dentistry, University of Queensland, Brisbane, Australia.
authors.forename: G J
authors.initials: GJ
authors.lastname: Seymour
authors.forename: E
authors.initials: E
authors.lastname: Gemmell
authors.forename: M
authors.initials: M
authors.lastname: Kjeldsen
authors.forename: K
authors.initials: K
authors.lastname: Yamazaki
authors.forename: T
authors.initials: T
authors.lastname: Nakajima
authors.forename: K
authors.initials: K
authors.lastname: Hara
mesh_terms: 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
chemical_list: D000942:Antigens, Bacterial; D016207:Cytokines; D000939:Epitopes