Cytokine expression in periodontal health and disease.
Soluble proteins that serve as mediators of cell function and are produced by various cell types, such as structural and inflammatory cells, are collectively called cytokines. Several lines of evidence have revealed that cytokines play important roles not only in tissue homeostasis but also in the pathogenesis of many infectious diseases. Recent research on biological activities in normal periodontium and the pathogenesis of periodontal diseases has clarified the involvement of various cytokines in the biological activities observed in the sites. Cytokines play crucial roles in the maintenance of tissue homeostasis, a process which requires a delicate balance between anabolic and catabolic activities. In particular, growth factors--such as fibroblast growth factor (FGF), platelet-derived growth factor (PDGF), insulin-like growth factor (IGF), transforming growth factor-beta (TGF-beta)--are thought to play important roles in modulating the proliferation and/or migration of structural cells in the periodontium and the production of various extracellular matrices by these cells. On the other hand, there is little doubt that excessive and/or continuous production of cytokines in inflamed periodontal tissues is responsible for the progress of periodontitis and periodontal tissue destruction. Particularly, inflammatory cytokines--such as IL-1 alpha, IL-1 beta, IL-6, and IL-8--are present in the diseased periodontal tissues, and their unrestricted production seems to play a role in chronic leukocyte recruitment and tissue destruction. It is possible that monitoring cytokine production or its profile may allow us to diagnose an individual's periodontal disease status and/or susceptibility to the disease. In addition, although the hypothesis is still controversial, it has been suggested that discrete T-cell subsets (Th1 and Th2) with different cytokine profiles play specific roles in the immunopathogenesis of periodontal diseases.
Department of Periodontology and Endodontology, Osaka University Faculty of Dentistry, Japan.
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Okada
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Murakami
D002455:Cell Division / Q000502:physiology; D002465:Cell Movement / Q000502:physiology; D016207:Cytokines / Q000235:genetics / Q000502:physiology*; D004198:Disease Susceptibility; D005109:Extracellular Matrix / Q000502:physiology; D005346:Fibroblast Growth Factors / Q000502:physiology; D005786:Gene Expression Regulation; D006706:Homeostasis / Q000502:physiology; D006801:Humans; D007375:Interleukin-1 / Q000502:physiology; D015850:Interleukin-6 / Q000502:physiology; D016209:Interleukin-8 / Q000502:physiology; D007962:Leukocytes / Q000502:physiology; D010510:Periodontal Diseases / Q000209:etiology / Q000503:physiopathology*; D010518:Periodontitis / Q000209:etiology / Q000503:physiopathology; D010519:Periodontium / Q000378:metabolism / Q000502:physiology*; D010982:Platelet-Derived Growth Factor / Q000502:physiology; D013002:Somatomedins / Q000502:physiology; D016176:T-Lymphocyte Subsets / Q000502:physiology; D016212:Transforming Growth Factor beta / Q000502:physiology
D016207:Cytokines; D007375:Interleukin-1; D015850:Interleukin-6; D016209:Interleukin-8; D010982:Platelet-Derived Growth Factor; D013002:Somatomedins; D016212:Transforming Growth Factor beta; D005346:Fibroblast Growth Factors