Journal of clinical periodontology · 2001
Cytokine gene expression in chronic periodontitis.
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Bickel M, Axtelius B, Solioz C, Attström R
Аннотация
BACKGROUND: Cytokines play an important rôle in controlling inflammatory processes and tissue homeostasis. Periodontitis, as any other chronic inflammatory disease, results from a disarrangement of host factors, mainly cytokines and the initiating agent. Modulation of the cytokines is not only controlled by the host but also by infecting bacteria and their products.
AIM: In the present study, we examined the cytokine mRNA expression profiles in six patients, each presenting sites affected with (1) severe progressive periodontitis, (2) chronic, but stable periodontal lesions, and (3) with healthy sites. Analysis using a quantitative RT-PCR included IFN-gamma, IL-1beta, IL-2, IL-4, IL-5, IL-6, and TNF-alpha.
MATERIAL AND METHODS: 6 patients with chronic periodontitis were following treatment observed for a period of six years for local sites staying healthy, local sites with periodontal pathology but without signs of progression of attachment loss and sites with verified progression were biopsied. The biopsies were lyzed and analyzed for levels of cytokine mRNAs.
RESULTS: Results revealed considerable variation not only between patients, but also between individual sites. Each patient's site has thus to be looked at as an independent entity.
CONCLUSIONS: The local action of cytokines, which is heavily dependent on recruitment, interaction and activation of immunocompetent cells can explain the site-specific nature of cytokine expression. Cytokine data from individual sites together with the local clinical status and data from the literature demonstrate the complexity of periodontal disease pathogenesis. To gain insight to specific mechanisms further studies are needed.
AIM: In the present study, we examined the cytokine mRNA expression profiles in six patients, each presenting sites affected with (1) severe progressive periodontitis, (2) chronic, but stable periodontal lesions, and (3) with healthy sites. Analysis using a quantitative RT-PCR included IFN-gamma, IL-1beta, IL-2, IL-4, IL-5, IL-6, and TNF-alpha.
MATERIAL AND METHODS: 6 patients with chronic periodontitis were following treatment observed for a period of six years for local sites staying healthy, local sites with periodontal pathology but without signs of progression of attachment loss and sites with verified progression were biopsied. The biopsies were lyzed and analyzed for levels of cytokine mRNAs.
RESULTS: Results revealed considerable variation not only between patients, but also between individual sites. Each patient's site has thus to be looked at as an independent entity.
CONCLUSIONS: The local action of cytokines, which is heavily dependent on recruitment, interaction and activation of immunocompetent cells can explain the site-specific nature of cytokine expression. Cytokine data from individual sites together with the local clinical status and data from the literature demonstrate the complexity of periodontal disease pathogenesis. To gain insight to specific mechanisms further studies are needed.