Interleukin-1 beta levels in gingival crevicular fluid in type 2 diabetes mellitus and adult periodontitis.


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Bulut U., Develioglu H., Taner I., Berker E.

Journal of oral science, cilt.43, sa.3, ss.171-177, 2001 (Scopus) identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 43 Sayı: 3
  • Basım Tarihi: 2001
  • Doi Numarası: 10.2334/josnusd.43.171
  • Dergi Adı: Journal of oral science
  • Derginin Tarandığı İndeksler: Scopus
  • Sayfa Sayıları: ss.171-177
  • Hacettepe Üniversitesi Adresli: Evet

Özet

Interleukin-1 beta (IL-1beta) is a potent bone-resorptive cytokine that also mediates soft-tissue destruction by stimulating prostaglandin production and inducing collagenase and other protease activity. The literature suggests that this substance may be an important mediator of attachment loss in human periodontitis, and indicates that IL-1beta may be useful for locating sites of periodontal disease activity. There is some evidence that IL-1beta is produced by cells of the periodontium, and that it can be detected in gingival crevicular fluid (GCF). Many factors are known to contribute to the destruction of periodontal tissue. One of the most important is immune deficiency in diabetes. The aim of this study was to measure and compare the concentration of IL-1beta in the GCF of patients with non-insulin-dependent diabetes mellitus (Type 2 DM), otherwise healthy adults with periodontitis, and individuals with no periodontal disease in order to assess whether diabetes alters IL-1beta levels. We also examined relationships between GCF levels and the clinical parameters of pocket depth, plaque index, and bleeding index in each group. Seventeen patients with Type 2 DM, 17 adult periodontitis patients (AP), and 17 healthy controls were selected. The levels of IL-1beta in the GCF were quantified by ELISA. The mean IL-1beta concentrations in the Type 2 DM, AP, and control groups were 200.1 +/- 65.34 pg/microl, 131.35 +/- 67.66 pg/microl, and 80.0 +/- 36.08 pg/microl, respectively. The levels in the diabetic patients were significantly higher than those in the AP and control subjects. There were no significant correlations between IL-1beta level and any of the clinical data parameters for each group. We believe that the macrophages may over produce IL-beta in Type 2 DM and increased IL-1beta levels in diabetic patients could be linked to altered immune function.