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Interleukin-11 and IL-17 and the Pathogenesis of Periodontal Disease

  • Autores: Dr. R.B. Johnson, N. Wood, F.G. Serio
  • Localización: Journal of periodontology, ISSN 0022-3492, Vol. 75, Nº. 1, 2004, págs. 37-43
  • Idioma: inglés
  • Enlaces
  • Resumen
    • Background: Interleukin (IL)-11 and IL-17 are cytokines that modulate the inflammatory process and have not been assessed within normal or inflamed gingival tissues. Our purpose was to compare concentrations of human IL-11 and IL-17 within healthy and diseased human gingiva to determine their possible role in the initiation or progression of periodontal diseases.

      Methods: Biopsies from healthy (non-hemorrhagic gingiva adjacent to a ≤3 mm gingival sulcus) and diseased gingiva (hemorrhagic gingiva adjacent to a ≥3 mm periodontal pocket) were studied. IL-11, IL-17, RANTES, and IL-6 concentrations were assessed within solubilized gingival biopsies by enzyme-linked immunosorbent assay. Data were compared by factorial analysis of variance and a post-hoc Tukey honestly significant difference (HSD) test. Regression analysis and partial correlation analysis (adjusted for sample weight) were also used to determine correlations between the variables.

      Results: Interleukin-11 concentrations were highest within gingiva adjacent to 3 mm diseased pockets (P <0.001), and IL-17 concentrations were highest at 4 to 5 mm sites compared to other sites (P <0.001). Gingival concentrations of both cytokines were significantly lower in gingiva adjacent to a ≥6 mm pocket. RANTES concentrations were significantly greater in gingiva adjacent to ≥6 mm pockets than in tissues derived from other sites (P <0.001). IL-11, IL-6, and RANTES concentrations were significantly correlated with sulcular depth.

      Conclusions: Gingival concentrations of IL-11 and IL-17 are different in diseased gingiva adjacent to 3, 4 to 5, and ≥6 mm pockets, suggesting that their concentrations change as a consequence of the progression of gingivitis to periodontitis and that both cytokines could have a significant role in this progression. These data may be useful for the design of procedures for prevention of periodontal disease. J Periodontol 2004;75:37-43.


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