Expression of suppressors of cytokine signaling in diseased periodontal tissues: a stop signal for disease progression?

J Periodontal Res. 2006 Dec;41(6):580-4. doi: 10.1111/j.1600-0765.2006.00908.x.

Abstract

Background and objective: Inflammatory cytokines are thought to trigger periodontal tissue destruction. In addition to being regulated by anti-inflammatory mediators, their activity is under the control of suppressors of cytokine signaling (SOCS), which down-regulate the signal transduction as part of an inhibitory feedback loop. We therefore investigated the expression of SOCS-1, -2 and -3, and the cytokines tumor necrosis factor-alpha (TNF-alpha) and interleukin-10, in different forms of human periodontal diseases.

Material and methods: Quantitative polymerase chain reaction (RealTime-PCR) was performed with mRNA from gingival biopsies of control subjects and from that of patients with chronic gingivitis and chronic periodontitis.

Results: Our results show that patients with chronic gingivitis and chronic periodontitis exhibit significantly higher SOCS-1, -2 and -3, TNF-alpha and interleukin-10 mRNA expression when compared with healthy controls. The data also demonstrate that SOCS-1 and -3 mRNA expression was higher in tissue from patients with chronic gingivitis than chronic periodontitis, while the levels of SOCS-2, TNF-alpha and interleukin-10 mRNA were similar in these groups.

Conclusion: The increased expression of SOCS-1, -2 and -3 mRNA in diseased periodontal tissues is believed to be involved in the down-regulation of inflammatory cytokine and Toll-like receptor signaling, and therefore in the attenuation of both the inflammatory reaction and disease severity. Furthermore, it is possible that variation in the levels of SOCS mRNA expressed in different forms of periodontal diseases may determine the stable or progressive nature of the lesions.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Case-Control Studies
  • Disease Progression
  • Female
  • Gingivitis / metabolism
  • Humans
  • Interleukin-10 / analysis*
  • Male
  • Middle Aged
  • Periodontitis / metabolism*
  • RNA, Messenger / analysis*
  • Suppressor of Cytokine Signaling Proteins / analysis*
  • Tumor Necrosis Factor-alpha / analysis*

Substances

  • RNA, Messenger
  • Suppressor of Cytokine Signaling Proteins
  • Tumor Necrosis Factor-alpha
  • Interleukin-10