Destructive and protective roles of cytokines in periodontitis: a re-appraisal from host defense and tissue destruction viewpoints

J Dent Res. 2010 Dec;89(12):1349-63. doi: 10.1177/0022034510376402. Epub 2010 Aug 25.


Periodontal diseases (PD) are chronic infectious inflammatory diseases characterized by the destruction of tooth-supporting structures, being the presence of periodontopathogens required, but not sufficient, for disease development. As a general rule, host inflammatory mediators have been associated with tissue destruction, while anti-inflammatory mediators counteract and attenuate disease progression. With the discovery of several T-cell subsets bearing distinct immunoregulatory properties, this pro- vs. anti-inflammatory scenario became more complex, and a series of studies has hypothesized protective or destructive roles for Th1, Th2, Th17, and Treg subpopulations of polarized lymphocytes. Interestingly, the "protective vs. destructive" archetype is usually considered in a framework related to tissue destruction and disease progression. However, it is important to remember that periodontal diseases are infectious inflammatory conditions, and recent studies have demonstrated that cytokines (TNF-α and IFN-γ) considered harmful in the context of tissue destruction play important roles in the control of periodontal infection. Therefore, in this review, the state-of-the-art knowledge concerning the protective and destructive roles of host inflammatory immune response will be critically evaluated and discussed from the tissue destruction and control-of-infection viewpoints.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Adaptive Immunity / immunology
  • Cytokines / immunology*
  • Disease Progression
  • Humans
  • Immunity, Innate / immunology
  • Inflammation Mediators / immunology
  • Interferon-gamma / immunology
  • Periodontitis / immunology*
  • Periodontitis / microbiology
  • T-Lymphocytes, Helper-Inducer / immunology
  • T-Lymphocytes, Regulatory / immunology
  • Tumor Necrosis Factor-alpha / immunology


  • Cytokines
  • Inflammation Mediators
  • Tumor Necrosis Factor-alpha
  • Interferon-gamma