Evidence of the presence of T helper type 17 cells in chronic lesions of human periodontal disease

Oral Microbiol Immunol. 2009 Feb;24(1):1-6. doi: 10.1111/j.1399-302X.2008.00463.x.

Abstract

Introduction: Periodontal disease is a chronic inflammation of the attachment structures of the teeth, triggered by potentially hazardous microorganisms and the consequent immune-inflammatory responses. In humans, the T helper type 17 (Th17) lineage, characterized by interleukin-17 (IL-17) production, develops under transforming growth factor-beta (TGF-beta), IL-1beta, and IL-6 signaling, while its pool is maintained by IL-23. Although this subset of cells has been implicated in various autoimmune, inflammatory, and bone-destructive conditions, the exact role of T lymphocytes in chronic periodontitis is still controversial. Therefore, in this study we investigated the presence of Th17 cells in human periodontal disease.

Methods: Gingival and alveolar bone samples from healthy patients and patients with chronic periodontitis were collected and used for the subsequent assays. The messenger RNA expression for the cytokines IL-17, TGF-beta, IL-1beta, IL-6, and IL-23 in gingiva or IL-17 and receptor activator for nuclear factor-kappaB ligand in alveolar bone was evaluated by real-time polymerase chain reaction. The production of IL-17, TGF-beta, IL-1beta, IL-6, and IL-23 proteins was evaluated by immunohistochemistry and the presence of Th17 cells in the inflamed gingiva was confirmed by immunofluorescence confocal microscopy for CD4 and IL-17 colocalization.

Results: Our data demonstrated elevated levels of IL-17, TGF-beta, IL-1beta, IL-6, and IL-23 messenger RNA and protein in diseased tissues as well as the presence of Th17 cells in gingiva from patients with periodontitis. Moreover, IL-17 and the bone resorption factor RANKL were abundantly expressed in the alveolar bone of diseased patients, in contrast to low detection in controls.

Conclusion: These results provided strong evidence for the presence of Th17 cells in the sites of chronic inflammation in human periodontal disease.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Alveolar Bone Loss / immunology*
  • Alveolar Bone Loss / metabolism
  • Case-Control Studies
  • Chronic Periodontitis / immunology*
  • Female
  • Fluorescent Antibody Technique
  • Gene Expression
  • Humans
  • Immunohistochemistry
  • Interleukin-17 / biosynthesis*
  • Interleukin-1beta / biosynthesis
  • Interleukin-23 / biosynthesis
  • Interleukin-6 / biosynthesis
  • Male
  • Microscopy, Confocal
  • RANK Ligand / biosynthesis
  • RNA, Messenger / biosynthesis
  • T-Lymphocytes, Helper-Inducer / immunology*
  • T-Lymphocytes, Helper-Inducer / metabolism
  • Transforming Growth Factor beta / biosynthesis

Substances

  • Interleukin-17
  • Interleukin-1beta
  • Interleukin-23
  • Interleukin-6
  • RANK Ligand
  • RNA, Messenger
  • Transforming Growth Factor beta