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

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-β (TGF-β), IL-1β, 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-β, IL-1β, IL-6, and IL-23 in gingiva or IL-17 and receptor activator for nuclear factor-κB ligand in alveolar bone was evaluated by real-time polymerase chain reaction. The production of IL-17, TGF-β, IL-1β, 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-β, IL-1β, 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.