The Th17/Treg cell balance: crosstalk among the immune system, bone and microbes in periodontitis

Periodontopathic bacteria constantly stimulate the host, which causes an immune response, leading to host-induced periodontal tissue damage. The complex interaction and imbalance between Th17 and Treg cells may be critical in the pathogenesis of periodontitis. Furthermore, the RANKL/RANK/OPG system plays a significant role in periodontitis bone metabolism, and its relationship with the Th17/Treg cell imbalance may be a bridge between periodontal bone metabolism and the immune system. This article reviews the literature related to the Th17/Treg cell imbalance mediated by pathogenic periodontal microbes, and its mechanism involving RANKL/RANK/OPG in periodontitis bone metabolism, in an effort to provide new ideas for the study of the immunopathological mechanism of periodontitis.

Automated summary

Periodontopathic bacteria stimulate host immunity, leading to periodontal tissue damage. Imbalance between Th17 and Treg cells is critical in periodontitis pathogenesis, and the RANKL/RANK/OPG system plays a significant role in periodontitis bone metabolism. The mechanism involving Th17/Treg cell imbalance and RANKL/RANK/OPG may provide new insights into the immunopathological mechanism of periodontitis.