Journal
JOURNAL OF PERIODONTAL RESEARCH
Volume 57, Issue 2, Pages 246-255Publisher
WILEY
DOI: 10.1111/jre.12958
Keywords
OPG; Periodontitis; RANK; RANKL; Th17 cell; Treg cell
Categories
Funding
- Scientific Research Project of Guangdong Provincial Administration of Traditional Chinese Medicine [20201107]
- Guangdong Foundation for Basic and Applied Basic Research [2019A1515110161]
- Fundamental Research for the Central Universities [21619344, 21621410]
- Guangzhou Science and Technology Plan Foundation and Application Foundation Research Project [202102020020]
- National Nature Science Foundation [81804153]
Ask authors/readers for more resources
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.
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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available
Share Paper
