Abstract
The alveolar bone resorption is a distinctive feature of periodontitis progression and determinant for tooth loss. Regulatory T lymphocytes (Tregs) display immuno-suppressive mechanisms and tissue repairing functions, which are critical to support periodontal health. Tregs may become unstable and dysfunctional under inflammatory conditions, which can even accelerate tissue destruction. In this study, experimental periodontitis was associated with the progressive and increased presence of Th17 and Treg-related mediators in the gingiva (IL-6, IL-17A, IL-17F, RANKL, IL-10, TGF-β and GITR; P < 0.05), and the proliferation of both Treg and Th17 cells in cervical lymph nodes. Tregs from cervical lymph nodes had reduced Foxp3 expression (> 25% MFI loss) and increased IL-17A expression (> 15%), compared with Tregs from spleen and healthy controls. Tregs gene expression analysis showed a differential signature between health and disease, with increased expression of Th17-associated factors in periodontitis-derived Tregs. The ex vivo suppression capacity of Tregs on osteoclastic differentiation was significantly lower in Tregs obtained from periodontally diseased animals compared to controls (P < 0.05), as identified by the increased number of TRAP+ osteoclasts (P < 0.01) in the Tregs/pre-osteoclast co-cultures. Taken together, these results demonstrate that Tregs become phenotypically unstable and lose anti-osteoclastogenic properties during experimental periodontitis; thus, further promoting the Th17-driven bone loss.
Highlights
The alveolar bone resorption is a distinctive feature of periodontitis progression and determinant for tooth loss
We used a ligature-induced periodontitis model to assess the impact of periodontal inflammation on the phenotype and functions of cervical lymph node-derived T regulatory (Treg)
The overall number of Tregs increased during periodontitis progression, a critical number of Tregs lost their immunesuppressive properties without fully transdifferentiating into Th17-like cells
Summary
The alveolar bone resorption is a distinctive feature of periodontitis progression and determinant for tooth loss. The ex vivo suppression capacity of Tregs on osteoclastic differentiation was significantly lower in Tregs obtained from periodontally diseased animals compared to controls (P < 0.05), as identified by the increased number of TRAP+ osteoclasts (P < 0.01) in the Tregs/pre-osteoclast co-cultures Taken together, these results demonstrate that Tregs become phenotypically unstable and lose anti-osteoclastogenic properties during experimental periodontitis; further promoting the Th17-driven bone loss. Tregs are a subset of C D4+ T lymphocyte with immunosuppressive functions that contribute to the maintenance of peripheral tolerance, prevention of autoimmunity, and limitation of chronic inflammation Tregs express their signature transcription factor forkhead box P3 (Foxp3) and interleukin-2 receptor alpha chain, termed CD257. The maintenance of the Treg phenotype has multiple clinical implications, Scientific Reports | (2020) 10:19018
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
