Abstract:

Objective To analyze the effect of rheumatoid arthritis （RA） on the phenotypes of plasma cells of gingiva and expression of receptor activator of nuclear factor-κB ligand（RANKL） in the patients with periodontitis，and to clarify its possible mechanism. Methods Sixty subjects who came to our hospital were selected and divided into healthy group， periodontitis group and periodontitis+RA group according to inclusion criteria， and there were 20 subjects in each group.The gingival index （GI）， probing depth （PD）， bleeding on probing （BOP） and clinical attachment loss （CAL） of the subjects were recorded. The expression levels of proliferation inducing ligand（APRIL） and B lymphocyte stimulator（BLyS） in gingiva tissue of the subjects in various groups were detected by real-time fluoresence quantatitive PCR（RT-qPCR） method；the percentages of CD38+ cells， CD138+ cells in gingiva tissue of the subjects in various groups were analyzed by flow cytometry；the percentages of RANKL+ cells in the gingival plasma cells and the RANKL levels in plasma cells of gingiva of the subjects in various groups were detected by flow cytometry and enzyme-linked immunosorbent assay（ELISA） methods； the growth of osteoclasts in the subjects in various groups was observed by anti-tartrate acid phosphatase （TRAP） staining； the expression levels of RANKL， receptor activator of nuclear factor-κB（RANK） and tumor necrosis factor associated factor 6（TRAF6） mRNA in plasma cells of gingiva of the subjects in various groups were detected by RT-qPCR method. Results Compared with healthy group， GI， PD， BOP and CAL of the patients in periodontitis group and periodontitis+RA group were significantly increased （P<0.05）； compared with periodontitis group，the PD and CAL of the patients in periodontitis+RA group were increased（P<0.05）.Compared with healthy group， the expression levels of APRIL and BLyS mRNA in gingiva tissue of the patients in periodontitis group and periodontitic+PA group were increased（P<0.05）；compared with periodontitis group，the expression level of APRIL mRNA of the patients in periodontitis+RA group was increased（P<0.05）.Compared with healthy group， the percentages of CD38+ cells and CD138+ cells in gingiva tissue of the patients in periodontitis group and periodontitis+RA group were significantly increased（P<0.05）；compared with periodontitis group， the percentage of CD138+ cells in gingiva tissue of the patients in periodontitis+RA group was increased （P<0.01）.Compared with healthy group， the percentages of RANKL+ cells in plasma cells of gingiva of the patients in periodontitis group and periodontitis+RA group were increased（P<0.05）；compared with periodontitis group， the percentage of RANKL+ cells in the plasma cells of gingiva the patients in periodontitis+RA group was increased（P<0.05）. Compared with healthy group， the percentages of RANKL in plasma cells of gingiva of the patients in periodontitis group and periodontitis+RA group were increased（P<0.05）. Compared with healthy group， the number of normal induced TRAP+osteoblast-like cells of the patients in periodontitis group and periodontitis+RA group were increased（P<0.05）； compared with periodontitis group， the number of normal induced TRAP+ osteoblast-like cells of the patients in periodontitis+RA group was increased （P<0.05）； compared with the normal induced cells， the numbers of anti-RANKL induced TRAP+osteoblast-like cells in various groups were decreased（P<0.05）.Compared with healthy group，the expression levels of RANKL， RANK， and TRAF6 mRNA in the plasma cells of gingiva of the patients in periodontitis group and periodontitis+RA group were significantly increased （P<0.05）；compared with periodontitis group， the expression levels of RANKL， RANK， and TRAF6 mRNA in the plasma cells of gingiva of the patients in periodontitis+RA group were increased （P<0.05）. Conclusion The differentiation level and the ability on promoting osteoclastogenesis of plasma cells of gingival of the patients with periodontitis complicated with RA are higher than those in the patients with single periodontitis， which may be a potential cause for RA aggravating periodontal tissue destruction in the patients with periodontitis.

Key words: Periodontits, Rheumatoid arthritis, Plasma cell, Receptor activator of nuclear factor-κB ligand