Chemerin contributes to inflammatory responses and suppresses osteogenic differentiation in chronic periodontitis

Background Chronic periodontitis (CP) is a common disease of oral cavity, and approximately 35% of adults suffered from CP. Therefore, its underlying mechanism needs to be explored for new therapeutic approaches. Chemerin, as a multifunctional adipokine, is found to be highly expressed in the gingival crevicular fluid (GCF), gingival tissues and the plasma of periodontitis patients. Thus, we aimed to uncover the underlying mechanism of chemerin in CP. Methods Thirty six CP patients and 25 healthy volunteers were enrolled. Periodontal ligament stem cells (PDLSCs) were isolated from CP patients and healthy ones, respectively. Then, normal PDLSCs or PDLSCs-differentiated osteoblasts were treated with different doses of recombinant human chemerin. Results Chemerin and inflammatory cytokines, including interleukin-1 beta, interleukin-6, and tumor necrosis factor-alpha, were higher in the GCF and serum of CP patients than healthy ones. Moreover, chemerin was positively correlated with these three inflammatory cytokines, respectively, in CP patients. PDLSCs isolated from CP patients had higher expressions of chemerin and these cytokines than the ones isolated from normal individuals. Furthermore, chemerin dose-dependently increased inflammatory responses and inhibited osteogenic differentiation of PDLSCs. Conclusion Chemerin accelerated inflammatory responses and suppressed osteogenic differentiation of PDLSCs, thus chemerin might sever as a therapeutic target of CP.

Automated summary

This study found that levels of chemerin and inflammatory cytokines were higher in the gingival crevicular fluid and serum of chronic periodontitis (CP) patients, and were positively correlated with each other. Periodontal ligament stem cells (PDLSCs) isolated from CP patients had higher expressions of chemerin and these cytokines compared to healthy individuals. Furthermore, chemerin dose-dependently increased inflammatory responses and inhibited osteogenic differentiation of PDLSCs.