Protective effect and related mechanisms of curcumin in rat experimental periodontitis

Background: Curcumin exhibits anti-inflammatory effects and has been suggested as a treatment for inflammatory diseases. The aim of this study was to investigate the effects of curcumin on the lipopolysaccharide induced inflammatory response in rat gingival fibroblasts in vitro and ligation-induced experimental periodontitis in vivo, and to speculate the possible anti-inflammatory mechanism of curcumin. Methods: The gingival fibroblasts were incubated with different concentrations of curcumin in the absence or presence of lipopolysaccharide (LPS). Concentrations of interleukin-1 beta(IL-1 beta), tumor necrosis factor-alpha (TNF-alpha), osteoprotegerin (OPG) and soluble receptor activator of nuclear factor kappa-B ligand (RAMC) culture supernatants of rat gingival fibroblasts were determined by enzyme linked immunosorbent assay. The nuclear fraction of rat gingival fibroblasts was extracted and nuclear factor kappa-B (NF-KB) activation was assessed by western blotting to elucidate related mechanisms. Curcumin was given every two days by oral gavage. The gingival inflammation and alveolar bone loss between the first and second molars were observed by hematoxylin and eosin staining. Collagen fibers were observed by picro-sirius red staining. Alveolar bone loss was assessed by micro-CT analysis. Results: Curcumin attenuated the production of IL-1 beta and TNF-alpha in rat gingival fibroblasts stimulated by LPS, and inhibited the LPS-induced decrease in OPG/sRANKL ratio and NE-kappa B activation. Curcumin significantly reduced gingival inflammation and modulated collagen fiber and alveolar bone loss in vivo. Conclusions: curcumin modulates inflammatory activity in rat periodontitis by inhibiting NE-kappa B activation and decreasing the OPG/sRANKL ratio induced by LPS.