Astragalus polysaccharide alleviates alveolar bone destruction by regulating local osteoclastogenesis during periodontitis

Inflammatory imbalance of bone formation/resorption leads to alveolar bone destruction. Astragalus polysaccharide has been confirmed to have anti-inflammatory effects. We sought to disdose the protective effect and its potential mechanisms of astragalus polysaccharide in the periodontitis model. Experimental periodontitis was induced by cotton ligatures for this study. We measured the alveolar bone damage rate, periodontal osteoclasts, proportion of CD4+Foxp3+, CD4+IL-10+, CD4+TGF-beta+ subsets in the gingiva, and RANKL, OPG, TGF-beta+, and IL-10+ level in the gingiva. We also cultured osteoclast precursor cells in the presence of RANKL and astragalus polysaccharide. Osteodasto-like cells were identified by TRAP staining, mRNA of RANK, TRAP, and TRAF6 were evaluated by real time PCR. We found that astragalus polysaccharide caused significant protection of the alveolar bone via reducing local osteoclasts. It also decreased the proportion of CD4+Foxp3+ cells and upregulated the level of CD4+IL-10+ cells, reduced RANKL, and remedied IL-10 levels. In cell culture experiments, astragalus polysaccharide prohibited the RANKL mediated osteodast differentiation. The findings of this study disdose the functions and possible mechanisms of astragalus polysaccharide engaged in local osteodastogenesis, and reveal the considerable effect of astragalus polysaccharide in alveolar bone homeostasis and its likely contribution to host immuno-regulation in periodontitis.

Automated summary

Astragalus polysaccharide was found to protect alveolar bone in a periodontitis model by reducing local osteoclasts, modulating immune cell proportions, and influencing levels of inflammatory factors. Its potential mechanisms involve inhibition of osteoclast differentiation and regulation of immune responses.