Bone homeostasis is maintained through balanced interactions between osteoblasts and osteoclasts, whereas chronic inflammation disrupts this balance by enhancing osteoclast activity and bone loss. This study investigated the protective effects of Cibotii Rhizoma (CR) on inflammatory bone destruction and its underlying mechanisms. In vitro, CR suppressed receptor activator of nuclear factor kappa B ligand (RANKL)-induced osteoclastogenesis in bone marrow-derived monocyte/macrophage (BMM) cultures by downregulating NFATc1, c-Src, and TRAF6, thereby inhibiting osteoclast formation, podosomal actin ring assembly, and cell fusion. In vivo, administration of CR in an LPS-induced bone loss mouse model preserved bone microarchitecture, as confirmed by micro-CT and histological analyses, and significantly reduced osteoclast numbers and calvarial bone erosion. Immunohistochemical staining further revealed decreased RANK and NFATc1 activity in calvarial bone tissue following CR treatment. Collectively, these findings indicate that CR mitigates inflammatory bone loss by targeting RANK signaling to inhibit osteoclastogenesis and bone resorption, highlighting its potential as a therapeutic agent for inflammatory bone diseases.
Hong et al. (2026) studied this question.