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Abstract Title:

Rhoifolin ameliorates titanium particle-stimulated osteolysis and attenuates osteoclastogenesis via RANKL-induced NF-κB and MAPK pathways.

Abstract Source:

J Cell Physiol. 2019 08 ;234(10):17600-17611. Epub 2019 Mar 10. PMID: 30854667

Abstract Author(s):

Shijie Liao, Fangmin Song, Wenyu Feng, Xiaofei Ding, Jun Yao, Huijie Song, Yun Liu, Shiting Ma, Ziyi Wang, Xixi Lin, Jiake Xu, Jinmin Zhao, Qian Liu

Article Affiliation:

Shijie Liao

Abstract:

Prosthesis loosening is a highly troublesome clinical problem following total joint arthroplasty. Wear-particle-induced osteoclastogenesis has been shown to be the primary cause of periprosthetic osteolysis that eventually leads to aseptic prosthesis loosening. Therefore, inhibiting osteoclastogenesis is a promising strategy to control periprosthetic osteolysis. The possible mechanism of action of rhoifolin on osteoclastogenesis and titanium particle-induced calvarial osteolysis was examined in this study. The in vitro study showed that rhoifolin could strongly suppress the receptor activators of nuclear factor-κB (NF-κB) ligand-stimulated osteoclastogenesis, hydroxyapatite resorption, F-actin formation, and the gene expression of osteoclast-related genes. Western blot analysis illustrated that rhoifolin could attenuate the NF-κB and mitogen-activated protein kinase pathways, and the expression of transcriptional factors nuclear factor of activated T cells 1 (NFATc1) and c-Fos. Further studies indicated that rhoifolin inhibited p65 translocation to the nucleus and the activity of NFATc1 and NF-κB rhoifolin could decrease the number of tartrate-resistant acid phosphate-positive osteoclasts and titanium particle-induced C57 mouse calvarial bone loss in vivo. In conclusion, our results suggest that rhoifolin can ameliorate the osteoclasts-stimulated osteolysis, and may be a potential agent for the treatment of prosthesis loosening.

Study Type : In Vitro Study

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