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Lithium chloride inhibits titanium particle-induced osteoclastogenesis by inhibiting the NF-κB pathway

Osteoclast over-activation and inflammation responses promote peri-implant osteolysis (PIO), which is the leading cause of aseptic artificial joint loosening. We examined the effect of lithium chloride (LiCl) on wear debris-induced osteoclastogenesis and inflammation. Fifty-Six C57BL/6J male mice we...

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Detalles Bibliográficos
Autores principales: Hu, Xuanyang, Wang, Zhirong, Shi, Jiawei, Guo, Xiaobin, Wang, Liangliang, Ping, Zichuan, Tao, Yunxia, Yang, Huilin, Zhou, Jun, Xu, Yaozeng, Geng, Dechun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Impact Journals LLC 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5663567/
https://www.ncbi.nlm.nih.gov/pubmed/29137395
http://dx.doi.org/10.18632/oncotarget.20000
Descripción
Sumario:Osteoclast over-activation and inflammation responses promote peri-implant osteolysis (PIO), which is the leading cause of aseptic artificial joint loosening. We examined the effect of lithium chloride (LiCl) on wear debris-induced osteoclastogenesis and inflammation. Fifty-Six C57BL/6J male mice were randomly distributed into four groups: sham control (sham, treated with phosphate buffered saline [PBS]), vehicle (treated with titanium/PBS), low-LiCl (L-LiCl, titanium: 50 mg/kg LiCl) and high-LiCl (H-LiCl, titanium: 200 mg/kg LiCl). After 14 days, mouse calvaria were harvested for micro-computed tomography and histomorphological and molecular analyses. Bone marrow-derived macrophages (BMMs) were extracted to examine osteoclast differentiation, and the RAW264.7 cell line was used to investigate osteoclastogenesis mechanisms. LiCl reduced the number of osteoclasts, debris-induced osteolysis, and the expression of inflammatory factors, thereby preventing bone loss in vivo. In vitro, LiCl inhibited osteoclastogenesis and osteoclastic bone resorption by inhibiting the RANKL-induced NF-κB signaling pathway. LiCl's activation of the canonical Wnt/β-catenin signaling pathway was not associated with LiCl's inhibition of osteoclastogenesis. These results suggest that LiCl may be an effective agent for treatment of osteolytic diseases caused by chronic inflammation and over-activation of osteoclasts.