Strontium-substituted bioactive glass (Sr-BG) has shown superior performance in bone regeneration. Sr-BG-induced osteogenesis has been extensively studied; however, Sr-BG-mediated osteoclastogenesis and the underlying molecular mechanism remain unclear. It is recognized that the balance of osteogenesis and osteoclastogenesis is closely related to bone repair, and the receptor activators of nuclear factor kappaB ligand (RANKL) signaling pathway plays a key role of in the regulation of osteoclastogenesis. Herein, we studied the potential impact and underling mechanism of strontium-substituted sub-micron bioactive glass (Sr-SBG) on RANKL-induced osteoclast activation and differentiation in vitro. As expected, Sr-SBG inhibited RANKL-mediated osteoclastogenesis significantly with the experimental performance of decreased mature osteoclasts formation and downregulation of osteoclastogenesis-related gene expression. Furthermore, it was found that Sr-SBG might suppress osteoclastogenesis by the combined effect of strontium and silicon released through inhibition of RANKL-induced activation of p38 and NF-κB pathway. These results elaborated the effect of Sr-SBG-based materials on osteoclastogenesis through RANKL-induced downstream pathway and might represent a significant guidance for designing better bone repair materials.

中文翻译：

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锶取代的亚微米生物活性玻璃通过抑制RANKL诱导的信号通路抑制成骨细胞生成。

锶取代的生物活性玻璃（Sr-BG）在骨骼再生中表现出卓越的性能。Sr-BG诱导的成骨作用已被广泛研究。然而，尚不清楚Sr-BG介导的破骨细胞形成及其潜在的分子机制。公认的是，成骨和破骨细胞形成的平衡与骨修复密切相关，核因子κB配体（RANKL）信号通路的受体激活剂在破骨细胞形成的调节中起着关键作用。在本文中，我们研究了锶取代的亚微米生物活性玻璃（Sr-SBG）对RANKL诱导的破骨细胞体外活化和分化的潜在影响及其潜在机制。。如预期的那样，Sr-SBG显着抑制RANKL介导的破骨细胞形成，其实验性能是降低成熟的破骨细胞形成并下调与破骨细胞形成相关的基因表达。此外，还发现Sr-SBG可能通过抑制RANKL诱导的p38和NF-κB途径活化而释放的锶和硅的联合作用抑制破骨细胞的生成。这些结果阐述了基于Sr-SBG的材料通过RANKL诱导的下游途径对破骨细胞形成的影响，并可能为设计更好的骨修复材料提供重要指导。