INTRODUCTION: This study investigated whether calcium silicate cement extract exerted antiosteoclastogenic actions in murine RAW 264.7 macrophages cultured with receptor activator for nuclear factor kappaB (RANKL). METHODS: The RAW 264.7 macrophage cell was treated with RANKL to osteoclastogenesis. Then, cell viability, cell death, and cathepsin K expression were examined. RESULTS: The silicon (Si)-inhibited RANKL-induced formation of osteoclasts during the osteoclast differentiation process. It was also found that ≥4 mmol/L Si reduced RANKL-enhanced tartrate-resistant acid phosphatase (TRAP) activity in a dose-dependent manner. Furthermore, Si diminished the expression and secretion of cathepsin K elevated by RANKL and was concurrent with the inhibition of TRAF6 induction and nuclear factor kappaB activation. CONCLUSIONS: The current report shows that silicate abrogated RANKL-induced osteoclastogenesis by retarding osteoclast differentiation. The Si can modulate every cell through dose-dependent in vitro RANKL-mediated osteoclastogenesis, such as the proliferation and fusion of preosteoclasts, and the function of osteoclasts. Therefore, silicate-based materials may be a potential therapeutic agent targeting osteoclast differentiation in bone defects.
INTRODUCTION: This study investigated whether calcium silicate cement extract exerted antiosteoclastogenic actions in murine RAW 264.7 macrophages cultured with receptor activator for nuclear factor kappaB (RANKL). METHODS: The RAW 264.7 macrophage cell was treated with RANKL to osteoclastogenesis. Then, cell viability, cell death, and cathepsin K expression were examined. RESULTS: The silicon (Si)-inhibited RANKL-induced formation of osteoclasts during the osteoclast differentiation process. It was also found that ≥4 mmol/L Si reduced RANKL-enhanced tartrate-resistant acid phosphatase (TRAP) activity in a dose-dependent manner. Furthermore, Si diminished the expression and secretion of cathepsin K elevated by RANKL and was concurrent with the inhibition of TRAF6 induction and nuclear factor kappaB activation. CONCLUSIONS: The current report shows that silicate abrogated RANKL-induced osteoclastogenesis by retarding osteoclast differentiation. The Si can modulate every cell through dose-dependent in vitro RANKL-mediated osteoclastogenesis, such as the proliferation and fusion of preosteoclasts, and the function of osteoclasts. Therefore, silicate-based materials may be a potential therapeutic agent targeting osteoclast differentiation in bone defects.