An anti-c-Fms Antibody Inhibits Orthodontic Tooth Movement

正畸力诱导体内破骨细胞生成。最近有报道称，抗巨噬细胞集落刺激因子（M-CSF）受体c-Fms的抗体可阻断肿瘤坏死因子-α(TNF-α)诱导的破骨细胞生成和骨侵蚀。本研究旨在研究抗c- fms抗体对小鼠正畸牙齿运动模型中机械负荷诱导的破骨细胞生成和骨溶解的影响。在TNF受体1和2缺失小鼠中，我们发现正畸牙齿移动是由TNF-α介导的。我们在机械加载期间每天向局部注射抗c- fms抗体，持续12天。抗c- fms抗体能显著抑制正畸牙的运动，显著减少体内破骨细胞数量，抑制TNF-α-诱导的体外破骨细胞生成。这些结果表明，M-CSF在TNF-α介导的正畸牙齿运动过程中机械负荷诱导的破骨细胞发生和骨吸收中起重要作用。

Orthodontic force induces osteoclastogenesis in vivo. It has recently been reported that administration of an antibody against the macrophage-colony-stimulating factor(M-CSF)receptor c-Fms blocks osteoclastogenesis and bone erosion induced by tumor necrosis factor-α(TNF-α)administration. This study aimed to examine the effect of an anti-c-Fms antibody on mechanical loading-induced osteoclastogenesis and osteolysis in an orthodontic tooth movement model in mice. Using TNF receptor 1 and 2-deficient mice, we showed that orthodontic tooth movement was mediated by TNF-α. We injected anti-c-Fms antibody daily into a local site, for 12 days, during mechanical loading. The anti-c-Fms antibody significantly inhibited orthodontic tooth movement, markedly reduced the number of osteoclasts in vivo and inhibited TNF-α-induced osteoclastogenesis in vitro. These findings suggest that M-CSF plays an important role in mechanical loading-induced osteoclastogenesis and bone resorption during orthodontic tooth movement mediated by TNF-α.