Osteocyte regulation of orthodontic force-mediated tooth movement via RANKL expression.
Osteocyte regulation of orthodontic force-mediated tooth movement via RANKL expression.
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DOI：
10.1038/s41598-017-09326-7
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发表时间：
2017-08-18
影响因子：
4.6
通讯作者：
Nakashima T
中科院分区：
文献类型：
--
作者：
Shoji-Matsunaga A;Ono T;Hayashi M;Takayanagi H;Moriyama K;Nakashima T
正畸牙齿移动是通过重塑牙根周围的牙槽骨来实现的。在施加正畸力时，破骨细胞骨吸收发生在牙槽骨的受压侧，牙齿被驱动到该侧。然而，牙槽骨重塑调节机制的分子基础尚未得到充分阐明。破骨细胞生成受核因子-κB 配体受体激活剂 (RANKL) 的调节，据推测该受体激活剂由牙根周围的细胞表达。在这里，我们表明骨细胞是正畸牙齿移动期间牙槽骨重塑中 RANKL 的关键来源。使用一种新建立的从牙槽骨中分离牙周组织成分细胞的方法，我们发现骨细胞表达的 RANKL 量比牙周组织中的其他细胞高得多。骨细胞来源的 RANKL 的关键作用通过骨细胞中特别缺乏 RANKL 的小鼠正畸牙齿移动的减少得到证实。因此，我们为骨细胞衍生的 RANKL 在牙槽骨重塑中的关键作用提供了体内证据，为正畸力介导的骨吸收奠定了分子基础。
Orthodontic tooth movement is achieved by the remodeling of the alveolar bone surrounding roots of teeth. Upon the application of orthodontic force, osteoclastic bone resorption occurs on the compression side of alveolar bone, towards which the teeth are driven. However, the molecular basis for the regulatory mechanisms underlying alveolar bone remodeling has not been sufficiently elucidated. Osteoclastogenesis is regulated by receptor activator of nuclear factor-κB ligand (RANKL), which is postulated to be expressed by the cells surrounding the tooth roots. Here, we show that osteocytes are the critical source of RANKL in alveolar bone remodeling during orthodontic tooth movement. Using a newly established method for the isolation of periodontal tissue component cells from alveolar bone, we found that osteocytes expressed a much higher amount of RANKL than other cells did in periodontal tissue. The critical role of osteocyte-derived RANKL was confirmed by the reduction of orthodontic tooth movement in mice specifically lacking RANKL in osteocytes. Thus, we provide in vivo evidence for the key role of osteocyte-derived RANKL in alveolar bone remodeling, establishing a molecular basis for orthodontic force-mediated bone resorption.
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