The elucidation of sharing roles of periodontal ligament cells and alveolar bone osteoblasts in orthodontic-force responsive osteoclast formation.

正畸牙齿移动过程中，牙周膜细胞产生前列腺素E_2。前列腺素E_2是一种有效的破骨细胞诱导因子，可诱导RANKL。在这项研究中，我们比较了作为PGE_2暴露的直接影响的人PDLS(HPDL)和正常人成骨细胞(HOBS)在破骨细胞生成方面的功能差异。然后，将RAW264.7细胞与HPDL或经PGE_2处理的HOBS共培养。与HPDL相比，PGE_2可显著增加HOBS中RANKL的表达。经PGE_2处理后，RAW264.7细胞中抗酒石酸酸性磷酸酶染色的破骨细胞样细胞数量明显增加，而RANKL的小干扰RNA下调后，RAW264.7细胞中的破骨细胞样细胞数量明显减少。这些结果表明，与PDLS相比，成骨细胞强烈影响PGE2诱导的牙周组织中RANKL对破骨细胞生成的刺激。

Periodontal ligament cells (PDLs) produce PGE_2 during orthodontic tooth movement. PGE_2 is a potent osteoclast-inducing factor that induces RANKL. In this study, we compared the functional difference in osteoclastogenesis between human PDLs (HPDLs) and normal human osteoblasts (HOBs) as a direct effect of PGE_2 exposure.We examined the expression of RANKL with or without PGE_2 in HPDLs and HOBs. Then, RAW264.7 cells were co-cultured on HPDLs or HOBs pretreated with PGE_2. PGE_2 exposure increased significantly RANKL expression in HOBs compared with HPDLs. The number of tartrate-resistant acid phosphatase staining osteoclast-like cells from RAW264.7 cells increased significantly by PGE_2 pretreatment in HOBs and was reduced by small interfering RNA knockdown of RANKL. These results suggest that osteoblasts strongly influence the stimulation of osteoclastogenesis via RANKL, induced byPGE2 in periodontal tissues, compared with PDLs.