核因子-κB受体活化因子配体在大鼠正畸牙压力侧骨改建中的作用

目的：初步探讨在正畸牙移动压力侧核因子-κB受体活化因子配基(receptor activator of nuclearfactor-κB ligand，RANKL)的表达在破骨细胞诱导和骨改建中的调节作用。方法：建立大鼠正畸牙移动模型，利用免疫组化的方法对压力侧RANKL的表达及其变化进行检测；并进一步观察了RANKL对大鼠骨髓破骨细胞形成的影响。结果：正畸牙移动压力侧组化结果显示，RANKL阳性表达位于牙周膜细胞和位于骨陷窝内的破骨细胞中，在正畸牙移动第3、5和7天时呈强阳性表达。体外破骨细胞诱导实验结果显示，在巨噬细胞集落刺激因子(macrophage clone stimulating factor，M-CSF)协同作用下，RANKL呈剂量依赖型诱导TRAP阳性细胞生成。结论：大鼠正畸牙移动中，RANKL在压力侧的表达上调有诱导破骨细胞形成的作用，并导致牙槽骨吸收。

The Role of RANKL on Bone Remodeling at the Compression Sites during Tooth Movement in Rat.

Objective: To investigate the role of RANKL on the induction of osteoclasts and bone remodeling at the compression site during tooth movement. Methods: The orthodontic tooth movement of upper molars was performed in Wistar rats. The expression of RANKL protein at the compression sites was detected by immunohistochemical staining technique. Furthermore, we observed the effect of RANKL on the osteoclast formation in bone marrow culture of adult rats. Results: Immunohistochemical staining revealed that expression of RANKL protein was detected in periodontal ligament cells and osteoclasts which mostly located in resorption lacunae. RANKL protein was expressed strongly at the compressive site at 3, 5, and 7 days after experimental tooth movement, RANKL expression increased in parallel with the changes in the numbers of osteoclasts. When bone marrow cells were cultured with increasing concentrations of RANKL in the presence of M-CSF (50 ng/ml), TRAP-positive cells increased in a dose-dependent manner. Conclusion: We found that RANKL up-regulation at the compressive site of experimental tooth movement induced osteoclastogenesis, and brought about alveolar bone resorption.