Laboratory of Immunopharmacology, Department of Biochemistry and Immunology, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais, Brazil.
Am J Orthod Dentofacial Orthop. 2012 Feb;141(2):153-60. doi: 10.1016/j.ajodo.2011.07.019.
Cytokines and chemokines regulate bone remodeling during orthodontic tooth movement. CC chemokine ligand 2 (CCL2) is involved in osteoclast recruitment and activity, and its expression is increased in periodontal tissues under mechanical loading. In this study, we investigated whether the CC chemokine receptor 2 (CCR2)-CCL2 axis influences orthodontic tooth movement.
A coil spring was placed in CCR2-deficient (CCR2(-/-)), wild-type, vehicle-treated, and P8A-treated (CCL2 analog) mice. In a histopathologic analysis, the amounts of orthodontic tooth movement and numbers of osteoclasts were determined. The expression of mediators involved in bone remodeling was evaluated by real-time polymerase chain reaction.
Orthodontic tooth movement and the number of TRAP-positive cells were significantly decreased in CCR2(-/-) and P8A-treated mice in relation to wild-type and vehicle-treated mice, respectively. The expressions of RANKL, RANK, and osteoblasts markers (COL-1 and OCN) were lower in CCR2(-/-) than in wild-type mice. No significant difference was found in osteoprotegerin levels between the groups.
These data suggested a reduction of osteoclast and osteoblast activities in the absence of CCR2. The CCR2-CCL2 axis is positively associated with osteoclast recruitment, bone resorption, and orthodontic tooth movement. Therefore, blockage of the CCR2-CCL2 axis might be used in the future for modulating the extent of orthodontic tooth movement.
细胞因子和趋化因子在正畸牙齿移动过程中调节骨重塑。CC 趋化因子配体 2（CCL2）参与破骨细胞的募集和活性，其在机械加载下牙周组织中的表达增加。在本研究中，我们研究了 CC 趋化因子受体 2（CCR2）-CCL2 轴是否影响正畸牙齿移动。
在 CCR2 缺陷（CCR2（-/-））、野生型、载体处理和 P8A 处理（CCL2 类似物）小鼠中放置螺旋弹簧。在组织病理学分析中，确定正畸牙齿移动的量和破骨细胞的数量。通过实时聚合酶链反应评估参与骨重塑的介质的表达。
与野生型和载体处理的小鼠相比，正畸牙齿移动和 TRAP 阳性细胞数量在 CCR2（-/-）和 P8A 处理的小鼠中显著减少。与野生型小鼠相比，CCR2（-/-）小鼠中 RANKL、RANK 和成骨细胞标志物（COL-1 和 OCN）的表达较低。各组间骨保护素水平无显著差异。
这些数据表明 CCR2 缺失时破骨细胞和成骨细胞活性降低。CCR2-CCL2 轴与破骨细胞募集、骨吸收和正畸牙齿移动呈正相关。因此，阻断 CCR2-CCL2 轴可能用于未来调节正畸牙齿移动的程度。
