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CCR2 在正畸牙齿移动中的作用。

Role of CCR2 in orthodontic tooth movement.

机构信息

Laboratory of Immunopharmacology, Department of Biochemistry and Immunology, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais, Brazil.

出版信息

Am J Orthod Dentofacial Orthop. 2012 Feb;141(2):153-60. doi: 10.1016/j.ajodo.2011.07.019.

Abstract

INTRODUCTION

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.

METHODS

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.

RESULTS

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.

CONCLUSIONS

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.

摘要

简介

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。

方法

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。

结果

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。

结论

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。

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