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CCR5 down-regulates osteoclast function in orthodontic tooth movement.

机译:CCR5下调正畸牙齿运动中的破骨细胞功能。

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摘要

During orthodontic tooth movement, there is local production of chemokines and an influx of leukocytes into the periodontium. CCL5 plays an important role in osteoclast recruitment and activation. This study aimed to investigate whether the CCR5-receptor influences these events and, consequently, orthodontic tooth movement. An orthodontic appliance was placed in wild-type mice (WT) and CCR5-deficient mice (CCR5(-/-)). The expression of mediators involved in bone remodeling was evaluated in periodontal tissues by Real-time PCR. The number of TRAP-positive osteoclasts and the expression of cathepsin K, RANKL, and MMP13 were significantly higher in CCR5(-/-). Meanwhile, the expression of two osteoblastic differentiation markers, RUNX2 and osteocalcin, and that of bone resorption regulators, IL-10 and OPG, were lower in CCR5(-/-). Analysis of the data also showed that CCR5(-/-) exhibited a greater amount of tooth movement after 7 days of mechanical loading. The results suggested that CCR5 might be a down-regulator of alveolar bone resorption during orthodontic movement.
机译:在正畸牙齿移动期间,局部产生趋化因子,并且白细胞大量流入牙周。 CCL5在破骨细胞募集和激活中起重要作用。这项研究旨在调查CCR5受体是否会影响这些事件,进而影响正畸牙齿的运动。将正畸矫治器放置在野生型小鼠(WT)和CCR5缺陷型小鼠(CCR5(-/-))中。通过实时PCR在牙周组织中评估参与骨重塑的介质的表达。在CCR5(-/-)中,TRAP阳性破骨细胞的数量以及组织蛋白酶K,RANKL和MMP13的表达均显着较高。同时,CCR5(-/-)中两个成骨细胞分化标记物RUNX2和骨钙素的表达以及骨吸收调节剂IL-10和OPG的表达较低。数据分析还显示,在机械负载7天后,CCR5(-/-)的牙齿运动量更大。结果表明,CCR5可能是正畸运动过程中牙槽骨吸收的下调因子。

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