Induction of osteopenia during experimental tooth movement in the rat: alveolar bone remodelling and the mechanostat theory
Induction of osteopenia during experimental tooth movement in the rat: alveolar bone remodelling and the mechanostat theory
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DOI：
10.1093/ejo/cjp032
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发表时间：
2009-06-01
影响因子：
2.6
通讯作者：
Meikle, Murray C.
中科院分区：
文献类型：
--
作者：
Milne, Trudy J.;Ichim, Ionut;Meikle, Murray C.
骨应变增加到一定阈值以上对骨量有积极影响，而应变幅度的降低会导致骨丢失和骨质减少;术语“机械调节器”已被引入来描述这种组织水平的负反馈机制。骨，特别是牙槽骨的机械生物学知之甚少，以及mechanostat理论是否有任何相关性，以解释正畸牙齿移动过程中发生的骨质变化仍然不清楚。为了进一步研究这种关系，用螺旋弹簧对36只6周龄Wistar大鼠的上颌磨牙施加0.2N的扩张力。在第1、2、4和8天处死动物，并通过组织学、生物化学和有限元（FE）方法分析组织反应。组间的差异通过Student t检验（双尾）确定。该器具在8天后使磨牙间宽度平均增加0.5 mm。对照组大鼠的四环素摄取表明，牙根间区和骨-牙周膜界面的骨转换迅速。然而，在实验组中，四环素掺入到根间区域减少，常规组织学显示实验组和一组假处理阳性对照（使用无活性退火弹簧）中存在骨丢失和骨质减少的证据。在8天的时间过程中，实验组和假治疗组的血清碱性磷酸酶均显著下降，表明骨形成减少。血清酸性磷酸酶也下降，表明骨吸收随之减少。咬合（2 N）和正畸加载后骨中产生的应力的三维有限元分析表明，正畸力产生恒定的加载条件，保护骨的某些区域免受机械应力的影响。低机械刺激区与组织学观察到的骨丢失部位一致，而高负荷区骨量得以保留，这些结果表明：（1）骨丢失是由于矫治器对根间骨的应力遮挡所致;以及随后咬合负荷降低到维持正常骨结构所需的临界阈值以下，以及（2）可以使用机械力调节器模型来至少部分地解释骨对正牙负载的响应。
Increases in bone strains above a certain threshold have a positive effect on bone mass, whereas reductions in strain magnitude lead to bone loss and osteopenia; the term 'mechanostat' has been introduced to describe this tissue-level negative feedback mechanism. The mechanobiology of bone and particularly alveolar bone is poorly understood, and whether the mechanostat theory has any relevance to explaining the osseous changes that occur during orthodontic tooth movement remains unclear. To investigate the relationship further, an expansile force of 0.2 N was applied to the maxillary molars of 36, 6-week-old Wistar rats by helical coil springs. The animals were sacrificed at 1, 2, 4, and 8 days and the tissue response analyzed by histological, biochemical, and finite element (FE) methods. Differences between groups were determined by Student's t-test (two-tailed).The appliance produced an increase in the intermolar width averaging 0.5 mm after 8 days. Tetracycline uptake in the control rats suggested a rapid turnover of bone in both the interradicular domain and the bone-periodontal ligament interface. In the experimental group, however, incorporation of tetracycline into the interradicular domain was reduced and conventional histology revealed evidence of bone loss and osteopenia, in both the experimental and a group of sham-treated positive controls (with inactive, annealed springs). Serum alkaline phosphatase declined significantly in both experimental and sham-treated groups over the 8-day time course, indicating decreased bone formation. Serum acid phosphatase also declined, suggesting a concomitant decrease in bone resorption. Three-dimensional FE analysis of the stresses generated in the bone following occlusal (2 N) and orthodontic loading showed that the orthodontic force created a constant loading condition shielding some areas of bone from mechanical stress. Areas of low mechanical stimulation were coincident with sites of bone loss observed histologically, while bone mass was preserved in areas with higher levels of loading.These findings suggest that (1) the osteopenia resulted from stress shielding of the interradicular bone by the appliance, and a consequent reduction in occlusal loading below the critical threshold required for maintaining normal osseous architecture and (2) the mechanostat model can be employed to explain, at least in part, the response of the bone to orthodontic loading.