Intracortical remodeling in adult rat long bones after fatigue loading
Intracortical remodeling in adult rat long bones after fatigue loading
复制标题
DOI：
10.1016/s8756-3282(98)00104-5
复制
发表时间：
1998-09-01
期刊：
影响因子：
4.1
通讯作者：
Schaffler, MB
中科院分区：
文献类型：
--
作者：
Bentolila, V;Boyce, TM;Schaffler, MB
在成人骨骼中，皮质内重塑去除并替换了持续微损伤的密质骨区域。尽管已经在存在重塑活性的现有基线的动物物种中进行了研究，但由于缺乏哈弗氏重塑活性，实验室啮齿动物被认为作为皮质骨转换过程的模型具有有限的适用性。体内尺骨的超生理循环轴向负荷用于诱导弯曲，从而产生疲劳和微损伤，成年SD大鼠右侧尺骨疲劳负荷至尺骨全骨刚度下降30%的破坏前停止点，第一次负荷后10天，左侧尺骨在同一时间疲劳。立即采集尺骨肌，以比较左尺骨对疲劳负荷的即时反应和右腿对疲劳挑战的生物学反应。碱性品红染色骨切片的组织形态计量学和共聚焦显微镜用于评估皮质内重塑活性、微损伤和骨细胞完整性。骨微损伤（线性微裂纹，以及补丁的扩散碱性品红染色的皮质内）发生在疲劳加载的尺骨骨干，疲劳加载后10天，皮质内吸收被激活的尺骨皮质，皮质内吸收发生在优先与线性型微裂纹，与微裂纹数密度减少近40%疲劳后10天。在未检测到骨基质损伤的皮质区域内也始终观察到吸收空间。共聚焦显微镜研究显示骨细胞和骨小管的完整性改变周围的这些吸收空间。这些研究表明：（1）大鼠骨在高水平的周期性应变下发生皮质内重塑，这会诱导皮质的微损伤;（2）皮质内再吸收与骨微损伤和骨细胞完整性改变的区域相关。从这些研究中，我们得出结论，大鼠可以响应疲劳而在长骨中启动哈弗氏重建，并且骨细胞死亡或损伤可以为该过程提供刺激之一（Bone 23：275-281; 1998）（C）1998，Elsevier Science Inc，保留所有权利。
Intracortical remodeling in the adult skeleton removes and replaces areas of compact bone that have sustained microdamage. Although studies have been performed in animal species in which there is an existing baseline of remodeling activity, laboratory rodents have been considered to have limited suitability as models for cortical bone turnover processes because of a lack of haversian remodeling activity, Supraphysiological cyclic axial loading of the ulna in vivo was used to induce bending with consequent fatigue and microdamage, Right ulnae of adult Sprague-Dawley rats were fatigue-loaded to a prefailure stopping point of 30% decrease in ulnae whole bone stiffness, Ten days after the first loading, Left ulnae mere fatigued in the same may. Ulnae mere harvested immediately to allow comparison of the immediate response of the left ulna to the fatigue loads, and the biological response of the right leg to the fatigue challenge. Histomorphometry and confocal microscopy of basic fuchsin-stained bone sections were used to assess intracortical remodeling activity, microdamage, and osteocyte integrity. Bone microdamage (linear microcracks, as well as patches of diffuse basic fuchsin staining within the cortex) occurred in fatigue-loaded ulnar diaphyses, Ten days after fatigue loading, intracortical resorption was activated in ulnar cortices, Intracortical resorption occurred in preferential association with linear-type microcracks, with microcrack number density reduced almost 40% by 10 days after fatigue. Resorption spaces were also consistently observed within areas of the cortex in which no bone matrix damage could be detected. Confocal microscopy studies showed alterations of osteocyte and canalicular integrity around these resorption spaces. These studies reveal that: (1) rat bone undergoes intracortical remodeling in response to high levels of cyclic strain, which induce microdamage in the cortex; and (2) intracortical resorption is associated both with bone microdamage and with regions of altered osteocyte integrity. From these studies, we conclude that rats can initiate haversian remodeling in long bones in response to fatigue, and that osteocyte death or damage may provide one of the stimuli for this process, (Bone 23:275-281; 1998) (C) 1998 by Elsevier Science Inc, All rights reserved.