INCREASED INTRACORTICAL REMODELING FOLLOWING FATIGUE DAMAGE
INCREASED INTRACORTICAL REMODELING FOLLOWING FATIGUE DAMAGE
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DOI：
10.1016/8756-3282(93)90235-3
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发表时间：
1993-03-01
期刊：
影响因子：
4.1
通讯作者：
BURR, DB
中科院分区：
文献类型：
--
作者：
MORI, S;BURR, DB
我们之前已经证明，微裂纹与吸收间隙的共同发生频率比预期的要高，并提出疲劳损伤会引发重塑事件。然而，裂缝可能在先前存在的吸收空间部位累积，并且没有引发新的重塑。这项工作的目的是确定骨重建是否遵循微裂纹的积累，如预期的，如果微裂纹是负责启动骨重建，或如果它之前的微损伤积累。在13只犬的左侧肢体上施加三点弯曲载荷，在2 Hz下循环10000次，在颅侧桡骨表面上施加2500微应变。8天后，以相同的方式加载右侧肢体，在第二次加载事件后立即处死犬。非负荷组（n = 7）用作外部对照。对桡骨进行整体拉伸，以检测微损伤;收集与骨吸收、微损伤累积以及损伤与骨吸收相关的参数。数据表明，在微损伤产生之后，新的重塑事件显著增加。微裂纹和再吸收空间之间的这种时间关系与裂纹位于预先存在的再吸收空间的位置的假设不一致。这表明骨重建优先发生在疲劳损伤区域，并支持骨中微损伤的起始与其修复之间的直接因果关系。
We previously demonstrated that microcracks occurred in common with resorption spaces more often than expected by chance, and proposed that fatigue damage initiates remodeling events. However, it was possible that cracks accumulated at sites of preexisting resorption spaces and did not initiate new remodeling. The goal of this work was to determine whether osteonal remodeling follows the accumulation of microcracks, as expected if microcracks are responsible for initiation of bone remodeling, or if it precedes microdamage accumulation. A three-point bending load was applied to the left limb of 13 dogs for 10 000 cycles at 2 Hz with 2500 microstrain on the cranial radial surface. The right limb was loaded in the same manner eight days later, and the dogs sacrificed immediately after the second loading episode. A nonloaded groups (n = 7) was used as an external control. Radii were strained en bloc for microdamage; parameters related to bone resorption, microdamage accumulation, and the association of damage and resorption were collected. The data demonstrate a significant increase in new remodeling events subsequent to the generation of microdamage. This temporal relationship between microcracks and resorption spaces is inconsistent with the hypothesis that cracks localize at sites of preexisting resorption spaces. This demonstrates that bone remodeling occurs preferentially in fatigue-damaged regions, and supports a direct cause and effect relationship between the initiation of microdamage in bone and its repair.