Anderson Matthew J, Diko Sindi, Baehr Leslie M, Baar Keith, Bodine Sue C, Christiansen Blaine A
Department of Orthopaedic Surgery, University of California-Davis Medical Center, 4635 2nd Ave, Suite 2000, Sacramento, California, 95817.
Department of Neurobiology, Physiology, and Behavior; Department of Physiology and Membrane Biology, University of California-Davis, Davis, California.
J Orthop Res. 2016 Oct;34(10):1680-1687. doi: 10.1002/jor.23178. Epub 2016 Feb 10.
Development of osteoarthritis commonly involves degeneration of epiphyseal trabecular bone. In previous studies, we observed 30-44% loss of epiphyseal trabecular bone (BV/TV) from the distal femur within 1 week following non-invasive knee injury in mice. Mechanical unloading (disuse) may contribute to this bone loss; however, it is unclear to what extent the injured limb is unloaded following injury, and whether disuse can fully account for the observed magnitude of bone loss. In this study, we investigated the contribution of mechanical unloading to trabecular bone changes observed following non-invasive knee injury in mice (female C57BL/6N). We investigated changes in gait during treadmill walking, and changes in voluntary activity level using Open Field analysis at 4, 14, 28, and 42 days post-injury. We also quantified epiphyseal trabecular bone using μCT and weighed lower-limb muscles to quantify atrophy following knee injury in both ground control and hindlimb unloaded (HLU) mice. Gait analysis revealed a slightly altered stride pattern in the injured limb, with a decreased stance phase and increased swing phase. However, Open Field analysis revealed no differences in voluntary movement between injured and sham mice at any time point. Both knee injury and HLU resulted in comparable magnitudes of trabecular bone loss; however, HLU resulted in considerably more muscle loss than knee injury, suggesting another mechanism contributing to bone loss following injury. Altogether, these data suggest that mechanical unloading likely contributes to trabecular bone loss following non-invasive knee injury, but the magnitude of this bone loss cannot be fully explained by disuse. © 2016 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 34:1680-1687, 2016.
骨关节炎的发展通常涉及骨骺小梁骨的退变。在先前的研究中，我们观察到小鼠非侵入性膝关节损伤后1周内，股骨远端骨骺小梁骨（骨体积分数）损失了30%-44%。机械卸载（废用）可能导致这种骨质流失；然而，尚不清楚损伤后受伤肢体的卸载程度，以及废用是否能完全解释所观察到的骨质流失幅度。在本研究中，我们调查了机械卸载对小鼠（雌性C57BL/6N）非侵入性膝关节损伤后小梁骨变化的影响。我们在损伤后4天、14天、28天和42天，通过跑步机行走时的步态分析以及旷场分析来研究自发活动水平的变化。我们还使用显微计算机断层扫描对骨骺小梁骨进行定量，并对正常对照组和后肢卸载（HLU）小鼠膝关节损伤后的下肢肌肉进行称重以量化萎缩情况。步态分析显示受伤肢体的步幅模式略有改变，站立期缩短，摆动期延长。然而，旷场分析显示在任何时间点，受伤小鼠和假手术小鼠之间的自发活动均无差异。膝关节损伤和HLU均导致相当程度的小梁骨丢失；然而，HLU导致的肌肉损失比膝关节损伤严重得多，这表明损伤后骨质流失还有另一种机制。总之，这些数据表明机械卸载可能导致非侵入性膝关节损伤后的小梁骨丢失，但这种骨质流失的幅度不能完全用废用来解释。© 2016骨科学研究协会。由威利期刊公司出版。《矫形外科学研究》2016年第34卷：1680 - 1687页。
