Comparison of loading rate-dependent injury modes in a murine model of post-traumatic osteoarthritis.
Comparison of loading rate-dependent injury modes in a murine model of post-traumatic osteoarthritis.
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DOI：
10.1002/jor.22480
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发表时间：
2014-01
影响因子：
2.8
通讯作者：
Christiansen, Blaine A.
中科院分区：
文献类型：
--
作者：
Lockwood, Kevin A.;Chu, Bryce T.;Anderson, Matthew J.;Haudenschild, Dominik R.;Christiansen, Blaine A.
创伤后骨关节炎 (PTOA) 是前十字韧带 (ACL) 断裂等关节损伤的常见长期后果。在这项研究中，我们使用胫骨压缩过载小鼠模型来比较低速（1毫米/秒）引起的膝关节损伤（导致撕脱性骨折）和高速（500毫米/秒）引起的损伤（导致ACL中部撕裂）。损伤后 0 天、10 天、12 周或 16 周处死小鼠，并通过微型计算机断层扫描、全关节组织学和生物力学松弛测试来分析关节。两种损伤模式的膝关节损伤在受伤后 10 天时都会导致大量骨小梁丢失，其中低速损伤组（撕脱）的骨丢失量比高速损伤组（中间撕裂）要多。受伤后，两种损伤模式均导致 AP 关节总松弛度相对于对照膝关节增加了 2 倍以上。受伤后 12 周和 16 周，总 AP 松弛度恢复至未受伤时的对照值，这可能是由于骨赘形成使膝关节稳定所致。该模型提供了一个机会来探索有关骨转换在 PTOA 中的作用的基本问题，并且本研究的结果支持损伤后骨赘形成的生物力学机制。
Post-traumatic osteoarthritis (PTOA) is a common long-term consequence of joint injuries such as anterior cruciate ligament (ACL) rupture. In this study we used a tibial compression overload mouse model to compare knee injury induced at low speed (1 mm/s), which creates an avulsion fracture, to injury induced at high speed (500 mm/s), which induces midsubstance tear of the ACL. Mice were sacrificed at 0 days, 10 days, 12 weeks, or 16 weeks post-injury, and joints were analyzed with micro-computed tomography, whole joint histology, and biomechanical laxity testing. Knee injury with both injury modes caused considerable trabecular bone loss by 10 days post-injury, with the Low Speed Injury group (avulsion) exhibiting a greater amount of bone loss than the High Speed Injury group (midsubstance tear). Immediately after injury, both injury modes resulted in greater than 2-fold increases in total AP joint laxity relative to control knees. By 12 and 16 weeks post-injury, total AP laxity was restored to uninjured control values, possibly due to knee stabilization via osteophyte formation. This model presents an opportunity to explore fundamental questions regarding the role of bone turnover in PTOA, and the findings of this study support a biomechanical mechanism of osteophyte formation following injury.
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DOI：
10.2106/00004623-197456020-00002
发表时间：
1974-01-01
影响因子：
5.3
作者：
NOYES, FR;DELUCAS, JL;TORVIK, PJ
通讯作者：
TORVIK, PJ
影响因子：
--
作者：
Poulet, Blandine;Hamilton, Richard W.;Pitsillides, Andrew A.
通讯作者：
Pitsillides, Andrew A.
影响因子：
7
作者：
Christiansen, B. A.;Anderson, M. J.;Haudenschild, D. R.
通讯作者：
Haudenschild, D. R.
影响因子：
2.8
作者：
Furman, Bridgette D.;Strand, Lens;Olson, Steven A.
通讯作者：
Olson, Steven A.
影响因子：
7
作者：
Bolbos, R. I.;Zuo, Jin;Majumdar, Sharmila
通讯作者：
Majumdar, Sharmila