An Anterior Cruciate Ligament Failure Mechanism
An Anterior Cruciate Ligament Failure Mechanism
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DOI：
10.1177/0363546519854450
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发表时间：
2019-07-01
影响因子：
4.8
通讯作者：
Wojtys, Edward M.
中科院分区：
文献类型：
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作者：
Chen, Junjie;Kim, Jinhee;Wojtys, Edward M.
背景：近四分之三的前交叉韧带（ACL）损伤发生在常规运动操作中的“非接触性”失效。最近的体外研究表明，已知反复剧烈的次最大膝关节载荷尤其会使ACL应变，可能导致其疲劳失效，通常发生在ACL股骨端。假设：ACL失效可能由累积的组织疲劳损伤引起：具体而言，该疲劳过程的化学和结构证据将在测试的尸体膝关节的胫骨的股骨止点处以及从接受ACL重建的患者中取出的ACL取出物中发现。研究设计：对照实验室研究。研究方法：7对成人尸体膝关节中的每一对膝关节在4倍体重的模拟枢轴着陆下重复加载，已知这会使ACL产生次最大应变，而对侧未加载膝关节用作比较。与此相关的化学和结构变化的特点是在ACL股骨附着点在多个层次的胶原蛋白水平，采用原子力显微镜（AFM），AFM-红外光谱，分子靶向与荧光标记的胶原蛋白杂交肽，和二次谐波成像显微镜。5例非接触性ACL失效患者的损伤膝关节ACL股骨附着点的取出物也通过类似方法进行表征。结果如下：AFM-红外光谱和胶原杂交肽结合表明，特征性分子损伤是胶原分子三螺旋的解开。原子力显微镜检测到破坏的形式，减少地形表面厚度和诱导类似的30- 100-nm的空隙在胶原纤维基质中的机械测试样品的胶原纤维。二次谐波成像显微镜检测到类似的诱导10至100 μ m的区域，其中胶原蛋白的非中心对称结构已被破坏。这些机械诱导的变化，从分子到微观破坏正常胶原结构，代表了以前未报道的非接触ACL失效中组织疲劳损伤的一个方面。验证性证据来自5例接受ACL重建的患者的取出物，其表现出与机械测试尸体样本中检测到的分子、纳米级和微米级结构损伤相同的模式。结论：作者发现，在非接触性ACL失效手术时，ACL股骨止点处的胶原原纤维和纤维存在累积损伤的证据。这种组织损伤与在体外接受重复4倍体重脉冲三维载荷的供体膝关节中发现的组织损伤相似，已知这种载荷会导致ACL疲劳失效。
Background: Nearly three-quarters of anterior cruciate ligament (ACL) injuries occur as "noncontact" failures from routine athletic maneuvers. Recent in vitro studies revealed that repetitive strenuous submaximal knee loading known to especially strain the ACL can lead to its fatigue failure, often at the ACL femoral enthesis. Hypothesis: ACL failure can be caused by accumulated tissue fatigue damage: specifically, chemical and structural evidence of this fatigue process will be found at the femoral enthesis of ACLs from tested cadaveric knees, as well as in ACL explants removed from patients undergoing ACL reconstruction. Study Design: Controlled laboratory study. Methods: One knee from each of 7 pairs of adult cadaveric knees were repetitively loaded under 4 times-body weight simulated pivot landings known to strain the ACL submaximally while the contralateral, unloaded knee was used as a comparison. The chemical and structural changes associated with this repetitive loading were characterized at the ACL femoral enthesis at multiple hierarchical collagen levels by employing atomic force microscopy (AFM), AFM-infrared spectroscopy, molecular targeting with a fluorescently labeled collagen hybridizing peptide, and second harmonic imaging microscopy. Explants from ACL femoral entheses from the injured knee of 5 patients with noncontact ACL failure were also characterized via similar methods. Results: AFM-infrared spectroscopy and collagen hybridizing peptide binding indicate that the characteristic molecular damage was an unraveling of the collagen molecular triple helix. AFM detected disruption of collagen fibrils in the forms of reduced topographical surface thickness and the induction of similar to 30- to 100-nm voids in the collagen fibril matrix for mechanically tested samples. Second harmonic imaging microscopy detected the induction of similar to 10- to 100-mu m regions where the noncentrosymmetric structure of collagen had been disrupted. These mechanically induced changes, ranging from molecular to microscale disruption of normal collagen structure, represent a previously unreported aspect of tissue fatigue damage in noncontact ACL failure. Confirmatory evidence came from the explants of 5 patients undergoing ACL reconstruction, which exhibited the same pattern of molecular, nanoscale, and microscale structural damage detected in the mechanically tested cadaveric samples. Conclusion: The authors found evidence of accumulated damage to collagen fibrils and fibers at the ACL femoral enthesis at the time of surgery for noncontact ACL failure. This tissue damage was similar to that found in donor knees subjected in vitro to repetitive 4 times-body weight impulsive 3-dimensional loading known to cause a fatigue failure of the ACL.