Shear loads induce cellular damage in tendon fascicles.
Shear loads induce cellular damage in tendon fascicles.
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剪切载荷会引起肌腱束的细胞损伤。
DOI：
10.1016/j.jbiomech.2015.06.006
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发表时间：
2015
影响因子：
2.4
通讯作者：
VanderbyJr,Ray
中科院分区：
文献类型：
--
作者：
Kondratko-Mittnacht,Jaclyn;Lakes,Roderic;VanderbyJr,Ray
肌腱对肌肉骨骼功能至关重要，将负荷从肌肉转移到骨骼，以实现关节运动和稳定性。它是一种各向异性的、高度组织化的纤维结构，除了肌腱细胞和其他有助于维持和功能的细胞外基质成分外，还主要含有I型胶原蛋白。肌腱通常通过纵向方向上的法向应力加载。然而，某些情况下，包括纤维断裂，酶重塑，或肌腱病理可能会引入不同程度的其他加载方式，如在纤维水平的剪切滞后，潜在地影响细胞反应和随后的功能。从大鼠尾肌腱的筋膜被解剖，并放置在三个配对组之一：完整，单裂伤，或双裂伤。每一对都有一个机械测试样本和一个对照样本。单个撕裂束包含一个横向撕裂，以模拟部分撕裂。双撕裂束在对侧有重叠的纵向分离撕裂，导致束内剪切转移是主要的载荷机制。纤维束的弹性性能，例如峰值载荷、稳态载荷和刚度，从完整到单撕裂再到双撕裂组降低。令人惊讶的是，当剪切是主要的内部载荷传递机制时，保持了45%的完整强度。在两个撕裂组中，机械测试后细胞活力降低;细胞死亡主要出现在发生高剪切载荷转移的纵向平面中。这种细胞死亡延伸到远离损伤部位，并且可能通过酶促因子和随后与细胞坏死相关的重塑进一步损害已经受损的肌腱。
Tendon is vital to musculoskeletal function, transferring loads from muscle to bone for joint motion and stability. It is an anisotropic, highly organized, fibrous structure containing primarily type I collagen in addition to tenocytes and other extracellular matrix components contributing to maintenance and function. Tendon is generally loaded via normal stress in a longitudinal direction. However, certain situations, including fiber breakage, enzymatic remodeling, or tendon pathology may introduce various degrees of other loading modalities, such as shear-lag at the fiber level, potentially affecting cellular response and subsequent function. Fascicles from rat tail tendon were dissected and placed in one of three paired groups: intact, single laceration, or double laceration. Each pair had a mechanically tested and control specimen. Single laceration fascicles contained one transverse laceration to mimic a partial tear. Double laceration fascicles had overlapping, longitudinally separated lacerations on opposite sides to cause intra-fascicular shear transfer to be the primary mechanism of loading. Elastic properties of the fascicle,e.g.peak load, steady state load, and stiffness, decreased from intact to single laceration to double laceration groups. Surprisingly, 45% of the intact strength was maintained when shear was the primary internal load transfer mechanism. Cellular viability decreased after mechanical testing in both laceration groups; cell death appeared primarily in a longitudinal plane where high shear load transfer occurred. This cell death extended far from the injury site and may further compromise an already damaged tendon via enzymatic factors and subsequent remodeling associated with cell necrosis.