Chambers Neil C, Herod Tyler W, Veres Samuel P
Division of Engineering, Saint Mary's University, Halifax, Nova Scotia, Canada.
School of Biomedical Engineering, Dalhousie University, Halifax, Nova Scotia, Canada.
J Orthop Res. 2018 Nov;36(11):2842-2850. doi: 10.1002/jor.24067. Epub 2018 Jul 13.
Previous research has shown that both the mechanics and elongation mechanisms of tendon and ligament vary with strain rate during tensile loading. In this study, we sought to determine if the ultrastructural damage created during tendon rupture also varies with strain rate. A bovine forelimb model was used, allowing two anatomically proximate but physiologically distinct tendons to be studies: the positional common digital extensor tendon, and the energy storing superficial digital flexor tendon. Samples from the two tendon types were ruptured at rates of either 1%/s or 10%/s. Relative to unruptured control samples, changes to collagen fibril structure were assessed using scanning electron microscopy (SEM), and changes to collagen molecule packing were studied using differential scanning calorimetry (DSC). Rupture at 1%/s caused discrete plasticity damage that extended along the length of collagen fibrils in both the extensor and flexor tendons. Consistent with this, DSC showed molecular packing disruption relative to control samples. Both SEM and DSC showed that extensor tendon fibrils sustained more severe damage than the more highly crosslinked flexor tendon fibrils. Increasing strain rate during rupture decreased the level of longitudinal disruption experienced by the collagen fibrils of both tendon types. Disruption to D-banding was no longer seen in the extensor tendon fibrils, and discrete plasticity damage was completely eliminated in the flexor tendon fibrils, indicating a transition to localized point failure. Ultrastructural damage resulting from tendon rupture depends on both strain rate and tendon type. © 2018 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 36:2842-2850, 2018.
先前的研究表明，肌腱和韧带在拉伸加载过程中的力学和伸长机制会随应变率而变化。在本研究中，我们试图确定肌腱断裂过程中产生的超微结构损伤是否也随应变率而变化。使用了牛前肢模型，以便对两条解剖位置相近但生理功能不同的肌腱进行研究：位置性指总伸肌腱和储能性指浅屈肌腱。两种肌腱类型的样本分别以1%/秒或10%/秒的速率断裂。相对于未断裂的对照样本，使用扫描电子显微镜（SEM）评估胶原原纤维结构的变化，并使用差示扫描量热法（DSC）研究胶原分子堆积的变化。以1%/秒的速率断裂导致离散的塑性损伤，这种损伤在伸肌腱和屈肌腱中均沿胶原原纤维的长度延伸。与此一致的是，DSC显示相对于对照样本分子堆积受到破坏。SEM和DSC均显示，伸肌腱原纤维比交联程度更高的屈肌腱原纤维遭受的损伤更严重。断裂过程中应变率的增加降低了两种肌腱类型的胶原原纤维所经历的纵向破坏程度。在伸肌腱原纤维中不再看到D带的破坏，在屈肌腱原纤维中离散的塑性损伤完全消除，表明转变为局部点失效。肌腱断裂导致的超微结构损伤取决于应变率和肌腱类型。©2018骨科研究协会。由威利期刊公司出版。《矫形外科学研究》36:2842 - 2850，2018年。
