Department of Biomedical Engineering, University of Delaware, Newark, DE 19716.
Department of Orthopaedic Surgery, University of Pennsylvania, Philadelphia, PA 19104; Translational Musculoskeletal Research Center, CMCVAMC, Philadelphia, PA 19104.
J Biomech Eng. 2023 Aug 1;145(8). doi: 10.1115/1.4062523.
Tendon degeneration is typically described as an overuse injury with little distinction made between magnitude of load (overload) and number of cycles (overuse). Further, in vivo, animal models of tendon degeneration are mostly overuse models, where tendon damage is caused by a high number of load cycles. As a result, there is a lack of knowledge of how isolated overload leads to degeneration in tendons. A surgical model of synergist ablation (SynAb) overloads the target tendon, plantaris, by ablating its synergist tendon, Achilles. The objective of this study was to evaluate the structural and functional changes that occur following overload of plantaris tendon in a rat SynAb model. Tendon cross-sectional area (CSA) and shape changes were evaluated by longitudinal MR imaging up to 8 weeks postsurgery. Tissue-scale structural changes were evaluated by semiquantified histology and second harmonic generation microscopy. Fibril level changes were evaluated with serial block face scanning electron microscopy (SBF-SEM). Functional changes were evaluated using tension tests at the tissue and microscale using a custom testing system allowing both video and microscopy imaging. At 8 weeks, overloaded plantaris tendons exhibited degenerative changes including increases in CSA, cell density, collagen damage area fraction (DAF), and fibril diameter, and decreases in collagen alignment, modulus, and yield stress. To interpret the differences between overload and overuse in tendon, we introduce a new framework for tendon remodeling and degeneration that differentiates between the inputs of overload and overuse. In summary, isolated overload induces multiscale degenerative structural and functional changes in plantaris tendon.
肌腱退变通常被描述为一种过度使用损伤，而对负荷（过载）的大小和循环次数（过度使用）之间几乎没有区别。此外，在体内，肌腱退变的动物模型大多是过度使用模型，其中肌腱损伤是由高次数的负荷循环引起的。因此，对于孤立的过载如何导致肌腱退变，我们知之甚少。协同肌消融（SynAb）的手术模型通过消融其协同肌腱（跟腱）来使靶肌腱（跖肌）过载。本研究的目的是评估协同肌消融大鼠 SynAb 模型中跖肌腱过载后发生的结构和功能变化。通过纵向磁共振成像在手术后 8 周内评估肌腱横截面积（CSA）和形状变化。通过半定量组织学和二次谐波产生显微镜评估组织级别的结构变化。使用串行块面扫描电子显微镜（SBF-SEM）评估原纤维水平的变化。使用定制的测试系统在组织和微观尺度上进行张力测试，该系统允许视频和显微镜成像，评估功能变化。在 8 周时，过载的跖肌腱表现出退行性变化，包括 CSA、细胞密度、胶原损伤面积分数（DAF）和原纤维直径的增加，以及胶原排列、模量和屈服应力的降低。为了解释肌腱中过载和过度使用之间的差异，我们引入了一个新的肌腱重塑和退化框架，该框架区分了过载和过度使用的输入。总之，孤立的过载会导致跖肌腱发生多尺度退行性结构和功能变化。
