Leni & Peter W May Department of Orthopaedics Surgery Mount Sinai School of Medicine, New York, NY 10029, United States.
J Biomech. 2012 Jan 3;45(1):59-65. doi: 10.1016/j.jbiomech.2011.10.008. Epub 2011 Nov 4.
Damage accumulation underlies tendinopathy. Animal models of overuse injuries do not typically control loads applied to the tendon. Our in vivo model in the rat patellar tendon allows direct control of the loading applied to the tendon. Despite this advantage, natural variation among tendons results in different amounts of damage induced by the same loading protocol. Our objectives were to (1) assess changes in the initial mechanical parameters (hysteresis, stiffness of the loading and unloading load-displacement curves, and elongation) after fatigue loading to identify parameters that are indicative of the induced damage, and (2) evaluate the relationships between these identified initial damage indices with the stiffness 7 day after loading. Left patellar tendons of adult, female retired breeder, Sprague-Dawley rats (n = 68) were fatigue loaded per our previously published in vivo fatigue loading protocol. To induce a range of damage, fatigue loading consisted of either 5, 100, 500 or 7200 cycles that ranged from 1 N to 40 N. Diagnostic tests were applied before and immediately after fatigue loading, and after 45 min of recovery to deduce recoverable and non-recoverable changes in initial damage indices. Relationships between these initial damage indices and the 7-day stiffness (at sacrifice) were determined. Day-0 hysteresis, loading and unloading stiffness exhibited cycle-dependent changes. Initial hysteresis loss correlated with the 7-day stiffness. k-means cluster analysis demonstrated a relationship between 7-day stiffness and day-0 hysteresis and unloading stiffness. This analysis also separated samples that exhibited low from high damage in response to both high or low number of cycles; a key delineation for interpretation of the biological response in future studies. Identifying initial parameters that reflect the induced damage is critical since the ability of the tendon to repair depends on the damage induced and the number of applied loading cycles.
累积性损伤是导致腱病的原因。过度使用损伤的动物模型通常无法控制施加到肌腱上的负荷。我们在大鼠髌腱中的体内模型允许直接控制施加到肌腱上的加载。尽管有这个优势,但由于肌腱之间的自然差异,相同的加载方案会导致不同程度的损伤。我们的目标是:(1)评估疲劳加载后初始力学参数(滞后、加载和卸载载荷-位移曲线的刚度以及伸长率)的变化,以确定指示诱导损伤的参数;(2)评估这些确定的初始损伤指数与加载后 7 天刚度之间的关系。成年、雌性退休繁殖大鼠的左侧髌腱(n = 68)按照我们之前发表的体内疲劳加载方案进行疲劳加载。为了诱导一系列损伤,疲劳加载包括 5、100、500 或 7200 个循环,范围从 1 N 到 40 N。在疲劳加载前后以及 45 分钟恢复后进行诊断测试,以推断初始损伤指数的可恢复和不可恢复变化。确定这些初始损伤指数与 7 天刚度(在处死时)之间的关系。第 0 天滞后、加载和卸载刚度表现出与循环相关的变化。初始滞后损失与 7 天刚度相关。k-均值聚类分析显示 7 天刚度与第 0 天滞后和卸载刚度之间存在关系。该分析还将表现出低或高损伤的样本与高或低循环数区分开来;这是未来研究中解释生物学反应的关键区别。识别反映诱导损伤的初始参数非常重要,因为肌腱的修复能力取决于诱导的损伤程度和施加的加载循环数。