Safa Babak N, Lee Andrea H, Santare Michael H, Elliott Dawn M
Mem. ASMEDepartment of Mechanical Engineering,University of Delaware,Newark, DE 19716.
Department of Biomedical Engineering,University of Delaware,Newark, DE 19716e-mail:
J Biomech Eng. 2019 Oct 1;141(10):1010081-10100810. doi: 10.1115/1.4043520.
Inelastic behaviors, such as softening, a progressive decrease in modulus before failure, occur in tendon and are important aspects in degeneration and tendinopathy. These inelastic behaviors are generally attributed to two potential mechanisms: plastic deformation and damage. However, it is not clear which is primarily responsible. In this study, we evaluated these potential mechanisms of tendon inelasticity by using a recently developed reactive inelasticity model (RIE), which is a structurally inspired continuum mechanics framework that models tissue inelasticity based on the molecular bond kinetics. Using RIE, we formulated two material models, one specific to plastic deformation and the other to damage. The models were independently fit to published macroscale experimental tensile tests of rat tail tendons. We quantified the inelastic effects and compared the performance of the two models in fitting the mechanical response during loading, relaxation, unloading, and reloading phases. Additionally, we validated the models by using the resulting fit parameters to predict an independent set of experimental stress-strain curves from ramp-to-failure tests. Overall, the models were both successful in fitting the experiments and predicting the validation data. However, the results did not strongly favor one mechanism over the other. As a result, to distinguish between plastic deformation and damage, different experimental protocols will be needed. Nevertheless, these findings suggest the potential of RIE as a comprehensive framework for studying tendon inelastic behaviors.
诸如软化(即破坏前模量逐渐降低)等非弹性行为会出现在肌腱中,并且是退变和肌腱病的重要方面。这些非弹性行为通常归因于两种潜在机制:塑性变形和损伤。然而,尚不清楚哪一种是主要原因。在本研究中,我们通过使用最近开发的反应性非弹性模型(RIE)来评估肌腱非弹性的这些潜在机制,该模型是一个受结构启发的连续介质力学框架,基于分子键动力学对组织非弹性进行建模。使用RIE,我们制定了两个材料模型,一个特定于塑性变形,另一个特定于损伤。这些模型分别与已发表的大鼠尾腱宏观拉伸试验数据进行拟合。我们对非弹性效应进行了量化,并比较了这两个模型在拟合加载、松弛、卸载和重新加载阶段力学响应方面的性能。此外,我们通过使用所得的拟合参数来预测一组独立的斜坡至破坏试验的实验应力 - 应变曲线,从而对模型进行了验证。总体而言,这些模型在拟合实验和预测验证数据方面均取得了成功。然而,结果并没有强烈支持其中一种机制优于另一种机制。因此,为了区分塑性变形和损伤,将需要不同的实验方案。尽管如此,这些发现表明RIE作为研究肌腱非弹性行为的综合框架具有潜力。