In recent experimental studies a possible damage mechanism of collagenous tissues mainly caused by fatigue was disclosed. In this contribution, a multi-scale constitutive model ranging from the tropocollagen (TC) molecule level up to bundles of collagen fibers is proposed and utilized to predict the elastic and inelastic long-term tissue response. Material failure of collagen fibrils is elucidated by a permanent opening of the triple helical collagen molecule conformation, triggered either by overstretching or reaction kinetics of non-covalent bonds. This kinetics is described within a probabilistic framework of adhesive detachments of molecular linkages providing collagen fiber integrity. Both intramolecular and interfibrillar linkages are considered. The final constitutive equations are validated against recent experimental data available in literature for both uniaxial tension to failure and the evolution of fatigue for subsequent loading cycles. All material parameters of the proposed model have a clear physical interpretation.

Statement of significance

Irreversible changes take place at different length scales of soft fibrous tissues tissues under supra-physiological loading and alter their macroscopic mechanical properties. Understanding the evolution of those histologic pathologies under loading and incorporating them into a continuum mechanical framework appears to be crucial in order to predict long-term evolution of various diseases and to support the development of tissue engineering.

中文翻译：

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软纤维组织的疲劳：多尺度力学和本构模型

在最近的实验研究中，公开了主要由疲劳引起的胶原组织的可能损伤机制。在此贡献中，提出了从原胶原（TC）分子水平到胶原纤维束的多尺度本构模型，并将其用于预测弹性和非弹性的长期组织反应。通过非共价键的过度拉伸或反应动力学触发的三螺旋胶原分子构象的永久打开，阐明了胶原纤维的材料失效。在提供胶原纤维完整性的分子键的粘合剂分离的概率框架内描述了这种动力学。分子内和纤维间键都被考虑。最终的本构方程根据文献中针对单轴拉伸破坏和后续载荷循环疲劳发展的最新实验数据进行了验证。建议模型的所有材料参数都有清晰的物理解释。

重要声明

在超生理负荷下，不同长度尺度的软纤维组织组织发生不可逆变化，并改变其宏观力学性能。为了预测各种疾病的长期演变并支持组织工程的发展，了解负荷下这些组织病理学的演变并将其纳入连续的力学框架似乎至关重要。