On the mechanics of networked type II collagen: Experiments, constitutive modeling, and validation.

Phoebe Szarek, David M Pierce
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Abstract

In this study we investigate the mechanics of type II collagen fibrils, an essential structural component in many load-bearing tissues including cartilage. Although type II collagen plays a crucial role in maintaining tissue integrity, the stress-stretch and failure response of type II collagen fibrils in tension is not established in the current mechanics literature. To address this knowledge gap, we conducted tensile tests on isolated collagen networks from articular cartilage and established a validated constitutive model for type II collagen fibril. We identified two distinct failure mechanisms: one without softening before failure and another with pronounced softening. Our findings reveal that network morphology significantly influences the bulk mechanical response, providing a framework for modeling the complex behavior of collagen fibrils in both healthy and diseased tissues. The validated model enhances the accuracy of finite element models used in analyses of soft tissues and may deepen our understanding of the mechanical progression of diseases like osteoarthritis. Our results offer valuable insights into the mechanics of type II collagen, with implications for improving computational models and for guiding future studies in tissue regeneration and disease treatment.

网络型II型胶原的力学:实验,本构模型和验证。
在这项研究中,我们研究了II型胶原原纤维的力学,这是包括软骨在内的许多承重组织的基本结构成分。尽管II型胶原蛋白在维持组织完整性方面起着至关重要的作用,但目前的力学文献中尚未建立II型胶原原纤维在张力下的应力-拉伸和失效响应。为了解决这一知识空白,我们对关节软骨分离的胶原网络进行了拉伸试验,并建立了II型胶原纤维的有效本构模型。我们确定了两种不同的失效机制:一种在失效前没有软化,另一种有明显的软化。我们的研究结果表明,网络形态显著影响整体力学响应,为健康和病变组织中胶原原纤维的复杂行为建模提供了一个框架。该验证模型提高了用于软组织分析的有限元模型的准确性,并可能加深我们对骨关节炎等疾病的机械进展的理解。我们的研究结果为II型胶原蛋白的机制提供了有价值的见解,对改进计算模型和指导未来组织再生和疾病治疗的研究具有重要意义。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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