Adouni Malek, Dhaher Yasin Y
Northwestern University, Physical Medicine and Rehabilitation Department, 345 East Superior Street, Chicago, IL 60611, USA; Rehabilitation Institute of Chicago, Sensory Motor Performance Program, 345 East Superior Street, Chicago, IL 60611, USA.
Northwestern University, Physical Medicine and Rehabilitation Department, 345 East Superior Street, Chicago, IL 60611, USA; Rehabilitation Institute of Chicago, Sensory Motor Performance Program, 345 East Superior Street, Chicago, IL 60611, USA; Northwestern University, Biomedical Engineering Department, 2145 Sheridan Road, Evanston, IL 60208, USA.
J Biomech. 2016 Sep 6;49(13):2891-2898. doi: 10.1016/j.jbiomech.2016.06.031. Epub 2016 Jul 1.
Collagen damage is one of the earliest signs of cartilage degeneration and the onset of osteoarthritis (OA), but the connection between the microscale damage and macroscale tissue function is unclear. We argue that a multiscale model can help elucidate the biochemical and mechanical underpinnings of OA by connecting the microscale defects in collagen fibrils to the macroscopic cartilage mechanics. We investigated this connection using a multiscale fibril reinforced hyperelastoplastic (MFRHEP) model that accounts for the structural architecture of the soft tissue, starting from tropocollagen molecules that form fibrils, and moving to the complete soft tissue. This model was driven by reported experimental data from unconfined compression testing of cartilage. The model successfully described the observed transient response of the articular cartilage in unconfined and indentation tests with low and high loading rates. We used this model to understand damage initiation and propagation as a function of the cross-link density between tropocollagen molecules. This approach appeared to provide a realistic simulation of damage when compared with certain published studies. The current construct presents the first attempt to express the aggregate cartilage damage in terms of the cross-link density at the microfibril level.
胶原蛋白损伤是软骨退变和骨关节炎（OA）发病的最早迹象之一，但微观损伤与宏观组织功能之间的联系尚不清楚。我们认为，多尺度模型可以通过将胶原纤维中的微观缺陷与宏观软骨力学联系起来，帮助阐明OA的生化和力学基础。我们使用多尺度纤维增强超弹塑性（MFRHEP）模型研究了这种联系，该模型考虑了软组织的结构架构，从形成纤维的原胶原蛋白分子开始，一直到完整的软组织。该模型由报道的软骨无侧限压缩试验的实验数据驱动。该模型成功地描述了在无侧限和压痕试验中，低加载速率和高加载速率下观察到的关节软骨的瞬态响应。我们使用该模型来理解损伤的起始和传播与原胶原蛋白分子之间交联密度的关系。与某些已发表的研究相比，这种方法似乎提供了一种逼真的损伤模拟。当前的构建首次尝试根据微纤维水平的交联密度来表达总体软骨损伤。
