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The effect of fibrillar degradation on the mechanics of articular cartilage: a computational model

机译:原纤维降解对关节软骨力学的影响:计算模型

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The pathogenesis and pathophysiological underpinnings of cartilage degradation are not well understood. Either mechanically or enzymatically mediated degeneration at the fibril level can lead to acute focal injuries that will, overtime, cause significant cartilage degradation. Understanding the relationship between external loading and the basic molecular structure of cartilage requires establishing a connection between the fibril-level defects and its aggregate effect on cartilage. In this work, we provide a multiscale constitutive model of cartilage to elucidate the effect of two plausible fibril degradation mechanisms on the aggregate tissue: tropocollagen crosslink failure () and a generalized surface degradation (). Using our model, the mechanics of aggregate tissue shows differed yield stress and post-yield behavior after crosslink failure and surface degradation compared to intact cartilage, and the tissue-level aggregate behaviors are different from the fibrillar behaviors observed in the molecular dynamics simulations. We also compared the effect of fibrillar defects in terms of crosslink failure and surface degradation in different layers of cartilage within the macroscale tissue construct during a simulated nanoindentation test. Although the mechanical properties of cartilage tissue were largely contingent upon the mechanical properties of the fibril, the macroscale mechanics of cartilage tissue showed similar to 10% variation in yield strain (tissue yield strain: similar to 27 to similar to 37%) compared to fibrillar yield strain (fibrillar yield strain: similar to 16 to similar to 26%) for crosslink failure and similar to 7% difference for the surface degradation (yield strain variations at the tissue: similar to 30 to similar to 37% and fibril: similar to 24 to similar to 26%) at the superficial layer. The yield strain was further delayed in middle layers at least up to 30% irrespective of the failure mechanisms. The cartilage tissue appeared to withst
机译:软骨降解的发病机制和病理生理学基础尚不清楚。在原纤维水平的机械上或酶促介导的变性可以导致急性局灶性损伤,即加管,引起大量的软骨降解。了解外部负荷与软骨的基本分子结构之间的关系需要在纤维水平缺陷和软骨上的骨料效应之间建立连接。在这项工作中,我们提供了一种多尺度组织型模型的软骨,以阐明两种合理的原纤维降解机制对聚集组织的影响:Tropocollagen交联失效()和广义表面降解()。使用我们的模型,聚集组织的机制显示交联失效后的屈服应力和产率后行为与完整软骨相比,表面降解,组织级聚集行为与分子动力学模拟中观察到的纤维状行为不同。我们还将纤维型缺陷的效果与在模拟纳米凸起试验期间宏观组织构建中的不同包装层中的交联失效和表面劣化的效果。虽然软骨组织的机械性能大大于原纤维的机械性能,但是与纤维菌相比,软骨组织的宏观尺寸显示出类似于10%的产菌菌株的变化(组织产量菌株:与纤维节相似的27%)产生菌株(纤维状产菌菌株:与交联突变相似的16〜类似于26%),其表面劣化的7%差异(组织的产量应变变化:与37%和纤维相似:类似于在浅层层,24至26%)。不管发生故障机制,至少高达30%的中间层进一步延迟产株。软骨组织似乎是

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