Department of Computer Science, University of Oxford, Parks Road, OX1 3QD, Oxford, United Kingdom.
MMPE, MERF, Faculty of Engineering, Queensland University of Technology, QLD 4000, Brisbane, Australia.
J Mech Behav Biomed Mater. 2024 Aug;156:106575. doi: 10.1016/j.jmbbm.2024.106575. Epub 2024 May 13.
Articular cartilage tissue exhibits a spatial dependence in material properties that govern mechanical behaviour. A mathematical model of cartilage tissue under one dimensional confined compression testing is developed for normal tissue that takes account of these variations in material properties. Modifications to the model representative of a selection of mechanisms driving osteoarthritic cartilage are proposed, allowing application of the model to both physiological and pathophysiological, osteoarthritic tissue. Incorporating spatial variations into the model requires the specification of more parameters than are required in the absence of these variations. A global sensitivity analysis of these parameters is implemented to identify the dominant mechanisms of mechanical response, in normal and osteoarthritic cartilage tissue, to both static and dynamic loading. The most sensitive parameters differ between dynamic and static mechanics of the cartilage, and also differ between physiological and osteoarthritic pathophysiological cartilage. As a consequence changes in cartilage mechanics in response to alterations in cartilage structure are predicted to be contingent on the nature of loading and the health, or otherwise, of the cartilage. In particular the mechanical response of cartilage, especially deformation, is predicted to be much more sensitive to cartilage stiffness in the superficial zone given the onset of osteoarthritic changes to material properties, such as superficial zone increases in permeability and reductions in fixed charge. In turn this indicates that any degenerative changes in the stiffness associated with the superficial cartilage collagen mesh are amplified if other elements of osteoarthritic disease are present, which provides a suggested mechanism-based explanation for observations that the range of mechanical parameters representative of normal and osteoarthritic tissue can overlap substantially.
关节软骨组织在材料性能上表现出空间依赖性，而这些性能决定了其力学行为。本文针对正常组织，建立了一个在一维受限压缩测试下的软骨组织数学模型，该模型考虑了这些材料性能的变化。本文还提出了一些代表性的软骨组织病变机制的模型修正方法，使得该模型不仅可以应用于生理组织，还可以应用于病理组织，包括骨关节炎组织。将空间变化纳入模型需要指定比不存在这些变化时更多的参数。本文通过全局敏感性分析，确定了正常和骨关节炎软骨组织在静态和动态加载下的主要力学响应机制的参数。这些参数的最敏感参数在软骨的动态和静态力学之间存在差异，在生理和骨关节炎病理生理学之间也存在差异。因此，软骨结构变化引起的软骨力学变化，预计取决于加载的性质以及软骨的健康状况。特别是软骨的机械响应，尤其是变形，预计在软骨材料性能发生骨关节炎变化时，例如浅层区通透性增加和固定电荷减少，对浅层区软骨刚度的变化更为敏感。反过来，这表明如果存在其他骨关节炎疾病的因素，与浅层软骨胶原网格相关的刚度的任何退行性变化都会被放大，这为观察到正常和骨关节炎组织的机械参数范围可能存在显著重叠提供了一种基于机制的解释。
