Marchi Benjamin C, Arruda Ellen M, Coleman Rhima M
Department of Mechanical Engineering, University of Michigan, Ann Arbor, MI 48109.
Department of Mechanical Engineering, University of Michigan, Ann Arbor, MI 48109; Department of Biomedical Engineering, University of Michigan, Ann Arbor, MI 48109; Program in Macromolecular Science and Engineering, University of Michigan, Ann Arbor, MI 48109.
J Biomech Eng. 2020 Feb 1;142(2). doi: 10.1115/1.4044032.
Articular cartilage focal defects are common soft tissue injuries potentially linked to osteoarthritis (OA) development. Although several defect characteristics likely contribute to osteoarthritis, their relationship to local tissue deformation remains unclear. Using finite element models with various femoral cartilage geometries, we explore how defects change cartilage deformation and joint kinematics assuming loading representative of the maximum joint compression during the stance phase of gait. We show how defects, in combination with location-dependent cartilage mechanics, alter deformation in affected and opposing cartilages, as well as joint kinematics. Small and average sized defects increased maximum compressive strains by approximately 50% and 100%, respectively, compared to healthy cartilage. Shifts in the spatial locations of maximum compressive strains of defect containing models were also observed, resulting in loading of cartilage regions with reduced initial stiffnesses supporting the new, elevated loading environments. Simulated osteoarthritis (modeled as a global reduction in mean cartilage stiffness) did not significantly alter joint kinematics, but exacerbated tissue deformation. Femoral defects were also found to affect healthy tibial cartilage deformations. Lateral femoral defects increased tibial cartilage maximum compressive strains by 25%, while small and average sized medial defects exhibited decreases of 6% and 15%, respectively, compared to healthy cartilage. Femoral defects also affected the spatial distributions of deformation across the articular surfaces. These deviations are especially meaningful in the context of cartilage with location-dependent mechanics, leading to increases in peak contact stresses supported by the cartilage of between 11% and 34% over healthy cartilage.
关节软骨局灶性缺损是常见的软组织损伤,可能与骨关节炎(OA)的发展有关。尽管几种缺损特征可能导致骨关节炎,但其与局部组织变形的关系仍不清楚。我们使用具有各种股骨软骨几何形状的有限元模型,假设加载代表步态站立期最大关节压缩,探讨缺损如何改变软骨变形和关节运动学。我们展示了缺损与位置依赖性软骨力学相结合如何改变受影响和相对软骨的变形以及关节运动学。与健康软骨相比,小尺寸和中等尺寸的缺损分别使最大压缩应变增加了约50%和100%。还观察到含缺损模型的最大压缩应变空间位置发生了偏移,导致初始刚度降低的软骨区域承受负荷,以支持新的、升高的负荷环境。模拟的骨关节炎(建模为平均软骨刚度的整体降低)并未显著改变关节运动学,但加剧了组织变形。还发现股骨缺损会影响健康的胫骨软骨变形。与健康软骨相比,股骨外侧缺损使胫骨软骨最大压缩应变增加25%,而小尺寸和中等尺寸的股骨内侧缺损分别降低了6%和15%。股骨缺损还影响关节表面变形的空间分布。在具有位置依赖性力学的软骨背景下,这些偏差尤其有意义,导致软骨支撑的峰值接触应力比健康软骨增加11%至34%。