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The Effect of Articular Cartilage Focal Defect Size and Location in Whole Knee Biomechanics Models

软骨 骨关节炎 生物力学 背景(考古学) 变形(气象学) 膝关节 材料科学 运动学 解剖 刚度 生物医学工程 压缩(物理) 医学 复合材料 病理 外科 地质学 物理 经典力学 古生物学 替代医学
作者
Benjamin C. Marchi,Ellen M. Arruda,Rhima M. Coleman
出处
期刊:Journal of biomechanical engineering [ASM International]
卷期号:142 (2) 被引量:10
标识
DOI:10.1115/1.4044032
摘要

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.
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