The biomechanical role of the chondrocyte pericellular matrix in articular cartilage

被引:165
作者
Alexopoulos, LG
Setton, LA
Guilak, F
机构
[1] Duke Univ, Med Ctr, Dept Surg, Orthopaed Res Lab, Durham, NC 27710 USA
[2] Duke Univ, Dept Biomed Engn, Durham, NC 27708 USA
关键词
chondron; cell mechanics; micropipette; modulus; permeability; biphasic; finite element model; biomechanics; pericellular matrix; osteoarthritis; articular cartilage;
D O I
10.1016/j.actbio.2005.02.001
中图分类号
R318 [生物医学工程];
学科分类号
0831 ;
摘要
The pericellular matrix (PCM) is a narrow tissue region that surrounds chondrocytes in articular cartilage. Previous parametric studies of cell-matrix interactions suggest that the mechanical properties of the PCM relative to those of the extracellular matrix (ECM) can significantly affect the micromechanical environment of the chondrocyte. The goal of this study was to use recently quantified mechanical properties of the PCM in a biphasic finite element model of the cell-PCM-ECM structure to determine the potential influence of the PCM on the mechanical environment of the chondrocyte under normal and osteoarthritic conditions. Our findings suggest that the mismatch between the Young's moduli of PCM and ECM amplifies chondrocyte compressive strains and exhibits a significant stress shielding effect in a zone-dependent manner. Furthermore, the lower permeability of PCM relative to the ECM inhibits fluid flux near the cell by a factor of 30, and thus may have a significant effect on convective transport to and from the chondrocyte. Osteoarthritic changes in the PCM and ECM properties significantly altered the mechanical environment of the chondrocyte, leading to similar to 66% higher compressive strains and higher fluid flux near the cell. These findings provide further support for a potential biomechanical role for the chondrocyte PCM, and suggest that changes in the properties of the PCM with osteoarthritis may alter the stress-strain and fluid flow environment of the chondrocytes. (c) 2005 Acta Materialia Inc. Published by Elsevier Ltd. All rights reserved.
引用
收藏
页码:317 / 325
页数:9
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