Abstract

The aim of this study was to investigate if the experimentally detected altered chondrocyte volumetric behavior in early osteoarthritis can be explained by changes in the extracellular and pericellular matrix properties of cartilage. Based on our own experimental tests and the literature, the structural and mechanical parameters for normal and osteoarthritic cartilage were implemented into a multiscale fibril-reinforced poroelastic swelling model. Model simulations were compared with experimentally observed cell volume changes in mechanically loaded cartilage, obtained from anterior cruciate ligament transected rabbit knees. We found that the cell volume increased by 7% in the osteoarthritic cartilage model following mechanical loading of the tissue. In contrast, the cell volume decreased by 4% in normal cartilage model. These findings were consistent with the experimental results. Increased local transversal tissue strain due to the reduced collagen fibril stiffness accompanied with the reduced fixed charge density of the pericellular matrix could increase the cell volume up to 12%. These findings suggest that the increase in the cell volume in mechanically loaded osteoarthritic cartilage is primarily explained by the reduction in the pericellular fixed charge density, while the superficial collagen fibril stiffness is suggested to contribute secondarily to the cell volume behavior.

Highlights

  • Osteoarthritis (OA) is a progressive joint disease, in which the tissue composition, structure, and mechanical properties are altered significantly [1,2,3]

  • We found that the cell volume increased by 7% in the osteoarthritic cartilage model following mechanical loading of the tissue

  • These findings suggest that the increase in the cell volume in mechanically loaded osteoarthritic cartilage is primarily explained by the reduction in the pericellular fixed charge density, while the superficial collagen fibril stiffness is suggested to contribute secondarily to the cell volume behavior

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Summary

Introduction

Osteoarthritis (OA) is a progressive joint disease, in which the tissue composition, structure, and mechanical properties are altered significantly [1,2,3]. It has been suggested that the pericellular matrix (PCM) is changed in early OA [8,9,10]. These changes in ECM and PCM properties and structure lead to altered osmotic and mechanical environments for the chondrocytes [11,12,13,14,15], possibly altering chondrocyte volume, morphology, and biosynthesis [6, 11,12,13, 15, 16]. The ability of the PCM to protect cells may become weakened in OA [9, 10, 17,18,19,20,21], exposing cells to malfunction and death

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