For this study, we hypothesized that the depth-dependent compressive equilibrium properties of articular cartilage are the inherent consequence of its depth-dependent composition, and not the result of depth-dependent material properties. To test this hypothesis, our recently developed fibril-reinforced poroviscoelastic swelling model was expanded to include the influence of intra- and extra-fibrillar water content, and the influence of the solid fraction on the compressive properties of the tissue. With this model, the depth-dependent compressive equilibrium properties of articular cartilage were determined, and compared with experimental data from the literature. The typical depth-dependent behavior of articular cartilage was predicted by this model. The effective aggregate modulus was highly strain-dependent. It decreased with increasing strain for low strains, and increases with increasing strain for high strains. This effect was more pronounced with increasing distance from the articular surface. The main insight from this study is that the depth-dependent material behavior of articular cartilage can be obtained from its depth-dependent composition only. This eliminates the need for the assumption that the material properties of the different constituents themselves vary with depth. Such insights are important for understanding cartilage mechanical behavior, cartilage damage mechanisms and tissue engineering studies.

Since both the static and the time-dependent mechanical properties have now become fully dependent on tissue composition, the model allows assessing the mechanical consequences of compositional changes seen during osteoarthritis without further assumptions. This is a major step forward in quantitative evaluations of osteoarthritis progression.

Biological tissues like intervertebral discs and articular cartilage primarily consist of interstitial fluid, collagen fibrils and negatively charged proteoglycans. Due to the fixed charges of the proteoglycans, the total ion concentration inside the tissue is higher than in the surrounding synovial fluid (cation concentration is higher and the anion concentration is lower). This excess of ion particles leads to an osmotic pressure difference, which causes swelling of the tissue. In the last decade several mechano-electrochemical models, which include this mechanism, have been developed. As these models are complex and computationally expensive, it is only possible to analyze geometrically relatively small problems. Furthermore, there is still no commercial finite element tool that includes such a mechano-electrochemical theory. Lanir (Biorheology, 24, pp. 173-187, 1987) hypothesized that electrolyte flux in articular cartilage can be neglected in mechanical studies. Lanir's hypothesis implies that the swelling behavior of cartilage is only determined by deformation of the solid and by fluid flow. Hence, the response could be described by adding a deformation-dependent pressure term to the standard biphasic equations. Based on this theory we developed a biphasic swelling model. The goal of the study was to test Lanir's hypothesis for a range of material properties. We compared the deformation behavior predicted by the biphasic swelling model and a full mechano-electrochemical model for confined compression and 1D swelling. It was shown that, depending on the material properties, the biphasic swelling model behaves largely the same as the mechano-electrochemical model, with regard to stresses and strains in the tissue following either mechanical or chemical perturbations. Hence, the biphasic swelling model could be an alternative for the more complex mechano-electrochemical model, in those cases where the ion flux itself is not the subject of the study. We propose thumbrules to estimate the correlation between the two models for specific problems.

The collagen structure as predicted with the collagen remodeling algorithm corresponds very well with the collagen structure in healthy knee joints. This remodeling algorithm is therefore considered to be a valuable tool for developing loading protocols for tissue engineering of articular cartilage.

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