Numerous in vitro studies have demonstrated that chondrocytes react to mechanical stimuli. Compression of chondrocytes in an agarose gel induces disruption of the actin cytoskeleton [1]. In addition, chondrogenic gene expression decreases for chondrocytes cultured in monolayer, while inhibition of actin polymerization causes an increase in type II collagen and GAG production [2]. Despite such extensive in vitro investigations, the mechanisms by which chondrocytes actively respond to mechanical loading are not well understood. Simple hyperelastic and viscoelastic computational cell models have previously been used to model chondrocytes. However, such passive models ignore the key biomechanisms by which cells sense and react to external loads, and hence offer limited insight or predictive capability [3].

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