Abstract
Purpose: Despite extensive success of novel drugs in preclinical models of osteoarthritis (OA), none have successfully been translated into approved interventions effective at restoring cartilage or modifying the onset of joint structural damage. It is possible that the lack of disease-modifying OA drugs (DMOADs) may in part be explained by the inadequate ability of present preclinical OA models to reflect the physiological environment of the joint. Joint tissues, in particular cartilage, are subject to mechanical loading, which is a critical component in maintaining cartilage homeostasis.
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