The cation-selective chondrocyte transient receptor poten-tial (TRP) channels have important roles as controllers ofchondrocyte matrix metabolism, cell volume, andinflammatory/pain responses, through their regulation of theintracellular Ca2+concentration [96]. Many TRP channeltypes are sensitive to chondrocyte volume and morphologyand the finding that there are changes to expression levels ofTRP channels in native and cultured chondrocytes from OAcartilage [105] has stimulated interest in their potential role inthe progression of cartilage degeneration in animal models.Recent work has focussed on the vanilloid (TRPV) sub-family as the TRPV4 channel could be particularly importantin the transduction of the mechanical/osmotic loading of ar-ticular cartilage by permitting the generation of intracellularCa2+transients. In a mouse model, deletion of TRPV4 chan-nels leads to cartilage degeneration; [106]however,lossofthis channel does not prevent cartilage failure in the DMMmodel but interestingly reduces the severity of age-relatedcartilage degeneration in a mouse model of OA [107].