Sost mRNA suggesting that Sclerostin might be regulated by Wnt. We further observed an enhanced expression of Sclerostin in osteoarthritic cartilage compared to cartilage of control mice. Conclusions: We here show that Wnt3a increases the catabolic activity and inhibits the anabolic activity in murine chondrocytes. Sclerostin alleviates the expression of catabolic genes induced by Wnt and rescued proteoglycan production. Moreover, Sclerostin promotes the cartilage maintenance through the inhibition of chondrocyte hypertrophy. Finally, the expression of Sclerostin expression in osteoarthritic mice suggests that Sclerostin might be involved in the pathophysiology in cartilage damage and might constitute a target for the prevention of osteoarthritis.

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