Background: Visfatin regulates prostaglandin E 2 synthesis in chondrocytes, through unknown pathways. Results: We characterized insulin and IGF receptor signaling and Nampt activity involved in this response. Conclusion: Proinflammatory actions of visfatin in chondrocytes implicate IR pathways, possibly through control of Nampt activity. Significance: IR, IGF-1R, and other tyrosine kinase receptor pathways need to be considered to understand visfatin signaling.

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In conclusion, our data demonstrate that, in an inflammatory context, CS inhibits the production of PGE₂ and MMPs. Since CS has previously been shown to counteract the production of these mediators in chondrocytes, we speculate that the beneficial effect of CS in Osteoarthritis (OA) could not only be due to its action on cartilage but also on subchondral bone.

In an inflammatory context in murine osteoblasts, HA can inhibit the expression of MMP and ADAMTS. Because HA can counteract the production of these mediators in chondrocytes, its beneficial effect in osteoarthritis may be due to its action on cartilage and subchondral bone.