Other than DKK-1, FLS inhibit the Wnt pathway and osteoblast bone-forming properties by secreting a high amount of sclerostin [37], even though data regarding the inhibition or deletion of sclerostin in TNF-α-dependent models of arthritis (but not in TNF-α-independent arthritis models) induced acceleration of the synovial pannus formation and subsequent local inflammation and bone injuries, suggesting a more sophisticated role of sclerostin in the TNF-α signaling pathways [119]. Here, SOST is linked to arthritic joint disease.