Abstract
Axial spondyloarthritis (axSpA) is a disease characterised by new bone formation. Biologic agents targeting TNFα or IL-17 are used widely and are very effective in controlling symptoms and improving quality of life in these patients. However, the effect of biologics on radiographic progression is still not entirely known. The most crucial question to be addressed is whether new bone formation in the context of axSpA is linked to the inflammatory process. If new bone formation and inflammation are interconnected, then long-term suppression of inflammation with biologic agents may eventually lead to inhibition of ankylosis. On the other hand, if these processes are totally uncoupled then biologics may not have an obvious effect on radiographic progression. In this case, targeting pathways that control new bone formation may be a more feasible approach to retard radiographic progression in axSpA. The molecular mechanisms involved in new bone formation in axSpA have been extensively investigated throughout the last years. In this narrative review we summarise the data regarding the mechanisms of new bone formation in axSpA.