New cartilage and bone formation potentially leading to joint and spine ankylosis is an important feature of the human spondyloarthritides. Increasing evidence suggests that inflammation and remodeling of the joint are at least partially independent processes. Patient cohort data have not demonstrated an effect of the current therapeutic strategies, including anti-tumor necrosis factor on these important aspects of spondyloarthritis. In this article, we review the evidence that inflammation and new tissue formation are uncoupled and indicate potential new therapeutic targets to inhibit disease progression. Both bone morphogenetic protein and wingless-like signaling have been demonstrated to control the process of joint ankylosis in mouse models. However, translation of these concepts to human pathology remains a challenge.
Keywords: Spondyloarthritis, ankylosing spondylitis, psoriatic arthritis, enthesitis, bone remodeling, targeted therapy
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