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We read with great interest the editorial article by Schett et al,1 where the authors discuss the role of tumour necrosis factor (TNF) α blockers in reducing new bone formation in ankylosing spondylitis (AS). They described the pathophysiological process, where TNF-α is a key proinflammatory cytokine, but is also a potent inhibitor of bone formation. Therefore, it is unlikely that TNF-α blockers are effective in reducing syndesmophyte growth and bridging. In other words, would TNF-α blockers inhibit the progression of structural damage even though they are proven to be very efficient in diminishing the clinical parameters of AS activity, acute-phase reactants and also active …
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