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The introduction of targeted therapies against cytokine tumour necrosis factor (TNF) alpha has dramatically changed the management, prognosis and perspectives of patients with ankylosing spondylitis (AS) and related forms of spondyloarthritis.1 Both the soluble TNF receptor etanercept and the different anti-TNF antibodies are highly successful in reducing the signs and symptoms of disease, thereby improving quality of life, participation in the work force and the overall wellbeing of patients.2 3 Clinical evidence suggests that anti-TNF therapies are more successful and the effect more sustained than in other diseases such as rheumatoid arthritis (RA) and inflammatory bowel disease.4 However, in contrast to what is seen in patients with RA, anti-TNF does not appear to have an impact on the structural progression of disease, a process characterised by ankylosis of the spine and sacroiliac joints in spondyloarthritis patients.5,–,7 This aspect of the disease contrasts with the typical pattern of erosive joint destruction seen in patients with RA and with the associated protective effect of anti-TNF.8
Two hypotheses have been put forw to explain this clinical conundrum. The first hypothesis states that inflammation, including the upregulation of TNF, triggers local damage and subsequently repair leading to new bone formation and ankylosis, thereby establishing a causal coupling between inflammation and this process of ankylosis.9 A decrease in inflammation may be necessary for repair to occur, with TNF acting as a brake on the specific mechanisms involved.10 The second hypothesis states that a common trigger is responsible for both inflammation and new bone formation, but that both phenomena further develop in a largely molecularly independent way.11 The question asked by these hypotheses is critical for the …
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