New bone formation of the vertebral column is pathognomonic for ankylosing spondylitis (AS), while acute and/or chronic changes in the sacroiliac joints are relevant for diagnosis.
The ‘gold standard’ for assessment of structural changes in AS are conventional radiographs, while MRI is useful to assess inflammation. Recent MRI studies have shown that the lower half of the thoracic spine is most commonly affected in AS.
Scoring tools for spinal inflammation such as the ASspiMRI-a have been proposed, successfully used in large clinical trials and compared in a multireader experiment; none was finally preferred by OMERACT.
Quantification of structural spinal AS changes is performed by the modified Stokes AS Spine Score (mSASSS), which evaluates lateral cervical and lumbar radiographs. Two years was identified as the shortest possible follow-up time based on the reliability and sensitivity to change of the mSASSS. A potential disadvantage of the mSASSS is that the thoracic spine is not included. Recent data based on the mSASSS have suggested that tumour necrosis factor blockers do not inhibit radiographic progression in AS. Since the mean radiographic change is reported to be less than 1 syndesmophyte over 2 years, the sensitivity to change of the mSASSS has been questioned. However, in one study where continuous non-steroidal anti-inflammatory drugs use was compared with on-demand use, a difference between these two methods of drug intake was reported. The face and construct validity of the mSASSS has been criticised because a score of ´1´ contains a mixture of osteodestructive (erosions) and osteoproliferative changes (squaring and sclerosis). A new scoring system, the RASSS, which concentrates only on bone formation and which includes the lower part of the thoracic spine is currently being evaluated.
The relationship between inflammation and new bone formation in AS has recently been investigated. Low sclerostin and DKK-1 serum levels, both inhibitors of bone formation, were found to be associated with syndesmophyte formation in patients with AS.
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