More effective suppression of spinal inflammation may be required to inhibit structural damage in ankylosing spondylitis.
Thus, it seems still possible that more effective suppression of spinal inflammation may lead to a stronger inhibition of structural damage in AS.
It seems still possible that more effective suppression of spinal inflammation may lead to a stronger inhibition of structural damage in AS. 2yFU: 2-year follow-up; AS: ankylosing spondylitis; BL: baseline; CI: confidence interval; MRI: magnetic resonance imaging; OR: odds ratio; STIR: short-tau-inversion-recovery; T1-post-Gd: T1-post-gadolinium; TNF: tumour necrosis factor; VE: vertebral edge.
Recent evidence suggests that new bone formation may be more likely to occur at the sites of spinal inflammation in patients with AS; two studies reported that more syndesmophytes developed at inflamed vertebral edges than at noninflamed vertebral edges, although the majority of syndesmophytes developed at vertebral edges without inflammation at baseline [ 30, 31].
In summary, in patients treated with anti-TNF-α, new bone formation occurred almost threefold more often in regions with MRI-proven spinal inflammation at BL, and, in the same cohort, most of the newly developed syndesmophytes occurred in VEs without evidence of inflammation at BL.
In patients treated with anti-TNF-α, new bone formation seems to occur almost threefold more often in regions with MRI-proven spinal inflammation at BL. But, similarly, some of the newly developed syndesmophytes may also occur in VEs without evidence of inflammation at BL.
From the perspective of spinal inflammation at baseline (n = 153 vertebral edges), more syndesmophytes developed at vertebral edges with (6.5%) than without (2.1%) inflammation (P = 0.002, odds ratio 3.3, 95% confidence interval 1.5 to 7.4).
Furthermore, as indicated by the analysis of T1-post-Gd sequences, which are more specific but not as sensitive as STIR in the depiction of spinal inflammation in AS [ 9], formation of new syndesmophytes occurred in VEs with persistent inflammation after 2 years (4.3%), whereas this was not the case in edges without persistent inflammation.
The finding that early improvement in IL-6 was associated with improvement in both spinal inflammation and disease activity suggests that IL-6 may play an earlier and more central role in the inflammatory cascade than CRP.
But they also produced more spinal shrinkage.
