Abstract
To prevent spinal progression in ankylosing spondylitis, initiating TNF-inhibitor treatment as early as possible is suggested. However, the outcomes are inconsistent in previous clinical studies. Here, we investigated the effect of TNF inhibition alone on spinal progression when used during arthritis development in a murine model. We injected 8-week-old SKG mice with curdlan (curdlan group). We injected adalimumab at 3 and 9 weeks after the first curdlan injection (ADA group). The clinical scores of peripheral arthritis decreased in the ADA group at 3 weeks after first adalimumab injection. Using positron emission tomography–magnetic resonance imaging and histologic examination, spinal inflammation was observed in the curdlan group, and was significantly deceased in the ADA group. However, spinal osteoblast activities by imaging using OsteoSense 680 EX and bone metabolism-related cytokines such as receptor activator of nuclear factor-kappa B ligand, osteoprotegerin, Dickkopf-1, and sclerostin levels except IL-17A level were not different between the two groups. We conclude that treating TNF inhibitor alone reduced peripheral arthritis score and spinal inflammation in curdlan-injected SKG mice but did not decrease the spinal osteoblast activity, suggesting little effect on spinal ankylosis.
Highlights
To prevent spinal progression in ankylosing spondylitis, initiating TNF-inhibitor treatment as early as possible is suggested
Therapeutic effect on peripheral arthritis in adalimumab-treated mice was sustained for 16 weeks after injecting adalimumab 9 weeks after first injecting curdlan, while the clinical scores of arthritis remained constant in mice without adalimumab treatment
Previous clinical studies[5,6,7,8] have shown that TNF inhibition does not prevent spinal radiographic progression in patients with Ankylosing spondylitis (AS), while TNF inhibitors decelerated the progression of structural damages especially in early AS patients without syndesmophyte[17,18,19,20,21]
Summary
To prevent spinal progression in ankylosing spondylitis, initiating TNF-inhibitor treatment as early as possible is suggested. We conclude that treating TNF inhibitor alone reduced peripheral arthritis score and spinal inflammation in curdlan-injected SKG mice but did not decrease the spinal osteoblast activity, suggesting little effect on spinal ankylosis. Excessive bone formation is an important factor in disease prognosis because it can impair the mobility of the spine This disturbs daily activity and reduces the quality of life of patients[2]. Previous studies have reported inconsistent findings regarding the effect of TNF-α inhibitor treatment on spinal radiographic progression in patients with AS5–9, whereas TNF-α inhibitors have been effective in preventing structural damage as well as reducing disease activity in psoriatic arthritis and rheumatoid arthritis (RA), in which bone erosion dominates bone formation[10,11]. The effects of TNF inhibitors alone were difficult to verify clearly because standard treatments including nonsteroidal anti-inflammatory drugs were allowed in the clinical studies
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