Development of clinically apparent synovitis: A longitudinal study at the joint level during progression to inflammatory arthritis
Introduction Subclinical inflammation, detected by MRI, in patients with arthralgia is predictive for development of inflammatory arthritis (IA). However, within patients that develop IA, the course of inflammation at the joint level during this transition is unknown. This longitudinal study assessed progression of inflammation at the joint level. Methods 350 joints (unilateral metacarpophalangeals (MCPs), wrist, metatarsophalangeal (MTP) joints) of 35 patients presenting with clinically suspect arthralgia (CSA) that progressed to IA were studied at presentation with CSA and subsequently when clinical synovitis was first identified at joint examination (median time interval 17 weeks). At both time points, subclinical inflammation (bone marrow oedema, synovitis, tenosynovitis) was evaluated with MRI and joint examination was performed. Results At presentation with CSA, 71 joints showed subclinical inflammation. During progression to IA, 20% of these joints had resolution of inflammation, 60% had persistent inflammation and 20% progressed to clinical synovitis. Of all joints that had developed clinical synovitis (n = 45), no prior subclinical inflammation was detected in 69%. Similar results were observed for anticitrullinated protein antibodies (ACPA)-positive and ACPA-negative patients. Conclusions This longitudinal study demonstrated moderate correlations between joints with subclinical inflammation and joints that developed clinical synovitis. These data imply that IA development is a more systemic rather than a locally outgrowing process.
|Keywords||inflammation, mri, outcome measures, rheumatoid arthritis|
|Persistent URL||dx.doi.org/10.1136/rmdopen-2018-000748, hdl.handle.net/1765/110330|
Ten Brinck, R.M. (Robin M), Van Steenbergen, H.W. (Hanna W), & van der Helm-van Mil, A.H.M. (2018). Development of clinically apparent synovitis: A longitudinal study at the joint level during progression to inflammatory arthritis. RMD Open, 4(2). doi:10.1136/rmdopen-2018-000748