Background Subclinical joint inflammation in the phase of arthralgia preceding RA can comprise synovitis, bone marrow edema (BME) and/or tenosynovitis. It is unknown in what time order the different tissues in a joint become inflamed or progress with inflammation. It has been postulated that synovitis is an initial process that is succeeded by bone involvement (“outside-in hypothesis” presuming that synovitis precedes BME and erosions). Alternatively, it is suggested that inflammatory cells in the bone marrow migrate via bone pores to the synovium, promoting synovitis (“inside-out”, then BME precedes synovitis). Thirdly, these processes can occur or progress simultaneously. Serial MRI studies can reveal time-relationships. This longitudinal MRI study on patient-level determined the course of joint inflammation during progression from arthralgia to clinical arthritis.
Objectives To increase the comprehension on the course of MRI-detected subclinical joint inflammation during progression from arthralgia to clinical arthritis, both in ACPA-positive and ACPA-negative arthritis patients.
Methods We longitudinally followed 29 patients that all progressed from Clinically Suspect Arthralgia to clinical arthritis. 1.5T MRI on hand and foot joints was performed at presentation with arthralgia and subsequently at the development of clinical arthritis. MRIs were evaluated for BME, synovitis and tenosynovitis (summed in the total inflammation score) and erosions by three readers (ICCs 0.98, 0.96 and 0.97) that were blind to clinical data and the order in time. Analyses were repeated in arthritis patients that fulfilled the 2010 criteria for rheumatoid arthritis, and in ACPA-positive and ACPA-negative patients separately.
Results At presentation with arthralgia the mean age was 43 years, 72% was female, and 28% was ACPA-positive. Median duration to clinical arthritis was 17 weeks. At the time of arthritis development 65% fulfilled the 2010-criteria. During progression from arthralgia to clinical arthritis the median total inflammation score increased from 4.5 (IQR 2.8–7.8) to 6.0 (IQR 2.0–13.5), p=0.01. The BME score increased over time (p=0.04), as did the synovitis score (p=0.002). The tenosynovitis and erosion scores increased as well, though not statistically significant (p=0.10 and p=0.07 respectively). Analyses within the patients that developed 2010-RA revealed that BME (p=0.047), synovitis (p=0.005) and tenosynovitis (p=0.004) all increased significantly, in contrast to the erosion score. At presentation with arthralgia, BME and synovitis scores were higher in ACPA-positive than in ACPA-negative patients; during progression to clinical arthritis the different types of inflammation increased similarly in ACPA-positive and ACPA-negative patients.
Conclusions During progression from arthralgia to clinically evident rheumatoid arthritis, BME, synovitis as well as tenosynovitis progress simultaneously.
Disclosure of Interest None declared