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Objective To ascertain whether bone mineral density loss during the first year of treatment for early rheumatoid arthritis (RA) as assessed by dual x-ray absorptiometry (DXA) is associated with long-term function, quality of life, and radiographic progression. Methods Early RA patients, prior to commencing disease-modifying antirheumatic drug therapy, underwent evaluation with DXA scans of both hands, femoral neck, and lumbar spine at the time of diagnosis, then at 1 year and final followup at >6 years. Clinical and laboratory data and hands and feet radiographs were obtained at baseline and final followup. Results Sixty-four patients were assessed. At baseline, median disease duration was 6 months, mean 28-joint Disease Activity Score was 5.85, and median Health Assessment Questionnaire score was 1.38. Median followup was 6.4 years (range 5.1-7.2 years). For erosion scores, 86% of patients with hand bone density loss above the smallest detectable change after 1 year progressed versus 55% of those with no hand bone density loss ( P = 0.006). However, baseline radiographs showed a similar strength of association. Eighty-four percent of patients with erosions at baseline had erosion progression versus 57% of those with no baseline erosions ( P = 0.021). Additionally, first-year bone density loss was not associated with function and quality of life status at followup. Conclusion Hand bone loss during the first year of treatment in early RA, as assessed with DXA, was associated with a high likelihood of radiographic progression; however, in the current study this was not superior to baseline radiographs. Furthermore, it was not associated with patient-reported outcomes. [ABSTRACT FROM AUTHOR]

Objective: For patients with rheumatoid arthritis (RA) in remission who are receiving disease-modifying antirheumatic drugs (DMARDs), radiographic progression correlates with imaging-detected synovitis as measured by power Doppler activity. In contrast, patients with disease in remission who are receiving the combination of tumor necrosis factor (TNF) blockade with methotrexate (MTX) (combination treatment) have reduced radiographic damage for the equivalent clinical state. We undertook this study to determine whether the difference in radiographic outcome is a result of more complete suppression of imaging-detected synovitis., Methods: One hundred patients with RA in remission (Disease Activity Score in 28 joints [DAS28] <2.6) for at least 6 months while receiving either combination treatment (n = 50) or DMARDs (n = 50) were matched for clinical variables. Ultrasound of metacarpophalangeal joints 1-5 and the wrist joints was performed. Remission according to imaging results was defined as a score of 0 for both grey scale synovitis and power Doppler activity., Results: In patients receiving combination treatment or DMARDs (median DAS28 1.65 versus 1.78, median disease duration 120 months versus 90 months, and median duration of remission 13 months versus 18 months), the proportion with remission according to imaging results was not significantly different (10% versus 16%, respectively). The combination treatment group had more grey scale synovitis (P < 0.001) but similar power Doppler activity (48% versus 60%, respectively; P = 0.229) in any joint as compared with the DMARD group. Results were not affected by stratification for duration of disease or remission., Conclusion: In RA patients with disease in remission, imaging-detected synovitis persists, with power Doppler activity seen in >or=48% of the patients regardless of therapy. These results suggest that superior radiographic outcomes in patients treated with the combination of TNF blockade and MTX may not be due to complete suppression of imaging-detected synovitis.

Objective: To investigate the role of metacarpophalangeal (MCP) joint anatomic and biomechanical factors in the distribution of synovitis and bone erosion in early rheumatoid arthritis (RA)., Methods: Thirty-three patients with early RA with clinically diagnosed MCP joint disease and 28 healthy controls were examined by magnetic resonance imaging of the second to fifth MCP joints of the dominant hand. T1 and T2 fat-suppressed coronal sequences were obtained to assess erosion, and dynamic contrast-enhanced images were acquired to assess synovitis in all of the RA patients and in 8 of the controls. Erosions were defined as bone defects with sharp margins observed using T1-weighted imaging in 2 planes, with a cortical break seen in at least 1 plane. The location of erosions was recorded. The volume of synovitis surrounding each MCP joint (divided into 8 regions) was calculated by summation of voxels derived from the maximal enhancement parameters. The synovial volumes adjacent to MCP joint collateral ligaments were determined by correcting synovial volumes for the positions of asymmetrically placed flexor tendons., Results: In patients with early RA in whom bone erosions were present, there was a propensity for involvement of the radial side of the second (P < 0.0001), third (P = 0.002), and fourth (P = 0.056) MCP joints, but not the fifth. Fifty-two of the 110 erosions (47.3%) occurred adjacent to the radial collateral ligaments of the second, third, and fourth MCP joints. The volume of synovitis was also greater on the radial side of the second (P < 0.0001) and third (P < 0.001) MCP joints. A predilection for synovitis in all of the MCP joints adjacent to the radial collateral ligaments was evident when the positional effects of the flexor tendon were considered. The position of radial collateral ligaments had an effect on erosion formation that was independent of synovitis. A predilection for radial bone damage was also evident in the controls, although lesions were 5-fold less frequent, were generally smaller, and had well-defined margins., Conclusion: This study shows that there is a predilection for both synovitis and bone erosion formation on the radial side of the MCP joints in early RA, and that joint inflammation appears to drive the inherent tendency for bone damage on the radial side of joints. These findings have implications regarding the pathogenesis of joint damage in RA.