Distal interphalangeal (DIP) joints are commonly considered to be unaffected by rheumatoid arthritis (RA). Despite synovitis and bone marrow edema being associated with radiographic progression in hand osteoarthritis (OA) and hand RA, radiographic courses differ substantially. This study was undertaken to analyze incidence and progression of radiographically evident DIP joint OA in RA patients, in relation to RA activity and patient characteristics.
In sequential radiographs of 1,988 RA patients in the Swiss Clinical Quality Management in Rheumatic Diseases registry, we evaluated and scored 15,904 DIP joints. Scoring was based on the presence of central erosions and subchondral sclerosis and on the severity of osteophytes and joint space narrowing, according to the modified Kellgren/Lawrence (K/L) grade. The presence of DIP joint OA was defined as ≥1 joint with a K/L grade of ≥2, and progression was defined as an increase in a summed K/L grade. Adjusted odds ratios (ORs) and 95% confidence intervals (95% CIs) were calculated.
The median follow-up time was 4.5 years (interquartile range 3.1-7.0), and the mean ± SD age was 56.1 ± 11.1 years. DIP joint OA was present in 60% of patients at baseline. Higher mean age (OR 1.09 [95% CI 1.08-1.10]), female sex (OR 1.37 [95% CI 1.08-1.74]), and higher mean body mass index (OR 1.03 [95% CI 1.00-1.06]) were associated with the presence of DIP joint OA, but neither the presence of anti-citrullinated protein antibodies (ACPAs) (OR 0.72 [95% CI 0.50-1.03]) nor the presence of rheumatoid factor (OR 1.01 [95% CI 0.74-1.38]) were associated with it. Disease Activity Score using the erythrocyte sedimentation rate and metacarpophalangeal (MCP) joint erosions were not associated with DIP joint OA progression. RA disease duration had no relevant effect size associated with DIP joint OA progression (OR 0.97 [95% CI 0.96-0.99]).
Known risk factors for DIP joint OA were replicated in patients with RA. The observation that RA activity, the presence of ACPA, and MCP joint erosions were not associated with the prevalence or progression of DIP joint OA indicates that there are distinct roles of inflammation in the pathogenesis of RA and DIP joint OA.