Association of BMI with radiographic incidence and progression of distal interphalangeal joint osteoarthritis in rheumatoid arthritis patients.
Zübeyir Salis, Claire Daien, Leo Caratsch, Christian Lechtenboemer, Diego Kyburz, Ulrich A Walker, Jeroen Geurts, Thomas Hügle
Abstract
Open AccessWhile obesity is associated with increased risk of osteoarthritis (OA) and rheumatoid arthritis (RA), it paradoxically correlates with less structural joint damage in RA. Its impact on distal interphalangeal (DIP) joint OA in RA remains unclear. This study investigated the association between baseline body mass index (BMI) and DIP joint OA incidence and progression in RA patients. We analyzed RA patients with baseline BMI ≥ 18.5 kg/m2 from the Swiss Clinical Quality Management in Rheumatic Diseases registry. DIP joint radiographs were evaluated using the modified Kellgren/Lawrence grading system. The incidence cohort (1031 patients, median follow-up 5.0 years) included those without baseline DIP OA and the progression cohort (1481 patients, median follow-up 4.9 years) included those with DIP OA at baseline. Multivariable logistic regression assessed the association of BMI with incidence or progression, as well as with joint space narrowing (JSN), osteophytes worsening, subchondral sclerosis, and central erosions. Mean baseline BMI was 25.1 kg/m2 (incidence cohort) and 26.0 kg/m2 (progression cohort). At follow-up, 24.3% of patients developed DIP joint OA and 67.9% showed progression. BMI was not significantly associated with incidence (adjusted odds ratio [OR] 1.02, 95% confidence interval [CI] 0.98-1.06) or progression (adjusted OR 1.01, 95% CI 0.98-1.04). BMI was similarly unrelated to JSN, osteophyte worsening, subchondral sclerosis, or central erosions. BMI was not associated with DIP joint OA incidence or progression in RA patients. These findings suggest that DIP joint OA in RA may follow a distinct pathophysiological pathway, independent of BMI-related systemic mechanisms.