Work-related physical strain as novel risk factor for the severity of joint inflammation at diagnosis of anti-citrullinated protein antibodies-positive rheumatoid arthritis.

Ton, Dennis A; van Dijk, Bastiaan T; van Steenbergen, Hanna W; van der Helm-van Mil, Annette H M · Rheumatology (Oxford) · 2026

cross_sectional · Level IV

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Abstract

Increased work-related physical strain associates with higher subclinical joint inflammation in the RA at-risk phase of clinically suspect arthralgia and with progression to RA. Based on this, we hypothesized that work-related physical strain is also associated with the severity of joint inflammation at RA diagnosis. We studied this in ACPA-positive and ACPA-negative RA separately, because of differences in aetiopathology. A total of 197 ACPA-positive and 220 ACPA-negative consecutively diagnosed RA patients reported occupation. Physical strain was quantified as exposure using the International Standard Classification of Occupations 1988. Joint inflammation at diagnosis was measured with physical joint examination [swollen joint count of 44 joints (SJC44)] and with MRI of hands and forefeet (evaluating total inflammation, synovitis, tenosynovitis, osteitis and intermetatarsal bursitis). Associations between physical strain and joint inflammation were studied using negative binomial regression, yielding incidence rate ratios (IRR). In ACPA-positive RA at diagnosis, increased physical strain associated with more swollen joints (IRR 1.07, 95% CI 1.02-1.12). This was related to more swollen hand joints (IRR 1.07, 95% CI 1.01-1.13). Increased physical strain also associated with higher joint inflammation scores on MRI (IRR 1.05, 95% CI 1.01-1.09). This was particularly driven by higher osteitis scores (IRR 1.07, 95% CI 1.01-1.13). In ACPA-negative RA at diagnosis, work-related physical strain was not associated with joint inflammation at physical examination or on MRI. Physical strain is a risk factor for more severe joint inflammation at diagnosis in ACPA-positive, but not in ACPA-negative RA. This differential risk factor aggravating joint inflammation adds to the growing evidence of pathophysiological differences between the two RA entities.

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