Background/Purpose:

Anti-citrullinated protein antibodies (ACPA) are one of the most important serological markers for rheumatoid arthritis (RA) and have been suggested to play a pathophysiologic role in osteopenia, a common RA comorbidity, by directly binding to osteoclasts. However, the effect of ACPA on systemic bone mineral density and in particular their effect on changes in bone mineral density over time is currently unknown. Therefore, we determined whether ACPA associate with changes in bone mineral density over time in patients with rheumatoid arthritis.

Methods:

Yearly dual X-ray absorptiometry scores were performed during 5 years of follow-up in 412 patients with recent-onset RA participating in the IMPROVED study¹, a clinical trial in which patients were treated according to a remission-(disease activity score<1.6) steered strategy. The effect of the presence of ACPA on 1) Z-scores of lumbar spine and hip over time, and 2) prevalence of osteopenia/osteoporosis (defined as a T-score ≤-1) over time was analysed using generalized estimating equations. Analyses were adjusted for age, gender, BMI, and symptom duration (determined at baseline), as well as smoking status, disease activity, prednisone intake, bisphosphonate use, calcium intake, and serum 25-OH vitamin D levels (determined longitudinally).

Results:

ACPA-positive patients had a significantly lower lumbar spine (p=0.04) and hip (p=0.01) Z-score at baseline. There was no difference in prevalence of osteoporosis/osteopenia at baseline between ACPA-positive and ACPA-negative patients (OR (95% CI) 1.02 (0.55 to 1.19)). We hypothesised that ACPA-positive patients would have more bone loss over time compared to ACPA-negative patients. However, ACPA positivity did not associate with a stronger decline in Z-score over time at lumbar (p=0.43) or femoral sites (p=0.66). Additionally, no effect of anti-citrullinated protein antibody positivity was found on the development of osteoporosis/osteopenia over time (p=0.23).

Conclusion:

ACPA-positive patients have a significantly lower bone mineral density at baseline compared to ACPA-negative patients. Surprisingly, in this cohort of patients treated according to a tight control strategy, ACPA do not associate with a decrease in bone mineral density over time. These results indicate that in the absence of inflammation/disease activity, ACPA do not contribute to increased bone loss after disease onset.

References

¹ Wevers-de Boer et al. Ann Rheum Dis. 2012 Sep;71(9):1472-7.

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