Background Recently it has been described that anti citrullinated protein antibodies (ACPA) can induce differentation and activation of osteoclasts even before arthritis onset (1,2).
Objectives The aim of this study was to analyze the effect of ACPA on periarticular and systemic bone mineral density (BMD) in a large population from an early arthritis (EA) clinic.
Methods We analyzed data from patients belonging to PEARL (Princesa Early Arthritis Longitudinal) study. Demographic, clinical, laboratory and treatment data were collected per protocol. BMD was meaasured at the first visit of the following up through dual X-ray absorptiometry (DXA) (Hologic ©QDR-4500) at lumbar spine (LS), hip, forearm and hand. ACPAs were determined by ELISA. Multivariable analysis was performed adjusting for coufinding variables such as sex, age and body mass index (BMI) was performed using generalized linear models with the command glm of STATA 12.
Results We analyzed data from 474 patients (39.6% ACPA positive, 80% women). 56.1% of patients fulfilled the Rheumatoid Arthritis (RA) 2010 criteria at start of follow up. The other patients were undifferentiated arthritis, spondyloarthritis, connective tissue disease and other diagnostics. Median age at disease onset was 54 years [43 - 66 (p25 - p50)]. Symptom duration until BMD measurement was 5 months [6-8 (p25-p50)]. Median DAS28 in patients who fulfilled RA criteria was 4.98 [4-6 (p25-p50)] and 3.6 [3-4 (p25-p50)] in remaining patients. Likewise, HAQ score was higher in RA patients (median 0.750 vs 1.125 in non-RA group). However, neither of these two variables was significantly associated with baseline bone mass. We found ACPA positive patients had lower BMD in LS (beta coefficient -0.025; p=0.051), femoral neck (coef. beta: -0.02; p=0.053) and total hip (coef. beta. - 0.017; p=0.1). This association was not observed in the nondominant hand or forearm.
Conclusions Our data provide further support to Schett at al suggesting that ACPA may induce systemic osteoporosis even at very early stages of the disease in absence of a long term inflammatory state. Subsequently, bone loss mass would extend to more localized areas in relation to the persistence of inflammatory activity.
#S. Castañeda and I. González-Άlvaro share the direction of this work.
George Schett et al. J Clin Invest. 2012;122(5):1791-1802. doi: 10.1172/JCI60975.
George Schett et al. Ann Rheum Dis 2014 73: 854-860 originally published online March 21, 2013 doi: 10.1136/annrheumdis-2012-202958
Disclosure of Interest I. Llorente Cubas: None declared, L. Merino: None declared, A. M. Ortiz: None declared, E. Escolano: None declared, E. García Lorenzo: None declared, A. García-Vadillo: None declared, T. Velasco: None declared, E. Vicente: None declared, R. García de Vicuña: None declared, I. González-Άlvaro# Grant/research support from: Red de Inflamaciόn y Enfermedades Reumáticas (RIER, RD 12/0009/0017), S. Castañeda# Grant/research support from: ISCIII (FIS P112/01578); Pfizer (Spain)
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