Abstract
Since the previous studies showed that anti-citrullinated protein antibodies (ACPA) can induce osteoclasts differentiation and activation, even before arthritis onset, the aim of our study was to determine whether ACPA-positivity is associated with lower bone mineral density (BMD) at baseline visit of a register of early arthritis (EA) patients. The study population comprised 578 patients (80% females) from our EA clinic with a median disease duration, 5.1 months (p25–p75: 6–8); median age, 53.6 years (41.9–66.1), 38% ACPA-positive, and 55% fulfilling 2010 criteria for rheumatoid arthritis. BMD was measured using dual X-ray absorptiometry at lumbar spine, hip, and metacarpophalangeal (MCP) joints of the non-dominant hand to evaluate both systemic and juxta-articular bone mass. ACPA titers were determined through enzyme immunoassay. The effect of ACPA on BMD was analyzed using multivariable analysis based on generalized linear models adjusted for various confounders. ACPA-positive patients showed lower bone mass at lumbar spine and hip, but no differences were observed at MCP joints compared to ACPA-negative patients. However, ACPA-positive patients displayed higher disease activity and disability than ACPA-negative patients. After adjustment for gender, age, body mass index, and other bone-related variables, the presence of ACPA remained significantly associated with lower BMD at the lumbar spine, femoral neck, and hip but not at MCP joints. Disease activity was not associated with baseline bone mass. Our data reinforce the previous preclinical findings suggesting that the systemic bone loss detected at the initial phases of early ACPA-positive arthritis is independent of inflammatory status and, therefore, could be mediated by ACPA.
Highlights
Electronic supplementary material The online version of this article contains supplementary material, which is available to authorized users.Rheumatoid arthritis (RA) is a chronic inflammatory disease characterized by persistent inflammation of the synovial membrane and joint destruction, bone loss, and systemic complications
Methods calculated with the ESR [11] and the Hospital Universitario de La Princesa Index (HUPI) [12], that is an index for the assessment of disease activity in chronic polyarthritis that includes the same domains as DAS28 and SDAI but corrected by gender when considering tender joint count and erythrosedimentation rate (ESR)
Bugatti et al have published a study performed in a clinical setting demonstrating that the presence of anticitrullinated protein antibodies (ACPA) and high rheumatoid factor (RF) levels is associated with lower systemic bone mineral density (BMD), but not at juxta-articular bone level, in an early untreated RA population [17]
Summary
Electronic supplementary material The online version of this article (doi:10.1007/s00296-017-3674-9) contains supplementary material, which is available to authorized users. Rheumatoid arthritis (RA) is a chronic inflammatory disease characterized by persistent inflammation of the synovial membrane and joint destruction, bone loss, and systemic complications. Skeletal changes in RA include juxta-articular bone erosions, periarticular bone loss, and systemic osteoporosis [1, 2]. Until a few years ago, rheumatologists assumed that osteoporosis in RA was mainly derived from chronic inflammation, use of glucocorticoids or some disease-modifying anti-rheumatic drugs (DMARDs), and immobilization. In the light of current knowledge, bone destruction in arthritis seems to be caused by two main mechanisms: inflammation and autoimmunity [2, 3]. Pro-inflammatory cytokines such as TNF-α, IL-1, IL-6, and IL-8 enhance the proliferation and differentiation of the
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