Abstract

IntroductionJuvenile idiopathic arthritis (JIA) is a disease associated with loss of bone mass, deterioration in bone mass quality and an increased risk of fractures. The objective of this study was to evaluate factors that predict bone mineral density (BMD) alterations in young adult patients with active JIA before and during therapy with tumour necrosis factor α (TNFα) inhibitors.MethodsThirty-one patients (twelve males and nineteen females; mean age =25.1 ± 6.1 years) with active JIA (mean Disease Activity Score in 28 joints (DAS28) =6.36 ± 0.64; mean high-sensitivity C-reactive protein (hsCRP) =18.36 ± 16.95 mg/L) were investigated. The control group consisted of 84 healthy individuals matched by sex and age. BMD, bone turnover markers and serum concentrations of soluble receptor activator of nuclear factor κB ligand, osteoprotegerin, dickkopf Wnt signalling pathway inhibitor 1 (Dkk1) and sclerostin were evaluated.ResultsBaseline BMD values in the lumbar spine, proximal femur, femoral neck and distal radius were significantly lower in patients with JIA compared to healthy control participants. Baseline sclerostin serum concentrations were significantly higher in patients with JIA compared to control participants. After 2 years of treatment with TNFα inhibitors, BMD was significantly increased in the lumbar spine. This increase correlated with a drop in DAS28 score. A statistically significant correlation between hsCRP and Dkk1 was found at baseline, as well as during the 2-year follow-up period. A significant reduction in serum sclerostin after 1 year of therapy was predictive of a drop in DAS28 score observed with a 1-year delay after reduction of serum sclerostin.ConclusionA significant correlation between the sclerostin serum concentration and the number of tender and swollen joints, but not BMD, supports the hypothesis that chondrocytes and cells of the subchondral bone may contribute to circulating sclerostin in JIA.

Highlights

  • Juvenile idiopathic arthritis (JIA) is a disease associated with loss of bone mass, deterioration in bone mass quality and an increased risk of fractures

  • We enrolled 31 patients with JIA (12 males and 19 females) with a mean age of 25.1 ± 6.1 years who had high disease activity determined on the basis of highsensitivity C-reactive protein level, erythrocyte sedimentation rate (ESR) and Disease Activity Score in 28 joints (DAS28)

  • No significant differences in anthropometric parameters were observed between the control participants and patients with JIA

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Summary

Introduction

Juvenile idiopathic arthritis (JIA) is a disease associated with loss of bone mass, deterioration in bone mass quality and an increased risk of fractures. Juvenile idiopathic arthritis (JIA) is a systemic autoimmune inflammatory connective tissue disease with onset occurring before age 16 years. It is associated with a decrease in bone mass, thinning of the cortical bone [1,2], sarcopenia [3,4] and an increased risk of fractures [5]. The loss of bone mass may reflect a disorder of bone modelling and remodelling. This process involves proinflammatory cytokines produced by the

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