Serum sclerostin in rheumatoid-induced osteoporosis

Abstract

Background: Rheumatoid arthritis (RA) is characterized by presence of localized and generalized osteoporosis. The mechanism of decreased bone mass is complex and multifactorial, a possible mechanism behind increased bone loss in RA is upregulation of sclerostin. The aim of this work was to evaluate serum sclerostin level in RA patients and its relation with bone mineral density (BMD) and disease activity. Results: Serum sclerostin level in RA patients was significantly higher than the controls (p < 0.001). Osteopenia and osteoporosis were more prevalent in RA patients (22.5% and 7.5% respectively) compared to controls (15% and 2.5% respectively) (p = 0.006). Serum sclerostin level was significantly correlated with tender joint count (p = 0.014), swollen joint count (p = 0.036), erythrocytes sedimentation rate (p = 0.010), C reactive protein serum level (p = 0.025), disease activity score (DAS) 28-ESR (p = 0.018), DAS28-CRP (p = 0.005), and radiological modified Sharp erosion score (p = 0.049). The correlation of serum sclerostin level in RA patients with BMD and with T-score in all sites revealed an inverse relationship with p values insignificant. Conclusion: Serum sclerostin is a major player in bone metabolism as a negative regulator of bone growth through inhibition of Wnt signaling that is largely influenced by the disease activity. Controlling the disease activity is a major factor for prevention of local as well as generalized osteoporosis and is essential for the reparative local and systemic bone health.