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Biologics Treatment Limits Disease Activity and Bone Metabolism in Patients
with Rheumatoid Arthritis
Introduction: Generalized bone loss in rheumatoid arthritis (RA) is multi-factorial, and can be divided into erosions of the joint and osteoporosis. Biomarkers of bone remodeling provide a dynamic view of the remodeling process and they contribute to a better understanding of bone physiology and the pathogenesis of metabolic bone diseases. To examine whether treatment with biologics agents reduces of disease activity and changes the markers of bone metabolism, including osteocalcin (OC), N-terminal propeptide of type I procollagen (PINP), cross-linked Cterminal telopeptide of type I collagen (CTX), receptor activator of the NF-κB ligand (RANKL) and osteoprotegerin (OPG). Materials and methods: 125 patients with active RA, who were treated with DMARDs (44 patients) and biologics agents including 49 patients on Etanercept, 16 patients on Adalibumab/Golibumab/Infliksimab and 16 patients on Rytuksymab/Tocilizumab were included in this study. Clinical and laboratory parameters of disease activity were measured at baseline and after 90 days of treatment and an index of disease activity (DAS-28) calculated. Changes in bone markers levels were measured by ELISA before start the treatment and after. Results: As a result of treatment of the active RA with biologics agents, after 90 days, parameters such as DAS-28, VAS, number of swollen/tender joints, CRP and ERS decreased in the biologics group compared to the DMARDs group. The sRANKL/OPG ratio, and carboxylated (GLA)–OC and CTX levels were higher in RA patients compared to healthy subjects (p<0.001, p=0.02 and p=0.002, respectively). DMARDs therapy decreased the CTX level and sRANKL/OPG ratio in RA patients (p=0.006 and p=0.06, respectively). OPG was increased, whereas the sRANKL/OPG ratio was decreased in RA patients after 90 days biologics treatment. Conclusion: The biologics therapy has protective effect against clinical disease activity as well as joint damage compared to conventional DMARDs in patients with RA.