Abstract
The aim of this study was to evaluate the effect of anti-tumor necrosis factor α (anti-TNF-α) therapy in combination with methotrexate on bone remodeling and osteoclastogenesis in female patients with RA. Serum levels of bone turnover markers (i.e., C- and N-terminal propeptides of type I procollagen (PICP and PINP), C- and N-terminal cross-linking telopeptides of type I collagen (CTX-I and NTX-I), and soluble receptor activator of nuclear factor κB ligand (sRANKL) and osteoprotegerin (OPG)) were determined by immunoassay at baseline and 15 months after initiation of treatment. Bone mineral density was measured by dual-energy x-ray absorptiometry. We found a significant decrease in serum PINP levels, a biomarker of bone formation, and higher levels of CTX-I and sRANKL indicative of increased bone resorption in RA patients prior to TNFαI treatment compared to the controls. Anti-TNF-α therapy was effective in improving bone metabolism in RA patients as reflected in a decrease in CTX-I (at least partially due to the RANKL/OPG reduction) and a concomitant increase in PINP levels. The bone metabolism changes were independent of the type of TNFαI used. PINP and CTX-I were found to be useful markers of bone metabolism, which may prove the effectiveness of TNF-α therapy earlier than the bone density assessment.
Highlights
Accepted: 28 June 2021Rheumatoid arthritis (RA) is a chronic systemic autoimmune disease of connective tissue characterized by symmetrical synovitis, eventually leading to bone erosion and cartilage damage
We demonstrated that the effective 15-month anti-inflammatory treatment with TNF-α inhibitors (TNFαI) was associated with improvement in bone metabolism, assessed through serum levels of matrix products released during bone formation (PICP, PINP) and bone resorption (CTX-I, NTX-I)
Our study has shown that the sRANKL/OPG ratio was significantly higher in women with RA before and after 15 months of anti-tumor necrosis factor α (TNF-α) therapy when compared to healthy subjects
Summary
Rheumatoid arthritis (RA) is a chronic systemic autoimmune disease of connective tissue characterized by symmetrical synovitis, eventually leading to bone erosion and cartilage damage. It affects approximately 0.5–1.5% of the world’s population and is about. In the course of the disease, there are numerous extra-articular manifestations of the organs, which are the major causes of rapidly progressing disability, reduced quality of life, and increased mortality [1,2,3]. RA patients have more skeletal damage and a higher risk of fractures compared to the general population. High disease activity (persistent inflammation), long-term glucocorticoid therapy (>3 months), and the physical disability and immobility are the main factors that increase the risk of bone loss in patients with
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