Objective: Osteoprotegerin (OPG) is considered an important biomarker in cardiovascular (CV) disease. CV disease is the most common cause of mortality in patients with rheumatoid arthritis (RA), a consequence of accelerated atherosclerosis. The present study aimed to evaluate the relationship of serum OPG levels to arterial stiffness, carotid intima-media thickness (CIMT), and clinical and laboratory indices in RA patients.
Patients And Methods: Included in the study were 68 RA patients with no history or signs of CV disease and 48 healthy subjects Disease activity was assessed by the 28-joint disease activity score (DAS28) in RA patients. Serum OPG level was measured using enzyme-linked immunosorbent assay (ELISA). Carotid femoral pulse wave velocity (PWV) was measured as an index of arterial stiffness and CIMT was evaluated by carotid ultrasonography.
Results: The mean serum OPG level was significantly higher in RA patients than controls (p < 0.001). Mean PWV and CIMT were also significantly increased in RA patients compared to controls (both p < 0.001). In RA patients, serum OPG level was significantly correlated with PWV and CIMT, as well as rheumatoid factor (RF) and anti-cyclic citrullinated peptide (anti-CCP) antibody; but not with DAS28, high-sensitivity C-reactive protein (hsCRP), or erythrocyte sedimentation rate.
Conclusion: Serum OPG levels were increased and correlated with CIMT and PWV in RA patients. In addition to PWV and CIMT, OPG may be a useful biomarker for CV risk management in RA patients.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1007/s00393-015-1675-1 | DOI Listing |
J Bone Miner Res
January 2025
Cancer Ecosystems Program, Garvan Institute of Medical Research, Sydney, NSW, Australia.
Rebound bone loss following denosumab discontinuation is an important barrier in the effective long-term treatment of skeletal disorders. This is driven by increased osteoclastic bone resorption following the offset of RANKL inhibition, and sequential osteoclast-directed therapy has been utilised to mitigate this. However, current sequential treatment strategies intervene following the offset of RANKL inhibition and this approach fails to consistently prevent bone loss.
View Article and Find Full Text PDFJ Orofac Orthop
January 2025
Guangxi Key Laboratory of Oral and Maxillofacial Rehabilitation and Reconstruction & Department of Orthodontics, College and Hospital of Stomatology, Guangxi Medical University, 10 Shuangyong Road, 530021, Nanning, Guangxi, China.
Purpose: Interleukin (IL)-17 expression in the periodontal ligament is associated with orthodontically induced inflammatory root resorption (OIIRR). Seeking a convenient, rapid, and non-invasive IL-17 detection approach could help predict OIIRR. In this study, we assessed the potential of the IL-17 level in gingival crevicular fluid (GCF) to be an indicator of OIIRR.
View Article and Find Full Text PDFArthritis Res Ther
January 2025
Department of Rheumatology, the Fifth Affiliated Hospital of Sun Yat-sen University, 52 Meihua East Road, Zhuhai, People's Republic of China.
Background: Currently, the pathophysiology of new bone formation in radiographic axial spondyloarthritis (r-axSpA) remains unclear. Cellular elements and their secreted bone turnover markers might be one of the underlying mechanisms that drive the new bone formation. Our study aimed to investigate the role of bone turnover markers in r-axSpA patients with fatty lesions.
View Article and Find Full Text PDFRev Invest Clin
January 2025
Discipline of Clinical Pharmacy, School of Pharmaceutical Sciences, University Sains Malaysia, Penang, Malaysia.
Background: Limited information exists regarding the pathophysiological interactions between osteoporosis and chronic obstructive pulmonary disease (COPD). Objective: To study the association of Osteoprotegerin (OPG) and receptor activator of nuclear factor kappa-Β ligand (RANKL) in male COPD patients. Methods: An observational clinical study was conducted at Penang General Hospital in Malaysia.
View Article and Find Full Text PDFAlthough the toxic effect of Sedentary behavior (SED) on bone health has been demonstrated in the previous study, the underlying mechanisms of SED, or break SED to bone health remain unclear. In this study, we aim to investigate the effects of sedentary behavior (SED) on bone health, as well as the potential favor effects of moderate to vigorous physical activity (MVPA) and periodic interruptions of SED. To simulate SED, we used small Plexiglas cages (20.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!