Imbalance of osteoprotegerin/receptor activator of nuclear factor-κB ligand and oxidative stress in patients with obstructive sleep apnea-hypopnea syndrome

Abstract

Abstract. Background:. Obstructive sleep apnea-hypopnea syndrome (OSAHS) is associated with a higher prevalence of osteoporosis. However, the underlying mechanisms linking OSAHS with bone loss are still unclear. The aim of this study was to investigate the changes of receptor activator of nuclear factor-κB ligand (RANKL, an osteoclastogenesis-promoting factor) and osteoprotegerin (OPG, the decoy receptor for RANKL), oxidative stress and bone metabolism markers in OSAHS, in order to understand the potential mechanisms underlying bone loss in OSAHS patients. Methods:. Forty-eight male patients with OSAHS, confirmed by polysomnography (PSG) study, were enrolled. Twenty male subjects who were confirmed as not having OSAHS served as the controls. The subjects’ bone mineral density (BMD) was assessed in lumbar spine and femoral neck using dual-energy X-ray absorptiometry (DXA). Blood samples were collected from all subjects for measurement of RANKL, OPG, the bone formation marker bone-specific alkaline phosphatase (BAP), the bone resorption marker tartrate-resistant acid phosphatase 5b (TRAP-5b), and total antioxidant capacity (TAOC). Results:. The BMD and the T-score of the femoral neck and the lumbar spine were significantly lower in OSAHS patients as compared to the control group (P 0.05). The serum level of OPG and the OPG/RANKL ratio were lower in the OSAHS group compared to the control group (both P < 0.05). TAOC level was also decreased significantly in the OSAHS group (P < 0.05). Correlation analysis showed that the TAOC level was positively correlated with BAP in the OSAHS group (r = 0.248, P = 0.04), but there were no correlations between TAOC and the BMD or the T-scores. The correlations between the level of OPG (or the OPG/RANKL ratio) and BMD or TAOC did not reach significance. Conclusion:. In OSAHS patients, lower levels of TAOC were associated with decreased bone formation, suggesting a role of oxidative stress in bone loss, while the role of OPG/RANKL imbalance in bone metabolism in OSAHS needs further evaluation.