Effect of Obstructive Sleep Apnea on Bone Mineral Density.

Abstract

Objective: Various studies have suggested that obstructive sleep apnea (OSA) affects bone metabolism. One of the most significant factors is hypoxia which induces certain transcription factors that stimulate bone osteoclastic activity. It also induces respiratory acidosis and oxidative stress which enhances bone resorption. Leptin and melatonin secretions are regulated by the circadian system which is affected due to sleep fragmentation in OSA. Other comorbidities associated with OSA such as vitamin D deficiency, hypogonadism, obesity, and insulin resistance are indirect mechanisms that affect bone mineral density (BMD).

Material and methods: This is a prospective case-control study. All patients having symptoms of sleep-related breathing disorder (excluding post-menopausal females or patients with known case of osteoporosis or any other clinical illness which is a direct cause of osteoporosis) attending the Sleep Out Patient Department (OPD) were screened for OSA as per the STOPBANG questionnaire scoring system. Participants having score >2 constituted the final study population and were subjected to the polysomnography test. Participants with an apnea-hypopnea index (AHI) > 5 in polysomnography were considered as cases and those with AHI <5 were considered as controls. Both the groups were then subjected for dual-energy X-ray absorptiometry (DEXA) scan and vitamin D to establish a comparison.

Results: Out of 93 participants, 59 were taken as cases (OSA group), whose mean age was 48.02 (±8.435) years, mean body mass index (BMI) was 33.73 (±7.48) kg/m2, mean neck circumference was 37.8 cm (±5.08) as compared with the age, sex, and BMI matched non-OSA control group (n = 34). Mean BMD in the case group was found to be significantly on the lower side as compared with the control group (-2.02 ± 1.09 vs. -1.03 ± 0.97) (P < .001) when compared in Z score, while (0.885 ± 0.535 vs. 0.933 ± 0.616) when compared in g/cm2 (P < .001), with negative correlation between AHI and BMD (r = -0.507, P < .001). Mean vitamin D level in the case group was at a lower level as compared to the control group (21.02 ± 7.27 vs. 24.48 ± 6.92, P < .05), with negative correlation between AHI and serum vitamin D level (P < .001, r = -0.286).

Conclusion: OSA affects BMD by various pathophysiologic mechanisms. The AHI is inversely correlated with BMD; that is, with increasing severity of OSA, there is a decrease in BMD.