Sleep disruptions and bone health: what do we know so far?

Abstract

This review briefly summarizes the growing body of literature addressing the skeletal consequences of sleep and circadian disruption. The most recent data in the field suggest that the diurnal variation in bone turnover markers are because of endogenous circadian rhythmicity linked to clock genes in all bone cells; in a small human intervention study, cumulative sleep restriction with concurrent circadian disruption negatively alter bone turnover markers in a way that could explain the lower BMD and increased fracture risk identified in some prior night shift work studies; abnormal sleep duration and obstructive sleep apnea are associated with low BMD and increased fracture risk in some but not all studies. Normal physiology and some animal and human intervention studies suggest that sleep and circadian disruptions, such as night shift work, abnormal sleep durations and obstructive sleep apnea are detrimental to skeletal health. However, additional research in this area is needed to determine which sleep/circadian disturbances are most detrimental to skeletal health, the reversibility of such impairments, and underlying mechanisms.