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The effects of alcohol on bone mineral density (BMD) are well-known and well-studied in animal and human populations. Through direct and indirect pathways, prolonged ethanol exposure increases fracture risk by decreasing bone mineral density and promoting osteoporosis. Indirect effects of alcohol abuse occur via growth hormone, sex steroids, and oxidative stress.
Growth hormone is an important regulator of bone growth and remodeling in adults, and it acts via [[insulin plant]] like growth factor I (IGF1) to stimulate osteoblastic differentiation. Chronic alcoholism decreases the levels of IGF1, which suppresses the ability of GH to increase bone mineral density.
Increasing alcohol consumption is linked with decreasing testosterone and serum estradiol levels, which in turn lead to the activation of RANK (a TNF receptor) protein that promote osteoclast formation. Oxidative stress results when ethanol induces NOX expression, resulting in ROS production in osteoblasts which can untimately result in cell senescence. Direct effects of chronic alcoholism are apparent in osteoblasts, osteoclasts and osteocytes. Ethanol suppresses the activity and differentiation of osteoblasts.
