ETHANOL INDUCED ABNORMALITIES IN BONE-FORMATION, TURNOVER, MECHANICAL-PROPERTIES AND MINERALIZATION IN YOUNG-ADULT RATS

This manuscript reviews evidence in humans and animals that chronic heavy consumption of alcohol (ethanol) results in alteration of bone and mineral homeostasis, including hypocalcemia and hypomagnesemia, disturbed vitamin D metabolism, decreased bone formation, increased bone resorption, and osteopenia. Many of the changes in bone and mineral metabolism seen in the rat model of alcoholism are similar to changes seen in alcoholics. Cumulatively, these changes result in degradation of mechanical properties of the skeleton (humans and animals) and an enhanced risk for atraumatic bone fractures (human). New data are presented to support the hypothesis that ethanol acts directly on bone cells to inhibit bone formation, increase bone resorption and degrade bone mechanical properties. However, there is also evidence to suggest that reduced caloric intake is a major contributing factor to the skeletal changes observed in ethanol-treated growing rats. This latter observation is consistent with previous observations showing that some of the skeletal changes associated with short-term alcohol treatment resolve during long-term exposure.