ALCOHOL-INDUCED BONE-DISEASE - IMPACT OF ETHANOL ON OSTEOBLAST PROLIFERATION

The habitual consumption of even moderate quantities of alcohol (1 to 2 drinks/day) is clearly linked with reduced bone mass (osteopenia). B iochemical and histological evaluation of patients with alcoholic bone disease reveal a marked impairment in bone formation in the face of r elatively normal bone resorption, Experiments using well-defined osteo blastic model systems indicate that the observed reductions in bone fo rmation result from a direct, antiproliferative effect of ethanol on t he osteoblast itself. As bone remodeling and mineralization are depend ent on osteoblasts, it follows that the deleterious effect of alcohol on these cells would result in slowed bone formation, aberrant remodel ing of skeletal tissue and, ultimately, osteopenia and fractures. The skeletal consequences of alcohol intake during adolescence, when the r apid skeletal growth ultimately responsible for achieving peak bone ma ss is occurring, may be especially harmful. The specific subcellular m echanisms whereby ethanol inhibits cell proliferation are, as yet, unk nown. During the last few years, attention has shifted from nonspecifi c membrane perturbation effects to actions on certain signaling protei ns. Specifically, there is increasing evidence that ethanol may exert significant effects on transmembrane signal transduction processes tha t constitute major branches of cellular control mechanisms. At present , abstinence is the only effective therapy for alcohol-induced bone di sease. An improved understanding of the pathogenesis of alcohol-induce d bone disease may eventually result in alternative therapeutic avenue s for those who are unable to abstain.