The dose-response effects of ethanol on the human fetal osteoblastic cell line

Alcohol is a risk factor for the development of osteoporosis, especially in men. Chronic alcohol abuse decreases bone mass, which contributes to the i ncreased incidence of fractures. To better understand the mechanism of acti on of ethanol on bone metabolism, we have studied the dose-response effects of ethanol on conditionally immortalized human fetal osteoblasts (hFOB) in culture. Ethanol treatment had no significant effects on osteoblast number after 1 day or 7 days. Ethanol treatment did not reduce type I collagen pr otein levels at either time point at any dose but slightly reduced alkaline phosphatase activity after 7 days. The messenger RNA (mRNA) levels for alk aline phosphatase, type I collagen, and osteonectin were unaltered by 24 h of ethanol treatment but a high dose (200 mM) reduced mRNA levels for the t wo bone matrix proteins after 7 days. Ethanol treatment led to dose-depende nt increases in transforming growth factor beta1 (TGF-beta1) mRNA levels an d decreases in TGF-beta2 mRNA levels. The concentration of ethanol in the m edium decreased with time because of evaporation but there was little degra dation caused by metabolism. These results, which show that cultured osteob lasts are less sensitive than osteoblasts in vivo, suggest that the pronoun ced inhibitory effects of ethanol on bone formation are not caused by direc t cell toxicity.