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There is evidence that ethanol inhibits osteoblast function and that chronic ethanol consumption induces systemic bone loss and increases the risk of fracture in humans. The purpose of the present study was to determine whether chronic ethanol consumption also compromises the healing of injured bone. Male Sprague-Dawley rats, 8-10 weeks old, were placed into four feeding groups: group A received ethanol (36% of calories) as part of a liquid diet; group B was pair-fed to group A and received an isocaloric control diet containing maltodextrin; group C was fed the AIN-93M standard semi-purified liquid diet ad libitum; group D was fed the same ethanol diet as group A before bone injury, but after surgery (see below) these rats were given isocaloric control diet ad libitum. After 6 weeks on their respective diets, a bone repair model was surgically created at the midshaft in both fibulae of each rat. Seven weeks after injury the animals were euthanized and bone healing was evaluated by determining rigidity of the fibula by three-point bending, flexural modulus of the repair tissue and mineral content of the repair tissue. Rigidity of fibula in ethanol-fed rats and their pair-fed controls (groups A and B) were respectively 48 and 47% lower than in group C. Flexural modulus of the repair tissue in ethanol-fed rats had a 55% (P = 0.046) deficiency compared with their pair-fed controls. The mineral contents in groups A and B were respectively 16 and 13% lower than in group C. There were no significant differences in the results between groups C and D. Thus, the outcome of bone repair in ethanol-fed rats was deficient compared with rats receiving a standard maintenance diet. The repair tissue in ethanol-fed rats was mechanically inferior to that in pair-fed controls. This deficiency could not be attributed to the reduced food consumption of these animals. On the other hand, the restoration of normal bone healing in group D cannot be attributed solely to the cessation of ethanol feeding after bone injury because of the increased food consumption during this period.

The accuracy and consistency of the delivery of ethanol to cultured cells is important to determine effects on morphologic, biochemical and physiologic alterations. Open and closed chamber systems were evaluated to determine cytotoxic vs sublethal, potentially teratogenic effects on neonatal rat cardiac myocytes. The open system employed a variety of cell culture vessels. Cardiac cells were exposed directly to ethanol in the growth media at concentrations of 5-50 mM in Petri dishes, multiwell slides and multiwell chambers. Ethanol concentrations in the media in these open vessels decreased over 60% in a 24 hr incubation period. A closed system consisted of tightly sealed plastic containers in which the same vessels were used. The vessels were placed on a platform over a bath of ethanol-water. Cells were acclimated for 24 hr with ethanol in the bath at 200% of the final desired media concentration. Ethanol gradually diffused into the media to reach peak levels of 5, 10, 25 or 50 mM at 24 hr. After the 24 hr period, ethanol was added to both the media and bath at the desired concentration. Cells exposed gradually to ethanol in the closed chambers remained viable, but showed slower division and growth. A period of gradual acclimation is required to induce sublethal cellular effects rather than lethal effects. The diversity of cell systems and manipulations of cultures to study the potential teratogenic effects of ethanol are improved using such a closed chamber system.

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