Chronic ethanol consumption does not reduce true bone density in male Wistar rats.

Osteoporosis is characterized by reduced bone mineral density (BMD) and increased bone fragility, which may be modified by lifestyle behaviors. In observational studies, chronic moderate ethanol consumption is associated with higher BMD, but results are inconsistent and underlying mechanisms are unknown. To understand the influence of chronic ethanol consumption on true bone density (Archimedes principal), bone mechanical properties (Young's Modulus of bend), and osteogenic gene expression, 12-month-old male Wistar rats were randomly assigned to a control group or ethanol intervention (20% ethanol in drinking water on alternate days) group for 13 weeks and tibiae and femurs were collected. Blood was collected to assess alcohol content and antioxidant enzyme activities. We hypothesized that chronic ethanol consumption would increase true bone density and mechanical properties and increase osteoblastic gene expression and serum antioxidant enzyme activity. Ethanol consumption did not influence femoral or tibial true bone density but did result in lower tibial Young's modulus of bend (p = 0.0002). However, there was no influence of ethanol on other measures of mechanical properties. Femoral pro-osteoclastic gene expression of Dkk1 was lower (p = 0.0006) and pro-osteoblastic gene expression of Ctnnb1 was higher (p = 0.02) with ethanol consumption. We observed no differences in circulating antioxidant activities between groups, other than a tendency for greater (p = 0.08) glutathione peroxidase in the ethanol group. Results showed chronic ethanol consumption did not influence true bone density, only modestly reduced tibial mechanical properties (lower Young's modulus of bend), and moderately impacted expression of genes within the femur known to regulate both osteoblast and osteoclast activities.