Demonstration that ethanol inhibits bone matrix synthesis and mineralization in the rat

Abstract

Abstract The effects of ethanol on bone and mineral metabolism were investigated in 3 groups of male rats. The first group received ethanol administered as 36% of caloric content in a liquid diet for 3 weeks. A second group of pair-fed animals was given the same liquid diet, except that sucrose was substituted isocalorically for ethanol. A third group of rats was fed standard laboratory chow. The ethanol-treated rats gained significantly less weight than laboratory chow-fed controls but gained the same weight as the pair-fed animals. Ethanol-treated rats had a modest but significant decrease in mean serum calcium compared to pair-fed controls (10.3 ± 0.1 vs. 10.6 ± 0.1 mg/dl, p < .001). Mean serum phosphate, 25-hydroxyvitamin D, 1,25-dihydroxyvitamin D and immunoreactive parathyroid hormone were the same in the 3 groups. The ethanol-treated animals showed significant decreases in mean tibial length (1.88 ± 0.01 vs. 1.98 ± 0.02 cm, p < .01), mean endosteal bone formation rate (0.0006 ± 0.0001 vs. 0.0026 ± 0.0003 mm3/day, p < .001) and mean periosteal bone formation rate (0.022 ± 0.001 vs. 0.026 ± 0.001 mm3/day, p < .01) compared to the pair-fed controls. The ethanol-treated rats demonstrated significant decreases in mean periosteal mineralization rate (7.5 ± 0.3 vs. 10.3 ± 0.6 μm/day, p < .01) and mean periosteal apposition rate (8.5 ± 0.5 vs. 11.0 ± 0.8 μm/day, p < .05) and a significant increase in mean periosteal osteoid thickness (15.5 ± 1.4 vs. 10.4 ± 0.8 μm, p < .01) compared to pair-fed controls. The laboratory chow-fed controls had higher mean endosteal bone formation rate (0.0040 ± 0.0004 mm3/day, p < .01), mean periosteal bone formation rate (0.034 ± 0.001 mm3/day, p < .01), mean periosteal mineralization rate (12.5 ± 0.7 μm/day, p < .01) and mean periosteal apposition rate (13.0 ± 0.7 μm/day, p < .01) than the pair-fed control animals. The results are interpreted to mean that in the rat ethanol alters mineral homeostasis and diminishes formation of bone matrix and mineralization of osseous tissue. These effects cannot be accounted for by alterations in the metabolism of vitamin D. Further, caloric restriction and inhibition of growth themselves diminish formation of bone matrix and mineralization of osseous tissue.