The urinary excretion of the collagen degradation markers pyridinoline and deoxypyridinoline in an experimental rat model of alcoholic bone disease.

(1) The effect of chronic (6 weeks) ethanol feeding on whole-body skeletal tissue in the rat was studied by analysis of the urinary pyridinium crosslinks of collagen, pyridinoline (PYD; found predominantly in the collagens of cartilage and bone and to a lesser extent in other tissues) and deoxypyridinoline (DPD; found only in type I collagen of bone and dentine). (2) The urinary concentrations of total, free and conjugated PYD were unaltered by ethanol feeding. In contrast, there were significant reductions in total and conjugated DPD concentrations. The reduction in the concentration of free DPD did not achieve statistical significance. The urinary PYD/DPD molar ratios, of total and conjugated forms, were increased. (3) Alcohol feeding caused the total 24 hr urinary PYD excretion to fall slightly, by 15%. There were no statistically significant effects on excretion of free and conjugated forms of PYD, nor on the free/total, free/conjugated and conjugated/total molar ratios. In contrast, the 24 hr urinary excretion of total, free and conjugated DPD was significantly reduced by 25-55%. Furthermore, the free/total and free/conjugated molar ratios were significantly increased by 40% and 80%, respectively, and the conjugated/total molar ratio was significantly reduced by 16%. (4) Data from the analysis of plasma electrolytes, enzymes and metabolites did not support the contention that the effects on collagen degradation were a result of secondary organ dysfunction due to alcohol consumption. (5) The results suggest that chronic ethanol feeding for 6 weeks is having a primary effect on skeletal tissue. A reduction in the absolute rate of bone resorption is implicated and ethanol may inhibit the normal formation of the mature crosslinks.