Antioxidant therapy attenuates deficient bone fracture repair associated with binge alcohol exposure.

Abstract

Alcohol consumption is a known risk factor for traumatic injuries of all types and has been shown to produce detrimental effects on bone metabolism. Although the mechanisms responsible for these detrimental effects are not well characterized, oxidative stress from alcohol exposure appears to play a central role. This study was designed to examine the effect of a short-term binge alcohol consumption pattern on fracture repair and the effect of an antioxidant, N-acetylcysteine, on fracture healing after binge alcohol consumption. One hundred forty-four adult male Sprague-Dawley rats underwent unilateral closed femur fracture after injection of either saline or alcohol to simulate a binge alcohol cycle. Animals in the antioxidant treatment group received daily N-acetylcysteine after fracture. Femurs were harvested at 1, 2, 4, and 6 weeks after injury and underwent biomechanical testing and histologic analysis. Binge alcohol administration was associated with significant decreases in biomechanical strength at 1- and 2-week time points with a trend toward decreased strength at 4- and 6-week time points as well. Alcohol-treated animals had less cartilage component within the fracture callus and healed primarily by intramembranous ossification. Administration of N-acetylcysteine in alcohol-treated animals improved biomechanical strength to levels comparable to the control animals and was associated with increased endochondral ossification. Our results indicate that binge alcohol alters the quality of fracture healing after a traumatic injury and that concurrent administration of an antioxidant is able to reverse these effects.