• Acute Alcohol;
  • Alcoholic Myopathy;
  • Angiogenesis;
  • Antioxidant;
  • Binge Alcohol;
  • Bone Fracture Repair;
  • Canonical Wnt Signaling;
  • Chronic Alcohol;
  • Cytoprotection;
  • Extracellular Matrix;
  • Fracture Non Union;
  • Gastric Mucosa;
  • Glutathione;
  • Inflammation;
  • Myopathy;
  • Orthopedic Trauma;
  • p34cdc2 Kinase;
  • Oxidative Stress;
  • Survivin;
  • Tissue Injury;
  • Wound Healing

Tissue injury owing to acute and chronic alcohol consumption has extensive medical consequences, with the level and duration of alcohol exposure affecting both the magnitude of injury and the time frame to recovery. While the understanding of many of the molecular processes disrupted by alcohol has advanced, mechanisms of alcohol-induced tissue injury remain a subject of intensive research. Alcohol has multiple targets, as it affects diverse cellular and molecular processes. Some mechanisms of tissue damage as a result of alcohol may be common to many tissue types, while others are likely to be tissue specific. Here, we present a discussion of the alcohol-induced molecular and cellular disruptions associated with injury or recovery from injury in bone, muscle, skin, and gastric mucosa. In every case, the goal of characterizing the sites of alcohol action is to devise potential measures for protection, prevention, or therapeutic intervention.