Alcohol is considered to be a major cause of morbidity and mortality in adults in most parts of the world. Ethanol, the most common hepatotoxin, can injure the liver cells directly or through its toxic metabolites i.e., acetaldehyde and free radicals. Its effect begins on its exposure to oral mucosa, but liver is the main site for its metabolism and not surprisingly its toxicity. Besides promoting the formation of reactive oxygen species and reactive nitrogen species, long-term ethanol ingestion might deplete the hepatocyte of some important secondary component of the antioxidant defense system. Thus, alcohol and its metabolites tip the balance between the oxidative stress and the antioxidant defense system toward the net oxidant excess, which seems to be one of the contributing factors in the pathophysiology of periodontitis, oral cancer besides alcohol-induced liver disease.