Document Type : Review Article
Authors
1 Addiction Research Center and Department of Oral Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
2 Oral and Maxillofacial Diseases Research Center , Department of Oral Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
Abstract
Background: Various medical, psychiatric and social problems affecting alcohol abuser tend to overshadow their oral health. From an epidemiologic viewpoint, chronic consumption of alcoholic beverages is associated with an increased risk for the upper gastrointestinal tract cancer, and tobacco and alcohol are regarded as the major risk factors for oral cancer. The objective of this presentation is to express different hypotheses proposed to explain how ethanol, via oral or systemic route, can act as a risk factor for the development of oral cancer.
Methods: A web-based search for all types of articles published was initiated using Medline/PubMed, with the keywords such as "oral cancer", "alcohol consumption" and "prevention". The search was restricted to English articles published up to December 2013.
Results: Various hypotheses have been proposed in the explanation for ethanol acting as a risk factor, locally or systemically, in the development of oral cancer. The main local effects of ethanol are: increase in oral mucosa permeability, action of acetaldehyde, and the role of retinoid and the most important systemic effects are: liver suppression and salivary gland dysfunction. Alcohol and tobacco are considered as two principal risk factors in the development of oral cancer. Ethanol itself is not carcinogenic. However, its first metabolite (acetaldehyde) has recently been shown to be a local carcinogen in humans. Establishing a direct cause-effect relationship between both entities turns out to be difficult. This is due to the frequent association of alcohol with other risk bearing practices such as cigarette smoking. The alcohol in contact with the oral mucosa is capable of producing an alteration in morphology characterized by an epithelial atrophy, which means an increase in the susceptibility of the said tissue against other carcinogenic chemicals. In this manner, it was suggested that ethanol is capable of increasing the penetration of carcinogens through the oral mucosa.
Conclusion: A large body of evidence from epidemiological studies of different designs and conducted in different populations has consistently supported that alcohol consumption is strongly associated with an increase in risk of oral and pharyngeal cancer.
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