GABRIELE BARBERA
CLAUDIO MASSANO
ALCOHOL AND ORAL CAVITY
A general vision of the effects of alcohol assumption and of its pathogenetic mechanisms in the oral cavity
INTRODUCTION
Excessive use of alcohol has many harmful effects on health, some of which affect dental treatment. These include things like:
-Bleeding disorders resulting from damage to the liver and the bone marrow.
-Liver damage and disease which compromise general health and reduces resistance to infection.
-An increased risk of oral cancer.
-Increased likelihood of tooth decay and periodontal disease.
Heavy drinking can cause:
-Irritation of the gum, tongue and oral tissues.
-Poor healing after dental surgery.
-Poor dental health habits.
-Increase in tooth decay.
-Poor compliance in home care to obtain good oral health.
-Increases risk toward periodontal (gum) disease
Persons who abuse alcohol are at high risk of having seriously deteriorated teeth, gums and compromised oral health in general.
Besides persistent alcohol abuse increases periodontitis severe gum disease, development by heightening the loss of attachment through recession of gingival margins.
ETHANOL METABOLISM
Metabolism is divided into two stages: the first stage consists of the transformation of ethanol to acetaldehyde, which can be achieved in three ways:
-by alcohol dehydrogenase (ADH)
-by hepatic microsomal system (MEOS)
-by catalase enzyme.
The second stage is characterized by the oxidation of the earlier obtained acetaldehyde into acetate by means of the aldehyde dehydrogenase enzyme (ALDH).
Clik here for ethanol metabolism in italian.
EFFECTS IN THE ORAL CAVITY
There is a series of clinical signs and symptoms triggered by either the direct effect of alcohol in the organism or by the consequence of poor personal hygiene. In this manner, significant indices of caries, calculus, sialosis, bruxism, leukoplakia and erythroplasia are found in chronic alcoholics. With regards to lichen planus, ethanol could be implicated in its potential transformation process to malignancy.
CORRELATED STUDIES
Cavo orale e alcol di Guido Abate
Safety evaluation of topical applications of ethanol on the skin and inside the oral cavity
Effect of an alcoholic diet on dental caries and on Streptococcus of the mutans group. Study in rats
PATHOGENETIC MECHANISMS
Since the mouth is the external part of the body that is in contact with alcohol, the components that form part of the beverages are encountered here in their maximum concentration which later on undergo various transformation processes mediated by the enzymatic systems of the body.
There are three fundamental mechanisms:
1- Increase in permeability
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, due to both their increase in solubility and an increase in the permeability of the oral mucosa.
2- Action of acetaldehyde
Since ethanol by itself has not been proven to be carcinogenic, the role of its first metabolite, acetaldehyde, has been postulated as a potential factor implicated in the effects of the consumption of alcoholic drinks. The International Agency for Research on Cancer has established that sufficient evidence exists to identify acetaldehyde as carcinogenic in animals, being possibly carcinogenic to humans.
In short term cellular cultures it causes mutations and other damages to the DNA and initiate the transformation of rat kidney cells and inhibit the repair of DNA.
Acetaldehyde:
-interferes with the synthesis and reparation of DNA, and consecuently the development of tumors;
-induces interchanges in sister cromatids;
-produces specific gene mutations;
-inhibits the O6methylguanitransferase, enzyme responsible for repairing
the injury caused by alkylating agents;
-unites to cellular proteins and DNA provoking morphologic and cellular injury;
-its components are neoantigens that determine the production of antibodies, stimulating the immune system and inducing a cytotoxic immune response and it is also capable of in vitro follic acid destruction .
-3 Alteration in retinoid metabolism
A new route of investigation has been proposed with the role of retinoids in the development of precancerous lesions. Chronic consumption of ethanol is found associated with decreased levels of retinoids in the oral cavity. Any alteration in their metabolism and activation will reflect in an increase in the oral mucosa susceptibility to other carcinogens.
Ethanol is a competetive inhibitor of retinol metabolism, since the same enzyme (ADH) is in charge of catalyzing two reactions in which an accumulation of retinol will be produced, in the expense of the reduction of retinoic acid, making this the active form. At the same time, the first metabolite of ethanol, acetaldehyde, is also capable of inhibiting the generation of retinoic acid. On the other hand, ethanol apparently causes a deficiency of retinoic acid in the liver due to an increase in its catabolism mediated by the action of cytochrome P4502E1.
The low levels of retinoic acid suppose a lack of control in epithelial growth, which could initiate the development of malignant lesions. Presently retinoids are being employed in the treatment of cancerous and precancerous lesions with partial and total remissions of leucoplakia demonstrated in 40-60% of the patients in systemic vitamin A treatment, though their topical use seem to have a limited effect.
DISCUSSION
The relation of the studies that establish this connection is complicated due to both the confluence of various risk factors within the same person such as alcohol and tobacco, and to the lack of data that can be verifiable by the clinician. For this reason the exact pathogenic mechanism responsible for this increase of risk is not known since ethanol per se was not confirmed to be carcinogenic.
The increase in the oral mucosa permeability by local action of ethanol is demonstrated in the analyzed studies. However this action is not sufficient to explain the development of oral cancer.
Acetaldehyde, the first metabolite of ethanol, has been identified as carcinogenic in animals, for which any increase in its concentration will reflect on the oral mucosa. There are two ways in which we could arrive at this situation: an increase in its production and a decrease in its elimination.
A new route of research has come to light on the study of the retinoid metabolism. Fundamental molecules in the regulation of growth and the differentiation of the epitheliums, and whose normal activity could be seen interrupted by the ethanol transformation process upon producing a competitive inhibition in the participating enzymes.
BIBLIOGRAFIA/REFERENCES
Figuero Ruiz, Carretero-Pelaez MA, Cerezo-Lapiedra R,Esparza-Gomez G, Moreno-Lopez LA. EFFECTS OF THE CONSUMPTION OF ALCOHOL IN THEORAL CAVITY: RELATIONSHIP WITH ORAL CANCER. MED ORAL 2004;9:14-23
Homann N, Jousimies H, Jokelainen K, Heine R, Salaspuro M. High acetaldehyde levels in saliva after ethanol consumption; methodological aspects and pathogenic implications. Carcinogenesis 1997;18:1739-43
García García V,González-Moles MA, Bascones Martínez A.Bases moleculares del cáncer oral. Revisión bibliográfica.Avances en Odontoestomatología versión impresa ISSN 0213-1285
Seitz H. Alcohol and retinoid metabolism. GUT 2000;47:748-50.
Arthur Mashberg, D.D.S., Paolo Boffetta, M.D., M.P.H. *, Regina Winkelman, M.A., Lawrence Garfinkel, M.A.§ - Tobacco smoking, alcohol drinking, and cancer of the oral cavity and oropharynx among U.S. veterans NIH-National Institute for Dental Research-Veterans Administration Interagency; Grant Number: 1Y01-DE-001-02
