Short‐term exposure to alcohol increases the permeability of human oral mucosa

Howie, NM; Trigkas, TK; Cruchley, A. T.; Wertz, P. W.; Squier, C. A.; Williams, Dennis

doi:10.1034/j.1601-0825.2001.00731.x

Cited by 98 publications

(57 citation statements)

References 34 publications

(39 reference statements)

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“…It has been suggested that alcohol may modify the cellular metabolism of carcinogens, 32 that its metabolite, acetaldehyde, is responsible for enhanced risk, 33,34 that excessive use may lead to nutritional deficiencies enhancing risk, 35 and that alcohol itself may simply solubilize carcinogens and enhance their penetration into cells. 36 Our data suggest that alcohol may act as a selective agent, promoting growth of cells with SFRP1 promoter methylation, and that the effect is independent of the effect of tobacco, with both light and heavy drinking cases showing similar elevated relative risks of SFRP1 promoter methylation (ORs 3.7 and 3.5, respectively) compared to nondrinking cases. This activity may be mediated through an effect on the carcinogen penetration or metabolism or through another growth promoting mechanism such as injury response.…”

Section: Discussionmentioning

confidence: 73%

Epigenetic inactivation of the SFRP genes is associated with drinking, smoking and HPV in head and neck squamous cell carcinoma

Marsit

McClean

Furniss

et al. 2006

Intl Journal of Cancer

108

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The soluble frizzled receptor protein (SFRP) family encodes antagonists of the WNT pathway, and silencing of these genes, through promoter hypermethylation, leads to constitutive WNT signaling. In bladder cancers, hypermethylation of the SFRP genes occurs more often in current and former smokers and is a strong predictor of poor patient survival. Hence, we examined methylation of these genes in another tobacco-related epithelial cancer, head and neck squamous cell carcinoma (HNSCC), to determine if the pattern of tobacco exposure again predicts the epigenetic alteration of these genes. Using methylation-specific PCR, the prevalence of methylation of SFRP1, SFRP2, SFRP4 and SFRP5 was 35, 32, 35 and 29%, respectively among 350 HNSCC cases. Promoter methylation of SFRP1 occurred more often in both heavy (OR 3.5, 95% CI 0.9-13.7) and light drinkers (OR 3.7, 95% CI 1.0-14.3) compared to nondrinkers. SFRP4 promoter methylation, on the other hand, occurred at a higher prevalence in never smokers and former smokers than in current smokers, and also was independently associated with HPV16 viral DNA. A joint effects model of SFRP4 promoter methylation demonstrated that smoking status and HPV virus significantly interacted (p < 0.04) such that never smokers with HPV16 had an OR of SFRP4 methylation of 9.0 (95% CI 2.1-38.6). These results suggest that epigenetic alterations of the SFRP genes are highly prevalent in HNSCC, and that the clonal selection for these alterations is complex and may be related to the carcinogenic exposures that are known risk factors for this disease. ' 2006 Wiley-Liss, Inc.Key words: head and neck cancer; SFRP; hypermethylation; HPV; tobacco smoking; alcohol Head and neck squamous cell carcinoma (HNSCC) is the ninth most common cancer in men in the United States (U.S.) and in 2003 390,000 new cases of oral cancer and 160,000 cases of laryngeal cancer were diagnosed worldwide.1 In the U.S., it is estimated that in 2004 there were 28,260 new cases of oral and pharyngeal cancer (excluding cancers of the lip) and 10,270 laryngeal cancers, and the overall 5-year survival rate for oral and pharyngeal cancer is approximately 50%.2 HNSCC is causally linked to tobacco smoking and smokeless tobacco use, 3,4 as well as to alcohol consumption, which acts both independently and synergistically with tobacco smoking to contribute to disease. 5Human papillomavirus (HPV) infection and low dietary folate have also been implicated in the etiology of this disease. [6][7][8][9] The WNT signaling pathway, activated through the binding of WNT proteins to the membrane-bound Frizzled receptors, leads to the stabilization and increase in the levels of the transcription factor b-catenin protein. This, in turn, leads to the activation of an array of target genes involved in numerous cellular processes important in tumor development, such as cell growth and survival, intercellular adhesion and cellular morphogenesis.10 Disruption of this pathway, through activating mutations of CTNNB1 (encoding b-catenin) or loss-of-function...

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Section: Discussionmentioning

confidence: 73%

Epigenetic inactivation of the SFRP genes is associated with drinking, smoking and HPV in head and neck squamous cell carcinoma

Marsit

McClean

Furniss

et al. 2006

Intl Journal of Cancer

108

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“…Prolonged exposure may also sensitize peripheral nerve-endings, leading to diminished response, since ethanol destroys nervous tissue by extracting cholesterol and other lipids and by protein precipitation (21). There are several other mechanisms by which ethanol might affect oral mucosa, such as oxidizing activity that leads to changes by directly injuring DNA (22) and increased carcinogen penetration across the oral mucosa, perhaps due to increased mucosal permeability (23), which increases with increasing alcohol concentration (24). Kuyama et al (25) studied the effects of alcohol on oral mucosal cells in 125 subjects and found increased keratinization of oral mucosal cells.…”

Section: Discussionmentioning

confidence: 99%

Effect of alcohol consumption status and alcohol concentration on oral pain induced by alcohol-containing mouthwash

Satpathy¹,

Ravindra²,

Porwal

et al. 2013

J Oral Sci

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Alcohol exposure alters oral mucosa.Patient compliance with mouthwash use may be reduced by oral pain resulting from rinsing with alcohol-containing mouthwash. However, information regarding the effects of alcohol consumption and mouthwash alcohol concentration on oral pain is limited. In this double-blind, randomized, controlled cross-over study, we investigated the effects of alcohol consumption status and mouthwash alcohol concentration on response to and perception of oral pain induced by alcohol-containing mouthwash. Fifty healthy men aged 33 to 56 years were enrolled and classified as drinkers and nondrinkers according to self-reported alcohol consumption. All subjects rinsed with two commercially available mouthwash products (which contained high and low concentrations of alcohol) and a negative control, in randomized order. Time of onset of oral pain, time of cessation of oral pain (after mouthwash expectoration), and pain duration were recorded, and oral pain intensity was recorded on a verbal rating scale. Drinkers had later oral pain onset and lower pain intensity. High-alcohol mouthwash was associated with earlier pain onset and greater pain intensity. In addition, oral pain cessation was later and pain duration was longer in nondrinkers rinsing with high-alcohol mouthwash. In conclusion, alcohol consumption status and mouthwash alcohol concentration were associated with onset and intensity of oral pain. (J Oral Sci 55, 99-105, 2013)

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“…Another possible mechanism by which alcoholic beverages may increase the risk of cancer is the potential for such beverages to contain various carcinogenic congers and contaminants. In addition, alcohol may (a) interfere with nutritional intake or bioavailability, (b) enhance the penetration of carcinogens within the oral mucosa, (c) reduce immune function, (d) potentiate the genotoxicity of or activate carcinogenic agents, (e) interfere with DNA repair and (f) inhibit the detoxification of carcinogens [36][37][38][39].…”

Section: Alcohol Consumptionmentioning

confidence: 99%

Smoking and drinking in relation to oral cancer and oral epithelial dysplasia

Morse

Psoter

Cleveland

et al. 2007

Cancer Causes Control

142

125

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Objective-Risks associated with smoking and drinking are not necessarily constant over the multistage pathway to oral cancer. We investigated whether smoking and drinking patterns differ for persons with oral cancer (OC) relative to those with oral epithelial dysplasia (OED), a precancerous condition.Methods-Incident cases of OC and OED were interviewed using a questionnaire containing questions on smoking and drinking. Odds ratios (ORs) compared the odds of smoking and drinking among persons with OC relative to OED.Results-No adjusted ORs for smoking achieved statistical significance; however, most were <1.0. The odds of OC relative to OED increased with drinking level; the adjusted OR for 19+ drinks/week was 3.03 (1.56-5.87). Age drinking began and years of drinking were not notably different for OC and OED cases; a higher proportion of OC cases reported discontinuing alcohol for 9+ years before diagnosis. Conclusions-The relationship between smoking and OED was at least as strong as that for smoking and OC, suggesting that smoking may have its greatest impact on oral carcinogenesis prior

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Short‐term exposure to alcohol increases the permeability of human oral mucosa

Abstract: These results suggest that short-term exposure to ethanol may act as a permeability enhancer, possibly by causing molecular rearrangement of the permeability barrier, not as a result of lipid extraction.

Cited by 98 publications

References 34 publications

Epigenetic inactivation of the SFRP genes is associated with drinking, smoking and HPV in head and neck squamous cell carcinoma

Epigenetic inactivation of the SFRP genes is associated with drinking, smoking and HPV in head and neck squamous cell carcinoma

Effect of alcohol consumption status and alcohol concentration on oral pain induced by alcohol-containing mouthwash

Smoking and drinking in relation to oral cancer and oral epithelial dysplasia

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