The Effect of Chronic Ethanol Consumption on Salivary Gland Morphology and Function in the Rat

Maier, H.; Born, I. A.; Veith, S.; Adler, D.; Seitz, Helmut K.

doi:10.1111/j.1530-0277.1986.tb05117.x

Cited by 70 publications

(33 citation statements)

References 16 publications

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“…Our findings agree with the alcohol-induced SF reduction observed in experimental studies [35]. Our results are also consistent with the study reported by Dutta et al [36], in which chronic alcohol intoxication resulted in a reduction in the stimulated SF from parotid glands.…”

Section: Discussionsupporting

confidence: 83%

Decrease in salivary lactoferrin output in chronically intoxicated alcohol-dependent patients

Waszkiewicz

Zalewska-Szajda

Zalewska

et al. 2012

Folia Histochem Cytobiol.

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Salivary lactoferrin is a glycoprotein involved in the elimination of pathogens and the prevention of massive overgrowth of microorganisms that affect oral and general health. A high concentration of lactoferrin in saliva is often considered to be a marker of damage to the salivary glands, gingivitis, or leakage through inflamed or damaged oral mucosa, infiltrated particularly by neutrophils. We conducted a study to determine the effect of chronic alcohol intoxication on salivary lactoferrin concentration and output. The study included 30 volunteers consisting of ten non-smoking male patients after chronic alcohol intoxication (group A), and 20 control nonsmoking male social drinkers (group C) with no history of alcohol abuse. Resting whole saliva was collected 24 to 48 hours after a chronic alcohol intoxication period. Lactoferrin was assessed by enzyme-linked immunosorbent assay. For all participants, the DMFT index (decayed, missing, or filled teeth), gingival index (GI) and papilla bleeding index (PBI) were assessed. The differences between groups were evaluated using the Mann--Whitney U test. We noticed significantly decreased salivary flow (SF) in alcohol dependent patients after chronic alcohol intoxication (A), compared to the control group (C). Although there was no significant difference in salivary lactoferrin concentration between the alcohol dependent group A and the control group C, we found significantly decreased lactoferrin output in group A compared to group C. We found a significant correlation between the amount of daily alcohol use and a decrease in lactoferrin output. There was a significant increase in GI and a tendency of PBI to increase in group A compared to group C. We demonstrated that chronic alcohol intoxication decreases SF and lactoferrin output. The decreased lactoferrin output in persons chronically intoxicated by alcohol may be the result of lactoferrin exhaustion during drinking (due to its alcohol-related lower 249Alcohol and salivary lactoferrin

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Section: Discussionsupporting

confidence: 83%

Decrease in salivary lactoferrin output in chronically intoxicated alcohol-dependent patients

Waszkiewicz

Zalewska-Szajda

Zalewska

et al. 2012

Folia Histochem Cytobiol.

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“…Our results confirm the data in the literature [42,43], in which chronic alcohol consumption caused a reduction in SF. Morphological changes of salivary glands, such as those described above, are considered to be involved in SF reduction in people addicted to alcohol.…”

Section: Discussionsupporting

confidence: 83%

The effect of chronic alcohol intoxication and smoking on the activity of oral peroxidase

Waszkiewicz¹,

Zalewska²,

Szajda³

et al. 2012

Folia Histochem Cytobiol.

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Abstract:Peroxidase is the most important antioxidant enzyme in saliva. Through peroxidation of thiocyanate in the presence of H 2 O 2 , peroxidase catalyses the formation of bacteriocidic compounds such as hypothiocyanate. The purpose of this study was to evaluate the effect of chronic alcohol intoxication and smoking on the activity of oral peroxidase (OPO). A total of 37 volunteers participated in the study. This cohort consisted of 17 male alcohol-dependent smoking patients after chronic alcohol intoxication (AS group, alcohol + smoking) (mean age: 42 years; range: 26-55) (100-700 g/day of alcohol; 10-20 cigarettes/day) and 20 control male social drinkers (CNS group, control non-smokers) with no history of alcohol abuse or smoking (mean age: 42 years; range: 30-53). Salivary peroxidase activity was measured by the colorimetric method. The differences between groups were evaluated using the Mann-Whitney U test. There was significantly higher activity of OPO (p = 0.00001) and significantly lower salivary flow (SF) (p = 0.007) in alcohol-dependent smokers after chronic alcohol intoxication compared to the control group. OPO activity significantly correlated with the number of days of alcohol intoxication, but not with smoking. Gingival index (GI) was significantly higher in smoking alcohol-dependent persons than in the control group, and correlated with OPO activity. The sensitivity of the OPO test was 70% in smoking alcoholics, while specificity was 95%. The increased activity of OPO suggests chronic oxidative stress is more likely due to ethanol action than to smoking. Smoking alcohol-dependent persons have a worse periodontal status than controls. OPO activity as a marker of chronic alcohol abuse may help in the diagnosis of alcoholism.

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“…These results indicate a certain mutual effect between ethanol and oral microorganisms. Chronic alcohol consumption may increase bacterial concentrations through affecting salivary gland morphology and decreasing salivary flow (98,99).…”

Section: Interactions Between Alcohol Consumption and The Correspondimentioning

confidence: 99%

Alcohol consumption and corresponding factors: A novel perspective on the risk factors of esophageal cancer

2016

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Abstract. Esophageal cancer is the eighth most common type of cancer in the world, and the sixth most common cause of mortality from cancer. Alcohol consumption is the major risk factor for esophageal cancer, due to the worldwide prevalence and high carcinogenicity of the ethanol metabolite. In epidemiological studies, the efficiency of alcohol intake to enhance the risk of esophageal cancer is altered by daily ethanol consumption, type of alcoholic beverages ingested, time since quitting drinking, age of drinking initiation, differences in population and subtypes of esophageal cancer. Corresponding factors, including gene polymorphisms, tobacco smoking, oral microorganisms and folate deficiency, reveal a synergistic effect in concurrent alcohol users that may lead to an increased risk of developing esophageal cancer. Consequently, esophageal cancer prevention involves multiple aspects, including quitting drinking and smoking, maintaining an adequate oral health and ingesting adequate quantities of folate, particularly in genetically high-risk populations.

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The Effect of Chronic Ethanol Consumption on Salivary Gland Morphology and Function in the Rat

Cited by 70 publications

References 16 publications

Decrease in salivary lactoferrin output in chronically intoxicated alcohol-dependent patients

Decrease in salivary lactoferrin output in chronically intoxicated alcohol-dependent patients

The effect of chronic alcohol intoxication and smoking on the activity of oral peroxidase

Alcohol consumption and corresponding factors: A novel perspective on the risk factors of esophageal cancer

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