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      Cytomorphometric Study of Changes in Buccal Mucosal Cells in Alcoholics

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          Abstract

          Background:

          Chronic alcohol consumption carries a high risk for oral and pharyngeal cancers among persons who have never smoked. Excessive alcohol consumption displays cytogenetic changes in oral mucosa cells. Cytomorphometric analysis of oral mucosal cells helps in the early detection of cytomorphological transformations in alcoholics before and after the onset of carcinoma.

          Materials and Methods:

          A prospective, hospital-based, comparative study was done after written informed consent. Smears were obtained from the clinically normal buccal mucosa of 102 randomly selected alcoholic patients attending the medicine outpatient department aged above 25 years who consumed a minimum of 45 ml alcohol per day for at least 10 years and of 102 nonalcoholics as control. The slides were immediately fixed in absolute methanol and stained by the Papanicolaou (Pap) staining technique. PAP-stained smears were examined under the light microscope. Using the image J 1.47 image analysis software, a morphometric analysis of around 50 cells/case was done.

          Results:

          A statistically significant increase in mean cytoplasmic area ( P < 0.001), mean nuclear area ( P < 0.01), and cell-to-nuclear parameter ratio ( P < 0.001) was seen in the alcohol group in comparison with the control group.

          Conclusion:

          Prolonged consumption of alcohol produces cytomorphometric changes in buccal mucosal cells before the onset of premalignant lesions.

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          Most cited references30

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          Profiling early head and neck cancer.

          Head and neck squamous-cell carcinoma (HNSCC) is the sixth most common cancer worldwide and, disappointingly, survival rates are not improving. Moreover, HNSCC has a severe impact on the quality of life of patients and survivors, and the significant morbidity subsequent to treatment often mandates long-term multidisciplinary care, which places significant financial pressures on the treating institution. Therefore, prevention and early diagnosis of high-risk pre-malignant lesions are high priorities for reducing deaths due to head and neck cancer. Recent advances have begun to elucidate the different aetiologies of HNSCCs in relation to previous pre-malignancies and to identify which pre-malignant lesions are likely to progress to malignancy.
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            High acetaldehyde levels in saliva after ethanol consumption: methodological aspects and pathogenetic implications.

            Chronic ethanol ingestion leads to an enhanced risk of upper gastrointestinal tract cancer. Although many hypotheses for the tumor promoting effect of alcohol exist, the pathogenetic mechanisms remain unclear since alcohol in itself is not carcinogenic. Acetaldehyde, the first metabolite of ethanol, has been shown to have multiple mutagenic effects and to be carcinogenic to animals. Previous research has revealed that acetaldehyde can be formed from ethanol via microbial alcohol dehydrogenase. Thus, at least part of the proposed tumorigenic effect of ethanol may be linked to local production of acetaldehyde from ethanol by oral microflora. In this study we demonstrate the production of marked amounts of acetaldehyde in saliva after ingestion of moderate amounts of ethanol. Considerable inter individual variation in acetaldehyde production capacity is also shown. In vivo acetaldehyde production is significantly reduced after a 3-day use of an antiseptic mouthwash (chlorhexidine). In vitro acetaldehyde production was shown to be linear in time, inhibited by 4-methylpyrazole and it could not be saturated under ethanol conditions that are relevant in vivo. There was a significant positive correlation between salivary acetaldehyde production in vitro and in vivo. We conclude, that the microbial formation of acetaldehyde in saliva could be one explanation for the tumor promoting effect of ethanol on the upper gastrointestinal tract. Moreover, this may support the epidemiological finding, that poor oral hygiene is an independent risk factor for oral cavity cancer.
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              Alcohol metabolism and cancer risk.

              Chronic alcohol consumption increases the risk for cancer of the organs and tissues of the respiratory tract and the upper digestive tract (i.e., upper aerodigestive tract), liver, colon, rectum, and breast. Various factors may contribute to the development (i.e., pathogenesis) of alcohol-associated cancer, including the actions of acetaldehyde, the first and most toxic metabolite of alcohol metabolism. The main enzymes involved in alcohol and acetaldehyde metabolism are alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH), which are encoded by multiple genes. Because some of these genes exist in several variants (i.e., are polymorphic), and the enzymes encoded by certain variants may result in elevated acetaldehyde levels, the presence of these variants may predispose to certain cancers. Several mechanisms may contribute to alcohol-related cancer development. Acetaldehyde itself is a cancer-causing substance in experimental animals and reacts with DNA to form cancer-promoting compounds. In addition, highly reactive, oxygen-containing molecules that are generated during certain pathways of alcohol metabolism can damage the DNA, thus also inducing tumor development. Together with other factors related to chronic alcohol consumption, these metabolism-related factors may increase tumor risk in chronic heavy drinkers.
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                Author and article information

                Journal
                Adv Biomed Res
                Adv Biomed Res
                ABR
                Advanced Biomedical Research
                Wolters Kluwer - Medknow (India )
                2277-9175
                2020
                30 September 2020
                : 9
                : 48
                Affiliations
                [1] Department of Pathology, Indira Gandhi Medical College and Research Institute, Puducherry, India
                [1 ] Department of Medicine, JIPMER, Puducherry, India
                [2 ] Department of Medicine, Indira Gandhi Medical College and Research Institute, Puducherry, India
                [3 ] Department of Community Medicine, Indira Gandhi Medical College and Research Institute, Puducherry, India
                Author notes
                Address for correspondence: Dr. Banushree Chandrasekhar Srinivasamurthy, Department of Pathology, Indira Gandhi Medical College and Research Institute, Puducherry - 605 009, India. E-mail: drbanushree15@ 123456hotmail.com
                Article
                ABR-9-48
                10.4103/abr.abr_92_20
                7792866
                38cc89b1-c960-4664-8371-05ff4499d28c
                Copyright: © 2020 Advanced Biomedical Research

                This is an open access journal, and articles are distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as appropriate credit is given and the new creations are licensed under the identical terms.

                History
                : 28 April 2020
                : 19 May 2020
                : 02 June 2020
                Categories
                Original Article

                Molecular medicine
                oral neoplasm,alcoholism,carcinogenesis,computer-assisted,image processing
                Molecular medicine
                oral neoplasm, alcoholism, carcinogenesis, computer-assisted, image processing

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