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      Low caloric value of ethanol itself increases alveolar bone loss in ligature-induced periodontitis in male rats

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          Abstract

          This study aimed at morphometrically evaluating the influence of variable caloric values of ethanol consumption on alveolar bone loss in periodontitis in male rats. Thirty-six male rats were randomized into four groups of nine rats each, as follows: Test group A (low) - rats were fed an ethanol-containing liquid diet (ethanol representing 22% of total caloric value); Control group A -rats were fed a pair-fed control diet (ethanol replaced by isocaloric amounts of carbohydrate); Test group B (high) -rats were fed an ethanol-containing liquid diet (ethanol representing 36% of total caloric value); Control group B -rats were fed a pair-fed control diet for Test B. Following anesthesia, cotton ligatures were placed around the cervix of the right upper second molar. At eight weeks, the maxillary bones were removed and alveolar bone loss was analyzed by measuring the distance between the cementoenamel junction and the alveolar bone crest at buccal and palatal sites of the upper second molar. The unligated groups showed no significant differences between the bone loss values observed for the low and high caloric values of ethanol (p > 0.05). In the ligated groups, the rats receiving low caloric values of ethanol showed significantly greater bone loss compared to the isocaloric rats (p < 0.05); however, the rats receiving high caloric values of ethanol showed no significant differences compared to the controls. Analysis of the results demonstrated that, in male rats, ethanol itself affected ligature-induced bone loss when representing a low value in the total caloric value.

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          Most cited references29

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          Causation and pathogenesis of periodontal disease.

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            Current view of risk factors for periodontal diseases.

            R Genco (1996)
            Peridontal diseases are infections, and many forms of the disease are associated with specific pathogenic bacteria which colonize the subgingival area. At least two of these microorganisms, Porphyromonas gingivalis and Actinobacillus actinomycetemcomitans, also invade the periodontal tissue and are virulent organisms. Initiation and progression of periodontal infections are clearly modified by local and systemic conditions called risk factors. The local factors include pre-existing disease as evidenced by deep probing depths and plaque retention areas associated with defective restorations. Systemic risk factors recently have been identified by large epidemiologic studies using multifactorial statistical analyses to correct for confounding or associated co-risk factors. Risk factors which we know today as important include diabetes mellitus, especially in individuals in whom metabolic control is poor, and cigarette smoking. These two risk factors markedly affect the initiation and progression of periodontitis, and attempts to manage these factors are now an important component of prevention and treatment of adult periodontitis. Systemic conditions associated with reduced neutrophil numbers or function are also important risk factors in children, juveniles, and young adults. Diseases in which neutrophil dysfunction occurs include the lazy leukocyte syndrome associated with localized juvenile periodontitis, cyclic neutropenia, and congenital neutropenia. Recent studies also point to several potentially important periodontal risk indicators. These include stress and coping behaviors, and osteopenia associated with estrogen deficiency. There are also background determinants associated with periodontal disease including gender (with males having more disease), age (with more disease seen in the elderly), and hereditary factors. The study of risk in periodontal disease is a rapidly emerging field and much is yet to be learned. However, there are at least two significant risk factors-smoking and diabetes-which demand attention in current management of periodontal disease.
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              Relationships Between Nutrition, Alcohol Use, and Liver Disease

              Many alcoholics are malnourished, either because they ingest too little of essential nutrients (e.g., carbohydrates, proteins, and vitamins) or because alcohol and its metabolism prevent the body from properly absorbing, digesting, and using those nutrients. As a result, alcoholics frequently experience deficiencies in proteins and vitamins, particularly vitamin A, which may contribute to liver disease and other serious alcohol-related disorders. Furthermore, alcohol breakdown in the liver, both by the enzyme alcohol dehydrogenase and by an enzyme system called the microsomal ethanol-oxidizing system (MEOS), generates toxic products such as acetaldehyde and highly reactive, and potentially damaging, oxygen-containing molecules. These products can interfere with the normal metabolism of other nutrients, particularly lipids, and contribute to liver cell damage. Nutritional approaches can help prevent or ameliorate alcoholic liver disease. For example, a complete balanced diet can compensate for general malnutrition. Administration of antioxidants (e.g., precursors of the endogenous antioxidant glutathione) can help the body eliminate reactive oxygen molecules and other reactive molecules generated from abnormal lipid breakdown. New agents currently are being studied as promising nutritional supplements for alcoholics with liver disease.
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                Author and article information

                Contributors
                Role: ND
                Role: ND
                Journal
                bor
                Brazilian Oral Research
                Braz. oral res.
                Sociedade Brasileira de Pesquisa Odontológica - SBPqO (São Paulo )
                1807-3107
                December 2009
                : 23
                : 4
                : 460-466
                Affiliations
                [1 ] Christian Life University Foundation Brazil
                [2 ] Universidade Estadual Paulista Brazil
                Article
                S1806-83242009000400017
                10.1590/S1806-83242009000400017
                20027455
                f6d0a07b-1429-4f23-9087-9a7331494e96

                http://creativecommons.org/licenses/by/4.0/

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                SciELO Brazil

                Self URI (journal page): http://www.scielo.br/scielo.php?script=sci_serial&pid=1806-8324&lng=en
                Categories
                DENTISTRY, ORAL SURGERY & MEDICINE

                Dentistry
                Ethanol,Alveolar bone loss,Periodontitis
                Dentistry
                Ethanol, Alveolar bone loss, Periodontitis

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