Ethanol- and Cigarette Smoke-Related Alternations in Oral Redox Homeostasis

Abstract

Alcohol abuse as well as smoking cigarettes has been proven to negatively affect the oral environment. The aim of this work was to provide a systematic review of the literature on the influence of ethanol and cigarette smoking on oral redox homeostasis. A search was performed for scientific articles indexed in the PubMed, Medline and Web of Science databases. We identified 32,300 articles, of which 54 were used for the final review, including the results from 2000 to 2021. Among the publications used to write this article, n = 14 were related to the influence of alcohol consumption (clinical studies n = 6, experimental studies n = 8) and n = 40 were related to the influence of smoking (clinical studies n = 33, experimental studies n = 7) on oral redox homeostasis. The reviewed literature indicates that alcohol abusers and smokers are more likely to suffer from salivary gland dysfunction, as well as develop precancerous lesions due to DNA damage. Compared to alcohol abstainers and non-smokers, alcohol drinkers and smokers are also characterized by a deterioration in periodontal health measured by various indicators of periodontal status. In summary, alcohol abuse and smoking are associated with disrupted oral redox homeostasis, which may lead not only to tooth loss, but also contribute to various adverse effects related to mental health, digestive processes and chronic inflammation throughout the human body.

Do Circulating Redox Biomarkers Have Diagnostic Significance in Alcohol-Intoxicated People?

“…Acetaldehyde and acetic acid formed by the ADH and ALDH enzymes are mainly responsible for alcohol poisoning [ 2 ]. In alcohol oxidation, cellular stores of glutathione and NAD are depleted [ 3 ], inhibiting the breakdown of lactic acid and resulting in metabolic acidosis [ 4 ]. The reduction of glutathione reserves may also be associated with the overproduction of acetaldehyde, which, like other toxic compounds, is removed from the cell by glutathione S-transferase [ 5 , 6 ].…”

“…Alcohol is one of the most widely misused stimulants in developed and developing countries [ 1 ]. Chronic alcohol intake is associated with many pathophysiological changes, including central nervous system (CNS) disorders, cancers, pancreatic disease, liver cirrhosis, diabetes, osteoporosis, arthritis, kidney disease, gastrointestinal disorders, immune dysfunction, hypertension, and cardiomyopathy, as well as heart failure [ 2 , 3 , 4 , 5 , 6 , 7 , 8 , 9 , 10 ]. Annually, alcohol abuse leads to about 3.3 million deaths, accounting for 5.9% worldwide deaths [ 11 ].…”

Impact of gastroplasty on salivary characteristics, dental health status and oral sensory aspects: A controlled clinical study

“…The inclusion criteria were individuals with morbid obesity (BMI of 40 kg/m 2 or higher) of both sexes, with at least 20 natural teeth or who use dental prosthesis. The exclusion criteria included conditions that are known to affect salivary characteristics: individuals presenting epilepsy, cancer, rheumatoid arthritis, bucco‐dentofacial diseases or traumas, tobacco use, illicit drugs, Sjögren's syndrome, systemic lupus erythematosus, sarcoidosis, alcoholic beverage and extensive tooth loss 22,23 …”

“…The exclusion criteria included conditions that are known to affect salivary characteristics: individuals presenting epilepsy, cancer, rheumatoid arthritis, bucco-dentofacial diseases or traumas, tobacco use, illicit drugs, Sjögren's syndrome, systemic lupus erythematosus, sarcoidosis, alcoholic beverage and extensive tooth loss. 22,23 The sample consisted of patients who were candidates for gastroplasty, allocated into two groups according to the stage of treatment. The Control group (CG; n = 34) included participants who were followed-up during a 6-months dietary programme prior to gastroplasty, and were evaluated at baseline, and 3 and 6 months later; the Gastroplasty group (GG; n = 39) included other participants who also participated in a 6-months dietary programme and were evaluated three times: immediately before, and 3 and 6 months after the gastroplasty.…”

Еxperimental justification of the efficacy of cocarnite for correction of disorders in rat periodont tissues under alcohol neuropathy

“…Отже, етанол-індукована полінейропатія викликає розвиток оксидативного стресу у м'яких тканинах пародонта, що підтверджується іншими дослідниками, які вивчали вплив етанолу на окисно-відновлювальні процеси в органах порожнини рота тварин [29,30]. Введення Кокарніту запобігало розвиткові оксидативного стресу у щурів за умов АПН, про що свідчить вірогідне зменшення вмісту ТБК-активних продуктів, молекул середньої маси та ОМБ порівняно з тваринами, яким моделювали алкогольну нейропатію без корекції (табл.…”