Dental and anesthesiology problems in nicotine dependents (literature review)

Nowadays, smoking is one of the significant factors for the development of inflammatory periodontal diseases. The effect of nicotine on the microcirculation is manifested in the deterioration of the trophic level of the gums and a decrease in their resistance to infection. Atrophy of acinar parts of small salivary glands develops and other morphological changes characteristic of progressive sialadenitis occur. A change in the microflora of the oral cavity was found depending on the duration of smoking. Epithelial dysplasia, which covers the entire thickness of the epithelium, but does not affect the connective tissue, is called carcinoma. Worldwide, more than 300 million people use smokeless tobacco. Malignant changes at the site of precancerous diseases occur after a couple of years of using the product. In smokers, nicotine blocks H-cholinergic receptors and reduces sensitivity to local anesthetics. Nicotine promotes the production of the CYP2E1 enzyme, which is responsible for the metabolism of halogen anesthetics: halothane, enflurane, diethyl ether, trichlorethylene, chloroform, isoflurane and methoxyflurane. Chronic smokers show reduced pain tolerance. Before morphine loading, the assessment of pain threshold in nicotine-dependent individuals was significantly lower than in non-smokers. Smokers require higher doses of opiates and benzodiazepines than nonsmokers. Smoking reduces the potency of aminosteroid muscle relaxants, the required doses of vecuronium and rocuronium in smokers were 25 % higher than in patients leading a healthy lifestyle. Smokers also need more frequent doses to maintain neuromuscular block. Quitting smoking 4–6 weeks (ideally 8 weeks) before general anesthesia reduces the frequency of peri- and postoperative complications.