Polysomnographic Assessment of Effects of Tobacco Smoking and Alcohol Consumption on Sleep Bruxism Intensity.

Abstract

Sleep bruxism (SB) is a common sleep-related movement behavior with a complex etiology. A recent hypothesis suggests psychoactive substance usage, tobacco smoking, and alcohol intake are risk factors for SB. This study aimed to evaluate SB intensity in tobacco smokers and alcohol drinkers. A total of 133 adults underwent full-night audio- and video-polysomnography, and the polysomnograms were evaluated using the American Academy of Sleep Medicine guidelines. The study group was divided into smoker and nonsmoker groups as well as drinker and non-drinker groups. The results of the polysomnographic analysis confirmed that tobacco smoking has a significant effects on SB. Tobacco smokers showed increased bruxism intensity (5.50 ± 4.71 vs. 3.83 ± 3.26, p < 0.05), especially the mixed phenotype (0.93 ± 1.00 vs. 0.59 ± 0.59, p < 0.05), in the N1 sleep stage (22.84 ± 20.45 vs. 15.66 ± 13.60, p < 0.05) and the nonsupine position (4.93 ± 5.56 vs. 2.50 ± 2.31, p < 0.05). They also showed a higher number of bruxism episodes with arousal compared with nonsmokers (2.91 ± 2.83 vs. 1.61 ± 1.49, p < 0.05), indicating increased sleep fragmentation. However, no significant effect of alcohol on SB intensity was observed, and the bruxism episode index was similar in alcohol drinkers and nondrinkers. In addition, electrolyte disturbances and lipid disorders were evaluated. Compared with nonsmokers, tobacco smokers showed a higher concentration of plasma triglycerides (177.67 ± 106.9 vs. 129.18 ± 65.61) and lower levels of iron and magnesium (96.68 ± 43.58 vs. 123.83 ± 52.36 and 1.85 ± 0.22 vs. 1.96 ± 0.21, respectively). In summary, this study showed that tobacco smoking, but not alcohol consumption, is related to bruxism intensity and lipid and electrolyte disturbances in individuals with sleep disorders.