Simple snoring is defined as the production of sound in the upper aerodigestive tract during sleep, not accompanied by other pathologies. Sleep bruxism (SB) refers to repetitive phasic, tonic, or mixed masticatory muscle activity during sleep. In this study, we investigated the relationship between simple snoring and SB in patients without obstructive sleep apnea (OSA). A total of 565 snoring subjects underwent polysomnography. After examination, individuals with OSA were excluded from the study group. Finally, 129 individuals were analyzed. The bruxism episode index was positively correlated with maximum snore intensity. Phasic bruxism was positively correlated with snore intensity in all sleep positions. Bruxers had a significantly decreased average and minimum heart rate compared with non-bruxers. Supine sleep position seemed to have a significant impact on snore intensity and SB. In summary, our study showed the relationship between SB, snore intensity, and body position. Phasic bruxism was positively correlated with snore intensity despite the body position, which is an interesting and novel finding.

Purpose: Sleep bruxism (SB) is characterized by repetitive phasic, tonic, or mixed masticatory muscle activity during sleep with multifactorial etiology. Previous studies have shown that the complex origin of SB can be related to the psychological features of the affected individual, consumption of caffeine and alcohol, smoking, obstructive sleep apnea, diabetes, increased body mass index, hypertension, thyroid diseases, and probable genetic vulnerability. This study aimed to investigate the inflammatory markers, hormonal disturbances, and sleepiness associated with SB, which have a potential effect on the total cardiovascular (CV) risk among relatively young and healthy patients. Patients and Methods: A total of 74 individuals with probable SB were subjected to single-night polysomnography, followed by blood panel and 24-h urinary excretion tests. The level of daytime sleepiness was assessed in the participants using the Epworth Sleepiness Scale. Results: SB was found in 78.4% of participants. The bruxism episode index (BEI) positively correlated with the concentrations of 17-hydroxycorticosteroids, C-reactive protein, and fibrinogen in the collected urine samples. A positive correlation was also found between phasic BEI and glucose concentration 2 h after the consumption of glucose solution. Sleep bruxers showed significantly increased sleepiness compared to nonbruxers (p = 0.02). The scores on sleepiness were positively correlated with mixed BEI, minimal oxygen saturation, and mean heart rate. Conclusion: The results of this study revealed that participants with SB had metabolic and hormonal disturbances, probably due to stress and sympathetic activity. Moreover, it was found that young sleep bruxers potentially have a high CV risk due to the increased level of inflammatory and stress markers.

Sleep bruxism is a common sleep-related behavior characterized as repetitive masticatory muscle activity. Genetic vulnerability to stress and anxiety is considered a basal component in the pathogenesis of bruxism events. Dysfunction of the autonomic nervous system related with an arousal during sleep is considered an underlying cause of the cardiovascular implications of sleep bruxism. Increased cardiovascular risk was previously linked with sleep conditions: for example, obstructive sleep apnea and insomnia, and sleep bruxism. The aim of present systematic review was to evaluate the current arguments on the relationship between sleep bruxism and cardiovascular diseases according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA). We have reviewed the Embase, PubMed (Medline) and Scopus databases to identify applicable articles (1994–2021). A total of 127 records in English language were identified, then after screening and exclusion of nonrelevant records, 19 full-text articles were evaluated. Finally, we included 12 studies for synthesis. Due to the heterogeneity of the compared studies, only a qualitative comparison and narrative summary were performed. In the majority of studies, increased sympathetic activity was successfully established to escalate heart rate variability, the inflammatory process, oxidative stress, endothelial remodeling and hormonal disturbances, leading to hypertension and other cardiovascular complications.

Objective: The aim of this research was to assess the relationship between prevalence and severity of obstructive sleep apnea (OSA) and insulin resistance among patients with increased risk of OSA without diabetes mellitus. Method and materials: our study group involved 102 individuals with suspected OSA, mean age 53.02 ± 12.37 years. Data on medical history, medication usage, sleep habits, sleep quality and daytime sleepiness, were obtained using questionnaires. All patients underwent standardized full night polysomnography. Serum fasting insulin and glucose concentration were analyzed, the homeostatic model assessment-insulin resistance (HOMA-IR) index was calculated. Results: polysomnographic study indicated that in the group with OSA mean values of apnea–hypopnea index (AHI), oxygen desaturation index (ODI), duration of SpO₂ < 90% and average desaturation drop were significantly higher compared to the group without OSA, while the minimum SpO2 was significantly lower. The carbohydrate metabolism parameters did not differ within those groups. Significantly higher fasting insulin concentration and HOMA-IR index were found in the group with AHI ≥ 15 compared to the group with AHI < 15 and in the group with AHI ≥ 30 compared to the group with AHI < 30. Higher AHI and ODI were independent risk factors for higher fasting insulin concentration and higher HOMA-IR index. Increased duration of SpO2 < 90% was an independent risk factor for higher fasting glucose concentration. Conclusions: Individuals with moderate to severe OSA without diabetes mellitus had a higher prevalence of insulin resistance.

Background: 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. Methods: 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. Results: 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). Conclusions: 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.

(1) Background: Sleep bruxism (SB) is a common sleep behavior. Obstructive sleep apnea (OSA) is a prevalent sleep-related breathing disorder with potential long-term major neurocognitive and cardiovascular sequelae. Although the co-occurrence of SB and OSA has been described previously, the exact relationship remains unclear. The present study aimed to evaluate the incidence of SB in different phenotypes of OSA. (2) Methods: The participants of this study were adult patients referred to the Department and Clinic of Internal Medicine, Occupational Diseases, Hypertension and Clinical Oncology at the Wroclaw Medical University. They underwent a single-night video polysomnography in a sleep laboratory. The data related to common OSA phenotypes were analyzed in two separate groups of patients: body position related (n = 94) and rapid eye movement (REM) related (n = 85). (3) Results: The obtained results showed that the incidence of SB and severe SB was higher for body position-related OSA phenotype (p < 0.05 for all comparisons). No statistically significant differences were observed for REM-related OSA phenotype (p > 0.05 for all comparisons). (4) Conclusions: Body position-related OSA phenotype seems to be associated with higher SB and severe SB incidence, but the relationship is not independent. However, in the light of the unclear relationship between SB and sleep-disordered breathing, the topic needs further study.