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Sleep bruxism (SB) involves involuntary jaw movements during sleep and is potentially caused by motor neuronal hyperexcitability and GABAergic system dysfunction. However, the molecular basis remains unclear. In this study, we aimed to investigate changes in the expression of several genes associated with the pathophysiology of SB. Bulk RNA sequencing (bulk RNA-seq) and single-nucleus RNA sequencing (snRNA-seq) of neurons derived from patient and control human induced pluripotent stem cells (hiPSCs) were performed to comprehensively assess gene expression and cell type-specific alterations, respectively. Bulk RNA-seq revealed significant upregulation of calcium signaling-related genes in SB neurons, including those encoding G protein-coupled receptors and receptor-operated calcium channels. snRNA-seq confirmed the increased expression of GRIN2B (an N-methyl-D-aspartate receptor subunit) and CHRM3 (an M3 muscarinic acetylcholine receptor), particularly in glutamatergic and GABAergic neurons. These alterations were linked to hyperexcitability, with GRIN2B contributing to glutamatergic signaling and CHRM3 contributing to cholinergic signaling. These findings suggest that disrupted calcium signaling and overexpression of GRIN2B and CHRM3 drive neuronal hyperexcitability, providing insight into the pathophysiology of SB. Targeting these pathways may inform therapeutic strategies for SB treatment.

Aim and Objective: Sleep bruxism is a complicated disease, and its cause remains controversial. If the etiology of bruxism is resolved, the treatment can be adjusted to the prevailing aetiological factor. Thus, the aim of this study was to evaluate the oxidative stress level and serum prolidase activity in patients with sleep bruxism., Materials and Methods: Seventy healthy subjects and 51 patients with sleep bruxism were included in this study, and blood samples from all patients were collected. Serum samples were analyzed for total antioxidant status (TAS), total oxidant status (TOS), oxidative stress index (OSI), and prolidase activity., Results: The prolidase, TOS, and OSI levels were significantly higher in patients with bruxism than in the healthy controls (p = 0.001, p = 0.001, p = 0.001, respectively). The TAS level was significantly lower in bruxism patients than in healthy controls (p = 0.003)., Conclusion: The increased TOS, OSI, and prolidase levels and decreased TAS levels could be assumed to result in oxidative injury in patients with sleep bruxism. However, the study could not determine whether oxidative imbalance and increased serum prolidase levels could be a cause or a result of bruxism., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Background: An increasing number of studies have indicated that the central and autonomic nervous systems play roles in the genesis of sleep bruxism (SB). The role of specific neurochemicals in SB has been a subject of interest., Objective: In this study, we use proton magnetic resonance spectroscopy ( 1 H-MRS) to determine whether the levels of γ-aminobutyric acid (GABA) and glutamate (Glu) are different in the brainstem and bilateral cortical masticatory area (CMA) between possible sleep bruxism (SB) patients and controls, and discuss whether the brainstem or cortical networks which may affect the central masticatory pathways are under the genesis of SB., Methods: Twelve possible SB patients and twelve age- and gender-matched controls underwent 1 H-MRS using the "MEGA-Point Resolved Spectroscopy Sequence" (MEGA-PRESS) technique in the brainstem and bilateral CMA. Proton magnetic resonance spectroscopy data were processed using LCModel. Because the signal detected by MEGA-PRESS includes contributions from GABA, macromolecules (primarily proteins) and homocarnosine, the GABA signal is referred to as "GABA+". The glutamate complex (Glx) signal contains both glutamate (Glu) and glutamine (Gln), which mainly reflect glutamatergic metabolism., Results: Edited spectra were successfully obtained from the bilateral CMA in all subjects. There were no significant differences in neurochemical levels between the left and right CMA in possible SB patients and controls. In the brainstem, significantly lower GABA+ levels were found in possible SB patients than in controls (P = .011), whereas there was no significant difference (P = .307) in Glx levels between the 2 groups., Conclusions: SB patients may possess abnormalities in the GABAergic system of brainstem networks., (© 2017 John Wiley & Sons Ltd.)

Objective: To determine whether there are in vivo differences of metabolites levels in bilateral cortical masticatory area(CMA) of patients with sleep bruxism, compared with healthy controls using proton magnetic resonance spectroscopy(1H-MRS). Accordingly to explore if cortical control of the central jaw motor system is abnormal in sleep bruxism patients., Methods: Fifteen sleep bruxism patients and fifteen age- and gender-matched healthy controls underwent 1H-MRS of bilateral CMA using J-difference edited point-resolved spectroscopy sequence(MEGA-PRESS) technique. Levels of metabolites were quantified from the ratio of the metabolite integral to the unsuppressed water signal. Differences of levels of γ-aminobutyric acid(GABA), glutmate(Glu) and N-acetyl aspartate(NAA) in bilateral CMA between sleep bruxism patients and healthy controls were tested using two-way ANOVA., Results: Edited spectra were successfully obtained from the bilateral CMA in all of the participants. Levels of GABA+, glutmate and NAA in right and left CMA in sleep bruxism patients were (2.45±0.48)×10(-3), (2.35±0.62)×10(-3), (10.65±1.84)×10(-3), (10.49±2.37)×10(-3), (10.70±3.61)×10(-3), and (11.26±4.01)×10(-3) respectively. In contrast, levels of GABA+, glutmate and NAA in right and left CMA in healthy controls were (2.63±0.68)×10(-3), (2.65±0.97)×10(-3), (11.19± 1.34)×10(-3), (10.58±3.14)×10(-3), (11.82±1.80)×10(-3), and (11.95±3.23)×10(-3). There were no differences in levels of GABA+(P=0.196), Glu(P=0.590), and NAA(P=0.292) between sleep bruxism patients and healthy controls, nor in inbilateral CMA(GABA+: P=0.837; Glu: P=0.510; NAA: P=0.628)., Conclusions: The results indicate the absence of any alteration of the cortical control of the central jaw motor system in the levels of GABA, Glu and NAA in patients with sleep bruxism.

Purpose: The aim of this study was to evaluate the relationship between sleep bruxism (SB) and perceived stress through the estimation of stress-related biomarkers (cortisol, α-amylase) in saliva., Materials and Methods: Forty-five volunteers (20 men, 25 women) participated in this study. Participants were divided into two groups (bruxers and nonbruxers) according to their answers in a standard bruxism assessment questionnaire outlined by the American Academy of Sleep Medicine. To confirm the preliminary diagnosis and to determine the severity of SB in the group of patients who had a positive self report for SB, a miniature, single-use electromyographic (EMG) device for SB detection (BiteStrip) was used. The perceived stress of the 45 participants was measured using the Perceived Stress Scale questionnaire. Unstimulated whole saliva was collected and levels of salivary cortisol and α-amylase were determined by enzyme-linked immunosorbent assay test and enzyme kinetic reaction, respectively. Nonparametric statistical methods were applied for data analyses., Results: Bruxers showed higher levels of perceived stress than nonbruxers (P < .001). There was a moderate positive correlation between the 25 bruxers' BiteStrip scores and the salivary cortisol levels (Spearman rank correlation = 0.401, P = .047). Additionally, bruxers showed higher levels of cortisol than nonbruxers (P < .001). On the contrary, salivary α-amylase levels were not significantly different in bruxers and nonbruxers (P = .414)., Conclusions: These findings suggest that SB activity was related to higher levels of perceived psychological stress and salivary cortisol. Despite the limitations of the EMG recording device, a moderate positive correlation between BiteStrip score and cortisol levels was observed in bruxers.

Purpose: The aim of this study was to evaluate the correlation between sleep bruxism (SB) frequency and serotonin transporter (SERT)-driven serotonin (5-HT)-uptake in platelets., Methods: Subjects were dental trainee residents and faculty members of Okayama University Hospital who were aware of having severe or no SB. SB frequency was assessed for 3-consecutive nights by a self-contained electromyographic detector/analyzer, which indicated individual SB levels as one of four grades (score 0, 1, 2 and 3). Subjects were classified as normal control (NC) when SB scores indicated only 0 or 1 during the 3 nights, or as severe SB for scores 2 or 3. Those subjects whose scores fluctuated from 0 to 3 during the 3 nights were omitted from further analysis. Fasting peripheral venous blood samples were collected in the morning following the final SB assessment. Amounts of SERTs proteins collected from peripheral platelets were quantified using ELISA, and SERTs transport activity was assessed by uptake assay using [3H]-5-HT., Results: Thirteen severe SB subjects and 7 NC subjects were eligible. Gender distribution, mean age, 5-HT concentration and total amounts of SERT protein in platelets showed no significant differences between NC and severe SB (p=0.85: Chi-squared test; p=0.64, 0.26, 0.46: t-test). However, [3H]-5-HT uptake by platelets was significantly greater in NC compared to severe SB subjects (12.79±1.97, 8.27±1.91 fmol/10(5) platelets/min, p<0.001, t-test)., Conclusion: The results of this pilot study suggest a possible correlation between peripheral platelet serotonin transporter uptake ability and SB severity., (Copyright © 2014 Japan Prosthodontic Society. Published by Elsevier Ltd. All rights reserved.)

Objective: We evaluated the relationship among sleep bruxism (SB), antioxidant/oxidant status, and anxiety level to determine whether antioxidant/oxidant status may be used as a biological marker of SB., Study Design: Thirty-three SB and 32 healthy patients of similar age, sex, and body mass index were enrolled, venous blood was collected, and anxiety scores were determined. Plasma samples were analyzed for total oxidant status, antioxidant status, and oxidative stress index., Results: In 2 of the 3 assays performed, SB patients exhibited an oxidative imbalance. A higher anxiety score was observed with SB (P < 0.05)., Conclusions: These results show that oxidant/antioxidant imbalance may be related to SB, either pathophysiologically or as an outcome of the condition. Further biochemical studies could prove useful in determining the importance of antioxidant drugs in the treatment of SB., (Copyright © 2012 Elsevier Inc. All rights reserved.)

Unlabelled: The study of factors potentially associated with sleep bruxism (SB) may contribute to a better understanding of its nature and etiology., Objectives: In this way, this cross-sectional study aimed to evaluate the association between SB and salivary cortisol levels, heart rate, and other parafunctional habits., Design and Methods: Data were collected in 100 healthy caries-free children of both genders, aged 7.23 ± 0.60 years, with (n=27) and without (n=73) signs and symptoms of SB by interview with the parents and clinical and physical examination. Salivary cortisol was measured immediately after waking up and 30min after awakening for the determination of the area under the response curve (AURC). Data were analyzed by descriptive statistics, normality test, and Spearman correlation test; a stepwise logistic regression model was used to verify the association between SB, as the dependent variable, and age, gender, body mass index (BMI), heart rate, presence of sucking habit, nail biting, enuresis, and AURC (α=0.05)., Results: AURC did not correlate with BMI and heart rate. Only AURC showed a significant negative association with SB, while age, gender, BMI, heart rate and other parafunctional habits did not associate with SB., Conclusion: In the studied sample, children with SB were more likely to present low concentrations of awakening salivary cortisol., (Copyright © 2012 The Canadian Society of Clinical Chemists. Published by Elsevier Inc. All rights reserved.)

The objective of this study was to examine the association between sleep bruxism and psychological stress. The subjects consisted of 76 volunteers, who were divided into those with and without bruxism according to the diagnostic criteria for sleep bruxism outlined by the American Academy of Sleep Medicine (AASM). Stress sensitivity was evaluated before and after an experimental stress task, which involved simple mathematical calculations. It was assessed objectively by measuring the subjects' salivary chromogranin A (CgA) levels and subjectively using a ten-division visual analog scale (VAS). Compared with those observed before the stress task, the mean salivary CgA levels of the non-bruxism group (n = 54) were not significantly increased after the stress task. Conversely, the mean salivary CgA levels of the bruxism group (n = 22) were significantly increased after the stress task (P < 0.01). The mean VAS scores of the groups without (n = 54) and with (n = 22) bruxism were significantly (P < 0.01) increased after the stress task compared with those observed before the stress task, but no differences were detected between the two groups in the stress task. These findings suggest that there is an association between sleep bruxism and psychological stress sensitivity.

Aims: First, to evaluate possible orofacial morphologic differences between sleep bruxers and non-bruxers, and second, to determine possible correlations between morphologic factors and striatal D2 receptor expression in persons with sleep-related oromotor activities., Methods: Twenty subjects were included in this study; half of them had polysomnographically confirmed oromotor values above the cutoff points for sleep bruxism. For all participants, 26 standard occlusal measures were recorded clinically and from dental study casts. In addition, 25 standard angular and linear measures were taken from standardized cephalometric films, and variables were derived to evaluate dental and skeletal relationships. Fourteen of the 20 participants had also participated in a previous study that included iodine-123-iodobenzamide (I-123-IBZM) and single-photon emission-computed tomography (SPECT). For them, the side-to-side difference in striatal D2 receptor binding was determined as the neurochemical outcome measure., Results: Following the classical Bonferroni adjustment for multiple testing, no morphologic differences were found between the sleep bruxers and the non-bruxers. In addition, none of the morphologic variables were significantly associated with the neuroimaging data., Conclusion: Taking into account the low power of this retrospective, exploratory study, the results suggest that the orofacial morphology of sleep bruxers does not differ from that of non-bruxers. In addition, morphologic factors are probably not involved in the asymmetry in striatal D2 receptor distribution that was previously observed in association with sleep bruxism.