Sleep Bruxism

In this issue, 1 we published a paper on sleep bruxism in children exposed to secondhand smoke (. see page 392. ). After publication, we received a letter ( below) raising questions about the ... Research paper: Association between exposure to secondhand

asked to continue smoking in the presence of their children for 6 months to evaluate if secondhand smoke ( SHS) exposure increased the risk of bruxism.1 It is surprising that after ... Editorial: Association between exposure to SHS and sleep bruxism in

To assess the impact of SHS on sleep bruxism in children, Montaldo.

Several movement disorders may occur during nocturnal rest disrupting sleep. A part of these complaints is characterized by relatively simple, non-purposeful and usually stereotyped movements. The last version of the International Classification of Sleep Disorders includes these clinical conditions (i.e. restless legs syndrome, periodic limb movement disorder, sleep-related leg cramps, sleep-related bruxism and sleep-related rhythmic movement disorder) under the category entitled sleep-related movement disorders. Moreover, apparently physiological movements (e.g. alternating leg muscle activation and excessive hypnic fragmentary myoclonus) can show a high frequency and severity impairing sleep quality. Clinical and, in specific cases, neurophysiological assessments are required to detect the presence of nocturnal movement complaints. Patients reporting poor sleep due to these abnormal movements should undergo non-pharmacological or pharmacological treatments.

Sleep bruxism (SB) is a common sleep-related motor disorder characterized by tooth grinding and clenching. SB diagnosis is made on history of tooth grinding and confirmed by polysomnographic recording of electromyographic (EMG) episodes in the masseter and temporalis muscles. The typical EMG activity pattern in patients with SB is known as rhythmic masticatory muscle activity (RMMA). The authors observed that most RMMA episodes occur in association with sleep arousal and are preceded by physiologic activation of the central nervous and sympathetic cardiac systems. This article provides a comprehensive review of the cause, pathophysiology, assessment, and management of SB.

The aim of the present study was to examine the role of genetic and environmental factors in the phenotypic variance of bruxism in a large population-based cohort of young adult twins in Finland.|The material of the present study derives from the FinnTwin16 cohort study consisting of five birth cohorts of twin pairs born in 1975-1979 who completed a questionnaire (at mean age 24, range 23-27 years) with data on frequency of sleep-related bruxism in 2000-2002. We used quantitative genetic modeling, based on the genetic similarity of monozygotic and dizygotic twins, to estimate the most probable genetic model for bruxism, based on decomposition of phenotypic variance into components:additive genetic effects (A), dominant genetic effects (D), and non-shared environmental effects (E).|On average, 8.7% experienced bruxism weekly, 23.4% rarely, and 67.9% never, with no significant gender difference (p = .052). The best fitting genetic model for bruxism was the AE-model. Additive genetic

The aim of this study was to evaluate the association between masticatory performance (MP) and bite force (BF) in children with sleep bruxism (SB) during the mixed dentition stage, considering also the occlusal characteristics. The sample was composed by 52 healthy children of both genders, aged 6-10years. From those, 22 presented signs and symptoms of SB and 30 were the controls. SB diagnosis consisted of both parental report and presence of tooth wear. MP was evaluated by the individual's ability to communicate an artificial chewable test material for determining the median particle size (X50) and distribution of particles in the different sieves (b). BF was measured using a digital gnathodynamometer with fork strength of 8mm. The results were submitted to descriptive statistics, Mann-Whitney and chi-square tests, Spearman's correlation and multiple logistic regression. Mean BF and X50 did not differ between groups with and without SB. A significant negative correlation was

This study was conducted to verify the results of a preceding retrospective pilot study by means of a prospective controlled investigation including a larger sample size. Therefore, the aim of this clinical investigation was to analyze the relationship between sleep bruxism and several functional and occlusal parameters. The null hypothesis of this study was that there would be no differences among sleep bruxism subjects and non-sleep bruxism controls regarding several functional and occlusal parameters. Fifty-eight sleep bruxism subjects and 31 controls participated in this study. The diagnosis sleep bruxism was based on clinical criteria of the American Academy of Sleep Medicine. Sixteen functional and occlusal parameters were recorded clinically or from dental study casts. Similar to the recently published retrospective pilot study, with a mean slide of 0.77mm (s.d., 0.69mm) in the sleep bruxism group and a mean slide of 0.4mm (s.d., 0.57mm) in the control group, the

Sleep bruxism, an intensified manifestation of rhythmic masticatory muscle activity, characterized by tooth grinding or clenching during sleep, lacks a definitive physiological purpose. This paper posits that physiologically, sleep bruxism is an autonomic self-regulatory response to nighttime occurrences of tachycardia stemming from the brain experiencing microarousals during sleep. Sleep bruxism by triggering the trigeminal cardiac reflex leads to bradycardia. Rhythmic masticatory muscle activity-sleep bruxism, thereby, serves to slow the heart rate when brain microarousals cause tachycardia.

To explore the relationship between sleep bruxism (SB), painful temporomandibular disorders (TMD) and psychologic status in a cross-sectional study. The sample consisted of 272 individuals. The Research Diagnostic Criteria for TMD (RDC/TMD) was used to diagnose TMD; SB was diagnosed by clinical criteria proposed by The American Academy of Sleep Medicine. The sample was divided into four groups: (1) patients without painful TMD and without SB, (2) patients without painful TMD and with SB, (3) patients with painful TMD and without SB and (4) patients with painful TMD and with SB. Data were analysed by Odds Ratio test with a 95% confidence interval. Patients with SB had an increased risk for the occurrence of myofascial pain (OR = 593, 95% CI: 319-1102) and arthralgia (234, 158-346). Group 3 had an increased risk for moderate/severe depression and non-specific physical symptoms (101, 367-2779; 147, 539-3992, respectively), and this risk increased in the presence