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ABSTRACT: 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.
Dental clinics of North America 04/2012; 56(2):387-413.
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ABSTRACT: Sleep bruxism, a well-known burden for dentists, is commonly observed in pediatric populations. Dentists are responsible for the detection and prevention of the detrimental consequences on the stomatognathic system that may occur in some patients with sleep bruxism. However, sleep bruxism is much more than tooth wear, since it is frequently associated with orofacial pain, headaches, and other more severe sleep disorders, such as sleep-disordered breathing. Although the mechanisms underlying the possible interactions among sleep bruxism, headaches, and sleep-disordered breathing need further research, these conditions are often concomitant. A literature search was performed to identify relevant publications related to the topic, which have been integrated in this topical review. The aim of this article was to provide a brief overview on sleep bruxism, headaches, and sleep-disordered breathing in pediatric patients and to promote a multispecialist approach (including dentists, sleep specialist physicians, and psychologists) in the diagnosis and management of these frequently associated disorders.
Journal of orofacial pain 01/2012; 26(4):267-76. · 2.59 Impact Factor
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ABSTRACT: Sleep bruxism (SB) is a movement disorder identified by grinding of teeth and rhythmic masticatory muscle activity (RMMA). RMMA is associated with body movements and cortical arousals. Increases in autonomic sympathetic activities that characterize sleep cortical arousal precede RMMA/SB. Based on these findings, this study examined whether RMMA/SB episodes are also associated with significant changes in arterial blood pressure (BP).
Participants underwent 3 nights of full polysomnography that included noninvasive beat-to-beat BP recording. Single RMMA/SB episodes and arousal episodes were analyzed in stage 2 sleep and categorized as: (i) RMMA/SB + arousal; (ii) RMMA/SB + body movement; (iii) RMMA/SB + arousal + body movement; or (iv) arousal alone. Sleep and RMMA/SB data were compared to a Non SB group. RMMA/SB clusters (RMMA/SB episodes ≤ 30 sec apart) were also analyzed.
Sleep Laboratory at l'Hôpital du Sacré-Coeur de Montréal.
Ten young, healthy participants with SB (mean age = 26 ± 1.8 years) and 9 without SB (mean age = 29 ± 1.2 years).
N/A MEASUREMENTS AND RESULTS: BP increased with all RMMA/SB and arousal episodes (P ≤ 0.05). The average maximum BP surges (systolic/diastolic ± SE mm Hg) were: 25.6 ± 3.3/12.6 ± 2.0 for RMMA/SB + arousal; 30.1 ± 1.7/19.1 ± 1.9 for RMMA/SB + body movement; 26.0 ± 2.8/15.1 ± 2.0 for RMMA/SB + arousal + body movement; 19.4 ± 2.3/8.9 ± 1.2 for arousal alone; and for RMMA/SB clusters: Episode: 1: 26.2 ± 8.7/16.4 ± 5.7; Episode 2: 21.1 ± 7.9/12.6 ± 6.4.
Rhythmic masticatory muscle activity/sleep bruxism (RMMA/SB) is associated with blood pressure fluctuations during sleep. Arousals and body movements often occur with RMMA/SB and can impact the magnitude of this BP surge.
Sleep 01/2012; 35(4):529-36. · 5.05 Impact Factor
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ABSTRACT: Sleep-related bruxism (SB) and wake-time tooth clenching (TC) have been associated with temporomandibular disorders (TMDs), headache, and sleep and behavioral complaints. This study aimed to assess the prevalence and risk factors of these signs and symptoms in a 7- to 17-yr-old population (n = 604) seeking orthodontic treatment. Data were collected by questionnaire and by a clinical examination assessing craniofacial morphology and dental status. Sleep-related bruxism was reported by 15% of the population and TC was reported by 12.4%. The SB group (n = 58) was mainly composed of children (67.3% were ≤12 yr of age) and the TC group (n = 42) was mainly composed of adolescents (78.6% were ≥13 yr of age). The craniofacial morphology of over 60% of SB subjects was dental class II and 28.1% were a brachyfacial type. Compared with controls (n = 220), SB subjects were more at risk of experiencing jaw muscle fatigue [adjusted OR (AOR) = 10.5], headache (AOR = 4.3), and loud breathing during sleep (AOR = 3.1). Compared with controls, TC subjects reported more temporomandibular joint clicking (AOR = 5), jaw muscle fatigue (AOR = 13.5), and several sleep and behavioral complaints. Sleep- and wake-time parafunctions are frequently associated with signs and symptoms suggestive of TMDs, and with sleep and behavioral problems. Their clinical assessment during the planning of orthodontic treatment is recommended.
European Journal Of Oral Sciences 10/2011; 119(5):386-94. · 1.88 Impact Factor
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ABSTRACT: The majority of patients suffering from musculoskeletal chronic widespread pain (CWP) are females, and they tend to report poor sleep. We tested the hypothesis that the poor sleep of female patients reporting CWP is gender specific for changes in (1) electroencephalograph (EEG) features and (2) heart rate variability (HRV).
Twenty-four normal sleepers were compared to 24 patients with CWP who complained of poor sleep. Patients were referred from general practice and were matched for age (41-47 years) and gender (25 W, 23 M). Sleep variables and spectral EEG activity analyses were performed during 1 night of sleep recording. Time-domain cardiac RR interval and spectral autoregressive analyses were also performed from the same data set.
Compared to normal females, female patients with CWP had significantly shorter sleep duration (-68 min), lower sleep efficiency (-9.9%), twice the awakenings and a trend for more periodic limb movements per hour of sleep. Daytime napping was reported by 78% of CWPs. Compared to all controls, females with CWP had significantly less power in the EEG delta band in the first and second non-REM sleep cycle. Although RR interval analysis revealed that CWP patients had a faster heart rate, neither the sympathetic nor sympathovagal analysis reached statistical significance for gender or pain status comparisons.
Female CWP patients have shorter sleep duration with many awakenings and lower sleep EEG delta activity without gender difference in HRV.
Sleep Medicine 02/2011; 12(2):179-85. · 3.40 Impact Factor
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ABSTRACT: Clonidine disrupts the NREM/REM sleep cycle and reduces the incidence of rhythmic masticatory muscle activity (RMMA) characteristic of sleep bruxism (SB). RMMA/SB is associated with brief and transient sleep arousals. This study investigates the effect of clonidine on the cyclic alternating pattern (CAP) in order to explore the role of cyclic arousal fluctuation in RMMA/SB.
Polysomnographic recordings from a pharmacological study.
University sleep research laboratory.
Sixteen SB subjects received a single dose of clonidine or placebo at bedtime in a crossover design.
Sleep variables and RMMA/SB index were evaluated. CAP was scored to assess arousal instability between sleep-maintaining processes (phase A1) and stronger arousal processes (phases A2 and A3). Paired t-tests, ANOVAs, and cross-correlations were performed. Under clonidine, CAP time, and particularly the number of A3 phases, increased (P≤0.01). RMMA/SB onset was time correlated with phases A2 and A3 for both placebo and clonidine nights (P≤0.004). However, under clonidine, this positive correlation began up to 40 min before the RMMA/SB episode.
CAP phase A3 frequency increased under clonidine, but paradoxically, RMMA/SB decreased. RMMA/SB was associated with and facilitated in CAP phase A2 and A3 rhythms. However, SB generation could be influenced by other factors besides sleep arousal pressure. NREM/REM ultradian cyclic arousal fluctuations may be required for RMMA/SB onset.
Sleep 12/2010; 33(12):1711-6. · 5.05 Impact Factor
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ABSTRACT: Between 50% and 89% of chronic pain patients report unrefreshing sleep. The aim of this retrospective analysis was to compare the sleep of normal subjects with the sleep of a clinical population presenting musculoskeletal chronic widespread pain (CWP), psychophysiological insomnia and restless legs syndrome/periodic limb movements during sleep (RLS/PLMS) in order to identify sleep variables that may explain the poor sleep complaints of CWP patients.
Sleep data from 10 normal subjects and 37 patients (mean age 55+/-3 yo), matched for age and sex, were retrieved from our sleep data bank. Sub-analysis controlled for the effects of medication.
In comparison to normal subjects, sleep duration was shorter in CWP patients (-71 min; p<0.01); sleep efficiency was significantly lower in CWP and insomnia patients (-10.1% and -11.1%, respectively; p<0.05). CWP and PLMS patients lost one non-rapid eye movement (REM) to REM sleep cycle (p<0.04). An intermediate level of PLM was observed during the sleep of CWP patients in comparison to normal subjects (8.8/h vs. 2.0/h) and PLMS patients (33/h). Regular use of non-narcotic analgesics did not seem to interfere with sleep variables.
The sleep of middle-aged patients with CWP is comparable to that of insomnia patients. The moderate level of PLM during sleep suggests that such sensory motor activity needs to be evaluated in patients suffering from chronic pain.
Sleep Medicine 05/2008; 9(4):352-61. · 3.40 Impact Factor
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ABSTRACT: Sleep bruxism may lead to a variety of problems, but its pathophysiology has not been completely elucidated. As such, there is no definitive treatment, but certain preventive measures and/or drugs may be used in acute cases, particularly those involving pain. This article is intended to guide clinician scientists to the treatment most appropriate for future clinical studies. To determine the best current treatment, 2 measures were used to compare the results of 10 clinical studies on sleep bruxism, 3 involving oral devices and 7 involving pharmacologic therapy. The first measure, the number needed to treat (NNT), allows several randomized clinical studies to be compared and a general conclusion to be drawn. The second measure, effect size, allows evaluation of the impact of treatment relative to a placebo using different studies of similar design. Taking into account the NNT, the effect size and the power of each study, it can be concluded that the following treatments reduce sleep bruxism: mandibular advancement device, clonidine and occlusal splint. However, the first 2 of these have been linked to adverse effects. The occlusal splint is therefore the treatment of choice, as it reduces grinding noise and protects the teeth from premature wear with no reported adverse effects. The NNT could not be calculated for an alternative pharmacologic treatment, short-term clonazepam therapy, which had a large effect size and reduced the average bruxism index. However, the risk of dependency limits its use over long periods. Assessment of efficacy and safety of the most promising treatments will require studies with larger sample sizes over longer periods.
Journal (Canadian Dental Association) 11/2007; 73(8):727-30. · 1.00 Impact Factor
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ABSTRACT: This is a short review paper presenting hypothesis to explain the mechanism that may be involved in the genesis of sleep bruxism (SB). In humans, SB is a repetitive sleep movement disorder mainly characterized by rhythmic masticatory muscle activity (RMMA) at a frequency of 1Hz and by occasional tooth grinding. Until recently, the mechanism by which RMMA and SB episodes are triggered has been poorly understood. It is reported that during light sleep, most SB episodes are observed in relation to brief cardiac and brain reactivations (3-15s) termed "micro-arousals". We showed that RMMA are secondary to a sequence of events in relation to sleep micro-arousals: the heart (increase in autonomic sympathetic activity) and brain are activated in the minutes and seconds, respectively, before the onset of activity in suprahyoid muscles and finally by RMMA in jaw closing masseter or temporalis muscles. In non-human primate study, we have shown that the excitability of cortico-bulbar pathways is depressed during sleep; no rhythmic jaw movements (RJM) are observed following intracortical microstimulation (ICMS) of cortical masticatory area (CMA) during sleep compared to the quiet awake state. The above results suggest that the onset of RMMA and SB episodes during sleep are under the influences of brief and transient activity of the brainstem arousal-reticular ascending system contributing to the increase of activity in autonomic-cardiac and motor modulatory networks.
Archives of Oral Biology 05/2007; 52(4):381-4. · 1.60 Impact Factor
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ABSTRACT: To examine whether 2 sympatholytic medications decrease sleep bruxism and prevent the rise in sympathetic activity preceding the onset of sleep bruxism: propranolol, a nonselective adrenergic beta-blocker, and clonidine, a selective alpha2-agonist.
Experimental randomized controlled crossover studies with placebo and active treatments (propranolol 120 mg; clonidine 0.3 mg).
Hospital-based sleep research laboratory.
Twenty-five subjects with a history and diagnosis of SLEEP BRUXISM (11 men, 14 women; age range, 21 to 31 years).
Polygraphic study.
Polygraphic sleep laboratory recordings were done for 4 nights: the first night was habituation, the second, sleep bruxism diagnosis; and 3 and 4 were study nights. The sleep bruxism index was estimated using masseter muscle activity. Heart rate variability was estimated with spectral analysis of RR intervals. Sleep and sleep bruxism variables were not significantly influenced by propranolol. A reduction of the mean RR intervals and of the sympathetic dominance (p < .05) was seen. Under clonidine, duration of sleep stage 2 was prolonged, whereas REM sleep was suppressed in 14 of 16 subjects with sleep bruxism. The sleep bruxism index was reduced by 61% (p < .05). Under clonidine, a reduction in heart rate and sympathetic dominance was observed in stable sleep and in the minute preceding the onset of sleep bruxism (p < .05).
Although propranolol did not affect sleep bruxism, clonidine decreased sympathetic tone in the minute preceding the onset of sleep bruxism, thus reducing sleep bruxism by preventing the sequence of autonomic to motor activation of sleep bruxism. This further supports the role of sympathetic activity in the pathophysiology of sleep bruxism. Because morning hypotension was seen in 19% of patients, further dose-dependant research is required to assess the safety of clonidine for the management of sleep bruxism.
Sleep 03/2006; 29(3):307-16. · 5.05 Impact Factor
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ABSTRACT: Sleep bruxism (SB) is an unusual orofacial movement described as a parafunction in dentistry and as a parasomnia in sleep medicine. Since several peripheral influences could be involved in sleep-wake regulation and the genesis of rhythmic jaw movements, the authors have reviewed the relevant literature to facilitate understanding of mechanisms possibly involved in SB genesis. Various animal and human studies indicate that during either wakefulness or anesthesia, orofacial sensory inputs (e.g., from periodontium, mucosa, and muscle) could influence jaw muscle activity. However, the role of these sensory inputs in jaw motor activity during sleep is unclear. Interestingly, during sleep, the jaw is usually open due to motor suppression; tooth contact most likely occurs in association with sleep arousal. Recent physiologic evidence supports an association between sleep arousal and SB; a sequential change from autonomic (cardiac) and brain cortical activities precede SB-related jaw motor activity. This suggests that the central and/or autonomic nervous systems, rather than peripheral sensory factors, have a dominant role in SB genesis. However, some peripheral sensory factors may exert an influence on SB through their interaction with sleep-wake mechanisms. The intent of this review is to integrate various physiologic concepts in order to better understand the mechanisms underlying the genesis of SB.
Journal of orofacial pain 02/2003; 17(3):191-213. · 2.59 Impact Factor
