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At least 19 recordsLinked to original sources
PubMed2003

Neurobiological mechanisms involved in sleep bruxism.

Sleep bruxism (SB) is reported by 8% of the adult population and is mainly associated with rhythmic masticatory muscle activity (RMMA) characterized by repetitive jaw muscle contractions (3 bursts or more at a frequency of 1 Hz). The consequences of SB may include tooth destruction, jaw pain, headaches, or the limitation of mandibular movement, as well as tooth-grinding sounds that disrupt the sleep of bed partners. SB is probably an extreme manifestation of a masticatory muscle activity occurring during the sleep of most normal subjects, since RMMA is observed in 60% of normal sleepers in the absence of grinding sounds. The pathophysiology of SB is becoming clearer, and there is an abundance of evidence outlining the neurophysiology and neurochemistry of rhythmic jaw movements (RJM) in relation to chewing, swallowing, and breathing. The sleep literature provides much evidence describing the mechanisms involved in the reduction of muscle tone, from sleep onset to the atonia that characterizes rapid eye movement (REM) sleep. Several brainstem structures (e.g., reticular pontis oralis, pontis caudalis, parvocellularis) and neurochemicals (e.g., serotonin, dopamine, gamma aminobutyric acid [GABA], noradrenaline) are involved in both the genesis of RJM and the modulation of muscle tone during sleep. It remains unknown why a high percentage of normal subjects present RMMA during sleep and why this activity is three times more frequent and higher in amplitude in SB patients. It is also unclear why RMMA during sleep is characterized by co-activation of both jaw-opening and jaw-closing muscles instead of the alternating jaw-opening and jaw-closing muscle activity pattern typical of chewing. The final section of this review proposes that RMMA during sleep has a role in lubricating the upper alimentary tract and increasing airway patency. The review concludes with an outline of questions for future research.

Adult↗
PubMed2006

A psychological study on patients with masticatory muscle disorder and sleep bruxism.

Sleep bruxism (SB) has been believed to be related to stress and psychosocial factors, however their implicit relationship has remained unclear. This study was conducted on patients visiting our clinic with SB and masticatory muscle disorders (MMD) for the purpose of clarifying personality and behavioral traits. This study was conducted on patients of MMD visiting our clinic. The Rosenzweig Picture-Frustration study was performed on each patient. Twenty-seven (27) patients were divided into two groups: 17 patients with SB and 10 patients without. The SB group showed a significantly lower level of E (extrapunitive) reaction than the nonSB group. SB patients showed a significantly higher level of M (impunitive) reaction than those without SB. Concerning the directions of aggression, the percentage of E-A (extraaggression) was significantly lower in SB patients than in those without. On the other hand, the percentage of I-A (intraaggression) was significantly higher in patients with SB than those without. Our study found a new aspect of the patients with MMD and SB: they are not only intraaggressive, but are also unable to be extrapunitive and extraaggressive. Consequently, they are unable to demonstrate adequate self-assertiveness in stressful situations.

Adolescent↗
PubMed2002

Sleep bruxism related to obstructive sleep apnea: the effect of continuous positive airway pressure.

Several studies have reported that sleep bruxism rarely occurs in isolation. Recently, in an epidemiological study of sleep bruxism and risk factors in the general population, it was found that among the associated sleep symptoms and disorders obstructive sleep apnea (OSA) was the highest risk factor for tooth grinding during sleep. The purpose of this report was to evaluate the effect of continuous positive airway pressure (CPAP) on sleep bruxism in a patient with both severe OSA and sleep tooth grinding. Two polysomnographic (PSG) recordings were carried out. The first showed 67 events of sounded tooth grinding, most of them appearing as an arousal response at the end of apnea/hypopnea events in both the supine and lateral postures. During the CPAP titration night most breathing abnormalities were eliminated and a complete eradication of the tooth grinding events was observed. The results of this study suggest that when sleep bruxism is related to apnea/hypopneas, the successful treatment of these breathing abnormalities may eliminate bruxism during sleep.

Journal Article↗
PubMed2000

Sleep bruxism in patients with sleep-disordered breathing.

The aim was to test the hypothesis of a direct association between sleep-disordered breathing and sleep bruxism. The frequency of masseter contraction (MC) episodes and rhythmic jaw movements (RJM) was measured in patients with mild and moderate obstructive sleep apnoea (OSA). The diagnosis of sleep bruxism was made from a combination of questionnaire, clinical observation and all-night polysomnographic recording which included masseter electromyography. A total of 21 patients (19 males/two females, mean age 40.0 years+/-9.2 SD) were randomly selected from a provisional diagnosis of snoring and OSA by a sleep physician. In the patients with mild OSA [n=11, mean apnoea hypopnoea index (AHI)=8.0+/-4.1 SD, body mass index (BMI)=29.1+/-5.0], the diagnosis of sleep bruxism was made in six out of 11 patients (54%); similarly, four out of 10 patients (40%) with moderate OSA (n=10, mean AHI=34.7+/-19.1, BMI=30.6+/-5.0) were identified as bruxists. Although the combination of clinical, subjective estimation and nocturnal electromyographic recording of masseter muscle might provide a more solid base for the diagnosis of sleep bruxism, the result is biased by the variation in the bruxing activity. MC episodes were associated with the termination of apnoea or hypopnoea episodes in only 3.5% of the mild group and 14.4% of the moderate group (p<0.05). It appears that sleep bruxism is rarely directly associated with apnoeic events, but is rather related to the disturbed sleep of OSA patients.

Adult↗
PubMed2003

Association between sleep bruxism, swallowing-related laryngeal movement, and sleep positions.

STUDY OBJECTIVE: To describe the relationships of sleep bruxism to swallowing and sleep positions. DESIGN: Controlled descriptive study. SETTING: Polysomnography and audio-video recordings were done in a hospital sleep laboratory. PARTICIPANTS: Nine patients with sleep bruxism and 7 normal subjects were matched for age and sex. INTERVENTIONS: n/a. MEASUREMENTS AND RESULTS: During sleep, patients with sleep bruxism showed a higher frequency of rhythmic masticatory muscle activity episodes (6.8 +/- 1.0 [SEM]/h) than did normals (0.5 +/- 0.1/h, p < 0.01). Swallowing-related laryngeal movements occurred more frequently in sleep of patients with sleep bruxism (6.8 +/- 0.8/h) than in normals (3.7 +/- 0.3/h, p < 0.01). In both groups, during sleep, close to 60% of rhythmic masticatory muscle activity episodes were associated with swallowing. In sleep bruxism patients, 68% of swallowing events occurred during rhythmic masticatory muscle activity episodes, while only 10% of swallowing events were associated with rhythmic masticatory muscle activity in normal subjects. Sleep bruxism patients and normals spent 95.5% and 87.3% of sleeping time in the supine and lateral decubitus positions, respectively. In both groups, up to 96% of rhythmic masticatory muscle activity and swallowing were observed in the supine and lateral decubitus position. In sleep bruxism patients, although sleeping time did not differ between the 2 sleeping body positions, 74% of rhythmic masticatory muscle activity and swallowing events were scored in the supine position compared to 23% in the lateral decubitus position. CONCLUSIONS: During sleep, rhythmic masticatory muscle activity is often associated with swallowing. In sleep bruxism patients, most of these oromotor events are observed in the supine position. The physiologic link between rhythmic masticatory muscle activity and swallowing and the clinical relevance of sleep position in sleep bruxism management need to be investigated.

Adult↗
PubMed2001

Risk factors for sleep bruxism in the general population.

OBJECTIVE: Sleep bruxism can have a significant effect on the patient's quality of life. It may also be associated with a number of disorders. However, little is known about the epidemiology of sleep bruxism and its risk factors in the general population. DESIGN: Cross-sectional telephone survey using the Sleep-EVAL knowledge based system. SETTINGS: Representative samples of three general populations (United Kingdom, Germany, and Italy) consisting of 158 million inhabitants. PARTICIPANTS: Thirteen thousand fifty-seven subjects aged > or = 15 years (United Kingdom, 4,972 subjects; Germany, 4,115 subjects; and Italy, 3,970 subjects). INTERVENTION: None. MEASUREMENTS: Clinical questionnaire on bruxism (using the International Classification of Sleep Disorders [ICSD] minimal set of criteria) with an investigation of associated pathologies (ie, sleep, breathing disorders, and psychiatric and neurologic pathologies). RESULTS: Grinding of teeth during sleep occurring at least weekly was reported by 8.2% of the subjects, and significant consequences from teeth grinding during sleep (ie, muscular discomfort on awakening, disturbing tooth grinding, or necessity of dental work) were found in half of these subjects. Moreover, 4.4% of the population fulfilled the criteria of ICSD sleep bruxism diagnosis. Finally, subjects with obstructive sleep apnea syndrome (odds ratio [OR], 1.8), loud snorers (OR, 1.4), subjects with moderate daytime sleepiness (OR, 1.3), heavy alcohol drinkers (OR, 1.8), caffeine drinkers (OR, 1.4), smokers (OR, 1.3), subjects with a highly stressful life (OR, 1.3), and those with anxiety (OR, 1.3) are at higher risk of reporting sleep bruxism. CONCLUSIONS: Sleep bruxism is common in the general population and represents the third most frequent parasomnia. It has numerous consequences, which are not limited to dental or muscular problems. Among the associated risk factors, patients with anxiety and sleep-disordered breathing have a higher number of risk factors for sleep bruxism, and this must raise concerns about the future of these individuals. An educational effort to raise the awareness of dentists and physicians about this pathology is necessary.

Adolescent↗
PubMed2001

Variability in sleep bruxism activity over time.

Sleep bruxism (SB) is an oral activity associated with jaw movements and tooth grinding. Sleep bruxism is believed to be highly variable over time, with subjects showing no activity on some nights and intense activity on others. Assessment of SB variability in individual patients is necessary for clinical trials designed to estimate the efficacy of SB management strategies. The present study analysed SB night-to-night variability over time in nine moderate to severe SB patients. Excluding the first night for habituation, a total of 37 nights were analysed, with a range of 2-8 nights per subject. The interval between the first and the last recording was between 2 months and 7.5 years. The outcomes were the number of SB episodes per hour, number of SB bursts per hour and number of SB episodes with grinding noise. The within subject variability of the three SB oromotor outcomes was evaluated using standard deviation (SD) and coefficient of variation. To verify the diagnosis of subjects over time, the values of the oromotor outcomes were compared with a standard research diagnostic cut-off: (1) Number of SB episodes per hour >4, (2) Number of SB bursts per hour >25, (3) Number of SB episodes with noise per night >1 (Lavigne et al. 1996). The mean coefficient of variation for the nine subjects was 25.3% for SB episodes per hour, 30.4% for SB bursts per hour and 53.5% for episodes with noise. Linear regression showed that the number of SB episodes per hour of stages 1 and 2 explains a large proportion of the variability. The SB diagnosis remained constant over time for every subject: 35 nights over 37 respected criteria 1 and 2, while grinding was present every night. These results indicate that while the SB diagnostic remains relatively constant over time in moderate to severe sleep bruxers, individual variability could be important in some SB patients.

Adult↗
PubMed2006

The effect of 2 sympatholytic medications--propranolol and clonidine--on sleep bruxism: experimental randomized controlled studies.

STUDY OBJECTIVE: 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. DESIGN: Experimental randomized controlled crossover studies with placebo and active treatments (propranolol 120 mg; clonidine 0.3 mg). SETTING: Hospital-based sleep research laboratory. PATIENTS: Twenty-five subjects with a history and diagnosis of SLEEP BRUXISM (11 men, 14 women; age range, 21 to 31 years). INTERVENTION: Polygraphic study. MEASUREMENTS AND RESULTS: 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). CONCLUSION: 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.

Adrenergic alpha-Agonists↗
PubMed1998

Sleep bruxism is a disorder related to periodic arousals during sleep.

There is evidence that sleep bruxism is an arousal-related phenomenon. In non-REM sleep, transient arousals recur at 20- to 40-second intervals and are organized according to a cyclic alternating pattern. Polysomnographic recordings from six subjects (two females and four males) affected by sleep bruxism (patients) and six healthy age-and gender-matched volunteers without complaints about sleep (controls) were analyzed to: (1) compare the sleep structure of bruxers with that of non-complaining subjects; and (2) investigate the relations between bruxism episodes and transient arousals. Patients and controls showed no significant differences in conventional sleep variables, but bruxers showed a significantly higher number of the transient arousals characterized by EEG desynchronization. Bruxism episodes were equally distributed between non-REM and REM sleep, but were more frequent in stages 1 and 2 (p < 0.0001) than in slow-wave sleep. The great majority of bruxism episodes detected in non-REM sleep (88%) were associated with the cyclic alternating pattern and always occurred during a transient arousal. Heart rate during the bruxism episodes (69.3+/-18.2) was significantly higher (p < 0.0001) than that during the pre-bruxing period (58.1+/-15.9). Almost 80% of all bruxism episodes were associated with jerks at the anterior tibial muscles. The framework of the cyclic alternating pattern offers a unified interpretation for sleep bruxism and arousal-related phenomena.

Adult↗
PubMed1997

Cigarette smoking as a risk factor or an exacerbating factor for restless legs syndrome and sleep bruxism.

Cigarette smoking has been associated with sleep disturbances. However, little is known about how smoking affects restless legs syndrome (RLS) and sleep bruxism, two movement disorders associated with sleep. From a nationwide survey of 2,019 Canadian adults, we estimated the prevalence of smoking to be 36%. Although there was no difference between smokers and nonsmokers for RLS prevalence, almost twice as many smokers (12%) as nonsmokers (7%) were aware of experiencing sleep bruxism. The estimated risk of a smoker suffering from RLS was nonsignificant. On the other hand, the risk of a smoker grinding his or her teeth was moderate (odds ratio = 1.9). Analysis of sleep laboratory findings revealed no differences in motor RLS and periodic leg movements in sleep (PLMS) indices between smoking and nonsmoking patients; after adjustment for age, there were no differences in sleep efficiency, latency, number of awakenings, or the arousal index for the RLS/PLMS patients. Among those suffering from bruxism, smokers had more tooth-grinding episodes than did nonsmokers (35.0 vs. 7.0; p = 0.056); none of the sleep variables differentiated sleep bruxism smokers from nonsmokers. It appears that cigarette smoking does not influence RLS/PLMS, whereas the risk that smoking and tooth grinding are concomitant is moderate. Smoking was not significantly associated with more motor activity in RLS/PLMS, but more grinding was noted in sleep bruxism.

Adult↗
PubMed2000

Sleep bruxism; an overview of an oromandibular sleep movement disorder. REVIEW ARTICLE.

Sleep bruxism (SB) is a stereotyped movement disorder characterized by grinding or clenching of the teeth during sleep. The majority of the population will at some time during their lifetime grind or clench their teeth. It becomes a pathological condition when the subject presents severe tooth damage or complains of non-restorative sleep. The prevalence of SB is difficult to estimate, since quite often the subjects are unaware of having the disorder. There is no gender difference. SB is more frequent in the younger generation, with a decline over age. The symptom recognized in children can persist in adulthood. The aetio-pathophysiology is still unclear. SB has been associated with tooth interference, psychosocial and environmental factors, brain transmitters and basal ganglia dysfunction. Attempts have been made to specify the personality traits of bruxers, reported to be greater anxiety or vulnerability to stress; however, this is still controversial. SB subjects were observed to present vigilance-sleepiness and somatic problems. However, they are generally good sleepers. Some authors reported SB during all sleep stages, others observed the majority of bruxe episodes during light sleep and REM and often associated with arousal transients. No abnormalities of the autonomic nervous system could be shown in awake SB subjects. While some studies have shown an association between SB and PLM or breathing disorders, others did not confirm this. There is no specific treatment for SB: each subject has to be individually evaluated and treated. Three management alternatives are used: dental, pharmacological and psychobehavioural.

Journal Article↗
PubMed2006

Sleep bruxism and temporomandibular disorder: Clinical and polysomnographic evaluation.

OBJECTIVE: To seek better understanding of chronic musculoskeletal facial pain and its relation to sleep bruxism, by comparing patients with sleep bruxism, with and without temporomandibular disorder. DESIGN: Forty sleep bruxism patients were evaluated according to the Research Diagnostic Criteria for Temporomandibular Disorders: group A-20 patients with myofascial pain, 3 men, 17 women; average age 32.7yr; mean duration of pain 4.37yr; group B-20 without myofascial pain, 5 men, 15 women; average age 30.8yr. Sleep and bruxism were evaluated in one-night polysomnography. RESULTS: There were no statistically significant differences for bruxism and sleep variables of the two groups: number of bursts and bruxism episodes per hour, amplitude and duration of bruxism episodes, sleep efficiency and latency, percentage of non-REM and REM sleep, respiratory events, periodic limb movements, and micro-arousals. CONCLUSIONS: The polysomnographic characteristics of patients with sleep bruxism, with and without orofacial pain, are similar. More studies are necessary to clarify the reasons why some sleep bruxism patients develop chronic myofascial pain, and others do not.

Adolescent↗
PubMed2005

[Influence of sleep bruxism on dislodgement of dental restorations].

PURPOSE: This study investigated the correlation between strength of sleep bruxism and dislodgement of dental restorations, by both using the facet index of occlusal splint for sleep bruxism and measuring the dislodgement rate of dental restorations. METHODS: Subjects consisted of 422 patients with 3673 dental restorations (inlay, crown, jointed crowns, and bridge) referred to the hospital from 1976 to 2004 who were randomly selected from 912 patients. All patients wore an occlusal splint during sleep. Ink was placed on the occlusal part of the splint and the strength of sleep bruxism was evaluated by the wearing away of the ink and indentation on the splint (Ikeda's method). The subjects were classified into the following four groups according to the evaluation: B-0: no facet on the splint, B-1: slight facet with wearing of the ink but no indentation on the splint, B-2: slight indentation on the splint, and B-3: notable indentation on the splint, and then the dislodgement rate between the groups was compared. The mean evaluation time in each patient was 10.1 years. RESULTS: The rate of patients with dislodgement was B-1: 12.7%, B-2: 35.1%, and B-3: 43.8%. The dislodgement rates of categorized restorations in groups B-1, B-2, and B-3 15 years after the placement were, restorations: 9%, 18%, and 24%, inlay: 19%, 24%, and 32%, and crown: 5%, 12%, and 13%, respectively. CONCLUSIONS: It is proved that the evaluation method using the facet index of occlusal splint for sleep bruxism is a reliable means of estimating how long the restoration will last. The results showed that sleep bruxism influences the dislodgement of restorations. To protect restorations, it might be effective to control the load from sleep bruxism.

Dental Restoration Failure↗
PubMed2002

Habitual snoring and sleep bruxism in a paediatric outpatient population in Hong Kong.

OBJECTIVE: To determine the prevalence of habitual snoring and sleep bruxism in children attending the out-patient clinics of a paediatric department. METHODOLOGY: A cross-sectional survey of parents was conducted with questionnaire administered by paediatric nurses. Parents were recruited when they brought their children to the out-patient clinics. Sex and age were recorded. Presence and absence of habitual snoring and sleep bruxism were noted. Types of diseases that brought the children to the out-patient clinics were also noted. RESULTS: Twenty-nine of the 200 recruited children were noted to have habitual snoring (14.5%, 95% C.I. 10%-20%). The mean age of these habitual snorers was 6.2 +/- 3.1 years. For habitual snorers, male to female ratio was 1.4 to 1. Sixteen of these 28 children accepted a sleep polysomnographic examination. Eleven children were found to have snoring during the night of study. Two were found to have obstructive sleep apnoea syndrome. Sleep bruxism was found in 17 children (8.5%, 95% C.I.5%-13%). Sleep bruxism was closely related to habitual snoring as 16 out of the 17 children with sleep bruxism were also habitual snorers (p < 0.0001). CONCLUSION: Habitual snoring and sleep bruxism were commonly found in children attending paediatric clinics. Paediatricians should be aware of these problems and be prepared to deal with them. Habitual snoring and sleep bruxism were closely related. Further studies into this relationship is needed.

Ambulatory Care Facilities↗
PubMedDate not supplied

Double-blind, crossover, placebo-controlled trial of bromocriptine in patients with sleep bruxism.

This study was designed to assess the effects of bromocriptine, a dopamine D2 receptor agonist, on sleep bruxism. Seven otherwise healthy patients with severe and frequent sleep bruxism participated in this randomized, double-blind, placebo-controlled study. The study used a crossover design that included 2 weeks of active treatment or placebo with a washout period of 1 week. To further evaluate whether bromocriptine influences striatal D2 receptor binding, we used iodine-123-iodobenzamide single photon emission computed tomography (SPECT) under both placebo and bromocriptine regimens. Bromocriptine did not reduce the frequency of episodes of bruxism during sleep (mean +/- SEM, 9.0 +/- 1.0 and 9.6 +/- 1.5 bruxism episodes per hour for placebo and bromocriptine, respectively) or the amplitude of masseter muscle contractions (root mean square values, 48.2 +/- 15.5 microV and 46.9 +/- 12.7 microV for placebo and bromocriptine, respectively). SPECT also failed to reveal that either treatment had any influence on striatal D2 binding (values for total binding in counts/pixel, 1.80 [1.72-1.93] and 1.79 [1.56-1.87] for placebo and bromocriptine, respectively). This study shows that a nightly dose of bromocriptine does not exacerbate or reduce sleep bruxism motor activity.

Adult↗
PubMed1997

Effects of the D2 receptor agonist bromocriptine on sleep bruxism: report of two single-patient clinical trials.

An altered dopamine receptor status has been associated with sleep bruxism. Evidence from a functional neuro-imaging study has implicated an abnormal side imbalance in striatal D2 receptor expression in its pathophysiology. To assess the significance of this finding, we studied the effects of short-term administration of the preferential dopamine D2 receptor agonist bromocriptine on sleep bruxism in a double-blind, placebo-controlled polysomnographic and neuro-imaging study with a single crossover design. Six otherwise healthy and drug-free patients with sleep bruxism were entered into the trial. One of the patients dropped out due to an intercurrent illness, while three others were discontinued from the study due to severe adverse reactions to bromocriptine. Because of the high frequency and intensity of the side-effects, the trial was interrupted. Two patients, however, completed the trial without any adverse reactions. Their outcome measures are presented as single-patient clinical trials. Following a two-week administration of bromocriptine, both patients showed a decrease in the number of bruxism episodes per hour of sleep of about 20% to 30% with respect to the placebo. WHile no significant differences between both conditions (i.e., placebo and bromocriptine) were found for the number of bruxism bursts per episode, significantly lower root-mean-squared EMG levels per bruxism burst occurred during bromocriptine use. In association with this polysomnographically established attenuation of sleep bruxism, bromocriptine afforded a decreased normal side distribution of striatal D2 receptor binding, as was evidenced by single-photon-emission computed tomography using the radioactive D2 receptor antagonist iodine-123-iodobenzamide. This study supports previous suggestions that the central dopaminergic system may be involved in the modulation of sleep bruxism. To see if the present findings apply across a population, investigators should use a peripheral D-2 antagonist to prevent side-effects.

Adult↗
PubMed1996

Striatal D2 receptor binding in sleep bruxism: a controlled study with iodine-123-iodobenzamide and single-photon-emission computed tomography.

The neurochemical mechanisms underlying sleep bruxism are little understood at present. However, recent pharmacologic evidence suggests that the central dopaminergic system may be involved in the pathophysiology of sleep bruxism. This possibility was further assessed by means of functional neuroimaging of dopamine D2 receptors with single-photon-emission computed tomography (SPECT). Ten controls and ten patients with polysomnographically confirmed sleep bruxism were injected intravenously with 185 MBq (5 mCi) iodine-123-iodobenzamide, a specific D2 receptor antagonist radioligand, and data acquisition was performed 90 min post-injection. Following image reconstruction, it was found that striatal D2 receptor binding potential (basal ganglia/background ratio) did not differ significantly between bruxism patients and controls. However, side-to-side differences between unilateral values of the striatal D2 binding potential ("highest side" values minus "lowest side" values) were significantly larger for the bruxism patients (p < 0.001, by two-independent-samples t test with pooled variances). It was concluded that an abnormal side imbalance in striatal D2 receptor expression can be associated with sleep bruxism. This reinforces the possibility that the central dopaminergic system plays a role in the pathophysiology of this disorder.

Adult↗
PubMed2002

Lower number of K-complexes and K-alphas in sleep bruxism: a controlled quantitative study.

OBJECTIVES: Although patients with sleep bruxism (SB) show a higher incidence of rhythmic masticatory muscle activity (RMMA) during sleep than matched normal controls, they are good sleepers. Sleep macrostructure (e.g. total sleep time, sleep latency, number of awakenings or sleep stage shifts and sleep stage duration) is similar between groups. Differences in sleep microstructure between SB patients and normals have been investigated only in few studies. The aim of the present study was to quantify number of microarousals, K-complexes, K-alphas, EEG spindles, and the density of slow wave activity, in both groups, in order to better understand the pathophysiology of SB. METHODS: Ten normal sleepers were matched for age and gender with 10 patients who exhibited frequent tooth-grinding during sleep. Using quantitative polysomnographic measures, we compared the above-mentioned sleep variables in both groups. Data are presented as indices for total sleep and for consecutive non-rapid eye movement (non-REM) episodes over non-REM to rapid eye movement (REM) cycles and per hour of sleep. RESULTS: SB patients showed 6 times more RMMA episodes per hour of sleep than normals (P<0.001), with a higher frequency in the second and third non-REM to REM cycles. SB patients presented 42.7% fewer K-complexes per hour of stage 2 sleep, but only normals showed a decline from the first to fourth non-REM episode. Only 24% of SB-RMMA episodes were associated with K-complexes in 60 s. The number of K-alphas was 61% lower in SB patients, no change across non-REM episodes was noted. While no difference in electroencephalographic (EEG) spindles or slow wave activity (SWA) was observed between groups, EEG spindles increased and SWA decreased linearly over consecutive non-REM to REM cycles. CONCLUSIONS: According to our observations, good sleep in SB patients is characterized by a low incidence of K-complexes or K-alphas and by the absence of any difference in other sleep microstructure variables or SWA.

Adult↗