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Sleep Bruxism: A Sleep-Related Movement Disorder
Abstract
Sleep bruxism (SB) is a sleep-related movement disorder characterized by rhythmic jaw muscle contractions with tooth-grinding sounds. SB may cause tooth wear, jaw muscle pain and discomfort, dental restoration failure, and temporal headache. A diagnosis of SB is confirmed using polysomnography and audio-video recordings. Although the causes of SB remain to be determined, the pathophysiology may be related to sleep homeostasis, neurochemicals, psychological factors, heritability, and the maintenance of oropharyngeal functions such as breathing and oral mucosa lubrication. The current trend in SB management is oriented toward the protection of orodental structures and the reduction of several risks rather than a cure. Behavioral, dental, and pharmacologic management is proposed because evidence-based data and safety assessments are missing.
... Bruxism, whether it occurs during wakefulness or sleep, is classifi ed into primary prevalence based on self-reports, a recent study has suggested that age is independently associated with the prevalence of SB. 11 Th e daytime form of bruxism, mainly characterized by clenching, is reported by 20% of the population with a gender diff erence (female more than male). 5 Daytime bruxism should be diff erentiated from SB because the two have been suggested to be diff erent entities. [3][4][5] Daytime clenching is mainly reactive and frequently induced in patients under life pressure or stress and anxiety, 4 whereas SB is involuntary and could be related to sleep-regulatory processes (e.g., sleep arousal). ...
... 5 Daytime bruxism should be diff erentiated from SB because the two have been suggested to be diff erent entities. [3][4][5] Daytime clenching is mainly reactive and frequently induced in patients under life pressure or stress and anxiety, 4 whereas SB is involuntary and could be related to sleep-regulatory processes (e.g., sleep arousal). [12][13][14] Patients with mild frequency of rhythmic jaw muscle activity during sleep, who also present tooth grinding related to a possible diagnostic of SB, do have more frequent self-reported awareness of daytime clenching than those with severe SB. 15 Th e interaction or relation between the two conditions, however, remains to be proven. ...
... Th e clinical diagnosis of SB is based on a suggestive history (e.g., self-reported tooth-grinding sounds, morning masticatory muscle fatigue) and a global orofacial examination (e.g., tooth wear, masseter muscle hypertrophy) (Table 41.2). 3,5 Th e history of tooth-grinding sounds reported by a sleep partner or parents is the most solid basis in recognizing a patient with SB. However, the presence of such sounds is variable over time (50%), and patients sleeping alone have no source of such history. ...
Sleep bruxism (SB) is a prevalent sleep related movement disorder, characterized by rhythmic jaw movements with intense jaw muscle contraction. It can damage tooth and dental prostheses, and trigger orofacial pain or headache. SB occurs in association with homeostatic sleep regulation and sleep instability (e.g., cyclic alternating patterns and micro-arousals). It is also under the modulatory influences of various networks of the autonomic and central nervous systems including several neurochemical substances, and it could be associated with psychological stress and oro-esopharyngeal functions (swallowing, breathing). SB can also occur with concomitant sleep disorders such as sleep disordered breathing (e.g., apnea), gastro-esophageal reflux, neurological (e.g., epilepsy, RBD) or psychiatric (e.g., depression and related medications, ADHD) disorders. A comprehensive clinical assessment (sleep or ambulatory recording) is mandatory if any concomitant medical disorder is suspected. Since no curative treatment for SB is recognized, the clinician needs to plan a multi-disciplinary approach for preventing damages to orofacial structures, and manage concomitant sensory and pain complaints.
... Another point that is usually overlooked in the clinical diagnosis of SB is whether or not patients have concomitant medical problems [32,35,36]. Thus, SB is regarded as primary type when no clear medical complications are present. ...
... Thus, clinical signs and symptoms for the clinical diagnosis of SB (e.g., frequent tooth grinding history, tooth wear, and morning masticatory muscle symptoms) can be found in patients with sleep disorders. Although sleep is disturbed and motor activity is often increased due to the distinct pathophysiological background in sleep disorders, evidence regarding co-morbidity with SB and increase of masticatory EMG activity has been gathered from case reports and subjective assessments; few electrophysiological assessments have been made [35]. Whether a concomitant presence of SB in sleep disorders is associated with secondary influence of sleep disruption (e.g., increased microarousals) or with common mechanisms for rhythmic oromotor activation remains to be investigated [97]. ...
... However, they may not ask about sleep. Although objective measurement of masticatory EMG activity during sleep is ideal, for clinical perspectives, sleep disorders can be screened by clinical interviews and oral examinations [32,35]. Patients with sleep disorder(s) often complain of common sleep problems (e.g., poor sleep, daytime sleepiness, fatigue, etc.) ( Table 2). ...
... The difference between the two types is that the latter has a totally involuntary motion. 2,3 Sleep disorders that have been reported to be concomitant with bruxism include obstructive sleep apnea, parasomnias, restless legs syndrome, oral mandibular myoclonus, and rapid eye movement behavior disorders. 3,4,5 Despite the controversy around the exact area of the nervous system where bruxism is triggered, i.e., peripheral or central, the main consequences of bruxism can be observed in the oral-dental area. ...
... 2,3 Sleep disorders that have been reported to be concomitant with bruxism include obstructive sleep apnea, parasomnias, restless legs syndrome, oral mandibular myoclonus, and rapid eye movement behavior disorders. 3,4,5 Despite the controversy around the exact area of the nervous system where bruxism is triggered, i.e., peripheral or central, the main consequences of bruxism can be observed in the oral-dental area. Such consequences may include tooth destruction, dental work failure, temporomandibular joint and jaw muscle pain or jaw movement limitation, and temporal headache. ...
... Such consequences may include tooth destruction, dental work failure, temporomandibular joint and jaw muscle pain or jaw movement limitation, and temporal headache. 3,4,5,6 The diagnosis and clinical assessment of bruxism is a complex process. What differentiates patients who were initially diagnosed with bruxism from others who were not diagnosed with the disorder despite exhibiting some degree of nocturnal parafunctional activity is the duration and intensity of muscular contractions, which are dramatically altered in patients suffering from bruxism. ...
This study evaluated the association of level of anxiety in children with and without sleep bruxism (SB). The study was performed with 84 six- to eigth-years-old children, divided into two groups: with bruxism (BG) and without bruxism (CG). Following the criteria purposed by American Academy of Sleep Medicine (AASM) to determine SB, the presence of tooth wear has been verified through clinical examinations, and the parents have answered a questionnaire about their children's behavior and habits. Additionally, the State-Trait Anxiety Inventory for Children (STAIC) was applied to parents of the selected patients. Data analysis revealed a statistical significant difference between the groups (Student's t-test, p = 0.0136). Based on the results, anxiety assessment revealed that children with bruxism have reached higher levels in the STAIC scale than the non-bruxism group. Therefore, it indicates a direct relationship between the presence of anxiety disorder and the onset of bruxism in children.
... [71][72][73][74][75] Hypersensitive teeth (eg, to cold), excessive teeth mobility and metallic taste are other reported symptoms. [76][77][78] Clinicians must also look for signs of teeth grinding. Teeth examination can reveal tooth wear and noncarious cervical defects. ...
... 77 It can thus be observed in about 40% of normal individuals and, among bruxers, does not reflect bruxism severity. 76,80 Jaw muscle examination can also be useful, showing tenderness to palpation or masseter hypertrophy during clenching. Tongue indentation, gum recession, limitation of mouth opening, and occlusal trauma are other signs to seek. ...
... Tongue indentation, gum recession, limitation of mouth opening, and occlusal trauma are other signs to seek. [76][77][78] Primary and Secondary Bruxism Different drugs, substances, sleep disorders, and movement disorders have been associated with bruxism (Box 11). 76,78 When no cause is found, bruxism is said to be primary. ...
Rhythmic movements of sleep are repetitive, stereotyped movements occurring mostly in children and usually represent a benign condition; however, other sleep-related disorders and psychiatric conditions can sometimes coexist and thus must be sought. Episodes occurring during sleep are often difficult to ascertain because of lack of witnesses or simple lack of awareness of the situation on the part of the individual. This article reviews symptoms and overall management related to pertinent conditions associated with rhythmic or periodic movement disorders of sleep.
... Sleep bruxism (SB) is defined as a stereotyped movement disorder occurring in sleep, frequently associated with tooth grinding [23]. SB should be differentiated from awake bruxism that is characterized by non-functional clenching habit during wakefulness [23,24]. ...
... Sleep bruxism (SB) is defined as a stereotyped movement disorder occurring in sleep, frequently associated with tooth grinding [23]. SB should be differentiated from awake bruxism that is characterized by non-functional clenching habit during wakefulness [23,24]. Tooth grinding can be reported in patients with medical diseases and drug treatment and such cases are classified as secondary or iatrogenic bruxism. ...
... Concomitant oromandibular myoclonus can be found in subpopulation of the patients with SB but is thought as a different entity from SB [25]. Primary type of sleep bruxism (e.g., no medical background) is reported by approximately 5-10% of adult population with a agerelated decrease from children (15-20%) to the elderly (3%) [23]. Clinical problems associated with SB include tooth wear and fracture, temporomandbular disorders (odds ratio: 4-8), headache (65%), failures of dental prosthese and implants [23]. ...
In normal sleep, cortical EEG activity is influenced by the balance in the activities of subcortical neurons in relation to the cyclic changes of sleep states. As well, jaw motor excitability is altered under the activity of sleep regulatory mechanism. Transient arousals (e.g., micro-arousal) are associated with a brief change of cortical activity and an increase of jaw motor activity. During this period, various types of jaw motor activities are occasionally found to occur, with either non-specific or specific patterns such as rhythmic activations. Exaggeration of the jaw motor activities during sleep can be seen in patients with sleep bruxism. Although cortical activity reflects arousal level and is correlated with the activity level of jaw muscles during sleep, it remains to be investigated whether or not cortex plays one of the sources of descending excitatory drive shaping a variety of jaw motor activities.
... BS is an important factor in the onset and persistence of temporomandibular pain. It is a common source of microtrauma that generates alteration of the capsular ligaments, thinning of the articular disc and lack of muscle coordination (5). It presents tooth wear and mobility, as well as other clinical findings, such as in the tongue or cheeks, muscle hypertrophy, pain in the temporomandibular joint (TMJ), headaches and pain or fatigue of the chewing muscles (6). ...
... It is important to analyze the occlusion to determine how it is affected by the biomechanical load generated by bruxism (5). Examining the tooth wear pattern during BS and understanding the relationship between bruxism activity and individual occlusion patterns are important in clinical dental practice. ...
Antecedentes: El bruxismo del sueño (BS) es una actividad oromandibular con rechinamiento y apretamiento dental y una actividad muscular masticatoria. Genera disfunción temporomandibular (DTM), desgaste y movilidad dental, así como otros hallazgos clínicos. Es importante analizar la oclusión y la ATM para determinar cómo se afecta por la carga biomecánica generada por el bruxismo. Objetivo: Establecer la relación entre la posición condilar de la articulación temporomandibular (ATM) utilizando tomografías computarizadas de haz cónico (TCHC) con los patrones de desgaste dental determinados con el BruxChecker®, en sujetos con diagnóstico clínico de BS. Métodos: Estudio observacional, descriptivo, transversal, en 45 pacientes con diagnóstico clínico de bruxismo del sueño, según los criterios de diagnóstico del bruxismo de la AASM (American Academy of Sleep Medicine), con edad promedio de 34,9 ± 8,6. Se analizaron las TCHC, midiendo los espacios de la ATM en el plano sagital: anterior, superior y posterior (SA,SS,SP) y en el plano coronal: lateral, superior y medial (CL,CS,CM). Se clasificó el patrón de desgaste dental con el BruxChecker® dividiendo los sujetos en: Grupo 1, patrón canino (PC) con 19 sujetos y Grupo 2, patrón molar (PM) con 26 sujetos. Resultados: No se observaron diferencias significativas entre las medidas de los espacios articulares de cada grupo ni en la comparación entre los patrones PC vs PM. La posición sagital del cóndilo posterior/anterior (P/A) fue posterior y la coronal medial/lateral (M/L) fue medial para los dos grupos, al evaluar las ratios. Se encontró diferencia significativa (P<0,00) en los patrones PC y PM del lado derecho, al estimar la diferencia entre promedios de espacios medial y lateral. Conclusiones: La posición del cóndilo se encontró posterior y medial en la fosa articular, en los patrones PC derecho y PM izquierdo. Se evidenció una posición condilar lateral derecha significativa, en los patrones PC y PM. Estos hallazgos indican una posición condilar alterada en los sujetos con bruxismo, que se puede asociar con un desplazamiento del cóndilo dentro de la fosa articular, generada posiblemente por los movimientos excéntricos mandibulares constantes durante la actividad de bruxismo.
... The diagnosis of bruxism involves a thorough clinical judgement and knowledge of recent diagnostic modalities in the field. The criteria for screening patients with moderate to severe sleep bruxism are [30]-1) Tooth grinding sounds-3 to 5 nights per week for over 6 months. ...
... In non bruxers it was 0.7 hertz while in bruxers it was 0.9 hertz. [30]Lavinge et al. reported that mean activity of masseter EMG burst in RMMA is 30-40% higher in bruxers than nonbruxers. [36] ...
ABSTRACT
Radiology is an essential tool in the dental clinical practice as most structures harbouring disease are not
visible to the naked eye. There are various entities that are generally not noticed until periapical pathology occurs. Under such circumstances, the diagnosis is difcult, as they mimic various other conditions. One of such condition is root fracture after an endodontic treatment of tooth. Vertical root fracture (VRF) usually starts from an internal dentinal crack and develops over time, due to masticatory forces and occlusal loads. Here in this paper we will discuss how we stepwise diagnostic radiographic modalities are used to see the actual cause of pain in a 60 year old male patient. Cone Beam Computed Tomography (CBCT) was done to view in 3D which revealed VRF of tooth. Throughout the paper the edge of CBCT over other diagnostic modalities is discussed till we get our diagnosis.
... PSG not only allows the evaluation of sleep architectures but also the differential diagnosis of sleep disorders [10,11]. The advantages of PSG in the diagnosis and assessment of SB are important in research settings for assessing treatment effects and clarifying pathophysiology [12]. Increased knowledge of SB and sleep disorders may reveal that it is not rare for a patient to exhibit SB with comorbid sleep disorders (ie, sleep apnea and insomnia etc.) or to have sleep disorders mimicking SB with similar symptoms (ie, parasomnias) [9,13e15]. ...
... Based on previous studies, oromotor events were scored based on masseter electromyographic activity and video recordings [16,17]. RMMA consisted of the following patterns: phasic typethree or more phasic bursts (duration 0.25e2 s), mixed typephasic and tonic bursts (duration 2 s or more) and tonic typesingle tonic burst [12,16,17,31]. RMMA episodes with teeth grinding noise were identified by the audio data. ...
Objective
This study investigated the first night effect on the polysomnographic diagnosis of sleep bruxism (SB).
Methods
Polysomnographic recordings were performed for two consecutive nights in forty-three subjects (mean age 23.7 ± 0.32 years [range: 20.0 - 33.0]). Sleep variables and rhythmic masticatory muscle activity (RMMA) were scored for two nights. The diagnosis of SB was graded by the frequency of RMMA with cut-off values of 2 and 4 times per hour of sleep.
Results
Participants were classified into control (n=15), low (n=13) and moderate-high (n=15) groups. Among the three groups, the concordance of the SB diagnosis was compared between the two nights. Sleep variables showed a significant first-night effect with lower sleep efficiency, longer sleep latency and higher frequency of arousals. The frequency of RMMA significantly increased from the first to the second night in the moderate-high SB group only. The concordance rate of the severity between the two nights was 93.3% (14/15) in the control group, 76.9% (10/13) in the low SB group and 60% (9/15) in the moderate-high SB group. When the severity was determined on the first night, it remained the same on the second night in 77.8% (14/18) of the control group, 66.7% (10/15) of the low SB group and 90.0% (9/10) of the moderate-high SB group.
Conclusion
The results showed that the first night effect on the occurrence of RMMA differed among the different degrees of the RMMA frequency, and suggest that, due to the first night effect, single-night polysomnography may underestimate the moderate-high level of SB but differentiate the low level of SB from controls.
... Nevertheless, it is worth noting that this may be an underestimation because people are often not aware of their habit to grit their teeth and/or lack a bed partner to draw their attention to the gnashing noise (e.g., Lavigne and Montplaisir, 1994;Kampe et al., 1997;Bader and Lavigne, 2000). Kato and Lavigne (2010) listed clinical features for evaluation and diagnosis of sleep bruxism which include: self-report from sleep partners or parents who complain about grinding sounds, various conditions reported by bruxers upon awakening (e.g., jaw muscle discomfort, fatigue or stiffness, and tooth hypersensitivity), clinical observations (e.g., visual inspection), and miscellaneous (e.g., dental restoration failure or fracture). The possibility that many people grind their teeth, although they are not aware of it, may be the explanation for the commonness of TD, if they are in fact related to dental irritation. ...
... Somewhat surprisingly, in contrast to a previous finding (Coolidge and Bracken, 1984), at least in our preliminary study, TD were not associated with psychological distress at all, nor were there any correlations with specific psychological symptom subscales. This is in spite of the fact that psychological distress was indeed (weakly) related to sensitivity or tension in teeth, supporting the claim that anxiety and stress are related to teeth grinding (Ohayon et al., 2001;Manfredini et al., 2005;Kato and Lavigne, 2010). Again, to the extent that these preliminary findings will be replicated in future studies, this negates the potential confounding effect of psychological distress as an explanation for the relation of TD with teeth tension. ...
Teeth dreams (TD), i.e., dreams of teeth falling out or rotting, are one of the most common and universal typical dream themes, yet their source remains unknown and they have rarely been studied empirically. They are especially enigmatic as they do not readily fall under the rubric of the “continuity hypothesis”, i.e., dreams of current and salient waking-life experiences. The aim of the present study was to explore two possible hypotheses for the origin of TD; specifically, TD as incorporation of dental irritation into dreaming, and TD as a symbolic manifestation of psychological distress. Dream themes, dental irritation, psychological distress, and sleep quality were assessed among 210 undergraduates. TD were related to dental irritation (specifically, tension sensations in the teeth, gums, or jaws upon awakening), whereas other dream types were not. Conversely, TD were unrelated to psychological distress, whereas other dream types were (specifically, dreams of being smothered and dreams of falling). This disparity in the correlates of TD existed despite a small but significant relationship between psychological distress and dental irritation. Albeit preliminary, the present findings support the dental irritation hypothesis and do not support the symbolic hypothesis regarding the origins of TD. Research on TD portrays one path through which the mind may distort somatosensory stimuli and incorporate them into dreams as a vivid and emotionally salient image; these preliminary findings highlight the potential of studying TD in order to broaden our understanding of the cognitive mechanisms governing dream production.
... As tooth attrition is a cumulative record of both functional and parafunctional tooth wear, the evaluation of tooth attrition to establish a diagnosis of ongoing SB and its severity remains controversial (Carra et al., 2011;Johansson et al., 2008;Kato and Lavigne, 2010). Some studies have reported finding a positive relationship between tooth attrition and selfreported bruxism (Carlsson et al., 1985;Ekfeldt et al., 1990); however, those studies did not differentiate between sleep and waking bruxism. ...
... The clinical diagnosis of hypertrophy is often accompanied by difficulty in appropriate confirmation due to vague standards, so diagnosis may depend entirely upon the evaluations of clinicians. In addition, severe or frequent tooth-clenching during wakefulness is known as one of the most important contributors to morphological change, such as masseter muscle hypertrophy (Bas et al., 2010;Clark et al., 1981;Kato and Lavigne, 2010). In fact, this clinical sign was also found in our control subjects. ...
The aim of this study was to investigate the association between patterns of jaw motor activity during sleep and clinical signs and symptoms of sleep bruxism. A total of 35 university students and staff members participated in this study after providing informed consent. All participants were divided into either a sleep bruxism group (n = 21) or a control group (n = 14), based on the following clinical diagnostic criteria: (1) reports of tooth-grinding sounds for at least two nights a week during the preceding 6 months by their sleep partner; (2) presence of tooth attrition with exposed dentin; (3) reports of morning masticatory muscle fatigue or tenderness; and (4) presence of masseter muscle hypertrophy. Video-polysomnography was performed in the sleep laboratory for two nights. Sleep bruxism episodes were measured using masseter electromyography, visually inspected and then categorized into phasic or tonic episodes. Phasic episodes were categorized further into episodes with or without grinding sounds as evaluated by audio signals. Sleep bruxism subjects with reported grinding sounds had a significantly higher total number of phasic episodes with grinding sounds than subjects without reported grinding sounds or controls (Kruskal-Wallis/Steel-Dwass tests; P < 0.05). Similarly, sleep bruxism subjects with tooth attrition exhibited significantly longer phasic burst durations than those without or controls (Kruskal-Wallis/Steel-Dwass tests; P < 0.05). Furthermore, sleep bruxism subjects with morning masticatory muscle fatigue or tenderness exhibited significantly longer tonic burst durations than those without or controls (Kruskal-Wallis/Steel-Dwass tests; P < 0.05). These results suggest that each clinical sign and symptom of sleep bruxism represents different aspects of jaw motor activity during sleep.
... SB is more frequent in smokers, those with high consumption of caffeine or alcohol, and in individuals taking neuroactive chemicals that affect the CNS (6)(7)(8)(9)(10). Clenching and grinding of teeth activities are often seen in individuals with stress and anxiety disorders (11)(12)(13) and are comorbid with restless leg syndrome, sleep apnea, oromandibular myoclonus, rapid eye movement behavior disorder, and other parasomnias (10,14). Iatrogenic secondary causes of such activities may include delivery/cessation of neuroactive medications (15), certain dental procedures, and treatment for temporomandibular disorder (TMD) (16)(17)(18). ...
... The role of neurochemicals in anxiety-related behaviors such as bruxism has been and continues to be of intense interest for some time now (9,(28)(29)(30)(31)(32)(33)(34). The exact neurochemical mechanisms that cause certain selective serotonin reuptake inhibitors (SSRIs) to manifest sleep bruxism is a focus of research efforts (9,31,33) as are those involved in the important comorbid factors of sleep regulation, endocrine systems, autonomic functions, stress/ anxiety, and motor control (14,15,(35)(36)(37). As demonstrated by the bruxism-ameliorating effects of the drugs gabapentin, tiagabine, gamma-hydroxybutyrate, diazepam, and lorazepam, the major neurotransmitter γ-aminobutyric acid (GABA) is suggested to play a critical role in bruxism (9). ...
... For a long time, only sleep bruxism had been researched [40,41], although, in 2012, awake bruxism came to the attention of researchers [38,40]. In 2012, an attempt was made to establish an international consensus regarding the definition of bruxism, its diagnostic system, and the consideration of awake bruxism [40]. ...
Background/Objectives: Bruxism is a masticatory muscle activity, phasic or tonic, with/without teeth contact, that appears in sleep or an awake state. An instrumental technique used to measure the surface electromyographic (sEMG) activity of the masseter muscle is used to diagnose bruxism activity during sleep and while awake. The objective of this study was to compare the variation in bruxism (sleep and awake) indices and masseter activity indices in low sleep bruxism and moderate sleep bruxism before and after wearing an occlusal appliance (OA) for 3 months each night. Methods: A clinical interventional study was designed in which subjects diagnosed with sleep bruxism were randomly selected to be included in the study. After the first sEMG recording, two groups were formed: a low sleep-bruxism group (number of sleep-bruxism events/h between 2 and 4) and a moderate sleep-bruxism group (number of sleep-bruxism events/h equal or higher than 4). All subjects received treatment with a 3D-printed occlusal appliance and wore it each night for 3 months, at which point the second sEMG recording was performed. For each participant of this study, a chart was created that included anamnestic data, clinical data, and sEMG data. The data were statistically analyzed with SPSS, using the Mann–Whitney U and Wilcoxon signed-rank tests. Results: A total of 21 participants were included in the final analysis, 18 women and 3 men, with a mean age of 24.5 ± 2.7 years. The OA lowered all bruxism indices in the whole group, but clusters analysis showed a significant reduction in sleep-bruxism indices in the moderate sleep-bruxism group, while in the low-bruxism group, the sleep and awake indices varied insignificantly, and the number of sleep-bruxism events/h remained constant. Conclusions: The 3D-printed occlusal appliances significantly lowered the sleep-bruxism indices and sleep masseter activity indices recorded with a portable sEMG device in the moderate sleep-bruxism group. The OA lowered the awake-bruxism indices and awake masseter activity indices in the moderate sleep-bruxism group.
... Literature suggests that tooth indentations might be related more to anatomical and physiological factors of the tongue itself (width at rest) than to SB (30). In a review, both masseter hypertrophy and tooth indentations might be also associated with daytime-wake oral parafunctions (tooth clenching, tongue pushing, and excessive swallowing) (31). The results of all measures of validity assessed in this study (Table 4) demonstrated that none of the five SB signs and symptoms questionnaire areas, when analyzed individually, reached acceptable results, including Area 1 (24). ...
Background: Sleep bruxism is a major research area in dentistry today and needs valid clinical means of diagnosis against valid instrumental methods. Purpose: To assess the validity of the most commonly reported sleep bruxism (SB) signs and symptoms in the literature against a polysomnography (PSG) validated portable electromyographic (EMG) device (BiteStrip®). Material and Methods: Fifty young adults (40 women & 10 men, 18-30 years old) volunteered for the sequential and simultaneous administration of the SB signs and symptoms questionnaire versus the BiteStrip®. The SB signs and symptoms questionnaire was comprised of 19 items divided in 5 areas: a) Area 1: self-awareness of tooth grinding , clenching, and/or tooth sounds/noises, b) Area 2: headaches and/or facial pain, c) Area 3: muscle fatigue and/ or hypertrophy, d) Area 4: clicking, crepitation and/or locking in the TMJ, and e) Area 5: tooth sensitivity, tooth wear/breaking, and/or cheek/tongue indentations. A cross-tabulation between the dichotomic test results (positive = 1, negative = 0) between the all five SB areas separately using quartiles (positive test result=75th percentile or higher, negative test result=50th percentile or lower) versus a positive test result of the BiteStrip® (score=1 or higher) was performed.
... A more detailed understanding of the mechanisms underlying SB requires analyses of the relationship between the sleep architecture and RMMA. To describe sleep-related brain states in humans, polysomnographic recordings, including electroencephalograms, electro-oculogram, and submental muscle electromyograms, are used to identify and classify brain states [17,22,29]. Sleep begins with stage N1 non-rapid eye movement (REM) sleep, a transition from wakefulness, followed by stage N2 non-REM sleep, which accounts for approximately 50% of the total sleep time and features occasional K-complexes and spindles. ...
Background:
Sleep bruxism (SB) is a common sleep disorder that affects approximately 20% of children and 10% of adults. It may cause orodental problems, such as tooth wear, jaw pain, and temporal headaches. However, the pathophysiological mechanisms underlying SB remain largely unknown, and a definitive treatment has not yet been established.
Highlight:
Human studies involving polysomnography have shown that rhythmic masticatory muscle activity (RMMA) is more frequent in otherwise healthy individuals with SB than in normal individuals. RMMA occurs during light non-rapid eye movement (non-REM) sleep in association with transient arousals and cyclic sleep processes. To further elucidate the neurophysiological mechanisms of SB, jaw motor activities have been investigated in naturally sleeping animals. These animals exhibit various contractions of masticatory muscles, including episodes of rhythmic and repetitive masticatory muscle bursts that occurred during non-REM sleep in association with cortical and cardiac activation, similar to those found in humans. Electrical microstimulation of corticobulbar tracts may also induce rhythmic masticatory muscle contractions during non-REM sleep, suggesting that the masticatory motor system is activated during non-REM sleep via excitatory inputs to the masticatory central pattern generator.
Conclusion:
This review article summarizes the pathophysiology of SB and putative origin of RMMA in both human and animal studies. Physiological factors contributing to RMMA in SB have been identified in human studies and may also be present in animal models. Further research is required to integrate the findings between human and animal studies to better understand the mechanisms underlying SB.
... Another limitation of the study was that the self-reporting of bruxism was based on a questionnaire that only included information regarding the presence of symptoms of bruxism, with no additional questions regarding its frequency and timeframe. This may be significant because self-reporting based only on the prevalence of symptoms of bruxism may lead to an overestimation of the number of patients with bruxism [39,71,72]. Instrument-based studies have shown that people who reported the occurrence of SB on the questionnaires more than once a week are more likely to have moderate-to-high frequency SB on polysomnography than low frequency SB [73][74][75]. ...
The study assessed masticatory muscle electromyographic (EMG) activity in both children diagnosed with pain-related temporomandibular disorders (TMD-P) and awake bruxism (AB) and in children without TMD, as well as the diagnostic value of surface electromyography (sEMG) in diagnosing TMD-P in subjects with AB. After evaluation based on the Axis I of the Research Diagnostic Criteria for Temporomandibular Disorders (RDC/TMD), 30 children diagnosed with myofascial pain were included in the myofascial pain group and 30 children without TMD diagnosis comprised the control group (mean age of 9.49 ± 1.34 years). The activity of the anterior temporal (TA) and masseter (MM) muscle was assessed bilaterally using a DAB-Bluetooth device (zebris Medical GmBH, Germany) at rest and during maximum voluntary clenching (MVC). The receiver operating characteristic (ROC) curve was used to determine the accuracy, sensitivity, and specificity of the normalized sEMG data. Statistically significant intergroup differences were observed in TA and MM muscle EMG activity at rest and during MVC. Moderate degree of sEMG accuracy in discriminating between TMD-P and non-TMD children was observed for TAmean, left MM, and MMmean EMG muscle activity at rest. sEMG can be a useful tool in assessing myofascial TMD pain in patients with AB.
... The gold standard in the detection of bruxism is polysomnography (PSG) [8], which involves multi-modal measurements of such parameters as electroencephalography (EEG), electromyography (EMG), electrocardiography (ECG), air flow monitoring and audio-video recording, and it is adopted to detect increased masseter and temporalis muscular activity during sleep typical of bruxism events [11]. This system is quite cumbersome due to the number of electrode channels and sensors required to be worn by the patients and is typically conducted in a laboratory environment as a result. ...
... The most common symptoms of awake bruxism include an unpleasant noise made by tooth grinding, jaw muscle pain or stiffness, headache, TMJ noise, difficulty when moving the mandible, tooth hypersensitivity, tooth chipping and cervical defects [5]. Moreover, tongue indentation, bilateral masseter muscle hypertrophy with jaw muscle tenderness to palpation [5], TMJ palpation pain, as well as fracture or failure of dental restorations might be observed [6]. Its prevalence among the general population reaches between 20% and 31.4% [7,8]. ...
The aim of this pilot study was to evaluate the short-term effectiveness of two different occlusal devices and their impact on the pressure pain threshold (PPT) values among patients who reported to the Dental Prosthetics Outpatient Clinic of Pomeranian Medical University (Szczecin, Poland) and who were diagnosed with probable bruxism. Two groups were formed (A and B) to which patients were assigned randomly. Each group used a different occlusal splint for bruxism management. The occlusal appliance by Okeson, or the bimaxillary splint, was used overnight by each patient for 30 days of the study. The PPT was measured twice, at the first visit and after 30 days of using each occlusal device, with Wagner Paintest FPX 25 algometer. Bruxism was diagnosed based on data from the patient’s medical history and from the physical examination. Nocturnal Bruxism Criteria according to the International Classification of Sleep Disorders (Third Edition) was used for the patient’s evaluation. Results: similar pain factor (PF) reduction was observed in both the examined groups, regardless of the device used; canine guidance and no guidance were similarly effective in terms of increasing pain resilience.
... Over the years, several management strategies have been proposed for clinically controlling primary SB activity. 43 ...
It becomes increasingly clear that some sleep disorders have important diagnostic and/or management links to the dental domain, hence the emergence of the discipline ‘Dental Sleep Medicine’. In this review, the following topics are discussed: 1. the reciprocal associations between orofacial pain and sleep; 2. the associations between sleep bruxism and other sleep‐related disorders; 3. the role of the dentist in the assessment and management of sleep bruxism; and 4. the dental management of obstructive sleep apnea. From these topics’ descriptions, it becomes clear that the role of the dentist in the recognition and management of sleep‐related orofacial pain, sleep bruxism, and obstructive sleep apnea is large and important. Since many dental sleep disorders can have severe consequences for the individual’s general health and well‐being, it is imperative that dentists are not only willing to take on that role, but are also able to do so. This requires more attention for Dental Sleep Medicine in the dental curricula worldwide, as well as better postgraduate training of dentists who are interested in specializing in this intriguing domain. This review contributes to increasing the dental researcher’s, teacher’s, and care professional’s insight into the discipline ‘Dental Sleep Medicine’ as it has taken shape in the 21st century, to the benefit of all patients suffering from dental sleep disorders.
... Tanı tamamen klinisyenin değerlendirmesine bağlıdır (9). Ek olarak uyanıklık bruksizminde masseter hipertrofisi en önemli morfolojik değişimlerden biri olarak kabul edilmektedir (39,40). Yoshida ve ark. ...
Amaç: Bruksizm tanısı konulan hastalara ait klinik bulguların araştırılması amaçlanmıştır.Yöntem: Ocak 2018-Aralık 2018 tarihleri arasında Adıyaman Üniversitesi Diş Hekimliği Fakültesi Ağız, Diş ve Çene Cerrahisi kliniğine başvuran Amerikan Uyku Tıbbı Akademisi tanı kriterlerine göre uyku bruksizmi tanısı konulan 110 hasta çalışmaya dahil edildi. Bruksizm tanısı konulan hastaların klinik muayenesinde, dişlerde aşınma varlığı, dilin lateral kenarlarında diş izleri, yanak mukozasında ısırma sonucu oluşan linea alba varlığı, periodontal hastalık, dişlerde hassasiyet, çiğneme kaslarında ağrı, temporomandibular eklemde ağrı, masseter kaslarında hipertrofi ve baş ağrısı değerlendirildi.Bulgular: Yaş ortalaması 32.95±12.34 olan, 78’i kadın 32’si erkek olan uyku bruksizmi tanısı konulan 110 hasta çalışmaya dahil edildi. Bruksizm tanısı konulan 110 hastanın 81’inde (%73.6) dişlerin insizal yüzeylerinde aşınma, 70’inde (%63.6) dilin lateral kenarlarında girintiler, 55’inde (%50) yanak mukozasında linea alba varlığı, 29’unda (%26.4) periodontal hastalık, 29’unda (%26.4) diş hassasiyeti, 77’sinde (%70) çiğneme kaslarında ağrı, 67’sinde (%60.9) TME bölgesinde ağrı, 27’sinde (%24.5) masseter kaslarında hipertrofi, 53’ünde (%48.2) ise baş ağrısı bulunmaktaydı. Sonuç: Bruksizmli hastalarda klinik bulgulardan en fazla diş aşınması, daha sonra ise çiğneme kaslarında ağrı, dil lateral kenarlarında girinti ve TME ağrısı eşlik etmektedir.
... However, it cannot be overlooked that both phenomena have important differences, such as the association with specific sleep disorders, cyclic alternating pattern onset and the absence of studies finding common gene variants. [5][6][7] Additionally, recent findings showed that patients with sleep bruxism shown impaired sleep architecture and often reported tiredness and sleepiness during the day. 8,9 ...
The recently published international consensus on bruxism assessment aimed to summarise the current understanding of sleep and awake bruxism. The consensus gathered some of the most renowned international experts with the intention of clarifying certain aspects of the definition, current status, grading system and future research perspectives on bruxism. Some interesting conclusions and concepts arose from this work; however, while analysing the concepts proposed, many critical questions regarding the definitions and clinical applicability seemed unresolved, giving way to speculations on whether or not the conclusions convened help clinicians or not.
... El bruxismo se puede clasificar como primario o idiopático, cuando no hay comorbilidades médicas asociadas o causas claras identificables; secundario o iatrogénico, cuando se relaciona a condiciones psicosociales o médicas como los trastornos respiratorios del sueño, problemas neurológicos, condiciones psiquiátricas y el consumo de drogas o medicamentos (11,12). También se ha clasificado como bruxismo céntrico o de apretamiento, cuando existe presión sobre los dientes en posición de intercuspidación y está relacionado a la función anormal de los músculos masetero y temporal y bruxismo excéntrico, cuando existe presión fuera del área de oclusión habitual, relacionado a la función anormal los músculos masetero, temporal y pterigoideos (13). ...
Bruxism is defined as a repetitive activity of the chewing muscles characterized by clenching or grinding of the teeth and/or by striking and swinging the jaw. It is of multifactorial etiology and it is considered that there is a physiological bruxism necessary for the development of the face of children. These two aspects complicate the diagnosis that is fundamentally based on a questionnaire to the parents and on the clinical examination of the child. When the physiological wear does not differentiate in time from the parafunctional wear, it has negative consequences in the child that alter their quality of life, requiring an adequate multidisciplinary management. Considering that it is necessary to know the fundamental characteristics of bruxism in children and adolescents, the objective of this review article is to update its circadian manifestations, classifications, prevalence, etiology, risk factors, diagnosis and treatment that will serve the dentist for the early identification and treatment.
... Sixth, data were collected from a single truck stop in North Carolina, which may have compromised the representativeness of these data; however, given the mobility of long-haul truck drivers, biases which would normally accompany single-location data collection methods are less relevant. Finally, the subjective sleep problem questions in the survey did not span the full spectrum of symptomology of sleep disorders, and the symptomology of some sleep disorders (e.g., grinding teeth due to sleep bruxism) are not typically recognized by the individuals themselves (Kato and Lavigne, 2010). ...
... Etiologically, bruxism can be divided into primary idiopathic bruxism, which occurs for no clearly identifiable reason 3 , and secondary bruxism, which may be associated with a number of other conditions such as extrapyramidal movement disorders 4 . Bruxism may also occur as a side effect of certain drugs 5 and other substances or chemicals 6 . ...
In routine dental practice, bruxism is generally diagnosed based on patient-reported signs and symptoms as well as clinical examination findings indicative of bruxism. According to the present-day definition of bruxism, current bruxism activity can be identified with high probability based on an evaluation of these findings. The Bruxism Status Examination Protocol (BSEP) is a two-part procedure consisting of a history interview and a clinical examination. It also includes an evaluation for treatment-related risk factors and comorbidi-ties, and a thorough assessment of the masticatory muscles, oral cavity, teeth, and oral soft tissue for signs of bruxism activity. This structured procedure not only serves to identify bruxism activity, but also makes it possible to distinguish between awake bruxism (AB) and sleep bruxism (SB), and to ascertain the predominant type of bruxing action (clenching or grinding). Another indication is for bruxism-specific risk assessments in dental restoration and denture planning.
... The American Academy of Sleep Medicine, in 1990, defined sleep bruxism (SB) as a parasomnia because it is an undesirable physical phenomenon which occurs predominantly during sleep [1]. In 2010, another study defined sleep bruxism as the stereotyped oromandibular activity during sleep, characterized by teeth grinding and clenching [2]. In 2013, bruxism was also defined as the repetitive jaw-muscle activity characterized by clenching or grinding of the teeth and/or by bracing or thrusting of the mandible, in an international consensus [3]. ...
Background
Bruxism is a sleep disorder characterized by grinding and clenching of the teeth that may be related to irreversible tooth injuries. It is a prevalent condition occurring in up to 31% of adults. However, there is no definitive answer as to which of the many currently available treatments (including drug therapy, intramuscular injections, physiotherapy, biofeedback, kinesiotherapy, use of intraoral devices, or psychological therapy) is the best for the clinical management of the different manifestations of bruxism. The aim of this systematic review and network meta-analysis is to answer the following question: what is the best treatment for adult bruxists?
Methods/design
Comprehensive searches of the Cochrane Library, MEDLINE (via PubMed), Scopus, and LILACS will be completed using the following keywords: bruxism and therapies and related entry terms. Studies will be included, according to the eligibility criteria (Controlled Clinical Trials and Randomized Clinical Trials, considering specific outcome measures for bruxism). The reference lists of included studies will be hand searched. Relevant data will be extracted from included studies using a specially designed data extraction sheet. Risk of bias of the included studies will be assessed, and the overall strength of the evidence will be summarized (i.e., GRADE). A random effects model will be used for all pairwise meta-analyses (with a 95% confidence interval). A Bayesian network meta-analysis will explore the relative benefits between the various treatments. The review will be reported using the Preferred Reporting Items for Systematic Reviews incorporating Network Meta-Analyses (PRISMA-NMA) statement.
Discussion
This systematic review aims at identifying and evaluating therapies to treat bruxism. This systematic review may lead to several recommendations, for both patients and researchers, as which is the best therapy for a specific patient case and how future studies need to be designed, considering what is available now and what is the reality of the patient.
Systematic review registration
PROSPERO CRD42015023308
Electronic supplementary material
The online version of this article (doi:10.1186/s13643-016-0397-z) contains supplementary material, which is available to authorized users.
... El BS presenta una etiología multifactorial, involucrando procesos fisiológicos multisistémicos muy complejos (Klasser et al., 2015). Debido a esto, se ha dividido en dos grandes clasificaciones: BS primario o idiopático del sueño, cuando no hay causas claras identificables, y BS Secundario, en el que sí está aso-ciado a una condición socio-psicológica o médica, como los trastornos respiratorios del sueño, problemas neurológicos o condiciones psiquiátricas y el consumo de drogas o medicamentos (Lavigne et al., 2005;Kato & Lavigne, 2010;Lobbezoo et al., 2013). ...
Sleep Bruxism (SB) is the act of grinding and clenching teeth during sleep, which could lead serious consequences in children, such a tooth wear and muscle pain. The objective of this research was to determine the prevalence of SB in children, and to relate the presence of signs of temporomandibular disorders (TMD) and daytime oral parafunctions. The sample consists of 369 students of 614 years old. SB diagnosis is based on the inclusion criteria of the American Academy of Sleep Medicine, with parent report indicating the history of tooth clenching/grinding, presence of awake oral parafunctions and medical history. The information was complemented by clinical examination of signs of TMD and tooth wear. For statistical analysis chi-square test and Odds Ratio Test was used, with a confidence interval of 95 %. The prevalence of SB was 32 %. Children 6 years old had the highest prevalence (38 %), and children 14 years old had less (27 %). Individuals with SB, 77 % showed signs of TMD (p
... If the result of screening is positive, the dentist can subsequently evaluate for individual risk factors that contribute to the development and maintenance of bruxism, which include psychogenic factors (eg, stress at home or at work) 13 , and exogenous factors, such as certain medications (eg, antidepressants of the selective serotonin reuptake inhibitor [SSRI] type, and attention deficit hyperactivity disorder [ADHD] medications 14 ), as well as alcohol 15 and tobacco abuse 16 . If comorbidities, such as TMD or sleep disorders, are suspected, further studies must be performed. ...
In previous clinical practice, findings of tooth damage and pain associated with temporomandibular disorders (TMDs) were the primary indications to search for further signs of bruxism. Today, however, it appears more prudent to perform a prospective evaluation (ie, screening) of patients for current bruxism activity before the start of treatment, for a number of reasons. First, if the screening test is positive, early preventive or curative measures (such as splint therapy or restoration of anterior canine guidance) can be planned, signs and symptoms of TMDs detected, and high-risk treatment options excluded from the outset. Second, a positive screening result gives the dentist an opportunity to educate bruxism patients about their individual risks at an early stage and include them in treatment planning. Finally, bruxism may be associated with obstructive sleep apnea, the treatment of which can contribute greatly to improving the quality of life and general health of the patient.
... El bruxismo se puede encontrar hasta en un 10% de pacientes con apnea central del sueño, y hasta en un 9% asociado a enfermedad cardiovascular, la fisiopatología de esta alteración no es clara, se sugiere que la hipoxemia durante las apnea, con la consecuente generación de microdespertares, genera un aumento de la actividad simpaticomimética, con una elevación de los niveles de dopamina (17). Este neurotransmisor estimula la vía directa e indirecta del tálamo y de los ganglios basales en el sistema extrapiramidal generando la producción de movimientos anormales principalmente a nivel de la musculatura mandibular (músculo masetero), condición similar a la ocurrida en el enfermedad de Parkinson (18). ...
Se presenta el caso de una mujer de 59 años con diagnóstico de encefalopatía anóxico-isquémica, quien se encuentra en estado vegetativo persistente y epilepsia secundaria de difícil control, quien en el transcurso de su evolución clínica desarrolla apnea central del sueño con índice de apnea hipopnea (IAH) de 87.86/h con patrón de respiración de Cheyne-Stokes (RCS) y bruxismo severo documentado mediante polisomnografía, alteraciones que mejoraron tras la administración de oxigeno por cánula nasal a 1 L/min. La asociación de bruxismo con respiración de Cheyne-Stokes y la respuesta simultánea y completa de las dos alteraciones a la administración de oxigeno suplementario no ha sido reportada previamente
... El bruxismo se puede encontrar hasta en un 10% de pacientes con apnea central del sueño, y hasta en un 9% asociado a enfermedad cardiovascular, la fisiopatología de esta alteración no es clara, se sugiere que la hipoxemia durante las apnea, con la consecuente generación de microdespertares, genera un aumento de la actividad simpaticomimética, con una elevación de los niveles de dopamina (17). Este neurotransmisor estimula la vía directa e indirecta del tálamo y de los ganglios basales en el sistema extrapiramidal generando la producción de movimientos anormales principalmente a nivel de la musculatura mandibular (músculo masetero), condición similar a la ocurrida en el enfermedad de Parkinson (18). ...
The case of a 59 year old female diagnosed with anoxic-ischemic encephalopathy, who is in
a persistent vegetative state and secondary epilepsy difficult to control, who in the course of her
clinical evolution develops central sleep apnea with apnea hypopnea index (AHI) of 87.86 / h with
Cheyne-Stokes pattern and severe bruxism documented by polysomnography, alterations that improved
after administration of oxygen by nasal cannula at 1 L / min., is presented.
The association of bruxism with Cheyne-Stokes respiration and the simultaneous and complete
response of the two alterations to the administration of supplemental oxygen has not been reported
previously.
... 2 Bruxism may also entail temporomandibular disorders (TMDs) or chronic myofascial pain in the masticatory muscles. [7][8][9] Even though bruxism as a whole is commonly considered the most harmful parafunctional activity of the temporomandibular joint (TMJ), there are many unsolved issues concerning the actual causal relationship between bruxism and TMD. 6,10 The main uncertainties are due to lack of knowledge on the aetiology and diagnosis of bruxism and TMD. ...
A finite element model of the temporomandibular joint (TMJ) and the human mandible was fabricated to study the effect of abnormal loading, such as awake and asleep bruxism, on the articular disc. A quasilinear viscoelastic model was used to simulate the behaviour of the disc. The viscoelastic nature of this tissue is shown to be an important factor when sustained (awake bruxism) or cyclic loading (sleep bruxism) is simulated. From the comparison of the two types of bruxism, it was seen that sustained clenching is the most detrimental activity for the TMJ disc, producing an overload that could lead to severe damage of this tissue.International Journal of Oral Science advance online publication, 14 March 2014; doi:110.1038/ijos.2014.4.
Background:
Sleep on the first night in a sleep laboratory is characterized by a lower sleep quality and frequency of rhythmic masticatory muscle activity (RMMA) than that on the second night in moderate to severe sleep bruxism (SB) patients.
Objective:
The aims of this study was to clarify the physiological factors contributing to the first night effect on oromotor activity during sleep and investigate whether physiological factors involved in the first night effect differed between rhythmic and non-rhythmic oromotor activities.
Methods:
Polysomnographic data collected on two consecutive nights from fifteen moderate to severe SB subjects (F 7: M 8; age: 23.2±1.3 [mean ± SD] years) were retrospectively analyzed. Sleep variables, RMMA, and non-specific masticatory muscle activity (NSMA) were scored in relation to episode types (i.e., phasic or tonic and cluster or isolated), sleep architecture, and transient arousals. The relationships between nightly differences in oromotor and sleep variables were assessed. The distribution of oromotor events, arousals, cortical electroencephalographic power, RR intervals, and heart rate variability were examined in relation to sleep cycle changes. These variables were compared between the first and second nights and between RMMA and NSMA.
Results:
Sleep variables showed a lower sleep quality on Night 1 than on Night 2. In comparisons with Night 1, the RMMA index increased by 18.8% (p <0.001, the Wilcoxon signed-rank test) on Night 2, while the NSMA index decreased by 17.9% (p = 0.041). Changes in the RMMA index did not correlate with those in sleep variables, while changes in the NSMA index correlated with those in arousal-related variables (P <0.001, Spearman's rank correlation). An increase in the RMMA index on Night 2 was found for the cluster type and stage N1 related to sleep cyclic fluctuations in cortical and cardiac activities. In contrast, the decrease in the NSMA index was associated with increases in the isolated type and the occurrence of stage N2 and wakefulness regardless of the sleep cycle.
Conclusion:
Discrepancies in first night effect on the occurrence of RMMA and NSMA represent unique sleep-related processes in the genesis of oromotor phenotypes in SB subjects.
Objectives
To quantitatively measure temporomandibular joint (TMJ) disk stiffness in adolescents with bruxism using shear wave elastography (SWE) and examine the relationship between elastography values, patient age, and duration of bruxism.
Study Design
This prospective study evaluated 120 TMJ disks of 60 adolescents (30 patients with bruxism and 30 controls). Stiffness of the anterior, intermediate, and posterior parts of the disk was measured. The patient and control groups' respective quantitative SWE values of elasticity (kilopascals (kPa) and velocity (meters/second (m/s)) were compared.
Results
Elasticity and velocity values of the anterior and intermediate parts were significantly higher in patients than in controls (P <.013), with no significant difference in the size of the joint space (P = .886). Receiver operating characteristic analysis resulted in sensitivity for the anterior part of 0.80 for kPa and 0.83 for m/s, with specificity of 0.57 (kPa) and 0.60 (m/s). For the intermediate part, sensitivity was 0.80 for kPa and 0.86 for m/s, with specificity of 0.64 (kPa) and 0.57 (m/s). No correlations were found between SWE values and patient age (P ≥ 0.098) or duration of bruxism (P ≥ 0.134).
Conclusions
SWE may be useful in the evaluation of TMJ disk stiffness in patients with bruxism.
Zusammenfassung
Bruxismus kann sowohl als Wach- (WB) wie als Schlafbruxismus (SB) auftreten. Die Prävalenz differiert je nach Untersuchungsmethode und wird bei WB mit 22,1–31% und bei SB mit 12,8±3,1% angegeben. Die Ätiologie des Bruxismus ist nur unvollständig bekannt, jedoch ist von einem multifaktoriellen Geschehen auszugehen. In diesem Artikel werden die Risikofaktoren vorgestellt. Des Weiteren werden neuroevolutionäre und paläoanthropologische Perspektiven erläutert und Einblicke in die Diagnostik gegeben. Zuletzt werden Behandlungsansätze beschrieben und das LEIT-Reset (Liem extrinsic and intrinsic TMJ-Reset) vorgestellt, bei dem extrinsische (osteopathisch manuelle Techniken – OMT) und intrinsische Kiefertechniken (Selbsthilfetechniken) aufeinander abgestimmt angewendet werden.
Sleep bruxism (SB) is a type of sleep disorder. Because pharmacotherapy for sleep disorders (sleeping drugs, antidepressants etc.) is associated with strong side effects, a complementary therapy in the form of olfactory stimulation with aromas was focused on. The purpose of this study was to investigate how olfactory stimulation with aromas affects SB. The subjects were 26 healthy, dentulous individuals (male: 21, female: 5, mean age: 24.8±3.2 years). Before starting the experiment, SB was confirmed in all 26 subjects using polysomnography (PSG) during nighttime sleep. Lavender (LA) was used for olfactory stimulation, and deionized water was used as the control (CO). The 26 subjects were randomly divided into the LA group and the CO group, and a crossover test, in which olfactory stimulation alternatingly administered, was performed. To eliminate the influence of initial night effects and obtain baseline data, PSG and masseter electromyography (EMG) measurements were performed using a portable high-precision EMG device on three consecutive nights. When crossing over, to eliminate any carry-over effects of each condition, the olfactory stimulation type was switched after a 1-week washout period, and PSG and EMG measurements were performed in the same manner over two consecutive nights. Sleep variables were evaluated with PSG analysis, and the number of SB events was calculated based on masseter EMG analysis. This resulted in the following conclusions.
1. Olfactory stimulation with LA improved the sleep state significantly for five of six sleep variables.
2. As compared to the baseline and the CO group, the number of SB events in the LA group decreased significantly.
3. Results suggested that olfactory stimulation using LA may reduce the number of SB events regardless of a subjective sense of favorable or poor sleep.
The results demonstrated the possibility that olfactory stimulation with applying LA improves the sleep state while reducing the number of SB events.
Background: Rhythmic masticatory muscle activity (RMMA) in sleep is usually not considered pathological unless associated with bruxism. On the other hand, so-called sleep-related rhythmic movement disorders (SRRMD) are a recognized category of sleep disorders, which involve prolonged rhythmic activity of large muscle groups, such as the whole body, the head, or a limb, but typically not the masticatory muscles.
Clinical Presentation: A polysomnographic description of a patient with symptomatic RMMA without bruxism, fulfilling the diagnostic criteria of an SRRMD, is presented. The symptoms were initially misdiagnosed as bruxism and then as sleep-related epilepsy, which delayed an adequate treatment. Therapy of the comorbid obstructive sleep apnea with a positive airway pressure device (APAP) led to a self-reported improvement.
Conclusion: The differential diagnosis of jaw movement in sleep is vast; a correct diagnosis is of the essence for adequate treatment. The prevalence of isolated RMMA resulting in perturbation of sleep warrants further exploration.
Background:
Most sleep bruxism (SB) episodes are accompanied by an increase in sympathetic tone and heart rate (HR).
Objectives:
To characterize heart rate (HR) changes in relation to rhythmic masticatory muscle activities (RMMAs) in SB patients.
Methods:
Polysomnographic recordings were performed on 10 SB patients and 11 normal controls. The duration of movement events, amplitude and duration of HR increases, and time to reach HR peak associated with RMMAs and limb movements (LMs) were determined and the relationships of the parameters of HR increases with types of movements and RMMAs were analyzed.
Results:
All of the parameters of HR increases associated with the three types of movements (RMMAs, RMMAs + LMs and LMs) and masseter activities (phasic, tonic and mixed) were significantly different (Two way ANOVA, P<0.001 for all) in both SB patients and controls. The duration of RMMAs/LMs was positively correlated with the parameters (SB patients: R2 =0.24-0.85, P<0.0001; Controls: R2 =0.23-0.68, P<0.0001). The amplitude of HR increases was also positively correlated with respiration changes in the SB patients (R2 =0.3258, P<0.0001) and controls (R2 =0.09469, P<0.05). The proportions of phasic RMMAs associated with awakenings, microarousals and no cortical arousals were significantly different and so were the proportions of tonic and mixed RMMAs (Friedman's tests, P<0.05-0.001).
Conclusions:
The HR increases associated with RMMAs may be intrinsic to the cortical arousal response and autonomic activation, and differences in HR increases associated with different types of movements and RMMAs might be related to the changes in respiration and differences in cortical arousal levels.
Im zahnärztlichen Alltag wird man vor allen Dingen mit vermutlichen Folgeerscheinungen übermäßiger Bruxismusaktivität, wie Schäden an den Zähnen, den Restaurationen, dem Zahnersatz und Zahnhalteapparat, Kopfschmerzen oder kraniomandibulären Dysfunktionen, konfrontiert. Da gegenwärtig keine kausal wirkende Bruxismustherapie bekannt ist, zielt die Behandlung je nach Leitsymptom in erster Linie auf den Schutz der Zähne und der Restaurationen, die Minderung der Bruxismusaktivität und die Schmerzlinderung. Basierend auf dem aktuellen Stand der Wissenschaft werden im Folgenden Behandlungsmöglichkeiten vorgestellt, die, basierend auf einer soliden Diagnostik, nahtlos in den Praxisalltag integrierbar sind. Neben den klassischen Maßnahmen wie Beratung und Information, Verhaltenstherapie, Biofeedback, Schienentherapie sowie pharmakologische Intervention wird eine Übersicht über die Prävention und Behandlung des Abrasionsgebisses gegeben.
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. (1) H-MRS 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=0.011), whereas there was no significant difference (P=0.307) in Glx levels between the two groups.
Conclusions:
SB patients may possess abnormalities in the GABAergic system of brainstem networks. This article is protected by copyright. All rights reserved.
Purpose of review:
Review of the literature pertaining to clinical presentation, classification, epidemiology, pathophysiology, diagnosis, and treatment of sleep-related movement disorders and disturbances of motor control.
Recent findings:
Sleep-related movement disorders and disturbances of motor control are typically characterized by positive motor symptoms and are often associated with sleep disturbances and consequent daytime symptoms (e.g. fatigue, sleepiness). They often represent the first or main manifestation of underlying disorders of the central nervous system, which require specific work-up and treatment. Diverse and often combined cause factors have been identified. Although recent data provide some evidence regarding abnormal activation and/or disinhibition of motor circuits during sleep, for the majority of these disorders the pathogenetic mechanisms remain speculative. The differential diagnosis is sometimes difficult and misdiagnoses are not infrequent. The diagnosis is based on clinical and video-polysomnographic findings. Treatment of sleep-related motor disturbances with few exceptions (e.g. restless legs/limbs syndrome) are based mainly on anecdotal reports or small series.
Summary:
More state-of-the-art studies on the cause, pathophysiology, and treatment of sleep-related movement disorders and disturbances of motor control are needed.
Patient: The patient was a 66-year-old man, with masticatory disturbance on the left side due to the loss of upper left molars and a root fracture of the second premolar. To improve the occlusal support, three dental implants were placed after extraction of the premolar. To obtain proper lateral guidance for this patient, interim prostheses were applied on implants for about 3 months. Finally, the final prosthesis with the occlusal form transferred from the interim prostheses was applied.
Discussion: In this case without anterior guidance, it was considered that occlusal support remained stable in the maintenance period by implant prostheses with the characteristic occlusal form transferred from the interim prostheses.
Conclusion: For unilateral maxillary free-end missing without anterior guidance, occlusal support was improved by implant prostheses with the characteristic occlusal form transferred from the interim prostheses.
Today’s scientific community and practitioners have the advantage of having access to an improved definition of sleep bruxism (SB), its classification schemes, epidemiological perspectives and a greater depth of understanding regarding this sleep time activity. However, gaps in our knowledge remain. Currently, we do not fully grasp the totality of risk factors and comorbid conditions associated with SB. We continue to uncover etiological factors and pathophysiological processes. We are attempting to better comprehend and implement diagnostic armamentarium to aid in more reliable and accurate diagnosis to the benefit of our patients. Unfortunately, we are yet to find a reliable management strategy for SB as more robust and rigorous study protocols are necessary to determine efficacy as well as results from potential side effects. Future ongoing research will be of great assistance in filling such gaps.
The American Academy of Sleep Medicine defines general bruxism in the International Classification of Sleep Disorders (ICSD-3 available only on website at http://www.aasmnet.org/library/default.aspx?id=9) as the following: A repetitive jaw-muscle activity characterized by clenching or grinding of the teeth and/or by bracing or thrusting of the mandible. Furthermore, bruxism has been divided into two distinct categories based upon a 24 h circadian cycle as to when this activity occurs: sleep bruxism (SB – occurring during sleep) and awake bruxism (AB – occurring during wakefulness) [1].
Bruxism is extensively defined as a diurnal or nocturnal parafunctional habit of tooth clenching or grinding. The etiology of bruxism may be categorized as central factors or peripheral factors and according to previous research results, central factors are assumed to be the main cause. Bruxism may cause tooth attrition, cervical abfraction, masseter hypertrophy, masseter or temporalis muscle pain, temporomandibular joint arthralgia, trismus, tooth or restoration fracture, pulpitis, trauma from occlusion and clenching in particularly may cause linea alba, buccal mucosa or tongue ridging. An oral appliance, electromyogram or polysomnogram is used as a tool for diagnosis and the American Sleep Disorders Association has proposed a clinical criteria. However the exact etiology of bruxism is yet controversial and the selection of treatment should be done with caution. When the rate of bruxism is moderate or greater and is accompanied with clinical symptoms and signs, treatment such as control of dangerous factors, use of an oral appliance, botulinum toxin injection, pharmacologic therapy and biofeedback therapy may be considered. So far, oral appliance treatment is known to be the most rational choice for bruxism treatment. For patients in need of esthetic correction of hypertrophic masseters, as well as bruxism treatment, botulinum toxin injection may be a choice.
Since sleep bruxism (SB) is defined as a stereotyped movement and mainly associated with rhythmic masticatory muscle activity, the aim of this study was to get a better understanding on the subcortical and cortical networks related to the excitability of the central masticatory pathways in SB patients. Of 26 SB patients (12 females and 14 males; mean age: 24.9±4.0 years) and 30 normal subjects (18 females and 12 males; mean age: 24.1±3.1 years) selected, the motor evoked potentials (MEPs) elicited by transcranial magnetic stimulation (TMS) in masseter muscles, and the masseter inhibitory reflex (MIR) elicited by magnetic stimulation with single and double-shock techniques were studied. The MEPs elicited by TMS were similar in both SB patients and normal subjects. As for the MIR elicited by single magnetic stimulation, the latency and duration of the early silent periods (SP1) between the two groups were similar; but in 5 patients the late silent periods (SP2) was absent, and this difference in the frequency of absence of the SP2 between SB patients and normal subjects was significant; with double-shock technique, the recovery of SP2 was significantly lower in SB patients compared to normal subjects. These results suggested an abnormal excitability of the central masticatory in SB patients; and it is also indicated that SB may be mainly under the influence of brainstem networks rather than that of cortical networks.
OBJECTIVE:
An investigation was conducted on 105 subjects to assess the existence of an association between mood psychopathology and bruxism.
METHODS:
Validated clinical criteria were used to diagnose bruxism and a self-report validated questionnaire (MOODS-SR) was filled out by each patient for an evaluation of depression and mania symptoms of mood spectrum.
RESULTS:
Prevalence of mood psychopathology, as identified by MOODS-SR score> or =60, was significantly higher in bruxers (11/38, 28.9% vs. 6/67, 8.9%; P=0.007). Significant differences between bruxers and non-bruxers also emerged in total MOODS-SR (P=0.001) scores and in total scores of domains evaluating manic (P=0.001) and depressive symptoms (P=0.007).
CONCLUSIONS:
Support to the existence of an association between bruxism and mood disorders has been provided. Further studies are strongly needed to clarify mechanisms underlying the described association
As part of a larger study, polysomnographic and audiovisual data were recorded over 2 nights in 41 subjects with a clinical diagnosis of sleep bruxism (SB). Electromyographic (EMG) events related to SB were scored according to standard criteria (Lavigne et al. J Dent Res 1996;75:546–552). Post hoc analysis revealed that rapid shock-like contractions with the characteristics of myoclonus in the jaw muscles were observed in four subjects. EMG bursts characterized as myoclonus were significantly shorter in duration than bursts classified as SB. None of the subjects had any history of myoclonus while awake. Myoclonic episodes were more frequent in sleep stages 1 and 2 than in REM. Half of the episodes contained one or two contractions whereas the other half had three or more repetitive contractions. SB and myoclonus coexisted in one subject. To rule out sleep epilepsy, full electroencephalogram montage was done in three subjects and no epileptic spikes were noted. Our results suggest that approximately 10% of subjects clinically diagnosed as SB could present oromandibular myoclonus during sleep.
Sleep bruxism (SB) is a known parasomnia in sleep medicine reported by approximately 8% of the adult population. Sleep bruxism is characterized mainly by rhythmic masticatory muscle activity (RMMA), often associated with powerful tooth grinding. In dentistry, SB has been thought to be associated with tooth wear, dental restoration fractures, masticatory muscle and temporomandibular joint problems. Although pathophysiology of SB remains to be elucidated, recent studies have suggested that SB is a consequence of transient arousals during sleep. Several studies have reported that SB occurs concomitantly in obstructive sleep apnea–hypopnea syndrome (OSAHS) patients. In OSAHS, abnormal respiratory events are associated with arousals. However, SB episodes seem unlikely to be associated with arousals induced by abnormal respiratory events. Compared to wakefulness, oropharyngeal activities decrease during sleep; these are preserved for maintenance of upper airway patency and for protection of the upper alimentary tract. The association between SB and oropharyngeal functions remains to be studied, while several studies have suggested altered oropharyngeal sensory and motor functions in OSAHS. Among various treatment/management strategies, oral appliances are used as an effective and relatively safe option to manage patients with light to moderate OSAHS. In some OSAHS patients undergoing oral appliance therapy, however, oromandibular and intra-oral aversive effects (e.g. orofacial pain/discomfort, oral dryness) have also been reported. Currently, little data is available to clarify the causes of these aversive effects. The aim of this review is to make an overview of SB and to present its physiological and clinical relations to OSAHS.
This study investigated whether the presence of tooth wear in young adults can help to discriminate patients with sleep bruxism (SB) from control subjects.
The tooth wear clinical scores and frequency of sleep masseter electromyographic activity of 130 subjects (26.6 +/- 0.5 years) were compared in this case-control study. Tooth wear scores (collected during clinical examination) for the incisors, canines, and molars were pooled or analyzed separately for statistics. Sleep bruxers (SBrs) were divided into two subgroups according to moderate to high (M-H-SBr; n = 59) and low (L-SBr; n = 48) frequency of masseter muscle contractions. Control subjects (n = 23) had no history of tooth grinding. The sensitivity and specificity of tooth wear versus SB diagnosis, as well as positive and negative predictive values (PPV and NPV), were calculated. One-way analysis of variance and the Mann-Whitey U test were used to compare groups.
Both SBr subgroups showed significantly higher tooth wear scores than the control group for both pooled and separated scores (P < .001). No difference was observed between M-H-SBr and L-SBr frequency groups (P = .14). The pooled sum of tooth wear scores discriminates SBrs from controls (sensitivity = 94%, specificity = 87%). The tooth wear PPV for SB detection was modest (26% to 71%) but the NPV to exclude controls was high (94% to 99%).
Although the presence of tooth wear discriminates SBrs with a current history of tooth grinding from nonbruxers in young adults, its diagnostic value is modest. Moreover, tooth wear does not help to discriminate the severity of SB. Caution is therefore mandatory for clinicians using tooth wear as an outcome for SB diagnosis.
The objective of this experimental study was to assess the efficacy and safety of a reinforced adjustable mandibular advancement appliance (MAA) on sleep bruxism (SB) activity compared to baseline and to a mandibular occlusal splint (MOS) in order to offer an alternative to patients with both tooth grinding and respiratory disorders during sleep.
Twelve subjects (mean age: 26.0 +/- 1.5 years) with frequent SB participated in a short-term (three blocks of 2 weeks each) randomized crossover controlled study. Both brain and muscle activities were quantified based on polygraphic and audio/video recordings made over 5 nights in a sleep laboratory. After habituation and baseline nights, 3 more nights were spent with an MAA in either a slight (25%) or pronounced (75%) mandibular protrusion position or with an MOS (control). Analysis of variance and Friedman and Wilcoxon signed-rank tests were used for statistical analysis.
The mean number of SB episodes per hour was reduced by 39% and 47% from baseline with the MAA at a protrusion of 25% and 75%, respectively (P < .04). No difference between the two MAA positions was noted. The MOS slightly reduced the number of SB episodes per hour without reaching statistical significance (34%, P = .07). None of the SB subjects experienced any MAA breakage.
Short-term use of an MAA is associated with a significant reduction in SB motor activity without any appliance breakage. A reinforced MAA design may be an alternative for patients with concomitant tooth grinding and snoring or apnea during sleep.
We characterized sleep disorder rates in temporomandibular joint disorder (TMD) and evaluated possible associations between sleep disorders and laboratory measures of pain sensitivity.
Research diagnostic examinations were conducted, followed by two consecutive overnight polysomnographic studies with morning and evening assessments of pain threshold.
Orofacial pain clinic and inpatient sleep research facility.
Fifty-three patients meeting research diagnostic criteria for myofascial TMD.
N/A.
We determined sleep disorder diagnostic rates and conducted algometric measures of pressure pain threshold on the masseter and forearm. Heat pain threshold was measured on the forearm; 75% met self-report criteria for sleep bruxism, but only 17% met PSG criteria for active sleep bruxism. Two or more sleep disorders were diagnosed in 43% of patients. Insomnia disorder (36%) and sleep apnea (28.4%) demonstrated the highest frequencies. Primary insomnia (PI) (26%) comprised the largest subcategory of insomnia. Even after controlling for multiple potential confounds, PI was associated with reduced mechanical and thermal pain thresholds at all sites (P < 0.05). Conversely, the respiratory disturbance index was associated with increased mechanical pain thresholds on the forearm (P < 0.05).
High rates of PI and sleep apnea highlight the need to refer TMD patients complaining of sleep disturbance for polysomnographic evaluation. The association of PI and hyperalgesia at a nonorofacial site suggests that PI may be linked with central sensitivity and could play an etiologic role in idiopathic pain disorders. The association between sleep disordered breathing and hypoalgesia requires further study and may provide novel insight into the complex interactions between sleep and pain-regulatory processes.
Sleep bruxism (SB) is a prevalent sleep related movement disorder, characterized by rhythmic jaw movements with intense jaw muscle contraction. It can damage tooth and dental prostheses, and trigger orofacial pain or headache. SB occurs in association with homeostatic sleep regulation and sleep instability (e.g., cyclic alternating patterns and micro-arousals). It is also under the modulatory influences of various networks of the autonomic and central nervous systems including several neurochemical substances, and it could be associated with psychological stress and oro-esopharyngeal functions (swallowing, breathing). SB can also occur with concomitant sleep disorders such as sleep disordered breathing (e.g., apnea), gastro-esophageal reflux, neurological (e.g., epilepsy, RBD) or psychiatric (e.g., depression and related medications, ADHD) disorders. A comprehensive clinical assessment (sleep or ambulatory recording) is mandatory if any concomitant medical disorder is suspected. Since no curative treatment for SB is recognized, the clinician needs to plan a multi-disciplinary approach for preventing damages to orofacial structures, and manage concomitant sensory and pain complaints.
Motor activities during sleep are divided into physiological and pathologic types. Several physiological orofacial motor activities are known to occur during sleep. They play a role in protecting and integrating oroesophageal functions and tissues during sleep. However, their occurrence may become exaggerated in several sleep disorders. Abnormal orofacial movements in patients with neurological and psychiatric disorders can appear either during sleep or wakefulness, or both. The terminology of orofacial movement disorders in sleep used in this chapter generally extends to conditions with exaggerated normal motor activities, as well as conditions characterized by the presence of abnormal aimless (non-purposeful) movements.
This chapter aims to overview: 1) physiological orofacial motor activities and their relevance; 2) abnormal orofacial movements occurring in sleep disorders; and 3) concomitant movement disorders and other medical factors related to abnormal orofacial movements in sleep. Sleep bruxism (SB) is described in this chapter but can be regarded as a secondary rather than primary type, and is discussed in more details in chapter 12.
The parasomnias are classified as disorders of arousal, partial arousal, and sleep stage transition. Many of these parasomnias manifest dramatic symptoms causing an activation of central nervous system. Most parasomnias appear early in childhood. Some parasomnias, for example REM sleep behavior disorders (RBD) and sleep-related penile problems are seen in adult and aged people (Figure 1). Usually, these patients have predisposing factors including neurologic disorders and aging (Figure 2). Despite these explosive features, most of children with these parasomnias show spontaneous remission at the time of puberty.
This review discusses the clenching-grinding spectrum from the neuropsychiatric/neuroevolutionary perspective. In neuropsychiatry, signs of jaw clenching may be a useful objective marker for detecting or substantiating a self-report of current subjective emotional distress. Similarly, accelerated tooth wear may be an objective clinical sign for detecting, or substantiating, long-lasting anxiety. Clenching-grinding behaviors affect at least 8% of the population. We argue that during the early paleolithic environment of evolutionary adaptedness, jaw clenching was an adaptive trait because it rapidly strengthened the masseter and temporalis muscles, enabling a stronger, deeper and therefore more lethal bite in expectation of conflict (warfare) with conspecifics. Similarly, sharper incisors produced by teeth grinding may have served as weaponry during early human combat. We posit that alleles predisposing to fear-induced clenching-grinding were evolutionarily conserved in the human clade (lineage) since they remained adaptive for anatomically and mitochondrially modern humans (Homo sapiens) well into the mid-paleolithic. Clenching-grinding, sleep bruxism, myofacial pain, craniomaxillofacial musculoskeletal pain, temporomandibular disorders, oro-facial pain, and the fibromyalgia/chronic fatigue spectrum disorders are linked. A 2003 Cochrane meta-analysis concluded that dental procedures for the above spectrum disorders are not evidence based. There is a need for early detection of clenching-grinding in anxiety disorder clinics and for research into science-based interventions. Finally, research needs to examine the possible utility of incorporating physical signs into Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition posttraumatic stress disorder diagnostic criteria. One of the diagnostic criterion that may need to undergo a revision in Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition is Criterion D (persistent fear-circuitry activation not present before the trauma). Grinding-induced incisor wear, and clenching induced palpable masseter tenderness may be examples Of such objective physical signs of persistent fear-circuitry activation (posttraumatic stress disorder Criterion D).
This authoritative guide to sleep medicine is also available as an e-dition, book (ISBN: 1416003207) plus updated online reference! The new edition of this definitive resource has been completely revised and updated to provide all of the latest scientific and clinical advances. Drs. Kryger, Roth, and Dementand over 170 international expertsdiscuss the most recent data, management guidelines, and treatments for a full range of sleep problems. Representing a wide variety of specialties, including pulmonary, neurology, psychiatry, cardiology, internal medicine, otolaryngology, and primary care, this whos who of experts delivers the most compelling, readable, and scientifically accurate source of sleep medicine available today. Includes user-friendly synopses of important background information before all basic science chapters. Provides expert coverage of narcolepsy * movement disorders * breathing disorders * gastrointestinal problems * neurological conditions * psychiatric disturbances * substance abuse * and more. Discusses hot topics such as the genetic mechanisms of circadian rhythms * the relationship between obesity, hormones, and sleep apnea * sleep apnea and arterial hypertension * and more. Includes a new section on Cardiovascular Disorders that examines the links between sleep breathing disorders and cardiovascular abnormalities, as well as the use of sleep related therapies for congestive heart failure. Provides a new section on Womens Health and Sleep Disorders that includes information on the effects of hormonal changes during pregnancy and menopause on sleep. Features the fresh perspectives of 4 new section editors. Employs a more consistent chapter organization for better readability and easier navigation.
Patients with obstructive sleep apnea (OSA) develop repetitive pharyngeal airway closure during sleep. Sophisticated physiologic and imaging studies have significantly advanced our understanding of the anatomic risk factors for OSA and illuminated the biomechanical mechanisms by which therapeutic interventions for this disorder such as continuous positive airway pressure, weight loss, oral appliances, and surgery increase upper airway caliber. Pharyngeal airway patency is maintained by a balance of forces between the activity of the upper airway muscles that dilate and stiffen the airway and negative intraluminal pressure. However, this balance can be disturbed by abnormalities in upper airway anatomy and neural control. Patients with OSA have been shown to have a narrowed, more collapsible pharyngeal airway. Sleep-related reduction in upper airway dilating muscle activity can lead to greater negative intraluminal pharyngeal pressure that further narrows and completely closes the airway.
Parafunctional activity (toothgrinding, toothclenching and bruxism) is a common problem which may lead to masticatory muscle and temporomandibular joint pain, and may result from sleep arousal or disturbances. Sleep apnea is another common sleep disorder which results in disrupted sleep architecture and frequent arousals. Because sleep apnea leads to sleep arousals, and because sleep arousals are thought to result in increased parafunctional activity, we undertook the present study to determine the relationship between sleep apnea and parafunctional activity. We were also interested in assessing the effects of sleep posture on sleep disordered breathing and parafunctional activity. We prospectively studied 24 patients who were referred to the clinical sleep apnea laboratory for study. They underwent standard nocturnal polysomnographic examination; in addition, masticatory activity was measured with a masseter electromyogram. Patients slept in the supine and lateral decubitus positions. Nocturnal clenching was slightly higher in patients with sleep apnea than those without (12.2 vs 7.6 clenches/hr, p = 0.18), and there was a correlation between the clench index (Cl) and apnea plus hypopnea index (A + HI) by linear regression (r = 0.49, p<0.05). There were significant falls in both the A + HI (64.4 ±28.8 vs 36.5±36.7, p = 0.02) and Cl (12.5±12.1 vs 7.0±8.6, p = 0.04) in the lateral decubitus vs supine sleeping positions. We conclude that there is an association between obstructive sleep apnea and parafunctional activity, that sleep position affects the incidence of both sleep disordered breathing and parafunctional activity, and that analysis of apneas and hypopneas in both supine and lateral decubitus sleeping positions may be helpful.
Material circulation like compost recycling is one of the main methods of the watershed management to reduce the pollutant load. The authors developed a water quality management system to evaluate scenarios to improve water quality in the Kasumigaura basin, Japan. The watershed is divided into six sub-watersheds and the nitrogen effluent load of each is computed from the statistical database. Outflow load from the Kasumigaura basin was calculated using a water quality tank model classified by land use. Two scenarios of compost recycling were simulated, and outflow load from Kasumigaura basin was predicted for the long term. The results showed that the nitrogen load could be reduced about 0.1g⋅m–2 in the sub-watershed of high animal waste by the sharing compost within watershed. The model quantitatively evaluated the scenarios.
Lee SJ, McCall WD, Jr., Kim YK, Chung SC, Chung JW: Effect of botulinum toxin injection on nocturnal bruxism: A randomized controlled trial. OBJECTIVE:: To evaluate the effect of botulinum toxin type A on nocturnal bruxism. DESIGN:: Twelve subjects reporting nocturnal bruxism were recruited for a double-blind, randomized clinical trial. Six bruxers were injected with botulinum toxin in both masseters, and six with saline. Nocturnal electromyographic activity was recorded in the subject's natural sleeping environment from masseter and temporalis muscles before injection, and 4, 8, and 12 wks after injection and then used to calculate bruxism events. Bruxism symptoms were investigated using questionnaires. RESULTS:: Bruxism events in the masseter muscle decreased significantly in the botulinum toxin injection group (P = 0.027). In the temporalis muscle, bruxism events did not differ between groups or among times. Subjective bruxism symptoms decreased in both groups after injection (P < 0.001). CONCLUSIONS:: Our results suggest that botulinum toxin injection reduced the number of bruxism events, most likely mediated its effect through a decrease in muscle activity rather than the central nervous system. We controlled for placebo effects by randomizing the interventions between groups, obtaining subjective and objective outcome measures, using the temporalis muscle as a control, and collecting data at three postinjection times. Our controlled study supports the use of botulinum toxin injection as an effective treatment for nocturnal bruxism.
In a controlled polysomnographic (PSG) study that we recently performed in our laboratory, we noticed that some patients with a chief complaint of sleep bruxism reported concomitant non-myofascial pain in their masticatory muscles. To study the influence of such pain on the pattern of bruxism motor activity, we re-assessed the 2nd out of 2 consecutive PSG and masseter electromyographic (EMG) recordings of 7 bruxers without pain and 6 bruxers with concomitant jaw muscle pain. Among others, the selection of these patients was based on reports of current jaw muscle pain intensity, using 100-mm visual analogue scales. In our sample of bruxism patients with pain, levels of pain intensity did not differ significantly between bedtime and awakening in the morning. Although there were no significant differences between both subgroups of bruxers in the number of bruxism bursts per episode and the root-mean-squared EMG level per bruxism burst, bruxers with pain had 40% less bruxism episodes per hour of sleep. This suggests that non-myofascial jaw muscle pain decreases the number of initiations of bruxism episodes, but leaves their contents unaffected.
In clinical practice, parasomnias are often found to run in families and to co-occur. Several studies have indicated a role of genetic factors in them. In 1990, a questionnaire (response rate, 77%) sent to the Finnish Twin Cohort, a representative population sample aged 33-60 years, surveyed the frequency of five parasomnias (sleepwalking, sleeptalking, enuresis, bruxism, and nightmares) in childhood and as adults. In assessing the phenotypic covariation and shared genetic effects between the parasomnias, we used polychoric correlations and structural equation modelling. In childhood (n = 5856 individuals), co-occurrence is highest in sleeptalking with sleepwalking (R = 0.73), nightmares (R = 0.50), and bruxism (R = 0.43). As adults (n = 8567), the results are similar (R = 0.56, 0.43, and 0.39, respectively). The analyses of shared genetic effects included 815 monozygotic and 1442 dizygotic twin pairs with complete responses on four parasomnias as adults. The strongest genetic covariation was found in sleeptalking with sleepwalking, sleeptalking with bruxism, and in sleeptalking with nightmares. The estimated proportions of shared genetic effects were 50, 30, and 26%, respectively. The present results indicate that parasomnias share some common genetic background.
This cross-sectional study was conducted to investigate the influence of sleep habits, sleep problems, and lifestyle on sleep bruxism in Japanese elementary school children. In study 1, to confirm the reliability of replies provided by parents on children's sleep bruxism, we compared the scale of sleep bruxism frequency from questionnaires with actual sleep bruxism tooth wear in 49 elementary school children (22 males and 27 females). In study 2, a total of 1956 children (973 males, 983 females; mean age, 8.8 ± 1.8 years) and parents living in metropolitan Tokyo participated. Parents answered questionnaires on sleep habits, sleep problems, and lifestyle. Participants were classified as severe bruxism group (s-Bx) and non-severe bruxism group (ns-Bx) according to the frequency of sleep bruxism. The six grades were summarized into three categories: 1st/2nd grades (grades 1/2), 3rd/4th grades (grades 3/4), and 5th/6th grades (grades 5/6). The results suggest that the incidence of sleep bruxism in Japanese children living in Tokyo is strongly related to the disturbance of sleep habits and psychological stress, which can be caused by an owl-type lifestyle in children and parents.
The natural arousal rhythm of non-rapid eye movement (NREM) sleep is known as the cyclic alternating pattern (CAP), which consists of arousal-related phasic events (Phase A) that periodically interrupt the tonic theta/delta activities of NREM sleep (Phase B). The complementary condition, i.e. non-CAP (NCAP), consists of a rhythmic electroencephalogram background with few, randomly distributed arousal-related phasic events. Recently, some relation between CAP and autonomic function has been preliminarily reported during sleep in young adults by means of spectral analysis of heart rate variability (HRV). The present study was aimed at analysing the effects of CAP on HRV in a group of normal children and adolescents. Six normal children and adolescents (age range 10.0–17.5 y) were included in this study. All-night polygraphic recordings were performed after adaptation to the sleep laboratory. Six 5-min epochs were selected from sleep Stage 2 and six from Stages 3 and 4 (slow-wave sleep), both in CAP and NCAP conditions. From such epochs, a series of parameters describing HRV was then calculated, in both time and frequency domains, on the electrocardiographic R–R intervals. Statistical comparison between CAP and NCAP epochs revealed a significant difference for most of the frequency domain parameters (increase of the low-frequency band, increase of the low-frequency/high-frequency ratio and decrease in the high-frequency band during CAP) both in Stage 2 and in slow-wave sleep. Our results demonstrate that the physiological fluctuations of arousal during sleep described as CAP are accompanied by subtle, but significant, changes in balance between the sympathetic and vagal components of the autonomic system.
This paper attempts to draw attention to the rich tradition of grammar and dictionary writing which flourished in Scotland in the late eighteenth century. While the work of Elphinston and Buchanan is relatively well known, there is little on record concerning the large number of works written in Scotland in the period which set out not only to record the ‘deficiencies’ of Scottish English pronunciation (and syntax) but also to provide exemplification of a standard for emulation. That this endeavour was instigated and organized by the Select Society of Edinburgh gives Scotland a claim to have gone some way to actually setting up an equivalent to the proposed English Academy.
However, it has not been generally recognized that in many instances writers of Scottish grammars and pronouncing dictionaries were not holding up for emulation some version of London society English, but rather a Scottish standard of the type spoken by members of the clergy, the universities and the legal profession, probably based on upper class usage in Edinburgh and Glasgow. The phonological characteristics of this Scottish Standard, as they are evidenced in Alexander Scot's The Contrast, are the main subject of this paper.
Thirty healthy geriatric subjects were studied during a single night of sleep in a sleep laboratory. Unilateral masseter muscle activity was recorded in addition to the standard polysomnographic study. The geriatric subjects in this study exhibited fewer bruxing events than other subjects reported in the literature. Certain conditions that have not been previously investigated, such as sleep position, type of bruxing event, and relationship to the state of the dentition, are reported.
The aim of this study was to investigate the possible association between sleep bruxism and sleep-disordered breathing. Twenty-six patients who snored (nine women and 17 men) participated in this study. All-night polysomnographic recordings, including masseter electromyography (EMG), were performed in all subjects. The frequency of masseter contraction (MC) episodes was measured. Masseter contraction episodes were classified under the phasic and tonic forms. The analyzed data indicated that the termination of apnea and hypopnea events are often accompanied with tonic MC. It is suggested that tonic MCs can be linked to apnea and hypopnea episodes.
Purpose:
The purpose of this clinical pilot study was to evaluate the effect of a tricyclic antidepressant, amitriptyline, on pain-intensity level and level of stress in bruxers.
Materials and methods:
In a randomized, double-blind, crossover experimental design, 10 subjects received active (amitriptyline 25 mg/night) and inactive (placebo 25 mg/night) medication, over a period of 4 weeks.
Results:
The administration of amitriptyline for 4 weeks did not significantly (p >.05) reduce pain intensity. However, it significantly (p <.05) reduced the level of stress perception.
Conclusion:
The results of this limited study do not support the administration of small doses of amitriptyline over a period of 4 weeks for the management of pain resulting from sleep bruxism. However, the results support the administration of small doses of amitriptyline for the management of the perception of stress levels associated with sleep bruxism.
Eight confirmed bruxist subjects were investigated using portable electromyographic equipment. Nocturnal masseteric muscle activity, as measured by electromyography, was reduced immediately following the insertion of a full arch maxillary stabilization splint. It remained low until the splints were removed, at which time all but one subject's EMG values returned to pretreatment levels. Although the short term splint therapy did not show a permanent reduction in EMG levels, a dramatic reduction has been demonstrated during treatment.
Overnight EEG's were recorded on 12 subjects from 12–53 years of age. Records obtained before and after nocturnal behavior such as sleep-talking, bed-wetting, and tooth-grinding were analyzed in terms of frequency. (1) Immediately before sleep-talking occurred during activated sleep the theta wave component of desynchronization in relation to activated sleep decreased momentarily. (2) Adult enuresis occurred during the synchronization phase of activated sleep (episodical appearance of alpha waves). (3) Tooth-grinding was observed most frequently during the spindle phase and occasionally during activated sleep. In the spindle stage components of theta, alpha, and beta waves were augmented immediately before the tooth-grinding occurred and in activated sleep the theta wave component was suppressed. (4) A comparison of EEG before and after parasomnia behavior revealed a theta wave component in the cortical EEG. The theta wave component probably represents a cortical invasion by the hippocampal theta wave.
Simple sleep-related movement disorders must be distinguished from daytime movement disorders that persist during sleep, sleep-related epilepsy, and parasomnias, which are generally characterized by activity that appears to be simultaneously complex, goal-directed, and purposeful but is outside the conscious awareness of the patient and, therefore, inappropriate. Once it is determined that the patient has a simple sleep-related movement disorder, the part of the body affected by the movement and the age of the patient give clues as to which sleep-related movement disorder is present. In some cases, all-night polysomnography with accompanying video may be necessary to make the diagnosis. Hypnic jerks (ie, sleep starts), bruxism, rhythmic movement disorder (ie, head banging/body rocking), and nocturnal leg cramps are discussed in addition to less well-appreciated disorders such as benign sleep myoclonus of infancy, excessive fragmentary myoclonus, and hypnagogic foot tremor/alternating leg muscle activation.
All-night polysomnographic recordings were made of clinically diagnosed sleep bruxists (n = 23) and non-symptomatic controls (n = 6). The total duration of masseter contraction (MC) episodes during sleep was 11.6 minutes per night in bruxists and 6.6 in controls (P < 0.01). The mean frequency of MC episodes was 11.0 per hour of sleep in bruxists and 6.4 in controls (P < 0.05). The mean relative amplitude of MC episodes reflecting clenching strength was 0.81 in bruxists and 0.56 in controls (P < 0.01). The percentage distribution of mixed and phasic MC episodes was 94% among bruxists and 88% in controls. The remaining activity was classified as tonic in both groups. The subclassification of rhythmic jaw movements (RJM), defined as three or more separate rhythmic contractions during MC episode were also evaluated. The frequency of those MC episodes with RJM was 3.6 per hour of sleep in bruxists and 1.1 in controls (P < 0.001). The difference in the relative amplitude between the two study groups suggests that the amount of clenching force is the primary factor responsible for the harmful effects of sleep bruxism on the masticatory apparatus. The most significant difference was seen in those phasic and mixed MC episodes which also included the subclassification of rhythmic jaw movement. The result suggests that relative amplitude and rhythmicity of MC episodes can be used as a basis to confirm the diagnosis and to evaluate the treatment effects of suspected sleep bruxists.
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.
Although the relative incidence of violent behavior during sleep (VBS) is presumed to be low, no epidemiologic data exist to evaluate the prevalence of the phenomenon or to begin to understand its precursors or subtypes. This study examined the frequency of violent or injurious behavior during sleep and associated psychiatric risk factors.
A representative United Kingdom sample of 2078 men and 2894 women between the ages of 15 to 100 years (representing 79.6% of those contacted) participated in a telephone interview directed by the Sleep-EVAL expert system specially designed for conducting such diagnostic telephone surveys.
Two percent (N = 106) of respondents reported currently experiencing VBS. The VBS group experienced more night terrors and daytime sleepiness than the non-VBS group. Sleep talking, bruxism, and hypnic jerks were more frequent within the VBS than the other group, as were hypnagogic hallucinations (especially the experience of being attacked), the incidence of smoking, and caffeine and bedtime alcohol intake. The VBS group also reported current features of anxiety and mood disorders significantly more frequently and reported being hospitalized more often during the previous 12 months than the non-VBS group. Subjects with mood or anxiety disorders that co-occurred with other nocturnal symptoms had a higher risk of reporting VBS than all other subjects.
We have identified a number of sleep, mental disorder, and other general health factors that characterize those experiencing episodes of VBS. These findings suggest that specific factors, perhaps reflecting an interaction of lifestyle and hereditary contributions, may be responsible for the observed variability in this rare but potentially serious condition.
To evaluate the effect of botulinum toxin type A on nocturnal bruxism.
Twelve subjects reporting nocturnal bruxism were recruited for a double-blind, randomized clinical trial. Six bruxers were injected with botulinum toxin in both masseters, and six with saline. Nocturnal electromyographic activity was recorded in the subject's natural sleeping environment from masseter and temporalis muscles before injection, and 4, 8, and 12 wks after injection and then used to calculate bruxism events. Bruxism symptoms were investigated using questionnaires.
Bruxism events in the masseter muscle decreased significantly in the botulinum toxin injection group (P = 0.027). In the temporalis muscle, bruxism events did not differ between groups or among times. Subjective bruxism symptoms decreased in both groups after injection (P < 0.001).
Our results suggest that botulinum toxin injection reduced the number of bruxism events, most likely mediated its effect through a decrease in muscle activity rather than the central nervous system. We controlled for placebo effects by randomizing the interventions between groups, obtaining subjective and objective outcome measures, using the temporalis muscle as a control, and collecting data at three postinjection times. Our controlled study supports the use of botulinum toxin injection as an effective treatment for nocturnal bruxism.
The pathogenesis, pathophysiology, and pharmacotherapy of sleep bruxism (SB) are still not fully understood. We investigated symptomatology, objective and subjective sleep and awakening quality of middle-aged bruxers compared with controls and acute effects of clonazepam 1 mg compared with placebo by polysomnography and psychometry. Twenty-one drug-free bruxers spent 3 nights in the sleep lab, 21 age- and sex-matched controls 2 nights. Clinically, bruxers exhibited deteriorated PSQI, SAS, SDS and IRLSSG measures, polysomnographically impaired sleep maintenance, increased movement time, stage shift index, periodic leg movements (PLM) and arousals and psychometrically deteriorated subjective sleep and awakening quality, evening/morning well-being, drive, mood, drowsiness, attention variability, memory, and fine motor activity. As compared with placebo, clonazepam significantly decreased the SB index in all patients (mean: -42 +/- 15%). Sleep efficiency, maintenance, latency, awakenings and nocturnal wake time, the stage shift index, S1, PLM, the arousal index, subjective sleep and awakening quality, and fine motor activity improved.
To report a patient with bruxism possibly induced by the antidepressant venlafaxine.
A 62-year-old man developed severe bruxism that began 2 weeks after starting a therapy with venlafaxine because of depression and anxiety. After venlafaxine withdrawal, bruxism improved gradually and disappeared 2 months later.
Bruxism should be considered as a possible adverse effect of venlafaxine.
To summarize literature data about the role of psychosocial factors in the etiology of bruxism.
A systematic search in the National Library of Medicine's PubMed Database was performed to identify all peer-reviewed papers in the English literature dealing with the bruxism-psychosocial factors relationship. All studies assessing the psychosocial traits of bruxers (by using questionnaires, interviews, and instrumental and laboratory exams) and reviews discussing the contribution of those factors to the etiology of bruxism were included in this review.
A total of 45 relevant papers (including eight reviews) were retrieved with a search strategy combining the term "bruxism" with the words stress, anxiety, depression, psychosocial and psychological factors. The majority of data about the association between psychosocial disorders and bruxism came from studies adopting a clinical and/or self-report diagnosis of bruxism. These studies showed some association of bruxism with anxiety, stress sensitivity, depression and other personological characteristics, apparently in contrast with sleep laboratory investigations. A plausible hypothesis is that clinical studies are more suitable to detect awake bruxism (clenching type), while polysomnographic studies focused only on sleep bruxism (grinding type).
Wake clenching seems to be associated with psychosocial factors and a number of psychopathological symptoms, while there is no evidence to relate sleep bruxism with psychosocial disorders. Future research should be directed toward the achievement of a better distinction between the two forms of bruxism in order to facilitate the design of experimental studies on this topic.
To compare parental psychopathology and psychiatric disorders in ADHD children with and those without enuresis.
The participants of the clinical sample interviewed according to DSM-IV diagnostic criteria were 35 children with ADHD and enuresis, 153 ADHD children without enuresis, 115 fathers, and 172 mothers.
Only ODD comorbidity was the predictor of enuresis. Conduct disorder, tic disorder, major depressive disorder, separation anxiety disorder, bruxism, generalized anxiety disorder, obsessive compulsive disorder, and nail biting were not statistically more frequent in ADHD children with enuresis than in the ADHD children without enuresis. The only parental psychiatric disorder that was related to the groups was father's major depressive disorder.
Enuresis in ADHD has a relationship with ODD. Physicians who treat patients with ADHD and enuresis should routinely inquire about the presence of major depression in the fathers. (J. of Att. Dis. 2010; 13(5) 464-467).