Sleep-related bruxism …

Sleep Disorders

Updated 04.14.2024
Released 07.20.1994
Expires For CME 04.14.2027

Sleep-related bruxism

Authors: Cibele Dal Fabbro DDS PhD, Gilles Lavigne DMD PhD

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Editor: Federica Provini MD

Sleep-related bruxism

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Introduction

Overview

Bruxism is classically defined as an oral-jaw-muscle activity that can occur during wakefulness or sleep, and both forms may occur in the same individual. Bruxism tends to be variable in occurrence and magnitude over time. It is characterized during wakefulness by jaw clenching or bracing, with and without tooth contact, respectively. Bracing is an oral behavior that may or may not be included in the definition of bruxism in the literature. During sleep, it is characterized by tooth grinding, with or without sound, and jaw clenching. Bruxism is not a disorder for most individuals. For diagnosis coding purposes, the International Classification of Sleep Disorders included it in the section of sleep-related movement disorder as sleep-related bruxism. A 2018 dental sleep medicine consensus further defined it as an oral behavior. In an update, a re-emphasis was made that in the presence of other conditions or disorders, sleep-related bruxism is a “co-occurrence” instead of a comorbidity. Sleep-related bruxism is most likely an additional physiological activity that may be associated with, or may be a sign of, an underlying condition or disorder. There is no evidence that sleep-related bruxism is associated with a risk of mortality. Indeed, in most individuals, the most obvious consequences are tooth wear, grinding sounds, restoration damage, temporomandibular disorders, headaches, and orofacial pain.

It is clear in the era of personalized medicine that sleep-related bruxism is not caused by only one risk factor and cannot be explained by a single mechanism. The role of anxiety and stress are debated and may be dominant as a trigger in certain individuals. The use of antidepressive medication can be an additive risk factor. A series of physiological studies support a dominant role of sleep arousal in autonomic cardiorespiratory and brain sequences as a brief and transient facilitatory window to explain the onset of oral activity. Some evidence suggests serotonin, dopamine, or myosin as gene candidates.

The diagnosis of “possible” sleep-related bruxism is first based on reports of frequent tooth grinding by the patient and sleep partner or by the patient’s awareness of jaw clenching during sleep. A clinical examination helps to assess the level of dental damage and pain, supporting the concept of a “probable” condition. Sleep laboratory or home polysomnography can be indicated if the following co-occurring disorders are suspected: obstructive sleep apnea, comorbid obstructive sleep apnea and insomnia, or movement disorder (periodic limb movement during sleep, REM-sleep behavior disorder, or sleep-related epilepsy). Commercially portable devices can also help with diagnosis and monitoring. Devices collecting single EMG or tooth-contact data are clinically available tools. Treatment is protective, palliative, and multidisciplinary based, including oral appliances, biofeedback, behavioral therapies, and medications. The level of evidence is modest, and selection must be tailored based on consequences, health risk, and patient preference.

Key points

	• Sleep-related bruxism is an oral behavior most likely centrally regulated and frequently associated with sleep arousal.
	• The diagnosis is clinical, based on tooth-grinding reports, tooth wear or damage, pain, and grinding noise reported by bed partners.
	• One of the biological markers of jaw muscle activity related to sleep-related bruxism is the rhythmic masticatory muscle activity (RMMA). It is collected by surface activity of masseter or temporalis muscles via EMG.
	• Clinically, polysomnography with masseter or temporalis EMG (frequency and duration of RMMA) is not needed for most cases except when co-occurring sleep disorders are suspected (eg, obstructive sleep apnea, periodic leg movements, REM-sleep behavior disorder, or sleep-related epilepsy). It may also be done to assess the efficacy of treatment.
	• Treatment involves oral appliances, biofeedback, behavioral therapies, and medications. No definitive cure is expected, and multidisciplinary approaches are recommended.

Historical note and terminology

The first mention of teeth grinding occurs in the Bible, where the term “gnashing of teeth” is an expression of suffering (Luke 13:28, Matthew 13:41-2, Matthew 8:12, Matthew 13:50, Matthew 22:13, and Matthew 24:51). One of the first-recorded notations of this phenomenon was from Black, who commented that teeth abrasion tends to remove the cusps quite rapidly (16). French neurologist pioneers Marie and Pietkiewicz introduced the word bruxomania in 1907 (98). In 1938, Miller re-introduced the term bruxism for bruxomania or repetitive teeth grinding in a seminal book (104). In 1941, Bodecker described a patient whose bruxism had destroyed the clinical crowns of all the lower anterior teeth (17). In the 1940s to mid-1960s, many clinicians proposed a link between bruxism (either the wake or asleep form) and periodontal disease, headaches, and occlusion (132).

In 2013 and 2018, a group of international experts compiled a work-in-progress consensus to better define bruxism (82; 83). It was proposed that bruxism is a behavior in otherwise healthy individuals characterized by the presence of repetitive jaw muscle activities, such as clenching or grinding of the teeth or bracing or thrusting of the mandible. Bracing means forcefully maintaining a mandibular position, whereas thrusting means moving the jaw forward or laterally. These two last activities were considered oral behaviors and do not necessarily require tooth contact. Note that including these last two oral behaviors in sleep-related bruxism is not universally accepted; indeed, it is debated if the term bruxism should be limited to an oral activity limited to tooth contact.

Bruxism can occur during sleep (sleep-related bruxism) or during wakefulness (awake bruxism). Moreover, a clinically empirical diagnostic system suggested grading bruxism as “possible,” “probable,” or “definite.” Possible sleep or awake bruxism is based on a positive self-report. Probable sleep or awake bruxism is based on a positive clinical inspection, with or without a positive self-report. Definite is for sleep or awake bruxism based on a positive instrumental assessment, with or without a positive self-report or a positive clinical inspection (83). The last is more confirmatory than definitive and is challenged by the fact that sleep and wake bruxism do not occur regularly; indeed, its occurrence and magnitude can vary from night to night (77; 117; 118). The validity of any instrumental toll, questionnaire or examination system, or device used for diagnostic or treatment follow-up must consider such variability. Sleep and awake bruxism appear to be distinct behaviors with different underlying causes and require different management approaches (82; 83). Both consensuses remain “work-in-progress.” In November 2023, the same group published an update in the form of an editorial to more precisely define some key elements in the definition of bruxism. The main highlight is the “co-occurrence” of sleep-related bruxism with other conditions rather than labeling it as a comorbidity.

Table 1. Sleep-Related Bruxism Current Concepts

Jaw-muscle activities:
	• With tooth contact: tooth clenching, tooth grinding (high evidence)
	• With no teeth contact: bracing or thrusting of the mandible (both more present for awake bruxism) (low evidence)
Sleep-related bruxism can be:
	• Physiological
	• A sign of an associated or co-occurring underlying condition or disorder (eg, anxiety, stress, medication use, obstructive sleep apnea, gastroesophageal reflux disease, anxiety)
	• May be protective when associated with sleep-related breathing condition or disturbance
	• May have negative clinical consequences (eg, tooth damage, grinding sounds, pain)
Adapted from (92)

Clinical manifestations

Presentation and course

	• Sleep-related bruxism has been associated with dental damage and tooth wear, restoration fractures, temporomandibular disorders, headaches, and orofacial pain. Some patients may complain about masticatory muscle fatigue or tension, not necessarily pain. Sleep partners or family might complain about grinding sounds. Others may report sensitive teeth on waking and also muscle stiffness that limits the fluidity of mandibular movements. Jaw muscle hypertrophy can occur but most likely represents awake oral behavior, such as clenching, bracing, or gum chewing.
	• Evidence supports that sleep-related bruxism does not cause loss of bone support around teeth as a sign of periodontal disease. This is a frequent concern in patients diagnosed with periodontitis because it is believed that intense bruxism activities may aggravate the severity of periodontal disease.
	• Poor sleep quality is not the main complaint of individuals with sleep-related bruxism. When present, its co-occurrence with insomnia or sleep respiratory disorders should be evaluated.

Prognosis and complications

Tooth wear. In some individuals, the lateral grinding and occlusal compressive forces generated by sleep-related bruxism may be destructive, depending on the intensity, frequency, direction, duration, and type of jaw movements. Enamel hardness, oral dryness, and acidity may contribute to the magnitude of tissue damage. Experimental data indicate that bite force during sleep-related bruxism can exceed the maximum voluntary bite force during wakefulness (114). Abnormal tooth wear is a frequent clinical sign of sleep-related bruxism, usually observed on teeth surfaces that are in contact during jaw function (160).

Severe tooth wear on the anterior teeth may create more than an esthetic problem. In some cases, the loss of vertical height of the teeth leads to occlusal changes (134). Bruxism activities can also result in fracture of cusps and restorations and injury to the tongue, lips, and cheeks. Tooth pain and hypersensitivity are also frequent symptoms (12; 134).

Tooth wear has a multifactorial etiology, including an acidic diet, reflux, GERD, and daytime clenching and grinding (65; 115). The use of medication or illicit drugs may exacerbate tooth wear. Thus, this clinical sign indicates the amount of tooth surface loss but does not indicate whether the process is ongoing or a consequence of a previous one (168).

No strong and significant association between the polysomnographic parameters of possible sleep-related bruxism and the presence of tooth wear was found in adult patients with sleep-related bruxism (04; 65). A systematic review found that although dental wear is not necessarily associated with sleep-related bruxism in children, the most prevalent clinical sign of sleep-related bruxism is the wear on primary canines (158). These findings support that tooth wear should not be used alone for the diagnosis; tooth wear accuracy is about 50% (117; 118). The clinician should associate tooth wear with other assessment parameters through careful anamnesis and clinical examination before concluding on a sleep-related bruxism diagnosis (83).

Orofacial pain. Patients with sleep-related bruxism may present with pain or discomfort in the masseter and temporal muscle regions, morning headaches, and fatigue (20; 74). Studies based on self-reports tend to find a higher positive association between sleep-related bruxism and pain than those based on validated clinical examinations and instrumental evaluations of muscle activity (08). In a systematic review, about 30% of children aged 3 to 8 years reported symptoms such as headache and temporomandibular, facial, and masseter muscle pain. The least prevalent symptom among children was pain during jaw movement (158). Such associations seem to be low and may be present in some vulnerable individuals with co-occurring conditions (eg, anxiety, stress, and mood), yet no causality is demonstrated.

Temporomandibular disorders. Temporomandibular disorders are a subset of orofacial pain, including temporomandibular joint pain or sounds, myalgia, or arthralgia with occasional limitation in jaw function. Studies addressing the association between sleep-related bruxism and temporomandibular disorders are controversial. A scoping review concluded that the association between sleep-related bruxism and temporomandibular disorder depends on the assessment approach adopted for bruxism diagnosis (95). Investigations based on questionnaires or self-reports showed low specificity for sleep-related bruxism assessment. In general, they found a positive association with temporomandibular disorders. Conversely, instrumental studies employing polysomnography or electromyography reported a modest relationship between sleep-related bruxism and temporomandibular disorder (155).

Periodontal disease. Periodontal disease is inflammation and infection involving the gingiva and bone surrounding teeth. It can be associated with systemic conditions, such as cardiovascular diseases, type 2 diabetes mellitus, respiratory disorders (including sleep apnea), and chronic renal disease. Findings about the influence of sleep-related bruxism on periodontal tissues are controversial. Indeed, a systematic review supports that sleep-related bruxism is not a cause of periodontal disease (93). Indeed, the hypothesis is that in patients diagnosed with periodontal disease, the simultaneous presence of sleep and awake bruxism activities can exacerbate the damage to periodontal tissues, aggravating periodontitis (12; 111). A study from Portugal found that individuals with sleep-related bruxism exhibited a lower prevalence of periodontitis (18). Conversely, a cross-sectional study from Turkey found a prevalence of 36.6% of probable bruxism in a sample of 541 patients seeking periodontal care. In addition, patients with probable bruxism were 2.24 times more likely to be diagnosed with periodontitis (95%, CI: 1.465-3.434) (15). Some caution is needed to analyze such results. First, the prevalence of advanced-stage periodontitis in the sample was probably higher than in the general population because the participants sought periodontal treatment. Second, the cross-sectional design does not allow the determination of cause-and-effect relationships between the evaluated variables. This suggests the need for high-quality studies with robust study designs.

Poor sleep quality. Assessment of sleep quality should also be part of the evaluation of individuals with sleep-related bruxism. Approximately 25% to 50% of adult individuals with sleep-related bruxism report difficulty in maintaining sleep (88; 89; 70). Patients with sleep-related bruxism may present decreased sleep efficiency and higher sleep fragmentation, as well as poor sleep quality when compared to individuals without sleep-related bruxism (88; 89; 70; 112). Sleep partners may also complain of poor sleep quality or sleep fragmentation due to grinding teeth noise.

Other symptoms. Individuals with sleep-related bruxism may also present with daytime fatigue, sleepiness, and more affective symptoms than control subjects (112).

Clinical vignette

A middle-aged female psychology professor was seen by appointment in our university hospital service. Her main complaint was intense episodes of sleep bruxism (three times a week) reported as tooth grinding (confirmed by sleep partner) and morning jaw temporalis and masseter muscle tension that lasted 90 to 120 minutes. Social history was in the normal range. Examination of her familial structure revealed she was the mother of a 3-year-old boy who was a good sleeper, and she had a collaborative life partner for regular household responsibilities. Her medical history was negative, and no medication or drug use was reported. Excessive fatigue was also a major concern, and occasional snoring was reported. Recent blood tests were within normal limits, and no anemia was suspected. BMI was normal, but secondary concerns included a report of no time to relax via exercise, reading books, watching movies, or taking walks.

At the clinical oral and dental examination, tooth wear was observed on her lower incisors and upper cuspid teeth with dentin exposure. Occasional tooth sensitivity to cold water was reported. The patient also presented a lower jaw retrognathia, deep palate, and a modified Mallampati 3; tonsils were removed in childhood. The jaw and neck muscles and temporomandibular joint were sensitive to finger palpation, with pain reported at 4/10. Masseter muscles were hypertrophic when she clenched her teeth. The Stop Bang was at 4, moderate risk to obstructive sleep apnea; Epworth was below 10. The panoramic x-ray did not show temporomandibular joint, jaw bone, tooth, or sinus abnormality that can be visualized by this type of examination.

A 1-night home ambulatory, type 3, sleep recording was requested and done under medical supervision. The results confirmed snoring (three to four times per hour of sleep), an AHI of 7, and an index of jaw muscle contraction at six RMMA per hour of sleep. The contraction pattern was mostly phasic type and occurred in light sleep or in periods preceding REM onset. Mean oxygen saturation was 92% with few RMMA episodes where drops of more than 4% were observed. Most sleep time was in the supine position. Sleep onset was 14 minutes, and sleep efficiency at 94%. The arousal index was 19 per hour, with half of the events linked to respiration or RMMA. Few RMMA events were associated with big breaths.

The medical and dental diagnoses, based on clinical examination, history, and sleep recording, were mild obstructive sleep apnea, snoring, and moderate sleep bruxism with concomitant fatigue and jaw myalgia.

Medical and dental medicine management were done as follows:
(1)	Explication of the mild condition, its putative causes, mechanisms (university professors are curious), and risks. This was followed by sleep behavioral advice: relaxation at time of sleep, increased physical activity, avoidance of stimulants before sleep, etc. (The level of evidence for sleep-related bruxism is low; such empirical guidance is always welcomed by individuals with sleep-related bruxism.)
(2)	For jaw muscle pain, a referral to physical therapy was provided. She agreed to go as the service was covered by private insurance. We informed her that some jaw muscle exercises can also improve her breathing.
(3)	Due to snoring and mild obstructive sleep apnea, an upper jaw oral splint (bite splint, occlusal splint) was not recommended. A mandibular advancement device was proposed, and she was informed of possible tooth displacements. The higher cost of mandibular advancement devices was a concern; the patient told us she wanted to double-check with private insurance for coverage. One month later, a mandibular advancement device was inserted, with a recommended follow-up at 2 weeks for comfort and pain. Advancement of lower jaw titration was done at 1 month because she tolerated the device well. (The level of evidence for co-occurrent obstructive sleep apnea and management of sleep-related bruxism is moderate.)
(4)	A sleep position correction device was also proposed. She refused both the cushion and an electronic vibration device. (The level of evidence is high for obstructive sleep apnea and emerging for sleep-related bruxism.)
(5)	At the 6-month follow-up, she reported high satisfaction with the mandibular advancement device, that her sleep partner was happy because she no longer snored, and that she had less fatigue. Physical therapy was done once a month. Although she felt it useful, the benefit did not last more than a few days. A home sleep recording was suggested for the 1-year follow-up.
Notes: For jaw muscle pain and sleep-related bruxism, some individuals benefit from repeated injections of botulinum toxin. Cost is also a limitation because the injections must be repeated every 3 to 4 months. (The level of evidence is moderate.) Oral appliances with vibration or electric aversive stimulation biofeedback have been used with success. Fidelity (adherence) for nightly use is a concern. (The level of evidence is moderate.) No evidence yet supports the frequent prescribing of muscle relaxants (eg, cyclobenzaprine) whose efficacy and efficiency are under testing (Prof Conti PC et al, Brazil). In the presence of sleep instability with sleep-related bruxism, the occasional use of clonidine at low doses helps some patients. Obviously, medical supervision is recommended due to the risk of morning hypotension. (The level of evidence is modest.) In the presence of anxiety, cognitive and behavioral therapy or anxiolytic medication can be considered. (The level of evidence low.)

Biological basis

	• Sleep-related bruxism is mainly regulated by the central and autonomic nervous systems. The role of the peripheral nervous system is debated and lacks solid evidence.
	• Episodes of jaw muscle activities (RMMA) in young and otherwise healthy individuals are preceded by events related to sleep arousals, such as increases in the autonomic sympathetic cardiac activity, frequency of EEG and EMG activities, heart rate, blood pressure, first elevation of jaw-opening muscle activity and onset of RMMA (with phasic or tonic or mixed-burst pattern). In some cases, a rise in breathing amplitude is noted.
	• Sleep-related bruxism has a multifactor etiology, including influences from psychological and environmental-genetic factors.
	• Sleep-related breathing disorders, medications, and addictive substance use can be associated with sleep-related bruxism. The cause-and-effect relationship is not yet fully explained.
	• Polysomnographic studies with jaw muscle EMG revealed that sleep-related bruxism activities occur during all sleep stages despite being more common in non-REM stages 1 and 2 (N1 and N2). RMMA peaks in frequency in the short period before REM sleep onset. In otherwise healthy individuals, RMMA and tooth grinding are rare in REM sleep. When sleep-related bruxism occurs during REM sleep, the presence of REM sleep behavior disorders should be evaluated. REM sleep behavior disorders may present with co-occurring jaw muscle myoclonus and RMMA.

Etiology

Sleep-related bruxism has a multifactorial etiology that can vary from individual to individual.

Structural (skeletal shape such as retrognathia) and functional tooth-to-tooth occlusion have been proposed as etiologic models to explain the etiology of sleep-related bruxism. The structural etiologic model argues that dental defects and malocclusions could cause bruxism. However, systematic reviews and meta-analyses have failed to support the role of dentoskeletal malocclusion in sleep-related bruxism, and the role of dental occlusion remains debated (97; 138).

The functional etiologic model argues that psychological factors, such as personality traits and predisposition to stress, may play a role in the onset of sleep-related bruxism. There is growing evidence in the literature for such hypotheses in children and adults (149; 40; 120; 151; 128).

Associated factors

Psychological factors. Although there is controversy about the association between anxiety and sleep-related bruxism in adults, a systematic review showed that some specific symptoms, such as stress sensitivity, anxious expectation, and panic symptoms of anxiety, might be associated with probable sleep-related bruxism (128). In children older than 6 years of age, evidence suggests an association between psychological factors and sleep-related bruxism (40).

Individuals with sleep-related brusixm reported fewer positive coping strategies or a deficit of functional coping strategies than those without sleep-related bruxism (147). In adults, however, the association is modest, based on a systematic review and meta-analysis (28). Interestingly, another systematic review and meta-analysis found a low association of evidence between sleep-related bruxism and stress, although a positive association was observed with stress biomarkers, such as epinephrine, norepinephrine, cortisol, adrenaline, dopamine, noradrenaline, and prolidase enzyme levels (129). Caution in the interpretation of these findings is recommended, and causality needs to be demonstrated (28; 129).

Personality traits. Personality traits may also contribute to sleep-related bruxism in children and young adults because individuals with sleep-related bruxism tend to have a high level of neuroticism and responsibility compared to people without sleep-related bruxism (151). An epidemiologic study involving children demonstrated that teeth clenching at night seemed to be associated with emotional symptoms, peer problems, and higher total scores on the “Strength and Difficulties Questionnaire,” a tool used to evaluate mental health conditions (135).

Comorbidities. As listed above, co-occurring obstructive sleep apnea, restless legs syndrome or periodic limb movement during sleep, insomnia, REM behavior disorder, sleep-related epilepsy, and sleep-related gastroesophageal reflux were associated, in adults, to sleep-related bruxism in comparison to the general population (74). Although the pathways and causality underlying such associated observations have not yet been clarified, the authors suggest that sleep arousal may be a common factor linking sleep-related bruxism and the above-mentioned disorders; it is yet unknown for REM behavior disorder and Parkinson disease (74).

The occurrence of sleep-related bruxism with movement disorders suggests that it may occur with some disorders, such as Parkinson disease, although no link can be found between the two conditions (166).

A suggestion that sleep-related bruxism is linked to systemic inflammation was shown in a systematic review to be weak and not well demonstrated until now (46).

Sleep-related breathing disorders. The association between obstructive sleep apnea and sleep-related bruxism also appears to be present but low to moderate. A putative protective role has been suggested as a compensatory mechanism to maximize upper airway patency during sleep; this is based on the observation of breathing activity preceding RMMA (55; 79; 71; 94). Both disorders are associated with arousals, but the prevalence of obstructive sleep apnea increases with age, and the prevalence of sleep-related bruxism self-reports decreases with age.

It was suggested that 30% to 50% of adults and 26% of children with obstructive sleep apnea have sleep-related bruxism (125; 50). The odds of sleep-related bruxism for individuals with obstructive sleep apnea reach almost 4 (OR: 3.96; 95% C.l., 1.03-15.20; p< 0.05) in one paper from 2014 and less than 1 (OR: 0.15; 0.036-0.68; p< 0.05) in other papers (33). It is important to note that study methodology varies, including the studies cited here, leading to different conclusions.

Although the 2018 international consensus highlighted that sleep-related bruxism may be a putative protective factor for obstructive sleep apnea, a systematic review questioned this association. Indeed, in a survey of seven studies, four showed a positive association, and three showed no association (83; 86). Such discrepancy may be explained by different obstructive sleep apnea-related phenotypes among patients with co-occurring obstructive sleep apnea and sleep-related bruxism.

Further investigations challenged the putative contribution of RMMA-SRB to breathing to describe the change in breathing flow and to challenge the sequence of events, obstructive sleep apnea preceding or following RMMA-EMG observation as a cause-and-effect driver.

Parallel between changes in respiration and RMMA. A positive and significant correlation was found between the frequencies of RMMA episodes (as a sleep-related bruxism marker) and the amplitude of breath (R2 = 0.26; p = 0.02). Although it explained only 26% of the variability, the breath amplitude was 11 times higher when arousal was associated with RMMA compared to arousal alone (71). It must be highlighted that seconds before the onset of RMMA, the amplitude of inspiration has already increased (8% to 23%), being high at the onset of the suprahyoid activity (60% to 82%, 1 second before RMMA) and maximal during the RMMA episode (108% to 206%), followed by a rapid return to levels preceding RMMA (71).

Sequence of events between obstructive sleep apnea respiration and RMMA-sleep-related bruxism. In a study of individuals with both conditions, 80% of sleep-related bruxism events were scored close to obstructive sleep apnea events, and most of them (55%) occurred after obstructive sleep apnea events (143). Two other studies found that fewer than one of four episodes of sleep-related bruxism were temporally associated with obstructive sleep apnea episodes. Indeed, sleep-related bruxism episodes occurred 4 to 10 times more frequently after a respiratory event than the opposite (34; 172).

Snoring and respiratory disease. The inclusion criteria should carefully consider conditions such as snoring and upper airway resistance syndrome rather than strictly obstructive sleep apnea. For example, studies with children and adolescents demonstrated snoring as the highest risk factor associated with sleep-related bruxism (42; 130). Also, respiratory diseases (allergic rhinitis, otitis media, and asthma) might be more prevalent in children with sleep-related bruxism (109; 42). From our knowledge, no studies are available for such respiratory diseases and sleep-related bruxism in adults.

Although one study with no polysomnography found no association between sleep-related bruxism and snoring, two other studies with polysomnography did find an association (124; 103; 56). According to the data from the Poland group, sleep-related bruxism associated with snoring was more frequent in the supine position, and phasic events were positively correlated with snore intensity despite the body position (103).

Although the link between sleep-related bruxism and the airway is difficult to show, it may be either spurious or phenotype-dependent. Research is beginning to focus on different phenotypes to understand different profiles and to select individualized management (125).

Insomnia. Two analyses based on polysomnography data from a general population of Sao Paulo, Brazil, showed an association between sleep-related bruxism and insomnia (89; 27). Analyses revealed that such an association was present using self-reported data of awareness of sleep-related bruxism; polysomnography-confirmed occurrence of sleep-related bruxism was not associated with any of the included factors (27). However, a sub-group of middle-aged women seemed more vulnerable, and the use of self-report of both sleep-related bruxism and insomnia may guide clinicians to pay attention to such occurring conditions. A survey in the Netherlands with 2251 participants self-reporting an awareness of sleep-related bruxism revealed that an association with insomnia was only present when anxiety was concurrent (27).

Genetic factors. According to scientific evidence, environmental family-related factors can contribute to the occurrence of sleep-related bruxism behavior (70; 150; 53; 146). A cohort study conducted with twins showed that genetic components are responsible for half of the risk variation of the sleep-related bruxism phenotype (163). The presence of RMMA in the masseter and temporal muscles was higher in monozygotic twins when compared to dizygotic ones, suggesting a genetic influence on the triggering of sleep-related bruxism (05). Genetic studies on sleep-related bruxism cannot exclude the role of the environment (139).

A study collected in Poland suggested a possible genetic contribution of the dopamine receptor gene DRD1 that may predispose to sleep-related bruxism, whereas the serotonin subtype of the receptor encoding gene HTR2A may contribute to its genesis or to the overlap between sleep-related bruxism and obstructive sleep apnea (170).

One study performed the first genome-wide association analysis for probable sleep-related bruxism in a population of almost 400,000 individuals in Finland. Genetic association-correlations were made with responses to questionnaires, lifestyle, and clinical traits. The authors found an association with the expression of the myosin IIIB gene (161). No association was observed with previously identified gene candidates, such as serotonin or dopamine. The association with myosin seems complex and supports the fact that sleep-related bruxism is most likely a condition overlapping with others, such as concurrent pain, sleep apnea, reflux disease, upper respiratory diseases, psychiatric traits, and the use of antidepressants or sleep medications. Myosin III is a gene candidate with roles being explored, such as phototransduction and hearing ciliary activity (161).

Genetic twin association, population-driven polysomnography-confirming, and large sample size-based sleep-related bruxism studies also suggest that no single candidate can explain the genetics of sleep-related bruxism. The role of the environment and the presence of comorbidities, or co-occurring conditions, or medication use probably influence the equation.

Medications and addictive substances. Clinical reports or studies on the effects of medication or drugs suggested a central dopaminergic and serotonergic role in the pathogenesis of pharmacologically induced wake or sleep-related bruxism (45). A literature survey concluded that sleep-related bruxism can be induced or worsened by addictive substances, such as heroin, nicotine, and alcohol, and by some classes of medications, including anticonvulsants, phenethylamines, and serotonin reuptake inhibitors (38). There is, however, insufficient scientific evidence to confirm the risk and putative mechanisms (ie, whether medications can aggravate preexisting bruxism or trigger its activities). The individual variability and the presence of other conditions or morbidities increase the complexity.

Chronotype profiles. The interest of chronotype and sleep-related bruxism seems to be recent. Studies on this topic are based mainly on questionnaires of children or young individuals.

There are three different alert/sleep chronotype profiles: morning, intermediate, and evening types (11; 108). A study demonstrated that children aged 3 to 5 years with an evening chronotype tended to have more “possible” sleep-related bruxism. Among children with sleep-related bruxism, 12.5% had a morning profile, 26.4% had an intermediate profile, and 47.8% had an evening profile (137). In undergrad students, most studies did not report a difference between chronotype and sleep-related bruxism (63; 148; 72). An analysis in a general population subgroup from Brazil revealed that the preferred morning chronotype was associated with a modest 19% lower risk of reporting sleep-related bruxism (64).

Neurologic conditions

The occurrence of sleep-related bruxism in movement disorders and neurologic conditions such as REM-sleep behavioral disorder, Parkinson disease, parkinsonism, epilepsy, and acquired brain injury has been described in few case reports and series.

A study from our group found sleep-related bruxism in 25% of 25 patients with REM-sleep behavior disorder. Only patients with idiopathic REM-sleep behavior disorder had significantly more RMMA and oromandibular myoclonus during REM sleep (02).

For Parkinson disease, the data are controversial, but the literature is limited. One study found a prevalence of 4.7% for possible sleep-related bruxism in 661 patients with Parkinson disease, which was not higher than in healthy individuals (173). According to a study of 368 patients with Parkinson disease or parkinsonism and 340 controls collected in the Netherlands, the patients with Parkinson diesease or parkinsonism reported bruxism during sleep and wakefulness significantly more often than controls (166). It is also suggested that these patients frequently present with orofacial pain and temporomandibular disorders (166), although a systematic review (with only three studies included) failed to show this association (106).

One paper described that patients with severe acquired brain injury showed a remarkably high level of jaw muscle activity during sleep at admission, which remained high after 4 weeks of hospitalization, with a potential risk of tooth wear and pain. Interestingly, these findings were more present in individuals younger than 40 years of age (73).

The prevalence of sleep-related bruxism seems to be higher in patients with epilepsy (20% to 23.7%) compared to individuals without epilepsy (4.8 to 5.4%) (49; 69). Another rare condition reported in the literature is sleep-related facio-mandibular myoclonus, a rare and under-recognized stereotyped parasomnia. Sleep-related facio-mandibular myoclonus can present with isolated tongue biting, which can be misdiagnosed as epilepsy and sleep bruxism. The authors suggest a simultaneous video-EEG and surface EMG to confirm the diagnosis and clonazepam as a form of management (175).

Physio(patho) genesis

Strong evidence suggests that the central nervous system plays a dominant role in sleep-related bruxism. RMMA, followed by transient microarousal, occurs more often in young and otherwise healthy individuals with sleep-related bruxism than in control persons without awareness of tooth grinding or clenching. In both, muscle tone and heart rate increased during experimental arousal; in close to 80% of those with awareness of tooth grinding or clenching and elevated frequency of RMMA (two or more per hour of sleep), the oral activity is in phase with brief and transient sleep arousal. The last is a current and normal activity during sleep associated with a rise in autonomic cardiac, brain, and muscle activities that lasts between 3 and 15 seconds and can recur seven to 14 times per hour of sleep (67; 85; 79; 78; 24; 23; 102).

These results support the hypothesis that sleep-related bruxism is an exaggerated form of oromotor activity associated with sleep microarousal (67; 24; 102). RMMA-sleep-related bruxism can occur during all stages of sleep, despite being more common in non-REM stages 1 and 2 and in the ascending period preceding REM sleep stage (24). This period, typified by the shift from non-REM toward REM sleep, correlates with increased sympathetic and arousal activities (54).

Polysomnographic studies revealed an increase in sympathetic activity several minutes before bruxism events. Increases in sympathetic dominance, heart rate, and brain activity followed by a rise in suprahyoid muscle tone were observed in a dominant sequence (78; 24; 102). In individuals with sleep-related bruxism and moderate to high RMMA frequency (severe motor activity), a marked increase in sympathetic cardiac activity over parasympathetic activity precedes sleep-related bruxism (58). These experimental findings tend to support the idea that the onset of RMMA and sleep-related bruxism episodes are influenced by the recurrent-cyclic window of brief and transient activity of the brainstem arousal ascending system, controlling the autonomic-cardiac and motor networks (78). Notably, few RMMA episodes were associated with big breaths, suggesting that sleep-related bruxism may be a natural physiological activity associated with sleep homeostasis (71; 102). Sleep-related bruxism genesis is in phase with oscillations in the sleep stage and cycle as well as the occurrence of microarousal (176).

Recurrent episodes of RMMA tend to occur in clusters of phasic types of brief muscle contractions (three or more, 1 Hz). Although the last is dominant, some are observed as prolonged isotonic contractions of the jaw muscles and are named tonic types. The combination of both is named mixed. Not all masseter or temporalis EMG activities are associated with tooth grinding; indeed, only about 50% of those events seem to be associated with grinding. The night-to-night variability of RMMA is around 25%, and the variability of tooth grinding occurrence is about 50% (23; 102).

One possible phenotype of sleep-related bruxism is that the masseter EMG with tooth-grinding events was dominant in the phasic type of RMMA, whereas tooth attrition was associated with longer tonic bursts (174). The mandible may be either in neutral or eccentric positions. RMMA occurs more often in young and otherwise healthy individuals with sleep-related bruxism than in controls without awareness of tooth grinding or clenching.

Yet, the dominant trigger of RMMA related to bruxism is not identified and may not exist; most likely, it is not a single trigger; most likely, many bio-socio-psychological factors may contribute differently from individual to individual. Phenotype and endotype should to be identified (176).

Epidemiology

	• Different methodological approaches, clinical criteria, and study sampling reflect different prevalence rates among studies.
	• Sleep-related bruxism can occur at a particular point in life, and as age increases, the prevalence of this condition tends to fall as a self-reported condition. However, involvement in bruxism activities can resume in stressful situations.

Prevalence

Different methodological approaches, clinical criteria, study sampling, and age have led to discrepancies in the reported prevalence of sleep-related bruxism (158).

In babies, bruxism is considered physiological during the development of the primary incisors. When the posterior primary teeth erupt, the mandibular instability tends to cease, as do bruxism activities (97). The prevalence of sleep-related bruxism is around 31% in children, 16% in adolescents, and 20% in undergraduate students (169; 158).

The prevalence of “possible” teeth grinding among schoolchildren reached 36.8% of preschoolers and 49.6% of first-graders, reported at least once a week by parents (61). Studies show that male children aged 8 to 10 years have a higher prevalence of sleep-related bruxism (41; 157). Among children aged 0 to 12 years, being male can be considered a risk factor for sleep-related bruxism (53). During adolescence, boys reported a higher percentage of sleep-related bruxism than girls did (66).

In adults, the sleep-related bruxism prevalence is around 8% to 16% (88; 169). People can suffer from sleep-related bruxism at a particular point during their lives, and as age increases, the prevalence of self-reports tends to fall (88; 96; 37). Data from three populations with polysomnography and questionnaires showed that the RMMA prevalence drops in clinical research samples but not in the general population (37). This result suggests that patients who complain about sleep-related bruxism when they are young might have other comorbidities about which they start to complain as they age (37).

Some evidence, including a systematic review, showed that children with Down syndrome present high prevalence of sleep-related bruxism (142; 06). Another systematic review showed that patients with autism spectrum disorders are more likely to present with sleep-related bruxism than controls, although the quality of evidence is low (OR: 3.80; 95% CI: 2.06-7.01) (51).

COVID-19 pandemic updates

Due to the rapid spread of the COVID-19 disease, health authorities imposed social distancing as a preventive strategy (52). Emotional challenges, such as stress, anxiety, fear, and changes in daily routines, marked people's lives. Thus, psychosocial and sleep disturbances possibly increased, worrying researchers about the risk of developing or worsening bruxism during social distance (25). A Brazilian study showed that students with poorer sleep quality were more likely to have severe “possible” sleep-related bruxism. In addition, the use of smartphones contributed to the odds of reporting mild and moderate possible awake bruxism (bracing and thrusting) (81; 131).

It is important to mention the possibility that associations of sleep-related bruxism with COVID-19 may have been influenced by variables such as anxiety, poor sleep quality, increased consumption of drugs, or intense use of electronic devices. Health professionals should address the possibility of COVID-19-related bruxism overlapping with the different clinical conditions mentioned and the need for a multi-professional team to manage these patients (36).

Differential diagnosis

Confusing conditions

When considering a diagnosis of sleep-related bruxism, a differential diagnosis based on the following contributes to accuracy:

(i)	The collection of patient history, complaint, and motive of consultation can help asses a “possible” presence of sleep-related bruxism.
(ii)	Clinical examination of teeth and other oral structures to assess if the presence of sleep-related bruxism is “probable.”
(iii)	Recording the sleep-related bruxism oral activity during sleep can help to “confirm” if it is present and, more importantly, if co-occurring conditions are at risk of exacerbation.

Various questionnaires are used when a co-occurring condition or disorder is suspected. For example, the Brux Screen or STAB or BruxScreen and TWES are used for suspected bruxism and tooth wear, respectively; Stop Bang or Berlin and Epworth scales are used to determine the risk of obstructive sleep apnea and sleepiness, respectively; and the Insomnia Severity Scale for risk of insomnia. Also, sleep investigation tools (Type 1 to 4) are used when a co-occurring condition or disorder is suspected (10; 32; 31; 84; 140). The most frequent co-occurring conditions include anxiety, transient or chronic pain and headache, gastro-esophageal reflux disorder, and sleep breathing conditions, such as snoring, obstructive sleep apnea, and insomnia.

Although many co-occurring conditions can be observed with sleep-related bruxism, its clinical recognition is not associated with many confounding activities due to the clear RMMA pattern with tooth grinding observed with phasic (three bursts of 0.5 seconds or longer), tonic (bursts of 2 seconds or longer), or a combination of both, mixed EMG contraction patterns (24; 102).

To avoid recognition of confounding conditions, the recognition of the following is helpful. Clinical tooth damage can be due to other factors, such as erosion due to diet or gastric reflux, and wear can be exaggerated by concurrent low salivation/oral dryness, medication or drug use, and oral breathing (167). Tooth wear accuracy is about 50% in cases with sleep-related bruxism, confirmed by EMG recording (117; 118). Muscle hypertrophy is not a clear sign of sleep-related bruxism because it can be due to many other factors, such as wakeful clenching habits, jaw bracing during exercise, or gum chewing. Oro-pharyngeal sounds can be due to snoring, somniloquy, or tongue-clinking; these can be easily discriminated (43; 68). Report of the duration of transient wake time morning pain, soreness, or tenderness is different from usual myofascial or temporomandibular pain, or tension-type headache, or migraine (01; 154). EMG recordings of masseter, temporalis, and digastric-chin muscles help to discriminate RMMA from usual oral activities, such as swallowing or somniloquy. Most critical, due to the risk of morbidity, is the occurrence of jaw muscle myoclonus that can be observed with REM-sleep behavior disorder or sleep epilepsy. These conditions are rare, and the very short contractions (less than 0.25 sec) help to differentiate myoclonus from RMMA (02).

Associated or underlying disorders

It is important for the clinician to recognize conditions that co-occur with sleep-related bruxism. Some may be spurious and do not explain causality, such as obstructive sleep apnea, insomnia, GERD, or are rarely observed, as in REM-sleep behavior disorder, sleep epilepsy, and Parkinson disease.

Diagnostic workup

	• Self-reports of tooth grinding and jaw clenching and clinical observation of tooth damage are the most used diagnostic tools in clinical practice.
	• Bed partners or family members’ complaints of grinding noises due to teeth friction guide clinicians to a better certainty, although these vary from night to night and are not always a reliable measure because some patients may not have a sleep or bedroom partner.
	•Clinical inspection of dental wear does not allow a solid diagnosis because damage may be nonspecific to sleep-related bruxism and seems not to be correlated to the RMMA frequency over the sleep period (04).
	• Polysomnography (ideally including audio and video recordings) can be used to quantify sleep-related bruxism, and it is indicated especially when other sleep disorders may be present. It is, however, not a routine test in otherwise healthy individuals.

According to the International Classification of Sleep Disorders, proposed by the American Association of Sleep Medicine and revised in 2023, sleep-related bruxism diagnosis is clinical and requires polysomnography only in some cases. They suggest combining the criteria A and B:

A.	The presence of repetitive jaw-muscle activity characterized by grinding or clenching of the teeth in sleep.
B.	The presence of one or more of the following clinical symptoms or signs consistent with the above reports of tooth grinding or clenching during sleep: abnormal tooth wear, transient morning jaw muscle pain or fatigue, or temporal headache (07).

Establishing the diagnosis only based on self-report is challenging due to several factors. Patients may have been previously informed of the suspicion of sleep-related bruxism by a clinician or may be unaware of it, basing their report on information from a sleep partner. Furthermore, patients suffering from symptoms tend categorize their disorder into a classification (133). Nonetheless, self-report assessment of sleep-related bruxism is the most used tool in bruxism research and clinical practice. Although self-report predicts teeth-grinding sounds, self-reported sleep-related bruxism does not predict the presence or absence of moderate or severe cases assessed by polysomnography (88; 133). For example, a study demonstrated a poor association between parental reports and sleep-related bruxism confirmed by polysomnography in children (60). Parents seem to underreport tooth clenching and grinding by 56% and 73.7%, respectively, in children with sleep-related bruxism. However, the authors highlighted that over 83% of the parental reports regarding the audible sounds of teeth grinding were consistent with the diagnosis made by polysomnography (04; 60).

Health professionals should know that tooth wear is not an exclusive clinical sign of sleep-related bruxism; it may even be a natural process attributed to age. No direct correlation was found between the tooth wear severity and the number of sleep-related bruxism episodes per hour of sleep (65).

Several factors can also play a role in the tooth wear process and should be investigated during anamnesis, eg, acid diet, diagnoses of xerostomia or gastroesophageal reflux disease (GERD), or medication use. In addition, there are differences between the types of tooth wear, eg, attrition, erosion, abrasion, as well as mechanical or chemical wear (65).

The investigation may include the masticatory muscle hypertrophy and indentations on the tongue or lip or a white line on the inner cheek adjacent to the molars. As previously mentioned, patients with sleep-related bruxism may report sleep disturbances and difficulty initiating sleep; hence, a sleep history can be helpful and guide management.

The association between diagnosis clinical criteria and consequences has not been established. Neither the intensity nor the number of sleep-related bruxism events seems to predict risk and consequences (83; 76). For example, when gastroesophageal reflux precedes sleep-related bruxism activities, tooth erosion may be aggravated due to the rise in oral acidity (168).

There are efforts to develop standardized and validated metrics, eg, questionnaire or EMG-based, for the clinical diagnosis of sleep-related bruxism (91; 90; 76). As listed above, the clinical signs and symptoms are insufficient to determine a “definite-confirmatory” diagnosis of sleep-related bruxism (65). Therefore, to improve a “definite-confirmatory” sleep/awake bruxism diagnosis, positive instrumental assessments can be useful until they are validated (eg, EMG or tooth contact) (83). Ideally, the use of polysomnography with masseter EMG and audiovisual recordings contributes to better identification of orofacial movements unrelated to sleep-related bruxism or co-occurring conditions listed above. With breathing issues suspected, recording of breathing, heart rate, and brain activities is recommended (43; 145; 102; 07). It is important to note that bruxism events may not occur every night (77; 110).

Polysomnography is rarely required for sleep-related bruxism diagnosis in the absence of co-occurring conditions. However, overnight studies are useful to make a differential diagnosis when the patient has symptoms of other sleep disorders, such as obstructive sleep apnea (145; 07). In addition to cases of patients with a suspected seizure disorder or REM-sleep behavior disorder, video polysomnography or daytime EEG may provide clues to the possible underlying etiology (145).

Many devices are coming available on the market with the intent to help in the diagnosis of sleep and awake bruxism. Some are devices intended only to measure the number and intensity of sleep-related bruxism events, eg, superficial EMG (extra-orally), splints (intra-orally bite sensors), or jaw movement sensors (extra and intra-orally) (162; 14; 126; 99; 100; 35; 121). Additionally, some vibrate when the patient’s teeth touch the splint, with the intention of changing the habit (see the treatment section). Not all devices are on the market yet; more information can be found on Pubmed (116; 127).

An international group of experts developed a research instrument tool called STAB to evaluate sleep-related bruxism status, associated comorbidities, etiology, and consequences (91; 90). The STAB or Standardized Tool for the Assessment of Bruxism has two axes (A and B) with 14 domains and 66 items. Axis A evaluates self-reported sleep and awake bruxism, symptoms, and clinical and instrumental assessments (technological devices). Axis B gathers self-reports that might have an etiological or comorbid association with bruxism. This instrument is now ready to be tested in research and clinical fields (91; 90). However, these may be difficult to use in an active clinical practice. Other tools are available, such as the BruxScreen and the Paesani questionnaire (123; 84).

The questionnaire from Paesani is simple and can be used in clinics to begin to discriminate sleep-related bruxism and awake bruxism (123). It contains five items, with answers as yes or no:

1.	Sleep grinding item: Are you aware of the fact that you grind your teeth during sleep?
2.	Sleep grinding referral item: Did anyone tell you that you grind your teeth during sleep?
3.	Sleep clenching item: On morning awakening or on awakenings during the night, do you have your jaws thrust or braced?
4.	Awake clenching item: Do you clench your teeth whilst awake?
5.	Awake grinding item: Do you grind your teeth whilst awake?

Management

	• There is insufficient solid evidence to recommend a standard approach to sleep-related bruxism management in adults, children, and adolescents. It seems obvious that sleep-related bruxism should be managed in a personalized mode when tooth grinding sound is an issue for sleep partners or family, when tooth damage interferes with chewing function, and when esthetics or pain is exacerbated.
	• Sleep-related bruxism management consists of a conservative "multiple-P" approach: pep talk (counseling), plates (oral appliances), physiotherapy, psychotherapy, and pills (pharmacotherapy).

Indeed, there is insufficient evidence to recommend a standard, “one-size-fits-all” approach to the management of sleep-related bruxism (20; 74; 105; 26). Sleep-related bruxism management consists of a conservative "multiple-P" approach: pep talk (counseling), plates (oral appliances), physiotherapy, psychotherapy, and pills (pharmacotherapy) (74).

Counseling and psychotherapy. Psychological counseling may help control sleep-related bruxism and consists of initial therapeutic intervention. Sleep-related bruxism may be associated with poor sleep quality in children and adults (88; 89; 70; 112; 101; 131). Such findings highlight the importance of sleep routines, including sleep hygiene. Although it is intuitive that sleep hygiene advice regarding progressive relaxation techniques would help some individuals with bruxism to improve their sleep, a control trial over a 4-week observation period failed to show significant benefit (165). The strength of this study is to realize that one-time instruction without follow-up is not enough to change sleep-related behavior, as seen for insomnia management. Indeed, cognitive behavioral therapy for insomnia is usually administered over 8 weeks and is a management approach that induces benefit up to 6 months after treatment (09).

Oral appliances. A systematic review evaluated several types of splints used in randomized clinical trials: acrylic occlusal stabilization splint, palatal coverage splint, mandibular anterior repositioning splint, and anterior splint. Although the level of evidence is graded low, findings suggest that acrylic occlusal stabilization splints present a safe and relatively effective management approach to protect the teeth and to reduce the frequency and intensity of sleep-related bruxism evaluated by EMG in some patients (105). With this kind of splint, the frequency and intensity of sleep-related bruxism events may be present in some cases where the indication is based on teeth protection. Stabilization splints should be used cautiously because (1) some individuals may present occlusal alterations (change in bite), and (2) in patients with obstructive sleep apnea, it may aggravate apnea and hypopnea events; such vulnerability needs to be defined (47; 113).

Stabilization splint in acrylic

Private laboratory device. (Contributed by Dr. Cibele Dal Fabbro.)

Other oral appliances, like mandibular advancement devices, normally used to manage obstructive sleep apnea, seem to effectively reduce tooth damage and grinding sound plus jaw muscle activity (75; 156; 159; 105; 171). In a comparison between mandibular advancement device and maxillary occlusal splint, mandibular advancement devices induced a greater reduction in sleep-related bruxism episodes per hour after 3 months of use (156; 159). It is, however, less comfortable than a maxillary occlusal splint and this may reduce regular compliance (03).

Mandibular advancement device

Private laboratory device. (Contributed by Dr. Cibele Dal Fabbro.)

In children, the use of oral appliances for sleep-related bruxism intervention requires caution and frequent monitoring by a dentist. Inappropriate use may lead to impairment in the development of oral structures; thus, the indication should be personalized (30). A study demonstrated that rapid palatal expansion reduced the frequency of bruxing events in 65% of children 8 to 14 years old with maxillary insufficiency (13).

Biofeedback therapy. Contingent electrical stimulation as a form of biofeedback therapy, although the level of evidence is modest, significantly reduced sleep-related bruxism episodes after a short-term period (105). Long-term evaluations and studies of positive and adverse effects are needed to recognize its clinical application. Biofeedback therapy is a domain in full technological expansion, and further validation and independent studies are expected. Some use electrical stimulation, others use vibration devices inserted in an oral appliance, and others use sound (141; 162; 14; 116; 127). Some individuals can be more vulnerable to sleep fragmentation with these kinds of devices. One study showed no increase in sleep arousals and no decrease in the percentage of N3 or REM sleep stage (62). The mechanism of action of biofeedback for sleep-related bruxism remains to be demonstrated because some devices reduce the frequency, whereas others seem to reduce the duration of the episode.

The efficacy of most of these devices has been tested as proof of concept; it remains to be demonstrated that they would change daily practice, ie, are accessible, useable with reasonable compliance by the individual, and do not trigger other problems, such as poor sleep quality, tooth movements, or exacerbation of breathing due to palatal-lingual space invasion.

Pharmacotherapy. Overall, the strength of evidence for drug recommendations to control sleep-related bruxism is low (38; 105). Therefore, safe drug prescription should be limited to short periods and considered only when other conservative strategies have failed (12; 30). The following medications are cited in the literature with the potential to attenuate sleep-related bruxism: amitriptyline, botulinum toxin, buspirone, clonazepam, clonidine, clozapine, gabapentin, hydroxyzine, levodopa, propranolol, quetiapine, and trazodone (38; 105). Only a few have been tested under a randomized control study design. Table 2 shows the medications tested in controlled trials with positive and negative results and their efficacy in reducing frequency or sleep-related bruxism intensity. Only two drugs were tested in more than one randomized controlled trial, and in only four of the studies was the quality of evidence considered moderate (105). For the other medications, due to the fact they were shown in case reports or non-controlled studies, caution is recommended. Furthermore, none are officially approved by regulatory agencies for the management of sleep-related bruxism.

Table 2. Overview of Medications Used for Sleep-Related Bruxism Management

Drugs	Dose	Number of clinical trials	Results on sleep-related bruxism	Citation (only randomized controlled trials are cited)
Rabeprazole*	10 mg/night, orally	2	+++	(119)
Clonidine*	0.30 mg 0.15 mg	2	+++ +++	(58) (144)
Gabapentin*	100-300 mg, 8 weeks	1 (compared with occlusal splint)	+++	(87)
Clonazepam	1 mg	3	++	(144)
Botulinum toxin*	50-100 U, masticatory muscle injection, 4-12 weeks follow-up	4	+++ +++ +++ +++	(80) (153) (122) (152)
L-tryptophan	50 mg/weight(Kg), orally, 8 days	1	-	(44)
Bromocriptine	7.5 mg/night, 2 weeks	3	-	(77)
Propanolol	120 mg/night	2	-	(58)
Pramipexole	0.09-0.54 mg/night, 3 weeks	1	-	(21)
Amitriptyline	25 mg/night, 1-4 weeks	1	-	(107)

Note: None of these medications are officially approved by regulatory agencies for management of sleep-related bruxism
*Moderate level of evidence

An experimental mechanism-driven study, using polysomnographic recordings revealed that clonidine (0.3 mg) significantly reduced sleep-related bruxism compared to placebo. The drug decreased sympathetic tone prior to the onset of sleep-related bruxism activities, preventing sequential activation of the autonomic and motor systems (58b). In a randomized study, clonidine (0.15 mg) was shown to be more efficacious than clonazepam, decreasing more than 30% of RMMA episodes compared with placebo and clonazepam (144). With the lower dose (0.15 mg), the side effects of hypotension were not seen in comparison to the use of 0.3 mg (58b; 144). Medical supervision is highly recommended when such medication is prescribed.

It was demonstrated that botulinum toxin decreases the intensity of masseter muscle contractions; nonetheless, it does not reduce the RMMA event frequency (152). Because sleep-related bruxism events are centrally generated, botulinum toxin seems to be a palliative management option, mainly for patients who do not tolerate oral splints or appliances. It has been shown that botulinum toxin benefits persist from 4 to 8 weeks after the application. An oral appliance or splint exerts a more enduring effect, especially after 9 to 12 weeks, and both options can be used during different treatment times or even combined (29). Long-term evaluations are needed to assess the effects of continued re-administration, changes in muscle and adjacent bony structures, and response to treatment of individuals of different ages or genders (Beddis et 2018; 105; 29).

Although some clinicians prescribe cyclobenzaprine for sleep-related bruxism, solid evidence is not yet available. Research on this topic is ongoing (USP-Bauru lab from Professor PC Conti, Brazil).

Because sleep-related bruxism can be a sign of a co-occurring condition, such as obstructive sleep apnea and, rarely, sleep epilepsy or REM-sleep behavior disorder, management should address the putative association. The selection of the best and safest treatment should focus on an individual’s complaints, medical history, and possible comorbidities (102; 26).

Outcomes

The therapeutic options suggest that most management approaches (ie, oral appliance, cognitive therapy or biofeedback, medication) help to control sleep-related bruxism but do not cure or eliminate oral motor activities. As an example, oral splints primarily aim to protect the dentition from tooth wear or dental restoration damage and grinding “enamel to enamel” sounds; however, the strength of evidence for a reduction in muscle activity is low (mean reduction of 30% to 40%) (12; 105). It is important to note that the incidence of sleep-related bruxism is variable over time. Thus, multidisciplinary approaches are recommended, particularly when co-occurring conditions are suspected. Rigorous long-term follow-up clinical trials are needed to clarify the efficacy and safety of sleep-related bruxism management (102; 105).

Special considerations

Pregnancy

A study conducted with Chinese pregnant and nonpregnant women found a high prevalence of sleep disorder-related symptoms in pregnant women, but there was no significant difference in sleep-related bruxism prevalence (22). A similar result was found in a sample of 2225 women from Brazil. Within the 48-hour postpartum period, only 79 (3.6%) self-reported clenching or grinding their teeth during sleep (39).

Pediatric age group

Sleep-related bruxism is an important clinical condition in pediatric patients because it is highly frequent, and childhood is the most critical period for human growth and development (53).

The prevalence of sleep-related bruxism in children and adolescents depends on the age and the diagnostic approach. The prevalence of possible sleep-related bruxism is about 20.7% in pre-school-aged children, 20% to 35% in school-aged children, and 14% to 53% in teenagers. For probable sleep-related bruxism, the prevalence is 47.6% in preschool-aged children, 10% to 16% in school-aged children, and 5% to 13.7% in teenagers. School-aged children presented a prevalence of 32% of definitive sleep-related bruxism (57).

In children older than 6 years of age, evidence suggests an association between psychological factors, emotional symptoms, and sleep-related bruxism (40). Some studies with children and adolescents demonstrated snoring as the highest risk factor associated with sleep-related bruxism (42; 130). Also, respiratory diseases (allergic rhinitis, otitis media, and asthma) might be more prevalent in children with sleep-related bruxism than in those without (109; 42).

The main risk factors described in literature for sleep-related bruxism are the following (57):

(i)	Respiratory conditions: asthma, snoring, obstructive sleep apnea, impaired nasal breathing, respiratory allergies, adenotonsillar hypertrophy
(ii)	Sleep-related factors: restless sleep complaints, nightmares, agitation during sleep, drooling during sleep, evening chronotype.
(iii)	Behavioral factors: aggressive behavior, attention and behavioral problems, oral habits, such as nail biting.

Further studies are necessary to determine the relationship between the genetic factors associated with respiratory disturbances (eg, obstructive sleep apnea) and sleep-related bruxism in children (136).

No specific therapy has been established for children (19; 136; 57).

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Contributors

All contributors' financial relationships have been reviewed and mitigated to ensure that this and every other article is free from commercial bias.

Authors

Cibele Dal Fabbro DDS PhD

Dr. Fabbro of the Université de Montréal and the Center for Advanced Research in Sleep Medicine has no relevant financial relationships to disclose. Montreal, Canada
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Gilles Lavigne DMD PhD

Dr. Lavigne of the University of Montreal has no relevant financial relationships to disclose.
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Editor

Federica Provini MD

Dr. Provini of the University of Bologna and IRCCS Institute of Neurological Sciences of Bologna received speakers' fees from Idorsia, Italfarmaco, and NeoPharmed Gentili Spa.
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Former Authors

Michael S Aldrich MD
Bradley V Vaughn MD
Geoffrey E Gerstner PhD DDS MS
Matthew F Abts MD
Nkiruka Chukudebelu MD
Jonathan D Cogen MD MPH
John J Kelly DDS
Jamie Harris MD
Darius A Loghmanee MD
Junia Maria Serra-Negra PhD
Federica Provini MD
Clarissa Drumond PhD
Letícia Fernanda Moreira-Santos MD

Patient Profile

Age range of presentation: 1 month to 65+ years
Sex preponderance: The approximate ratio of male-to-female children: 95% CI 1.13 (1.02-1.26); P-value < 0.05 (Guo et al 2018)

Approximate ratio of male-to-female adults: No sex preponderance (Manfredini et al 2013a)
Heredity: Hereditary mechanism: incidence of sleep-related bruxism runs in families and is under environmental and genetic influences.
Population groups selectively affected: No population group selectively affected
Occupation groups selectively affected: No occupation group selectively affected

ICD & OMIM codes

ICD-9: Bruxism: 306.8

Sleep-related bruxism: 327.53
ICD-10: Sleep-related bruxism: G47.63

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Sleep-related bruxism

Associated Disorders

Attention deficit hyperactivity disorder
Autism spectrum disorder
Cerebral palsy
Down syndrome
Epilepsy
- Gastroesophageal reflux disease
- Insomnia
- Obstructive sleep apnea
- Temporomandibular disorders
- REM behavior disorder
- Restless leg syndrome

Differential Diagnosis

Awake bruxism
Sleep apnea
Partial complex seizure disorder
Generalized seizure disorder
Idiopathic myoclonus
- Parasomnias
- Sleep epilepsy
- Sleep talking
- Familial nocturnal faciomandibular myoclonus
- Other orofacial activities
- REM-sleep behavior disorder

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- Sleeptalking

Sleep-related bruxism

Introduction

Overview

Key points

Historical note and terminology

Table 1. Sleep-Related Bruxism Current Concepts

Clinical manifestations

Presentation and course

Prognosis and complications

Clinical vignette

Biological basis

Etiology

Associated factors

Neurologic conditions

Physio(patho) genesis

Epidemiology

Prevalence

COVID-19 pandemic updates

Prevention

Differential diagnosis

Confusing conditions

Associated or underlying disorders

Diagnostic workup

Management

Table 2. Overview of Medications Used for Sleep-Related Bruxism Management

Outcomes

Special considerations

Pregnancy

Pediatric age group

Media

References

Contributors

Authors

Editor

Former Authors

Patient Profile

ICD & OMIM codes

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Questions or Comment?

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