Version May 2024
INTRODUCTION — Sleep-related bruxism involves activation of the masticatory muscles, resulting in tooth clenching and grinding during sleep. The prevalence of bruxism during sleep peaks in childhood and progressively declines with age. Although often asymptomatic, frequent bruxism may become clinically significant when it interferes with sleep or results in tooth wear or jaw discomfort.
This topic will review the clinical presentation, diagnosis, and management of sleep-related bruxism. Temporomandibular disorders and other sleep-related movement disorders are reviewed separately. (See "Temporomandibular disorders in adults" and "Approach to abnormal movements and behaviors during sleep".)
DEFINITION — Bruxism is defined as repetitive jaw-muscle activity characterized by grinding or clenching of the teeth [1] and/or by bracing or thrusting of the mandible [2].
Bruxism is most common during sleep, when it is referred to as sleep-related bruxism. Wakeful bruxism is a circadian phenotype of bruxism and probably differs etiologically from sleep-related bruxism; it is seen primarily in association with neurodevelopmental disorders such as Rett syndrome. (See "Rett syndrome: Genetics, clinical features, and diagnosis".)
EPIDEMIOLOGY — Sleep-related bruxism is common, affecting approximately 15 to 40 percent of children and 8 to 10 percent of adults [3-8].
It may be noted as early as the appearance of the first teeth; the prevalence then rises to approximately 30 percent by the age of six years [9]. In adults, rates peak at about 12 percent in young adults and fall to 2 to 4 percent by age 60 years [4].
Prevalence may be higher among Asian Americans compared with other racial and ethnic groups, although data are limited [10,11]. Males and females are equally affected.
RISK FACTORS — The main risk factors for sleep-related bruxism are comorbid sleep disorders, especially parasomnias, anxiety, and other psychiatric and neurologic disorders (table 1) [12].
Obstructive sleep apnea (OSA), temporomandibular disorders, and certain medications and substances have historically been considered risk factors, although evidence for these associations has been mixed [13-17]; however, evidence for a relationship between sleep-related bruxism and OSA is growing. A prospective polysomnographic study of 914 adults found that 50 percent of the adults with OSA had comorbid sleep-related bruxism [18].
In a population-based study of over 13,000 individuals 15 years of age and older who were assessed for sleep-related bruxism and other comorbidities by telephone-based questionnaire, the following factors were associated with an increased risk of sleep-related bruxism [5]:
●OSA (odds ratio [OR] 1.8)
●Heavy alcohol use (OR 1.8)
●Loud snoring (OR 1.4)
●Caffeine intake (OR 1.4)
●Smoking (OR 1.4)
●Anxiety (OR 1.3)
●Highly stressful life circumstances (OR 1.3)
Evidence for a relationship between sleep-related bruxism and OSA has led some to suggest that sleep-related bruxism may play a protective role during respiratory-related arousals [19]. A study directly testing this relationship determined that apnea-hypopnea events were more strongly associated with oromotor activity other than sleep bruxism, suggesting that any causal relationship between the two is unclear [20]. On the other hand, a prospective study found that most rhythmic masticatory muscle activity (RMMA) events were time-related to arousals in adults with OSA [21].
Sleep-related bruxism has been reported in association with certain medications and substances, including amphetamines, antipsychotics, selective serotonin reuptake inhibitors, serotonin-noradrenaline reuptake inhibitors, noradrenaline-dopamine reuptake inhibitors, and drugs of abuse with catecholaminergic effects (eg, cocaine, 3, 4-methylenedioxymeth amphetamine [MDMA; commonly known as ecstasy]) [22-26]. The magnitude of risk is not well established, nor is it clear whether these medications exacerbate preexisting bruxism or cause de novo symptoms. A narrative review found only low-quality evidence to support or refute specific medications as risk factors for bruxism [15].
Bruxism occurs with increased frequency in patients with certain neurologic and psychiatric disorders, including Down syndrome, Rett syndrome, cerebral palsy, and attention deficit hyperactivity disorder (ADHD) [10,27-33]. In many of these cases, wakeful bruxism may be more prominent than sleep-related bruxism. In others, such as ADHD, medications used to treat the disorder (eg, stimulants) may contribute to bruxism, and it is not clear whether an independent association exists.
Additional risk factors in children include other parasomnias or sleep-related behaviors (eg, sleeptalking, sleepwalking, enuresis), enlarged tonsils and adenoids, and OSA [7,9,34-38].
Psychosocial risk factors include anxiety, stress, and competitive personality traits [39-41]. Bruxism has been reported with increased frequency among individuals with temporomandibular joint disorders, although the association is controversial and evidence is conflicting [13,14,16]. An association with gastroesophageal reflux disease has also been described [10].
Twin studies and parent-offspring studies suggest that genetics may play a role, although specific genetic risk factors have not been identified [7,42-44]. Twenty to fifty percent of patients with bruxism report at least one direct family member with a history of bruxism [1].
PATHOPHYSIOLOGY — Sleep-related bruxism is most likely a centrally-mediated phenomenon related to micro-arousals from sleep and activation of the autonomic nervous system.
Nearly all events occur during natural micro-arousals from sleep and are preceded by a predictable pattern of autonomic activity. The seconds before an event are characterized by rapid-frequency cortical electroencephalogram (EEG) activity, heart rate elevation, increased jaw and oropharyngeal muscle tone, and increased respiratory effort and nasal air flow [34,39,45-48]. This is followed by an increase in rhythmic masticatory muscle activity (RMMA) in the jaw muscles of such magnitude to produce tooth grinding [34]. Bruxism events tend to occur in clusters during a micro-arousal spanning 3 to 15 seconds [49].
Based on these observations, it is hypothesized that sleep-related bruxism is an exaggerated form of oromotor response to sleep micro-arousals under the influence of the brainstem reticular activating system, which contributes to increased activity in autonomic, cardiac, and motor networks [46]. It may even serve a physiologic function to improve airway patency during sleep in some cases [15]. Genome-wide analyses suggest that serotonin and dopamine pathways may be involved [50].
Additional support for a relationship to micro-arousal comes from the following observations:
●Experimentally induced micro-arousals lead to RMMA and tooth grinding in 70 percent of individuals with sleep-related bruxism but rarely in those without bruxism [51]
●Administration of the alpha-adrenergic agonist, clonidine, reduces cardiac sympathetic activity as well as the number of sleep bruxism episodes in individuals with bruxism [52,53]
●Elevated levels of urine catecholamines have been found in both adults and children with sleep-related bruxism [54-57].
There is no evidence to support a causal link between dental occlusion (ie, the way the upper and lower teeth contact each other) and sleep-related bruxism [58,59]. Although perceived stress and anxiety are often correlated with sleep-related bruxism in observational studies [9,60-62], a pathophysiologic basis for this association has not been established [63-65].
It is also noteworthy that other mammalian species manifest rhythmic jaw movements during sleep, which manifest very similar physiological profiles, suggesting that sleep bruxism may be a natural albeit misunderstood motor behavior [66].
CLINICAL FEATURES
Symptoms and signs — Sleep-related bruxism manifests as rhythmic, approximately one-per-second (1 Hz) contractions of the masticator muscles during sleep. Many patients are unaware of the episodes, but parents/caregivers or bed partners may complain of disturbance from the clicking or grating sound that occurs with about 20 percent of contractions.
The frequency of bruxism fluctuates from night to night and from week to week. Some patients may report that bruxism, or symptoms associated with bruxism, increase with levels of life stress and anxiety.
Extreme forms of sleep-related bruxism involve forceful rhythmical grinding or clenching of the teeth [67]. The forces generated during these episodes can exceed those of voluntary maximum biting or chewing, and patients may develop secondary morning headaches, jaw pain, and clicking in the temporomandibular joints.
Bruxism can have detrimental effects on the teeth, including damage to teeth and dental work, thermal sensitivity in the teeth, hypermobility, and need for dental restorations. Tooth wear is seen on tooth surfaces that contact during biting or chewing. Lateral grinding forces in particular can be particularly destructive. Tooth wear alone, however, is not specific to bruxism. (See 'Differential diagnosis' below.)
In severe cases, sleep-related bruxism can lead to injury to soft tissues of the mouth (tongue, lips, cheeks), dental fractures, tooth hypermobility and changes in the bite, difficulty with chewing, muscle pain and spasm, temporomandibular joint pain and dysfunction, and head and neck pain [67,68]. The relationship between bruxism and chronic craniofacial pain is controversial, however, and several studies have found no association or an inverse association between sleep-related bruxism and jaw pain or muscle fatigue [40,69].
There is some evidence that patients with bruxism may show skeletal and morphological changes that are radiographically evident, including bony exostoses of the mandibular angle, smaller condyles, and changes in cancellous and cortical mandibular bone [70].
Natural history — Sleep-related bruxism is most common during childhood but can begin at any age. It may be noted by parents as early as the appearance of the first primary upper and lower anterior teeth. Onset during adolescence or adulthood may be associated with risk factors such as obstructive sleep apnea or certain medications. (See 'Risk factors' above.)
The natural history is not well characterized but is usually benign. Although bruxism beginning in childhood often persists into adulthood, episodes may be infrequent or remain asymptomatic for most of the lifespan [1]. Some individuals report episodic worsening of sleep-related bruxism across the lifespan in relation to perceived life stress or anxiety; however, most studies indicate that prevalence decreases linearly with age [4,5].
Polysomnography — On polysomnography, sleep-related bruxism is characterized by rhythmic masticatory muscle activity (RMMA) that occurs at approximately 1 Hz and is usually concomitant with a micro-arousal from sleep, typically lasting 3 to 15 seconds (waveform 1) [46]. Bruxism can also manifest as prolonged isotonic contraction of the masticatory muscles, which may last for several minutes at a time [71].
Most events occur during stages N1 and N2 of non-rapid eye movement (NREM) sleep. Occurrence during REM sleep is rare except in association with medication-induced bruxism and neurodevelopmental disorders [39,45,71].
Additional surface electromyography (EMG) electrodes can be placed over the masseter and temporal muscles to increase the sensitivity of detecting bruxism episodes on polysomnography [72]. Audio-video recordings improve specificity and help distinguish bruxism from other orofacial and head movements, such as lip sucking, rhythmic movement disorders, chewing-like movements (waveform 2), swallowing, head rubbing and scratching, eye opening, and blinking [73,74]; however, EMG studies alone are not reliable [75]. (See "Polysomnography in the evaluation of abnormal movements during sleep", section on 'Sleep-related bruxism'.)
Of note, the terms sleep-related bruxism and RMMA are sometimes confused with each other or used interchangeably. RMMA refers only to the rhythmic EMG activity observed in the masticatory muscles during sleep, whereas sleep-related bruxism refers to the specific orofacial movements.
DIAGNOSIS — Sleep-related bruxism is a clinical diagnosis, established in most cases by a history of tooth grinding during sleep and corroboration by parents/caregivers or bed partners. In children, tooth wear is not a major sign of sleep bruxism and is not necessary for diagnosis [76,77].
Patients should be asked about risk factors and exacerbating factors, including poor sleep quality, signs and symptoms of obstructive sleep apnea (eg, loud snoring, witnessed pauses in breathing during sleep), and excess caffeine or alcohol intake. The medication list should be reviewed for potential contributors, including antipsychotic medications and serotonergic drugs (table 1). (See 'Risk factors' above.)
Formal criteria for sleep-related bruxism according to the International Classification of Sleep Disorders, Third Edition (ICSD-3), include the following [1]:
●The presence of repetitive jaw-muscle activity characterized by grinding or clenching of the teeth in sleep; and
●The presence of one or more of the following clinical symptoms or signs consistent with the report of tooth grinding or clenching during sleep:
•Abnormal tooth wear
•Transient morning jaw muscle pain or fatigue, or temporal headache
Of note, neither the presence of tooth wear nor temporomandibular discomfort is specific for sleep-related bruxism, and these features should not be equated with bruxism in isolation. (See 'Differential diagnosis' below.)
Polysomnography is not required for the diagnosis but may be useful when there is uncertainty about whether the described events are truly bruxism versus other orofacial movements during sleep, and when the clinical history is suggestive of a comorbid sleep disorder that may be exacerbating bruxism episodes. Importantly, overnight sleep studies are not highly sensitive for sleep-related bruxism, as episode frequency varies from night to night [78]. (See "Overview of polysomnography in infants and children" and "Overview of polysomnography in adults" and "Clinical presentation and diagnosis of obstructive sleep apnea in adults".)
DIFFERENTIAL DIAGNOSIS — The differential diagnosis of sleep-related bruxism includes a variety of alternative causes of orofacial movements during sleep, tooth wear, and jaw pain and fatigue.
●Other orofacial movements – A range of normal and pathologic orofacial movements during sleep can sometimes be confused with bruxism, including facial myoclonus, chewing-like movements, swallowing, sleep talking, expiratory groaning (catathrenia), other parasomnias, and rarely, nocturnal seizures [73,79-85].
Description of the movements and sounds by a bed partner or parent is often sufficient to distinguish these alternative diagnoses from bruxism, as the tooth grinding noises associated with sleep-related bruxism are remarkably loud and distinct, whereas tooth grinding noises are not a feature of the other orofacial movements. (See "Approach to abnormal movements and behaviors during sleep".)
Ictal bruxism has been reported rarely in association with temporal lobe seizures [85,86]. In such cases, additional clues that tooth grinding is not simple sleep-related bruxism are typically present, including other more classical symptoms of temporal lobe seizures (eg, rising epigastric sensation, déjà vu, altered awareness), and occurrence of events during both day and night. (See "Focal epilepsy: Causes and clinical features".)
●Other causes of tooth wear – The differential diagnosis of tooth wear is broad, and it can be difficult if not impossible for a dental clinician to distinguish bruxism-related tooth wear from other causes of tooth wear by examination alone. Distinguishing active versus chronic or static tooth wear is also difficult.
Patients should be asked about risk factors for other causes of tooth wear, including chemical erosion related to dietary factors (eg, soft drinks), gastroesophageal reflux, bulimia nervosa, or xerostomia; abrasion (wear caused by chewing abrasive substances); normal age-related tooth wear; and wakeful bruxism.
●Other causes of jaw pain and fatigue – Although the presence of morning pain or fatigue in the jaw muscles, teeth, and temples is part of the diagnostic criteria for sleep-related bruxism [1], these symptoms alone are not sufficient for diagnosis. In fact, some evidence suggests that patients with frequent sleep-related bruxism may be less prone to present with complaints of jaw muscle pain and fatigue compared with individuals without sleep-related bruxism. (See 'Symptoms and signs' above.)
Alternative causes of jaw muscle pain and fatigue, including temporomandibular disorders, can usually be differentiated from sleep-related bruxism based upon the absence of self-reported tooth grinding noises, absence of tooth wear, and negative findings on polysomnography. The clinical features and diagnosis of temporomandibular joint disorders are reviewed in detail separately. (See "Temporomandibular disorders in adults".)
MANAGEMENT — Many individuals with sleep-related bruxism do not require any specific treatment. Occasional bruxism is common, particularly during childhood, and often asymptomatic.
Treatment options for frequent or symptomatic sleep-related bruxism include behavioral modifications, oral devices to protect the teeth, and pharmacotherapy [23,87]. In cases of drug-induced sleep-related bruxism, symptoms may resolve after dose adjustments, withdrawal of the implicated medication or substance, or switch to an alternative or adjunctive medication [88].
Individuals with sleep-related bruxism should receive routine dental care to monitor for tooth wear and intervene when necessary. Excessively worn teeth may require dental restorative procedures.
Sleep hygiene and other behavioral measures — Sleep hygiene education and counseling is suggested in all patients, since bruxism tends to occur in association with arousals from sleep [23]. Avoidance of alcohol, caffeine, and tobacco before bedtime and other sleep hygiene recommendations are reviewed in detail separately. (See "Cognitive behavioral therapy for insomnia in adults", section on 'Sleep hygiene'.)
Evidence to support the effectiveness of sleep hygiene education for the specific outcome of sleep-related bruxism is limited, however. One small, randomized trial in 16 individuals with sleep-related bruxism found no improvement in any polysomnographic variables in patients who received sleep hygiene instructions and watched a 20-minute video on progressive relaxation techniques [89]. No patient-reported outcomes were measured.
Biofeedback therapy has shown some evidence of benefit in patients with sleep-related bruxism (see "Temporomandibular disorders in adults", section on 'Biobehavioral management for psychological contributors'). Other behavioral or complementary modalities, such as acupuncture, have not been well studied [90].
Bruxism associated with medications — Sleep-related bruxism has been reported as an adverse effect of several common classes of medications, including antidepressants and antipsychotics (table 1). The risk appears to be highest in adult women with comorbid psychiatric disorders [23]. (See 'Risk factors' above.)
A wait-and-see approach may be reasonable in many cases, as spontaneous remission after four weeks has been reported in at least one case of fluoxetine-induced sleep bruxism, with no interruption or decrease in fluoxetine dose [91].
If bruxism events persist, dose reductions may help to alleviate symptoms [23]. If dose reduction or discontinuation is not possible, case reports indicate that co-prescription of buspirone [88,92,93], tandospirone (not available in the United States) [94], or gabapentin [95-97] may reduce or eliminate symptoms.
Oral devices to protect the teeth — For individuals with frequent bruxism (eg, nightly) or related tooth wear, an oral device that covers the upper or lower teeth can be fitted by a dental clinician to protect the teeth from damage and reduce grinding noises associated with bruxism [23,87].
Despite their widespread use, relatively few studies have been performed, and most if not all studies have not measured pain or dental outcomes. The available data indicate that oral devices do not reduce the frequency of bruxism itself [98]. Anecdotally, however, many patients nonetheless find that they decrease morning jaw discomfort when used regularly, and they are fairly effective at controlling tooth wear.
Oral devices for bruxism fall into two categories: occlusal (bite) splints and mandibular advancement devices (MADs). Of these, occlusal splints are most commonly used and preferred in most cases; MADs may be less comfortable to wear than occlusal splints and are not typically used for bruxism unless there is comorbid obstructive sleep apnea (OSA) [99]. (See "Oral appliances in the treatment of obstructive sleep apnea in adults".)
The main goal of an occlusal splint is to protect the teeth from damage during bruxism episodes. Occlusal splints should be inspected periodically by a dental clinician, as they can wear out or become damaged with time due to ongoing bruxism. Children in a mixed dentition phase may benefit from a soft occlusal splint, which can be adapted to the dynamically changing bite.
Numerous other specialized oral devices exist; however, none of these has been shown to be effective in clinical trials, and some can induce irreversible changes in the bite. Thus, an occlusal splint is the most studied and safest device to use in virtually all cases where sleep bruxism is the sole entity being treated. Of note, over-the-counter "boil and bite" appliances, if used, should be supervised by a dental practitioner, as evidence indicates that such appliances cannot be formed correctly without the proper training.
The main contraindication to occlusal splints is OSA, which can be exacerbated by splint use [100]. An MAD or continuous positive airway pressure (CPAP) are better choices in such patients, as they address apneas and may reduce associated arousals, as well as protect the teeth (for MADs) [23,99,101-103]. The MAD is a custom, titratable device, and patients require follow-up visits with an appropriately trained dentist to confirm comfort during wear and to monitor for adverse effects. (See "Obstructive sleep apnea: Overview of management in adults" and "Oral appliances in the treatment of obstructive sleep apnea in adults".)
Oral devices should not be used or should be used with caution in patients with epilepsy, as the splints represent a foreign body in the mouth and might theoretically obstruct the airway during generalized seizures [23].
Refractory symptoms
Pharmacotherapy — A variety of drugs have been explored for management of sleep-related bruxism, but none has shown a consistently large effect and all have potential side effects. Pharmacotherapy should only be considered for the most severe cases, as sleep bruxism may be a natural behavior and serve to improve upper airway patency during sleep in some cases. (See 'Pathophysiology' above.)
Medication trials of either clonazepam or clonidine are typically reserved for rare patients with refractory symptoms despite the strategies described above, including regular use of an oral device. (See 'Oral devices to protect the teeth' above.)
A 2014 systematic review identified seven randomized trials in adults comparing one or more drugs versus placebo for treatment of sleep-related bruxism [104]. The number of participants ranged from 7 to 25, and no studies measured long-term outcomes. Included drugs were amitriptyline (three trials), bromocriptine, clonidine, propranolol, levodopa, and tryptophan. None of the trials found a significant decrease in electromyography (EMG)-determined bruxism episodes or improvement in patient-reported outcomes (eg, jaw pain). Clonidine (0.3 mg nightly) was associated with a trend towards benefit in the number of bruxism events per hour compared with placebo (mean difference -2.4, 95% CI -4.8 to 0.02) [105]. Three out of 16 patients developed prolonged morning hypotension.
In a subsequently published small, randomized trial, clonidine (0.15 mg) nightly for three nights reduced the relative frequency of rhythmic masticatory muscle activity by approximately 30 percent compared with placebo [53]. The most common side effects were dry mouth (16 percent) and dizziness (10 percent).
Anecdotal reports indicate that benzodiazepines such as clonazepam or diazepam may inhibit bruxism, although a limited number of small, randomized trials have been mixed. Two small trials in patients with sleep-related bruxism found that a single dose of clonazepam (1 mg) resulted in a 30 to 40 percent relative reduction in bruxism frequency compared with placebo [106,107], whereas a third trial showed no effect compared with placebo or clonidine [53]. A low dose of clonazepam (eg, 0.25 to 0.5 mg) before bedtime is likely sufficient and associated with lower risk of morning drowsiness and unsteadiness compared with higher doses.
In menopausal women with sleep-related bruxism, hormone therapy may improve bruxism, probably via a decrease in the number of arousals from sleep and hot flashes [108]. (See "Treatment of menopausal symptoms with hormone therapy".)
Dopamine agonists such as pramipexole appear to be ineffective in the treatment of bruxism [109]. Evidence for other drugs, such as topiramate and gabapentin, is limited to case reports [110,111].
Other therapies — Limited evidence, including a small, randomized trial, suggests that botulinum toxin type A injections into the temporalis and masseter muscles may provide symptomatic benefit in patients with refractory symptoms [112-118]. The mechanism of effect is to decrease the strength of the jaw-muscle contractions; as with oral devices, the number of sleep bruxism events does not appear to be reduced in most patients. Injections are typically given every six months by a movement disorder specialist with training in botulinum toxin A injections.
In a randomized trial of 23 adults with sleep-related bruxism, more patients assigned to onabotulinumtoxinA injections than placebo injections reported much or very much improved symptoms at four to eight weeks (6 of 13 versus 0 of 9 patients) [117]. Visual analog scores for pain and bruxism were also better in the active treatment arm. There was a trend towards decreased bruxism events by EMG, but night-to-night variability was high in both arms. Two patients had a cosmetic change in their smile (15 percent), and no patients reported dysphagia, masseter weakness, or dry mouth.
Nocturnal biofeedback therapy is an investigational approach involving use of an EMG sensor to recognize clenching and grinding and provide feedback during sleep, with the goal of interrupting the bruxism episode. Further study is needed, and its impacts on sleep quality are unknown [119].
Awake bruxism — Management of patients with neurological disorders, in whom awake bruxism may be the predominant feature, is individualized. As in sleep-related bruxism, an occlusal splint may help to reduce tooth wear [23]. (See 'Oral devices to protect the teeth' above.)
Based on case series, botulinum toxin A may be effective in managing severe bruxism in patients with movement disorders [120]. (See 'Other therapies' above.)
SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Parasomnias, hypersomnias, and circadian rhythm disorders".)
INFORMATION FOR PATIENTS: BASIC EDUCATIONAL MATERIALS — A useful reference on sleep-related bruxism for patients is available from the American Dental Association.
SUMMARY AND RECOMMENDATIONS
●Definition – Sleep-related bruxism involves repetitive jaw-muscle activity during sleep, characterized by involuntary clenching or grinding of the teeth. (See 'Definition' above.)
●Epidemiology – Sleep-related bruxism is most common during childhood, affecting up to one-third of early school-age children and approximately 8 percent of adults. (See 'Epidemiology' above.)
●Risk factors – Risk factors include comorbid sleep disorders; anxiety and other psychiatric and neurologic disorders; and possibly certain medications and substances, including selective serotonin reuptake inhibitors (SSRIs), antipsychotic drugs, and amphetamines (table 1). (See 'Risk factors' above.)
●Pathophysiology – Sleep-related bruxism is most likely a centrally-mediated phenomenon related to micro-arousals from sleep and activation of the autonomic nervous system. (See 'Pathophysiology' above.)
●Complications – When severe, sleep-related bruxism can do considerable damage to teeth and dental work and result in morning jaw pain or fatigue, temporal headaches, and jaw locking. (See 'Symptoms and signs' above.)
●Diagnosis – Sleep-related bruxism is a clinical diagnosis, established in most cases by a history of tooth grinding during sleep and corroboration by parents/caregivers or bed partners. Polysomnography is not required but is indicated when there is uncertainty as to the etiology of the sleep-related movements or if a comorbid sleep disorder is suspected. (See 'Polysomnography' above and 'Diagnosis' above.)
●Management – Many individuals with sleep-related bruxism do not require any specific treatment. Occasional bruxism is common, particularly during childhood, and often asymptomatic. (See 'Management' above.)
•Eliminate aggravating factors – Precipitating factors should be identified and eliminated or treated when possible, including excess alcohol intake, drugs of abuse, medications such as SSRIs and antipsychotics (table 1), and comorbid OSA. (See 'Sleep hygiene and other behavioral measures' above and 'Bruxism associated with medications' above.)
•Oral devices – For patients with frequent or symptomatic sleep-related bruxism, a simple oral appliance that covers the posterior dentition can be fitted by a dentist to protect the teeth and reduce grinding noises at night. Oral devices do not alter the frequency of bruxism episodes, but some patients find that they reduce morning jaw discomfort. (See 'Oral devices to protect the teeth' above.)
•Refractory symptoms – For rare patients with refractory bruxism despite conservative measures, we suggest a trial of either clonidine or clonazepam (Grade 2C). Botulinum toxin A injections may provide symptomatic benefit in patients with refractory symptoms. (See 'Pharmacotherapy' above and 'Other therapies' above.)
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