Parasomnia overlap disorder and status dissociatus
Sep. 01, 2022
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Sleep bruxism is a repetitive jaw-muscle activity characterized by clenching or grinding of the teeth or bracing or thrusting of the mandible. Sleep medicine defines bruxism as a sleep-related movement disorder characterized by repetitive movements and transient arousals during sleep. In dentistry, the current international consensus definition establishes that sleep bruxism is a behavior. A sequential shift in brain cortical and autonomic activities precedes sleep bruxism, suggesting that the central and autonomic nervous systems, rather than the peripheral system, play a dominant role in sleep bruxism onset. Polysomnography and electromyography are used to diagnose definite bruxism associated with the clinical signs of the stomatognathic system and the patient's self-report. Sleep bruxism can have consequences, such as tooth wear, fractures of restorations, temporomandibular disorders, headaches, and orofacial pain. Among associated factors that can be cited are psychological factors (eg, stress, personality traits, and anxiety), sleep-related breathing disorders, temporomandibular disorders, genetic factors, encephalopathies, and the use of medications and addictive substances. Treatment is palliative and multidisciplinary, including oral appliances, behavioral therapies, and medications.
• Sleep bruxism is a behavior mainly regulated by the central nervous center and associated with rhythmic activity of the masticatory muscles.
• Polysomnography and EMG are used to diagnose definite sleep bruxism associated with the clinical signs of the stomatognathic system and the patient's self-report.
• Sleep bruxism is often reported by bed partners due to teeth noises; self-report has a substantial false-negative rate.
• Snoring, sleeptalking, and nightmares are factors associated with sleep bruxism.
• Treatment is palliative and multidisciplinary and involves oral appliances, behavioral therapies, and medications.
The allusion to grinding and clenching of teeth comes from ancient times, where they are mentioned in the Bible in gospels such as Luke 13:28, Matthew 13:41-2, Matthew 8:12, Matthew 13:50, Matthew 22:13, and Matthew 24:51. In 1938, Miller introduced the term bruxism for bruxomania or repetitive teeth grinding (66). One of the first recorded notations of this phenomenon was from Black, who commented that abrasion of the teeth tends to remove the cusps quite rapidly (13). In 1941, Bodecker described a patient whose bruxism had destroyed the clinical crowns of all the lower anterior teeth (14).
In 2013, an international expert consensus examined several definitions of bruxism from sleep medicine and dental organizations and defined bruxism as a repetitive jaw-muscle activity characterized by clenching or grinding of the teeth or bracing or thrusting of the mandible. Bracing means forcefully maintaining a mandibular position, and thrusting means moving the jaw forward or laterally. These activities do not necessarily require tooth contact. According to its circadian phenotype, bruxism is classified as sleep bruxism or awake bruxism (51).
In the international consensus, experts defined bruxism as a behavior (52). According to the grading system, bruxism has three classifications: possible, probable, and definite. Possible sleep/awake bruxism is based on a positive self-report. Probable sleep/awake bruxism is based on a positive clinical inspection, with or without a positive self-report. Definite sleep/awake bruxism is based on a positive instrumental assessment, with or without a positive self-report or a positive clinical inspection. Sleep and awake bruxism appear to be distinct behaviors with different underlying causes and require a different management approach (52).
• Sleep bruxism has been associated with tooth wear, restoration fractures, temporomandibular disorders, headaches, and orofacial pain.
• Bruxism is not a cause of periodontal disease, but in patients diagnosed with periodontitis, bruxism activities can aggravate the severity of damage to periodontal tissues.
Tooth wear. Abnormal tooth wear is the most reported clinical sign of sleep bruxism, usually observed on teeth surfaces that come into contact during jaw function and in the cementoenamel junction, causing abfractions (99; 97). The lateral grinding and occlusal compressive forces generated by sleep bruxism activities may be destructive, depending on the intensity, frequency, direction, duration, and type of jaw movements. Data indicate that nocturnal bite force during bruxism can exceed the maximum voluntary bite force during the daytime (70).
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 (76). For example, interferences in posterior teeth can decrease oral volume and tongue space, leading to difficulty chewing. Bruxism activities can also result in tooth hypermobility, fracture of cusps and restorations, and injury to the tongue, lips, and cheeks. Pulpal exposure also may occur, resulting in pain, hypersensitivity, pulpitis, and pulpal death (08; 76).
A study concluded that there is no significant association between the polysomnographic parameters of possible sleep bruxism and the presence of tooth wear in adult patients (39). The authors highlighted that tooth wear is not an exclusive consequence of sleep bruxism. Tooth wear has a multifactorial etiology, including an acidic diet and daytime parafunction (nail-biting, biting hard objects, clenching, and grinding during the day) (39). Also, tooth wear is an irreversible condition. 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 (102). A systematic review found that tooth wear was the most prevalent clinical sign of sleep bruxism in children, mainly in primary canines. However, dental wear was not associated with sleep bruxism (96). These findings do not rule out the assessment of tooth wear but support that it should not be considered alone for the diagnosis. The clinician should associate tooth wear with other assessment parameters through careful anamnesis and clinical examination (52).
Orofacial pain. Pain in the mandible muscles, sensibility in the masseter and temporal muscle regions, morning headaches, and fatigue are symptoms often reported by individuals with sleep bruxism (91; 16; 97). Studies based on self-reports tend to find a higher positive association between sleep bruxism and pain than those based on validated clinical examinations and instrumental evaluations of muscle activity (06). In a systematic review, among children aged 3 to 8 years, headache (frontal muscle), temporomandibular pain, facial pain, and masseter muscle pain were the most reported symptoms, affecting around 30% of the participants. The least prevalent symptom among children was pain during jaw movement (96).
Temporomandibular disorders. Studies addressing the association between sleep bruxism and temporomandibular disorders are controversial. A scoping review concluded that the relationship between sleep bruxism and temporomandibular disorder depends on the assessment approach adopted for bruxism diagnosis (60). Investigations based on questionnaires or self-reports showed low specificity for sleep bruxism assessment. In general, they found a positive association with temporomandibular disorder. Conversely, instrumental studies employing polysomnography or electromyography reported a lower level or a negative relationship between sleep bruxism and temporomandibular disorder. Due to this inconsistency, future studies should consider sleep bruxism as a multifaceted behavior instead of using a simplified dichotomous presence or absence approach (60).
Periodontal disease. Findings about the influence of sleep bruxism on periodontal tissues are controversial, and there seem to be few studies on this topic (59). Indeed, sleep bruxism is not a cause of periodontal disease (59). The hypothesis is that in patients diagnosed with periodontal disease, the simultaneous presence of bruxism activities can exacerbate the damage to periodontal tissues, aggravating periodontitis (08; 69).
A cross-sectional study involving 541 adult patients seeking periodontal care found a prevalence of probable bruxism and periodontitis of 36.6% and 40.9%, respectively. Patients with probable bruxism were 2.24 times more likely to be diagnosed with periodontitis (95%, CI: 1.465-3.434) (12). Some caution is needed to analyze this result. 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 determining cause-and-effect relationships between the evaluated variables. It suggests the need for high-quality studies with robust study designs, such as randomized controlled trials (59; 12).
A 26-year-old male professional student reported morning stiffness in the cheeks and waking feeling unrefreshed; his wife reported that he made tooth-grinding noises while he slept. The patient reported a 2-year history of the pattern of morning stiffness and poor sleep, with these symptoms greatly exacerbated by stress brought about by school examinations and other family stressors. At the clinical evaluation, the patient showed a range of jaw motion (47 mm), which was increased with passive stretch to 52 mm. His canines and molar cusps showed signs of wear into the dentine, which were excessive for his age. Medical history revealed no significant findings. The patient was referred to a dental specialist for a bite splint and was enrolled in stress management sessions. Symptoms, compliance, and management will be reassessment as needed.
• Bruxism has a multifactorial etiology, including psychological and genetic factors, sleep-related breathing disorders, encephalopathies, medications, and addictive substances.
• Bruxism seems to be mainly regulated by the central nervous system, not the peripheral system.
• Rhythmic masticatory muscle activity episodes are preceded by events related to sleep arousals, such as increases in the autonomic sympathetic cardiac activity, frequency of ECM and EMG activities, heart rate, the activity of jaw-opening muscles, breathing amplitude, and blood pressure.
• Polysomnographic studies revealed that bruxism activities can occur during all stages of sleep, despite being more common in non-REM stages 1 and 2.
Sleep bruxism has a multifactorial etiology. The structural and functional etiologic models were proposed to explain the etiology of this behavior. The structural etiologic model argues that dental defects and malocclusions could cause bruxism. However, the researchers failed to prove that optimal occlusion could control the impact of sleep bruxism (47; 80). 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 bruxism. There is growing evidence in the literature of this model for children and adults (90; 10; 104; 87; 71).
Psychological factors. A systematic review of the association between anxiety and sleep bruxism in adults revealed controversies among researchers; however, it confirmed that specific symptoms, such as stress sensitivity, reassurance sensitivity, anxious expectation, and panic symptoms of anxiety, might be associated with probable sleep bruxism (72). In children over 6 years old, evidence suggests an association between psychological factors and sleep bruxism (25). Sleep bruxism is often related to stressful situations, such as school examinations, job difficulties, and marital strife. Once the stressful problem is solved, bruxism activities tend to cease.
In an animal model, stress-induced bruxism activity attenuated increases in adrenaline and cortisol levels and neutrophils in the blood, suggesting that bruxism may alleviate deleterious stress effects in other body systems (85). Similarly, children with sleep bruxism are more likely to have lower levels of early-morning salivary cortisol than controls (20). In this case, stress-elicited bruxism may be a beneficial tool that relieves sympathetic pressure and restores autonomic balance during sleep.
Personality traits may also contribute to the etiology of bruxism (88). People with bruxism tend to have a high level of neuroticism and responsibility compared to people without bruxism (90). An epidemiologic study involving children demonstrated that teeth clenching at night seem 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 problems (77).
Sleep-related breathing disorders. In polysomnographic studies, 805 or more of the bruxing events were related to respiratory events (42). The association between obstructive sleep apnea and sleep bruxism appears to be related to a compensatory mechanism to maximize upper airway permeability during sleep. Not all studies evaluating the association between sleep-disordered breathing and sleep bruxism demonstrate a relationship (83). However, the authors appear to recognize the importance of carefully selected inclusion criteria in studies and consider conditions such as snoring and upper airway resistance syndrome rather than strictly obstructive apnea or hypopnea syndrome. For example, studies demonstrated snoring as the highest risk factor associated with sleep bruxism (22; 27; 73). Also, upper and lower respiratory diseases (allergic rhinitis, otitis media, and asthma) might be more prevalent in children with sleep bruxism (68; 27).
Although the 2018 international consensus considers sleep bruxism a protective factor for obstructive sleep apnea (52), a systematic review questioned this association (57). The authors found no scientific evidence to support a conclusive relationship and also suggested future clinical studies with control groups to investigate possible common mechanisms for sleep bruxism and obstructive sleep apnea (57).
The link between sleep bruxism and the airway is difficult to show because sleep bruxism minimizes the degree of obstruction and flow restriction (93; 27). A statistically significant association is found when respiratory effort-related arousals are included in the apnea-hypopnea index. However, 4 seconds before rhythmic masticatory muscle activity, respiration amplitude has already increased (8% to 23%). The rise is higher at the onset of the suprahyoid activity (60% to 82% one second before rhythmic masticatory muscle activity), and it is maximal during rhythmic masticatory muscle activity (108% to 206%), followed by a rapid return to levels preceding rhythmic masticatory muscle activity (44). A positive and significant correlation was found between the frequencies of rhythmic masticatory muscle activity episodes and the amplitude of breath (R2 = 0.26; p = 0.02). The amplitude of respiration changes was 11 times higher when arousal was associated with rhythmic masticatory muscle activity compared to arousal alone (44). Sleep bruxism acts to protect the airway rather than solve the obstruction (94).
Comorbidities. Although the pathogenesis of bruxism remains unclear, the occurrence of sleep bruxism with encephalopathies and movement disorders suggests that it may occur because of loss of cortical or basal ganglia inhibition of brainstem motor generators. This finding reinforces the observation that patients with bruxism have significantly more body and orofacial movements during sleep than those without bruxism. Most otherwise healthy patients, however, do not show signs of cortical or nigrostriatal dysfunction (28).
Obstructive sleep apnea, restless leg syndrome, periodic limb movement during sleep, sleep-related gastroesophageal reflux disease, REM behavior disorder, and sleep-related epilepsy were higher in adult patients with sleep bruxism than in the general population. Although the pathways underlying this association have not yet been clarified, the authors suggest that sleep arousal may be a common factor linking sleep bruxism and the above-mentioned disorders, except REM behavior disorder and Parkinson disease (45).
Genetic factors. According to scientific evidence, sleep bruxism appears to be determined by genetics, indicating that family factors can contribute to this behavior (56; 91; 31; 86). A cohort study conducted with twins showed that genetic components are responsible for half of the risk variation of the phenotype for sleep bruxism (98). The percentage of rhythmic activity of the masseter and temporal muscles was higher in monozygotic twins when compared to dizygotic ones, which suggests the genetic influence on the triggering of sleep bruxism (03).
A systematic review concluded that sleep bruxism in parents is a potential risk factor for childhood sleep bruxism (31). Another study reported that first-degree relatives are twice as likely to have sleep bruxism than non-first-degree relatives (43). An association between bruxism and single nucleotide polymorphisms in dopamine receptor D2 was proposed (86). A previous study also demonstrated that 6- to 8-year-old children with bruxism have higher catecholamine levels (epinephrine and dopamine) (101).
Regarding awake bruxism, a study revealed an association between perceived stress level and awake bruxism and its clinical signs (tooth wear and tongue impressions). The authors concluded that polymorphic variants in genes related to coping with stress might be correlated with susceptibility to awake bruxism through elevated levels of perceived stress (58).
Medications and addictive substances. Image studies that evaluated the relationship between bruxism and chronic use of medications with antidopaminergic properties suggested that an imbalance in centrally acting neurotransmitters, such as dopamine and serotonin, may play a role in bruxism activities (55; 53). Conversely, psychostimulant drugs have been associated with bruxism, possibly because they upregulate serotoninergic pathways (29). There is insufficient scientific evidence to define drugs and addictive substances as risk factors for sleep bruxism. Thus, the magnitude of the risk and specific mechanisms (whether medications can aggravate preexisting bruxism or start its activities) are not well established. Sleep 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 (24).
Chronotype profiles. Sleep bruxism may be associated with several sleep characteristics that alter sleep patterns, influencing the internal biological clock and the chronotype profile. The chronotype profile is an individual's preference for establishing their favorite times to sleep, wake up, and perform daily activities. There are three different chronotype profiles: morningness, eveningness, and intermediate. A study demonstrated that children aged 3 to 5 years with an evening chronotype tended to have possible sleep bruxism. In addition, there was a proportional difference between the chronotype profiles of children with and without sleep bruxism. Among children with sleep bruxism, 12.5% had a morning profile, 26.4% had an intermediate profile, and 47.8% had an evening profile (79).
Facial profiles. A study involving Brazilian adolescents investigated whether facial profiles influence clinical signs of bruxism. Brachycephalic bruxists were more likely to report temporal muscle pain and have more wear facets on posterior teeth than mesocephalic ones. Dolichocephalics reported pain in the masseter muscle and were more likely to drool on the pillow when compared to mesocephalics (97).
Evidence suggests that the central nervous system plays a dominant role in sleep bruxism (54). Rhythmic masticatory muscle activity, followed by transient microarousal, occurs more often in patients with sleep bruxism than in controls. In both, muscle tone and heart rate increased during experimental arousal. These results support the hypothesis that sleep bruxism is an exaggerated form of oromotor activity associated with sleep microarousal (41). The bruxism activities and microarousals are often simultaneous, lasting about 3 to 15 seconds (47; 19). Bruxism can occur during all stages of sleep, despite being more common in non-REM stages 1 and 2, especially in the ascending period within a sleep cycle. This period, typified by the shift from non-REM toward REM sleep, is correlated with increased sympathetic and arousal activities (32).
Polysomnographic studies revealed an increase in sympathetic activity several minutes before bruxism events. Increased brain activity followed by increased activity in suprahyoid muscles was also observed (47). In moderate to severe sleep bruxism subjects, a marked increase in sympathetic activity precedes sleep bruxism (35). Also, the onset of rhythmic masticatory muscle activity and sleep bruxism episodes are influenced by the brief and transient activity of the brainstem arousal ascending system, contributing to the increase of activities in autonomic-cardiac and motor modularly networks (46).
During episodes of bruxing, rhythmic masticatory muscle activity or prolonged isotonic contractions of the jaw muscles may occur. Masseter’s EMG showed that grinding events were more characterized as phasic, whereas tooth attrition was associated with longer tonic bursts (105). The mandible may be either in intercuspal neutral or eccentric positions. Rhythmic masticatory muscle activity occurs at about 1 Hz, the rhythmic frequency close to human mastication; however, sustained contractions (clenching) may last several minutes (81).
• Different methodological approaches, clinical criteria, and study sampling reflect different prevalence rates among studies.
• Bruxism can occur at a particular point in life, and as age increases, the prevalence of this condition tends to fall. However, involvement in bruxism activities can resume in stressful situations.
Different methodological approaches, clinical criteria, and study sampling have led to discrepancies in the reported prevalence of sleep bruxism (96). For example, reliance on self-report and sleep partner reports of teeth grinding can underestimate sleep bruxism prevalence (63). People can suffer from bruxism at a particular point during their lives, and as age increases, the prevalence of this condition tends to fall (61). Children can stop bruxing activities and resume behavior between adolescence and adulthood (18). In a 20-year prospective study, bruxism was considered a persistent trait. It suggests that the original cause or the adaptive process underlying childhood bruxism may persist throughout life (34).
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 (62). In 2013, a systematic review identified several studies with a large sample that reported a bruxism prevalence of 8% to 31.4% (63). In children, the prevalence of sleep bruxism is around 31%; prevalence is 16% in adolescents and 20% in undergraduate students (103; 96). In adults, a systematic review showed that the prevalence of sleep and awake bruxism ranges from 8% to 31.4% and 22.1% to 31%, respectively (63; 61).
Studies show that male children aged 8 to 10 years have a higher prevalence of sleep bruxism (89; 26; 95). Among children aged 0 to 12 years, being male can be considered a risk factor for sleep bruxism (31). During adolescence, boys reported a higher percentage of sleep bruxism than girls (40). In adults, sex seems not to be a reliable risk factor for sleep bruxism (07; 64; 100), although there is a moderate association with the female sex (02).
Bruxism has shown a variable prevalence in different countries. The prevalence of teeth grinding among schoolchildren aged 2 to 12 years was estimated to be higher in preschoolers from Brazil and the United States, 34% to 40% and 36.8%, respectively (89; 38). Bruxism occurs in approximately 30% of children aged 5 or 6 years when late adenoid and tonsillar hypertrophy occurs (48). In patients with Down syndrome, bruxism has a high prevalence (51.8%) (82).
Due to the rapid spread of the COVID-19 disease, health authorities imposed social distancing as a preventive strategy (30). Emotional challenges such as stress, anxiety, fear, and changes in daily routines marked people's life. Thus, psychosocial and sleep disturbances possibly increased, worrying researchers about the risk of developing or worsening bruxism during social distancing (21). A Brazilian study showed that students with poorer sleep quality were more likely to have severe possible sleep bruxism (bracing, grinding, and thrusting). In addition, the use of smartphones contributed to the odds of reporting mild and moderate possible sleep bruxism (bracing and thrusting) (74). Another study evaluated adolescents before and after the completion of lockdown. Results revealed that increased state anxiety and use of social media at night were associated with self-reported sleep bruxism (21). In a longitudinal study involving children aged 8 to 10 years, access to electronic devices may have nearly doubled the risk of developing sleep bruxism during the pandemic (50). These findings suggest that exposure to screens before falling asleep can influence sleep patterns and bruxism activities due to the delay in sleep onset, its discontinuity, and the increase in the number of nocturnal awakenings. Furthermore, increased screen time at night plays a moderating role between anxiety and bruxism (21).
• Prevention approaches for sleep bruxism focus on identifying risk factors related to psychological factors, sleep-related breathing disorders, comorbidities, genetic factors, medications, and addictive substances.
Prevention approaches focus on identifying risk factors for sleep bruxism. Several medical conditions are associated with bruxism: Down syndrome, autism spectrum disorders, attention deficit hyperactivity disorder, epilepsy, schizophrenia, posttraumatic stress disorder, and other forms of chronic encephalopathies. Other potential risk factors can be cited: tension-type headaches, tardive dyskinesia, snoring, hypertension, hyperthyroidism, deficiencies, psychological stress, phobias, anxiety, and smoking (82; 24).
The differential diagnosis of sleep bruxism requires observation of the moment when the events occur and the presence of noises. Sleep bruxism occurs during sleep and may be loud and annoying, whereas awake bruxism occurs during wakefulness and is usually silent. Characteristic rhythmic jaw movements of sleep bruxism can also be associated with other sleep-related disorders. Thus, patients may have sleep conditions that are similar to bruxism. Restless legs syndrome, focal or generalized seizures, idiopathic oromandibular myoclonus, and parasomnias are examples. Unlike sleep bruxism, in nocturnal oromandibular myoclonus, the muscle activation spreads from the masseter to the orbicularis oris and oculi muscles (01).
• Definite sleep bruxism is based on self-report, clinical inspection, and polysomnography (ideally including audio and video recordings).
• Self-report assessment of sleep bruxism is the most used tool in bruxism research and clinical practice.
• Bed partners or family members may complain of noises due to teeth friction, but this is not always a reliable measure.
According to the International Classification of Sleep Disorders, which was proposed by the American Association of Sleep Medicine, the diagnosis of sleep bruxism requires reporting regular or frequent teeth grinding sounds during sleep and clinical signs, including abnormal tooth wear or transient morning jaw muscle pain or fatigue with or without temporal headache or jaw locking on awakening (04). Severe cases involve forceful rhythmic grinding or clenching of the teeth with audible tooth contact in about 20% of the episodes (19). The teeth in contact during eccentric movements (usually canines, but often incisors, premolars, molars, or a combination of these) are the first to show wear, demonstrating facets of the incisal surfaces (76). Health professionals should know that tooth wear is not an exclusive clinical sign of sleep bruxism; it may even be a natural process attributed to age. Several factors can also play a role in the tooth wear process and should be investigated during anamnesis as follows: acid diet, the diagnoses of xerostomia, gastroesophageal reflux disease, and medication use. In addition, there are differences between the types of tooth wear (attrition, erosion, and abrasion) (88; 39). Additional evidence also supports the investigation of masticatory muscle hypertrophy and indentations on the tongue or lip or a linea alba on the inner cheek adjacent to the molars (02; 52). Patients with sleep bruxism often also report sleep disturbances and difficulty initiating sleep; hence, a sleep history can be necessary.
Establishing the diagnosis by self-report is challenging due to several factors. Patients may have been previously informed of the suspicion of sleep 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 to be “intuitive epidemiologists” looking for their cause (75). Nonetheless, self-report assessment of sleep bruxism is the most used tool in bruxism research and clinical practice (52). The data suggest that, although self-report predicts teeth grinding sounds, self-reported sleep bruxism did not predict the presence or absence of moderate or severe cases assessed by polysomnography (75). Bed partners or family members may complain of noises due to teeth friction, but this is not always a reliable measure (52). For example, a study demonstrated a poor association between parental reports and sleep bruxism confirmed by polysomnography in children (37). Parents seem to underreport 56% and 73.7% of children with sleep bruxism regarding tooth clenching and grinding, respectively. 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 (37).
Alone, the clinical signs and symptoms mentioned above are insufficient to diagnose definite sleep bruxism, as most of them are based on the patient's report and can also be associated with factors other than sleep bruxism activities (39). Therefore, definite sleep bruxism assessment is based on self-report, clinical inspection, and polysomnography (52). Ideally, polysomnography includes both EMG of the masseter muscle and audio and video recordings to identify orofacial movements unrelated to bruxism (28; 04). It is important to note that the absence of muscle activity does not exclude the diagnosis, as bruxism may not occur every night. Also, bruxism is often incidentally observed as an EEG artifact due to temporalis muscle rhythmic contraction.
Polysomnography is rarely required for diagnosis. However, overnight studies are needed to make a differential diagnosis (if the events reported are sleep bruxism or other orofacial movements during sleep) and when the patient has symptoms of other sleep disorders (04). For example, patients should be asked about symptoms of obstructive sleep apnea, as this sleep disturbance can exacerbate bruxism. In addition to cases of patients with a suspected seizure disorder, video polysomnography or daytime EEG may provide clues to the possible underlying etiology (47).
• There is insufficient evidence to recommend a standard approach to the treatment of sleep bruxism.
• Sleep bruxism management consists of a conservative "multiple-P" approach, as follows: pep talk (counseling), plates (oral appliances), physiotherapy, psychotherapy, and pills (pharmacotherapy).
Clinical criteria have not yet been established to determine how many or how often bruxism activities can result in sequelae. The level of EMG activity seems to represent a risk factor, not the number of sleep bruxism events (52). In addition, defining cut-off points for clinical consequences may not be applicable in a clinical setting because bruxism interacts with other conditions (52). For example, when gastroesophageal reflux precedes sleep bruxism activities, the tooth wear is possibly worse. Teeth grinding will occur in the presence of stomach acid, accelerating the hard tissue loss (102). Thus, healthcare practitioners must guide the decision-making according to the particularities of each patient and consider the need for a multi-professional team. There is insufficient evidence to recommend a standard approach to the treatment of sleep bruxism (16; 45; 67). To date, sleep bruxism management consists of a conservative "multiple-P" approach, as follows: pep talk (counseling), plates (oral appliances), physiotherapy, psychotherapy, and pills (pharmacotherapy) (45).
Counseling and psychotherapy. In stress-related bruxism, psychological or psychiatric counseling may help control sleep bruxism and consists of initial therapeutic intervention. Psychological therapy has no side effects and does not interfere with maxillofacial growth and development, making it an appropriate approach for children (23). A study found that children who do not play sports are almost twice as likely to be diagnosed with probable sleep bruxism (49). Thus, physical activities may be encouraged because of increased circulation and oxygen supply to the brain, improving bone and muscle density, breathing, and stress tolerance (11).
Sleep bruxism may be associated with poor sleep quality in children and adults (65; 74). This finding highlights the importance of sleep routines, including sleep hygiene. This practice involves restrictions on electronic devices before bed, fixed hours to wake up and sleep, a comfortable bedroom concerning temperature, light, and noise, and avoiding heavy foods and drinking fluids at bedtime (65). Health professionals should inform patients about the potential effects of excessive use of screens, such as anxiety, physical inactivity, stress disorders, and daytime dysfunction (74).
Oral appliances. Oral appliances seem to be effective, despite the lack of studies with standardized methodology and knowledge about their mechanism of action (05). A systematic review evaluated several types of splints used in randomized clinical trials: palatal coverage splint, mandibular anterior repositioning splint, and anterior splint. The findings suggest that stabilization splints represent a safe and relatively effective management approach to reducing the frequency and intensity of sleep bruxism evaluated by EMG. The sample population consisted of subjects aged 20 to 40 years, so the effect on other age groups was not evaluated (67). In children, this intervention requires caution and frequent monitoring by the dentist. The inappropriate use and indication of occlusal splints may lead to impairment in the development of oral structures, thus, becoming more harmful than beneficial (23). A study demonstrated a reduction in the frequency of bruxing events in 65% of children with maxillary insufficiency who underwent rapid palatal expansion (09). These findings suggest that dentists should evaluate the cause of malocclusion or other potential etiologies. However, although maxillary expansion has shown success, there is no scientific evidence of an association between malocclusions (peripheral factor) and bruxism, as this behavior is related to the central nervous system (80).
Biofeedback therapy. Concerning biofeedback therapy, mainly contingent electrical stimulation significantly reduced sleep bruxism episodes after a short-term period. Long-term evaluations and studies of positive and adverse effects are needed to recognize its clinical application (67).
Pharmacotherapy. Overall, the strength of evidence for drug recommendations to control sleep bruxism is weak (67). Therefore, drug prescribing should be limited to short periods and considered when other conservative strategies have failed (08; 23). The following medications are cited in the literature with the potential to attenuate sleep bruxism: amitriptyline, botulinum toxin, buspirone, clonazepam, clonidine, clozapine, gabapentin, hydroxyzine, levodopa, propranolol, quetiapine, and trazodone (24; 67).
Polysomnographic recordings revealed that clonidine significantly reduced sleep bruxism when compared to placebo. The drug decreased sympathetic tone previously to the onset of sleep bruxism activities, preventing the sequential activation of the autonomic and motor systems (36). In a study, clonidine decreased more than 30% of rhythmic masticatory muscle activity episodes compared with placebo and clonazepam (84).
Applications of botulinum toxin in the masticatory muscles can reduce pain complaints related to sleep bruxism (16). Findings demonstrated that botulinum does not reduce rhythmic masticatory muscle activity events but decreases the intensity of masseter muscle contractions for at least 12 weeks (92). Thus, botulinum toxin seems to be a palliative management option, as it does not solve the cause of bruxism. Long-term evaluations are needed to assess the effects of continued reapplication and changes in muscle and adjacent bony structures (Beddis et 2018; 67).
The therapeutic options of the "multiple P" approach appear to control sleep bruxism but do not interrupt its activities. In addition, oral splints primarily aim to protect the dentition from tooth wear, and the evidence for a reduction in muscle activity is conflicting (78; 08; 67). It is important to note that bruxism can come and go in an individual's life. Thus, health professionals should maintain control consultations with a multidisciplinary team. Methodologically rigorous randomized large-sample long-term follow-up clinical trials are needed to clarify the efficacy and safety of sleep bruxism management (67).
A study conducted with Chinese pregnant and nonpregnant women found a high prevalence of sleep disorder-related symptoms in pregnant women. There was no significant difference in the prevalence of bruxism (17). A Finnish study showed that in the prepregnancy period, 25.8% of the women reported bruxism and only 19.9% during the first trimester (P=0.009). Therefore, there was a decrease in the prevalence of bruxism during pregnancy in this study (33).
Childhood is the most critical period for human growth and development; therefore, sleep bruxism is an important clinical condition in pediatric patients (31). To date, no specific therapy has been established for children (15).
Junia Maria Serra-Negra PhD
Dr. Serra-Negra of Universidade Federal de Minas Gerais, Brasil, has no relevant financial relationships to disclose.See Profile
Federica Provini MD
Dr. Provini of the University of Bologna and IRCCS Institute of Neurological Sciences of Bologna received speakers' fees from Italfarmaco and Pfizer.See Profile
Clarissa Drumond PhD
Dr. Drumond of Faculdade Santa Maria, Brasil has no relevant financial relationships to disclose.See Profile
Letícia Fernanda Moreira-Santos MD
Dr. Moreira-Santos of Federal University of Minas Gerais UFMG has no relevant financial relationships to disclose.See Profile
Federica Provini MD
Dr. Provini of the University of Bologna and IRCCS Institute of Neurological Sciences of Bologna received speakers' fees from Italfarmaco and Pfizer.See Profile
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