Morvan syndrome and related disorders associated with CASPR2 antibodies
Jan. 18, 2022
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Sleep bruxism is a repetitive jaw-muscle activity characterized by clenching or grinding of the teeth and/or by bracing or thrusting of the mandible. In sleep medicine, it has been described as a sleep-related movement disorder characterized by simple repetitive movements and transient arousals during sleep. In dentistry, according to the current international consensus, sleep bruxism has been described as a behavior. As for consequences, sleep bruxism may provoke tooth wear, fracture of restorations, temporomandibular disorder, headache, and muscular orofacial pain. Dental therapy involves palliative procedures such as protective plates and care for the temporomandibular joint, in addition to multidisciplinary care for associated factors. There is controversy among researchers about the association between emotional factors and bruxism. However, systematic reviews have proven that emotions act as a trigger for bruxism. A sequential change from autonomic and brain cortical activities precedes sleep bruxism, suggesting that the central and/or autonomic nervous systems, rather than peripheral sensory factors, have a dominant role in sleep bruxism onset. Therefore, the association between malocclusions and poorly adapted dental restorations was ruled out as being a peripheral factor. Comorbidities include snoring, hypertension, headaches, temporomandibular disorder, encephalopathy, epilepsy, affective disorders, psychological stress, personality traits, and anxiety. At this time, the diagnosis of definitive bruxism is made with polysomnography or with electromyography, associated with clinical signs of the stomatognathic system and the patient's self-report. Neuroimaging studies provide evidence of functional changes in oral motor cortical areas in patients with bruxism. Treatment of sleep bruxism includes dental plates, behavioral modification, and medication.
• Sleep bruxism is primarily associated with rhythmic masticatory muscle activity (RMMA).
• Bruxism is often reported or observed by sleep partners; self-reporting has a substantial false-negative rate. The clinical signs of the stomatognathic system associated with polysomnography or EMG are important.
• Snoring, sleeptalking, and nightmares are factors associated with sleep bruxism.
• Sleep bruxism is centrally rather than peripherally mediated.
• Treatment is palliative and involves intraoral appliances, behavioral therapies, and medications.
The allusion to grinding and clenching of teeth comes from ancient times, 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 (57). One of the first recorded notations of this phenomenon was from Black, who commented that "abrasion of the teeth may tend to remove the cusps of the teeth quite rapidly” (10). Later descriptions noted the potential effects of this disorder. In 1941, Bodecker described a patient whose bruxism had destroyed the clinical crowns of all the lower anterior teeth (11).
Sleep bruxism and awake bruxism were not differentiated for several decades; however, the sleep-wake state dependence appears to demonstrate that these are distinct disorders that have different underlying causes and require different treatments (45).
An international expert consensus examined several definitions of bruxism from sleep medicine and dental organizations and recommended that bruxism be defined as a repetitive jaw-muscle activity characterized by clenching or grinding of the teeth and/or by bracing or thrusting of the mandible (44). In the most recent publication of the international consensus, experts defined bruxism as a behavior (45).
Sleep bruxism is characterized by rhythmic masticatory muscle activity (RMMA) that occurs at about 1 Hz and is usually concomitant with microarousals that last about 3 to 15 s (42; 15). Sleep bruxism can occur during all stages of sleep, but is more common in non-REM stages 1 and 2. Sleep bruxism episodes are most frequently found 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 tone and arousal activity (28). Extreme forms involve forceful rhythmic grinding or clenching of the teeth with audible tooth contacts in about 20% of the episodes (15). Making this diagnosis by history is challenging, as most patients are completely unaware of these nocturnal contractions. Data suggest that although self-reporting was useful to predict tooth grinding sounds, it was not useful in identifying sleep bruxism noted via polysomnography (66). Bed-partners or family members may complain of disturbance from the noise and tooth friction, but this is not always a reliable measure. For example, 1 study demonstrated a poor association between parental report and bruxism (32). However, in the same study, the authors highlighted that 83% of the parents' reports regarding audible sound of teeth grinding of their children while sleeping were consistent with the diagnosis made by polysomnography. The same did not happen with patients who clenched their teeth while sleeping and this silent bruxism is only detected by polysomnography (32). Repetitive nocturnal grinding/clenching may be associated with headaches, jaw pain, tooth wear, and clicking in the temporomandibular joints (TMJ) (65). Forty-three percent of patients with temporomandibular disorders have 2 or more sleep disorders (84). Some patients present themselves for a visit because the bruxism has led to significant tooth wear, damage to previous dental work, dental thermal hypersensitivity, hypermobility, hypercementosis, muscle hypertrophy, or the need for dental restorations. Tooth wear generally occurs on tooth surfaces that come into contact during jaw function, as well as at the cemento-enamel junction causing abfractions (92; 87). The lateral grinding and occlusal compressive forces generated may be extremely destructive, depending on the intensity, frequency, direction, duration, and type of jaw movements. Data indicate that nocturnal bite force during bruxism can exceed the amplitude of maximum voluntary bite force during the daytime (61). Although sleep bruxism is a common disorder, it remains unclear how often it results in daytime sequelae.
Bruxism has been routinely cited as a pathogenic factor in the development of myofacial temporomandibular disorder. Most of the supporting evidence behind this hypothesis relies on self-reported bruxism rather than diagnostic polysomnography (67). However, the international consensus highlights the importance of a detailed anamnesis and evaluation of clinical signs in the stomatognathic system where the isolated diagnosis by polysomnography would not be sufficient to treat the patient (45).
Reports of regular or frequent sleep bruxism and presence of abnormal tooth wear and incidents of transient morning jaw pain were the best discriminatory items of sleep bruxism diagnosis (88). The abnormal wear of teeth is the most frequent sign of the disorder and is more common in male bruxers than in female bruxers. Severe wear on the anterior teeth may create an esthetic problem. In severe cases, the loss of vertical height of the teeth leads to occlusal changes, eg, interferences on posterior teeth. This loss of tooth height causes a decrease in oral volume and tongue space. The occlusal surfaces of the posterior teeth can be worn away, resulting in difficulty in chewing (87). In some patients, bruxism results in tooth hypermobility or fractured cusps and injury to the tongue, lips, and cheeks. Pulpal exposure also may occur, resulting in pain, hypersensitivity, pulpitis, and pulpal death. Sleep bruxism can be considered a factor that influences periodontal disease and a study suggested that patients with periodontal disease show more bruxism during wake than during sleep (60). Fracture of dental work and dental prostheses is also a major concern. Additionally, some patients may develop tenderness of the masseter or temporalis muscles that requires therapy. Changes in palatal growth and development may be a consequence of bruxism in children and mouth breathers appear to occur more commonly in bruxists (56). The facial profiles of the patients also influence their clinical signs. A study carried out with Brazilian adolescent bruxers demonstrated that brachycephalic adolescents were more likely to report pain in the temporal muscle and more facets of wear on posterior teeth compared to mesocephalic ones. Dolichocephalics reported pain in the masseter muscle and were more likely to drool on the pillow when compared to mesocephalics (87).
Bruxism has been routinely cited as a pathogenic factor in the development of myofacial temporomandibular disorder. Most of the supporting evidence behind this hypothesis relies on self-reported bruxism rather than diagnostic polysomnography (67).
A 26-year-old male professional student presented with reports of morning stiffness in the cheeks and waking feeling unrefreshed, along with a report from his wife 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 being greatly exacerbated by stress brought about by school examinations and other family stressors. On examination, the patient revealed a normal 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. The patient will be re-examined by the dentist and physician to evaluate symptoms, compliance, and management reassessment as needed.
Sleep bruxism has been attributed to numerous etiologies. The structural etiologic model argues that dentoskeletal defects or malocclusion were the root cause; however, this model has fallen out of favor due to lack of evidence (71). Idealizing occlusion may control the impact of sleep bruxism, but it has not been shown to lead to its resolution (42). The functional model argues that a combination of psychological stress and specific personality traits (eg, a predisposition to anxiety), may play a role, and there is growing evidence for this model both in children and in adults (80; 09; Wincour et al 2011; 62). A systematic review of the association between anxiety and bruxism in adults revealed that there are controversies among researchers; however, it confirmed that there is scientific evidence of the influence of some signs of anxiety in the onset of bruxism (64). A systematic review of the association between psychological factors and bruxism in children found that there is evidence in children over 6 years of age (19). Sleep bruxism has been associated with awake bruxism and snoring in adults and children (96; 65). From a respiratory standpoint, there tends to be a higher prevalence of upper and lower respiratory disease, such as allergic rhinitis, otitis media, and asthma, in children who have bruxism (59; 20). Additional risk factors include smoking or nicotine dependence (58), gastroesophageal reflux, movement disorders, affective disorders, alcohol abuse, loss of a significant other, use of certain medications, including serotonin reuptake inhibitors (SSRIs), amphetamines, and L-dopa (42; 34). Eating disorders have also been associated with sleep disorders and bruxism in Israeli women (22).
Although the pathogenesis of bruxism remains unclear, the occurrence of 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 notion is reinforced by the observation that patients with bruxism have significantly more body movements and orofacial movements during sleep than individuals without bruxism (21). Most otherwise healthy patients, however, do not show signs of cortical or nigrostriatal dysfunction. Some evidence suggests that children who brux are more likely to be hyperactive or restless (24). Imaging studies and the relation between bruxism and chronic use of medications with antidopaminergic properties suggest that CNS dopaminergic systems may play a role (48). Conversely, psychostimulant use has also been associated with bruxism, possibly because of upregulated serotoninergic pathways (23). When compared with nonbruxers, bruxers’ brains show activation patterns that are less extensive, suggesting central changes in motor systems reminiscent of those seen in “over-learned” tasks (97). Additionally, genetic factors have also been shown to have a role in the generation of bruxism in both children and adults (02). Khoury and colleagues also mentioned familial ties, showing that one-third of sleep bruxism subjects diagnosed by polysomnographic studies report that at least 1 first-degree relative also suffers from sleep bruxism (38).
Personality traits may also contribute to the pathogenesis of bruxism (78). People with bruxism tend to have a high level of neuroticism and responsibility compared to people without bruxism (80). Epidemiologic studies have demonstrated that bruxism can also be associated with emotional symptoms, peer problems, and higher total scores on a strength and difficulties questionnaire (69). Bruxism often becomes more pronounced during stressful periods, eg, school examinations, job difficulties, or marital strife. These symptoms may improve once the problem is resolved. One study examining stress-related hormones in 6- to 8-year-old children with bruxism revealed that urinary catecholamine levels (epinephrine and dopamine) were higher than in those children without evidence of bruxism (94). Similar results have been reported in adult bruxers. There are also findings of an association between dopamine and bruxism (76).
Bruxism appears to be regulated centrally, not peripherally. It also appears to be modulated by various neurotransmitters in the central nervous system (46). The central and/or autonomic nervous systems, rather than the peripheral sensory factors, have a dominant role in sleep bruxism. Evidence of central regulation shows that spontaneous rhythmic masticatory muscle activity (RMMA) during sleep occurs more frequently following spontaneous transient microarousal in patients with sleep bruxism and normal 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 (36). A cross correlation analysis revealed a shift of sympatho-vagal balance towards increased sympathetic activity starting 8 minutes before sleep bruxism onset. In moderate to severe sleep bruxism subjects, a clear increase in sympathetic activity precedes sleep bruxism (31). Also, the onset of RMMA and sleep bruxism episodes during sleep are under the influence of brief and transient activity of the brainstem arousal ascending system, contributing to the increase of activity in autonomic-cardiac and motor modularly networks (41). In bruxism patients, sympathetic cardiac activity was higher than in volunteers (55). In moderate to severe sleep bruxism subjects, a clear increase in sympathetic activity precedes sleep bruxism onset (31).
Polysomnographic investigations reveal that an increase in sympathetic activity occurs several minutes before most bruxing events with increased EEG rhythm frequency followed by increased activity in suprahyoid muscles, which appears seconds before bruxing events (42). This sequence of activity has led Lavigne and colleagues to suggest that bruxism is under the influence of brief and transient activity of the brainstem arousal-reticular ascending system that increases activity in autonomic-cardiac and motor modulatory networks. An investigative team has suggested that the A3 arousal phase is a window during which bruxing events can be elicited; however, the arousal does not act as a generator of bruxism (15).
During episodes of bruxing, rhythmic masticatory muscle activity (RMMA) or prolonged isotonic contractions of the jaw muscles may occur. Using masseter electromyography, grinding episodes were associated with a higher number of phasic episodes whereas tooth attrition was associated with longer tonic bursts (Yoshida et al 2017). The mandible may be either in intercuspal neutral or eccentric positions. RMMA occurs at about 1 Hz, which is near the rhythmic frequency of mastication in humans; however, sustained contractions (clenching) may last several minutes (72). The rhythmic nature of RMMA suggests involvement of masticatory timing networks in pontine and medullary trigeminal systems.
In a work with an animal model, it was demonstrated that sleep bruxism attenuated stress-related increases in adrenaline, cortisol, and neutrophils, suggesting that bruxism may alleviate deleterious stress effects in other body systems (75). Similarly, children with sleep bruxism are more likely to have lower levels of early-morning salivary cortisol then their nonbruxing controls (17). In this case, stress-elicited bruxism may be a beneficial tool that relieves sympathetic pressure and restores autonomic balance during sleep.
Bruxism occurs during microarousals from regular sleep patterns (42). Many factors may introduce microarousals, including reflux and tactile and auditory stimuli. The majority of sleep bruxism occurs during light non-REM sleep, and in polysomnographic studies 805 or more of the bruxing events have related respiratory events (37). The connection between obstructive sleep apnea and sleep bruxism appears to be related to a compensatory mechanism targeted at maximizing upper airway patency during sleep. Not every study evaluating the connection between sleep-disordered breathing and sleep bruxism demonstrates a relationship (74), but it seems that authors are recognizing the importance of carefully selected inclusion criteria and of considering conditions including snoring and increased upper airway resistance syndrome rather than strictly obstructive apnea/hypopnea syndrome. For example, studies demonstrated snoring as the highest risk factor associated with sleep bruxism (18; 20; 65). Although the 2018 international consensus considers bruxism to be a protective factor for obstructive sleep apnea (45), a systematic review questioned this association (50). This review found that there is no scientific evidence to support a conclusive relationship between sleep bruxism and obstructive sleep apnea. In addition, the authors concluded that future clinical studies with control groups should be encouraged to investigate whether there are possible common mechanisms for sleep bruxism and obstructive sleep apnea (50).
The link between sleep bruxism and the airway is difficult to show because sleep bruxism minimizes the degree of obstruction and flow restriction (82; 20). Only when respiratory effort-related arousals (RERAs) are included in the apnea-hypopnea index is a statistically significant association found. However, it has been shown that 4 seconds before RMMA muscle activity, the amplitude of respiration is already increased (8% to 23%); the rise is higher at the onset of the suprahyoid activity (60% to 82% 1 second before RMMA); the rise is maximal during RMMA (108% to 206%) followed by a rapid return to levels preceding RMMA (39). A positive and significant correlation was found between the frequency of RMMA episodes and the amplitude of breath (R(2) = 0.26; p = 0.02). The amplitude of respiratory changes was 11 times higher when arousal was associated with RMMA in comparison to arousal alone (39). Sleep bruxism acts to protect the airway rather than resolving the obstruction (83).
Most people brux at some point during their lives. In babies, the behavior of bruxism is considered physiological. During the development of the primary incisors there is mandibular instability that tends to cease when the posterior primary teeth erupt (52). Sleep bruxism is a frequent habit that affects a significant percentage of the population. It is initially suspected due to the presence of symptoms described by the patient. Only polysomnography (PSG) in a sleep laboratory can confirm a definite diagnosis (de la Hoz-Aizpurua et al 2011; 44). However, subjective reporting of bruxism is also considered a useful and valid diagnostic tool with a reported sensitivity and specificity of 78% and 94% respectively (69). Variations in methodological approaches, clinical criteria, and patient sampling have led to the discrepancies in the reported prevalence of bruxism. A 2013 systematic review of the literature identified several large survey studies that reported a bruxism prevalence of 8% to 31.4% (51). The prevalence of sleep bruxism is 35% in children, 16% in adolescents, and 20% in undergraduate students. There is a tendency for the prevalence of bruxism to fall as age increases (78; Aguiar et al 2019; 95).
A systematic review of the prevalence of bruxism among adults found a variation of 8% to 31.4% of sleep bruxism and 22.1% to 31% of awake bruxism. In children, a study showed a range of 3.5% to 40.6%. This discrepancy can be explained by methodological differences in diagnosis (51a; 51b). In patients with Down syndrome there is a high prevalence (51.8%) (73).
Bruxism has shown varying prevalence in different countries. The prevalence of tooth-grinding among school children aged 2 to 12 years old was estimated to be highest in preschoolers from Brazil and the USA, 34% to 40% and 36.8%, respectively (90). The reliance on self-reporting and sleep partners to report the presence of bruxism during sleep probably led to underestimation of the actual prevalence of the condition (51). Sleep bruxism usually results in moderate to severe tooth wear and orofacial muscle pain discomfort (87).
Bruxism occurs in up to 30% of children, often around ages 5 or 6 during late adenoid and tonsillar hypertrophy (43). Many childhood bruxers stop bruxing by their teens, although self-reported bruxism appears to increase between adolescence and young adulthood (14). In a 20-year prospective study it was determined that bruxism may be a persistent trait. This suggests that either the cause or the adaptive process to the original causal factor of childhood bruxism may persist.
Individuals with static encephalopathies have a high prevalence of bruxism with nearly 50% of institutionalized mentally retarded patients having significant tooth wear from bruxing. Bruxism is frequently associated with Down syndrome, autism spectrum disorders, headaches, and Rett syndrome as well as restlessness, hyperactivity, and attention deficit hyperactivity disorder (24; 73). Bruxism seems to be more common among late versus early postmenopausal women (27).
Approaches to prevention are currently focused on identifying and treating risk factors for sleep bruxism. Psychiatric conditions associated with increased risk for destructive sleep bruxism include Down syndrome, autism spectrum disorders, attention deficit hyperactivity disorder, and other forms of chronic encephalopathy. Other possible risk factors include tension-type headaches, schizophrenia, tardive dyskinesia, snoring, hypertension, epilepsy, posttraumatic stress disorder, hyperthyroidism, gastrointestinal disturbances, nutritional deficiencies, psychological stress, phobias, anxieties, internal aggression, and smoking (99). Medications such as selective serotonin reuptake inhibitors, antipsychotic agents, amphetamines, L-dopa, and alcohol also may increase the risk of developing bruxism (42).
The differential diagnosis of bruxism first requires identifying when the events occur. Typically, awake bruxism is silent, whereas nocturnal bruxism may be loud and annoying.
The nocturnal rhythmic jaw movements can be associated with other disorders (01). Patients may have other sleep issues such as restless legs syndrome. Bruxism-like movements also may be associated with focal or generalized seizures and can be confused with isolated sleep bruxism. Idiopathic oromandibular myoclonus and parasomnias can also be mistaken for bruxism. Familial nocturnal oromandibular myoclonus can also mimic sleep bruxism, but, unlike bruxism, the muscle activation spreads from the masseter to the orbicularis oris and oculi muscles. Numerous other orofacial activities that occur during sleep can mimic bruxism (01).
According to the ICSD-3, the diagnosis of sleep bruxism requires both the presence of regular or frequent tooth grinding sounds occurring during sleep and clinical signs, including: abnormal tooth wear consistent with reports of tooth grinding during sleep or transient morning jaw muscle pain or fatigue with or without temporal headache or jaw locking on awakening (05). The teeth in contact during eccentric movements (usually canines, but often anterior, premolars, molars, or a combination of these) are the first to show wear, demonstrating facets of the incisal surfaces and tooth hypermobility. Additional supportive evidence is gained by the observation of bite lesions and ridging of the lateral borders of the tongue and buccal mucosa adjacent to the molars. Tenderness or hypertrophy of the masseter or temporalis muscles may also aid in the diagnosis. Bruxers often report sleep disturbances and difficulty initiating sleep; hence, a sleep history can be useful in making the diagnosis.
When evaluating a patient for sleep bruxism it is important to remember that excessive dental wear can be due to multiple factors (eg, diet, soft drinks, xerostomia, medications, gastroesophageal reflux disease) and should not be used as exclusive evidence that bruxism is occurring. The dentist is able to observe the clinical differences of erosive dental wear caused either by chemicals or attrition (80; 78). Also, the relationship between bruxism and craniofacial pain or joint locking is controversial, and current pain symptoms should not be construed as positively indicating the presence of bruxism (89).
Overnight sleep studies are rarely necessary for the diagnosis of sleep bruxism unless the patient has symptoms of other sleep disorders. Often, bruxism is noted incidentally during polysomnography as an EEG artifact caused by rhythmic contraction of the temporalis muscle. Polysomnographic studies including EMG monitoring of masseter muscle activity may show episodes of rhythmic masseter and temporalis muscle activity during sleep, but the absence of such activity does not exclude the diagnosis because bruxism may not occur every night.
Patients suspected of having bruxism should be queried regarding symptoms of obstructive sleep apnea for the potential need of polysomnographic investigation. Ideally, polysomnography performed to evaluate bruxism would include masseter muscle activity recording (05), and audio-video recordings should be used to rule out nonbruxing orofacial movements (21). For patients in whom a seizure disorder is suspected, video-polysomnography or daytime EEG may give clues to potential underlying epileptic origins. It is hoped that continued research focused on the nature of sleep-arousal processes will produce useful diagnostic criteria (42).
Criteria for when bruxism becomes severe enough to be considered a disorder requiring treatment have not been established yet and are, therefore, subject to case-by-case clinical judgment. The bruxer should be followed up by a competent dentist who can monitor the dental wear and intervene when necessary. A review concluded that bite splints are the treatment of choice, with clonidine and mandibular advancement devices demonstrating some utility (86); however, the latter treatments have more side effects than does the splint (42). Although most patients continue to brux with the splint, tooth wear and other symptoms, such as pain, are usually reduced. In most cases, conservative, stabilizing splint designs are sufficient, if not best. In partially edentulous cases, splint-like removable prostheses may be used. In randomized, controlled studies propranolol did not affect sleep bruxism. Clonidine, on the other hand, decreased sympathetic tone in the minute preceding the onset of sleep bruxism by preventing the sequence of autonomic to motor activation, which further supports the role of sympathetic activity in the pathophysiology of sleep bruxism (33). Presently, there are no clearly superior methods to treat bruxism in children, though 1 study demonstrated a reduction in frequency of bruxing events in 65% of children with maxillary insufficiency who underwent rapid palatal expansion (08). This suggests that an approach to treating bruxism should include the evaluation and management of causes of malocclusion or other potential etiologies. Maxillary expansion in cases of atresia in children has shown success; however, a systematic review has shown that there is no scientific evidence of an association between malocclusions and bruxism. The explanation for this is that malocclusion is a peripheral disorder and bruxism is related to the central nervous system (71).
Some patients may require further therapy to reduce bruxism. In stress-related bruxism, psychological or psychiatric counseling may be helpful. Medications also may be necessary to reduce symptoms. Lorazepam is the only drug that has evidence-based proof of managing sleep bruxism in the short term. Intermittent use of diazepam (5 mg, 30 minutes before bedtime) may relieve anxiety, improve sleep, and reduce symptoms during acute exacerbations. Long-term benzodiazepine therapy is rarely indicated. Beneficial effects have been reported with medications such as propranolol, L-dopa, pergolide, gabapentin, tiagabine, and atypical antipsychotics such as clozapine (47; Kawashima et al 1999; 23). In other studies, neither propranolol nor amitriptyline showed statistical improvement of symptoms (42). In severely intractable patients, there is limited evidence that botulinum toxin (Botox) injections may show some benefit (68) but it is not recommended for treatment, as the risk to safety outweighs its effectiveness (40). For patients with SSRI-induced bruxism, buspirone appears to have relieved symptoms in a small series (12). Aripiprazole, a partial serotonin/dopamine agonist, has also been shown to effectively treat SSRI-induced awake bruxism (23). For postmenopausal women, estrogen plus progesterone appear to give relief from bruxism as well as from arousals (26). A variety of other treatments, such as nocturnal EMG biofeedback therapy, have shown some value in the treatment of bruxism.
In the dental field, occlusal splints are used in a palliative manner. Studies have observed that plate therapy does not stop bruxism but rather protects the tooth wear by attrition (70; 07). Excessive tasks should also be avoided to reduce stress. Sports activities are considered protective factors against bruxism (77). It is important to note that bruxism can come and go in an individual's life. The health professional must maintain control consultations with multidisciplinary support. Sleep hygiene practices should be adopted to improve the patient's quality of life. Stimulating foods consumed in bed time should be considered. In addition, the use of smartphones and media at night should be avoided. The blue light effect impairs melatonin secretion and consequently can affect sleep.
There may be a negative relationship between childhood bruxism and maternal age at birth (16). A study conducted in China in pregnant and nonpregnant women found several sleep disorders in a higher percentage of pregnant women than in nonpregnant women (13). It is interesting to note that a Finnish study showed that during 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 (29).
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
Junia Maria Serra-Negra PhD
Dr. Serra-Negra of Universidade Federal de Minas Gerais, Brasil, has no relevant financial relationships to disclose.See Profile
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