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lournalof Back and Musculoskeletal Rehabilitation Journal of Back and Musculoskeletal Rehabilitation 6 (1996) 165-176

Bruxism: A factor associated with temporomandibular disorders and orofacial pain Frank LobbezoOa,b,c, Jacques

Y.

Montplaisirb,c, Gilles J. Lavigne*a,b,c

a Faculte de Medecine Dentaire, Universite de Montreal, Quebec, Canada bCentre de Recherche en Sciences Neurologiques, Faculte de Medecine, Universite de Montreal, Quebec, Canada CCentre d'Etude du Sommeil, Departement de Psychiatrie, Hopital du Sacre·Coeur, Montreal, Quebec, Canada

Abstract Rhythmic masticatory muscle activities are probably part of normal jaw motor behavior. Certain factors, like disease, stress, personality, alcohol, and medication, may turn this normal activity into a condition that might include abnormal tooth wear, myofascial pain, and temporomandibular joint problems. This condition then corresponds with bruxism. Bruxism and masticatory muscle pain may reciprocally influence one another: although not a compulsory finding, bruxism may be associated with the predisposition, initiation, and perpetuation of temporomandibular disorders and orofacial pain. On the other hand, the presence of jaw muscle pain may reduce bruxism motor activity. Research on the integrity and nature of the relationship between bruxism and pain is hampered by controversies that exist regarding definition, diagnostic criteria, and measurement techniques. Moreover, the pathophysiology of bruxism and its association with other sleep-related and movement disorders are still unclear. Consequently, there is no real cure for bruxism, although several treatments may be used to control its adverse effects. However, there is very limited research to support the efficacy of behavioral, physical, dental, pharmacological, and orthopedic treatments. Probably the best current treatment modality for bruxism is the occlusal stabilization splint. Although such an orthopedic device may not actually prevent bruxism, it may help to reduce its symptoms. Keywords: Bruxism; Temporomandibular disorders; Sleep

1. Introduction

Bruxism, a disorder of the masticatory system involving tooth grinding or clenching, has been

* Corresponding author, Tel.: + 1 5143432310; Fax: + 1 514 3432233; E-mail:[email protected].

associated with the predisposition, initiation, and perpetuation of temporomandibular disorders (TMD) and orofacial pain [1-4]. According to some reports, the disorder is more prevalent in TMD patients than in the general population [1,5]. Intense bruxism has been hypothesized to cause postexercise muscle soreness (PEMS), a condition characterized by muscle fibre micro-

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trauma, pain, and dysfunction [6]. Ultimately, bruxism may result in masticatory muscle pain, temporomandibular joint noises (clicking or crepitus), and limitation of jaw movements [7]. Furthermore, bruxism has been proposed to cause myofascial pain and tension-type headaches [2]. Pain associated with bruxism is not a compulsory finding. In a polysomnographic study, about 70% of patients who appeared to brux nightly had no masticatory muscle pain at all [8], probably due to training of their jaw muscles, resulting in a high resistance to fatigue and damage [6]. Interestingly, it has recently been demonstrated that the number of bruxism episodes per hour of sleep is lower in the presence of jaw muscle pain [9]. Since evening and morning pain scores were similar, it was suggested that bruxism may not be the primary cause of jaw muscle pain and, by inference, that pain modulates the pattern of bruxism. In conclusion: the integrity and nature of the relationship between bruxism motor activity and masticatory muscle pain are not clear at this time. However, the evidence cited above suggests that bruxism and pain may reciprocally influence one another. Therefore, an overview of the literature on bruxism fits well into the theme of this issue of the Journal of Back and Musculoskeletal Rehabilitation. In this contribution, bruxism and oromandibular motor activity will be reviewed with regards to definition, epidemiology, diagnostic criteria, measurement techniques, concomitant disorders, pathophysiology, and management strategies. 2. Definition

The term 'bruxomania' was first employed by Marie and Pietkiewicz [10] to describe oromandibular movements associated with tooth grinding in patients with various neurological and mental health problems. More recently, bruxism was defined by the American Academy of Orofacial Pain (AAOP) as 'sustained or rhythmic contractions of jaw muscles accompanied by tooth contact' [4,11], This definition, however, is descriptive only and disregards any pathophysiological mechanism underlying the disorder. Moreover, it lacks specific criteria to discriminate nor-

mal from pathological oromandibular motor behavior that may occur during both sleep and wakefulness, such as swallowing, myoclonic contractions, or alternate opening and closing of the mouth [12,13]. A more operational definition for sleep-related bruxism was offered by the American Sleep Disorders Association (ASDA): 'bruxism is a periodic stereotyped movement disorder characterized by grinding or clenching of the teeth during sleep' [14]. Although this definition disregards diurnal bruxism, it appears to be the best currently available description for both research and clinical purposes [15]. However, it remains desirable from a clinical point of view to specify more clearly when rhythmic masticatory muscle activities become pathological in order to detcrmine the need for treatment. 3. Epidemiology

In this section, prevalence and incidence will be defined according to the AAOP glossary [4] as the number of positive cases at a given time and the number of new cases at a given time, respectively. The prevalence of bruxism, with either grinding or clenching, has been estimated to be in the 6-20% range. These figures are derived from studies of student populations [16,17], general dental practices [18], and general populations [3,19,20]. In a cross-sample of 2000 ll-year-old Quebec children, the prevalence of bruxism was 14.1 % [21]. Women report clenching more frequently than men [3], but no sex differences were observed for grinding [3,17,18]. The incidence of bruxism diminishes with age, especially after the age of 50 [20]. Interestingly, it was noted that in 17-20% of bruxers, associated oro facial pain is present [3]. The main limitation of most bruxism epidemiology surveys is that they are derived from patients' self-reports of clenching and grinding, a technique that is considerably sensitive for bias. Another important aspect is whether or not denture wearers grind. The reported reduction with age is probably not very accurate, because being edentulous is more common in elderly people. Moreover, some survey questions may be impre-

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cise because at present, many criteria for bruxism diagnosis are still in process of validation. In order to overcome such problems, J ennum and Sjol [22] supported the self-report data of their survey on snoring and sleep apnea by physiological evaluations in a subsample of their subjects, using the standard cut-off diagnostic criteria defined by the ASDA [14]. A similar approach to the study of bruxism should be considered. 4. Diagnostic criteria In the absence of validated criteria for bruxism diagnosis (for details on validation, sensitivity, and specificity, see [23,24]), the clinician or researcher must use criteria derived from the available literature. For the dental clinician, the clinical signs and reports may include the following (Table 1A): (a) abnormal tooth wear; (b) tooth or restoration fracture/failure; (c) tooth mobility; (d) masseteric (temporalis) muscle hypertrophy on voluntary contraction; (e) jaw tightness sensation; (f) myofascial pain and temporomandibular joint problems; and (g) grinding sounds as noted by a bed partner. These criteria were taken from the recent literature [2,13,25-27]. Their sensitivity and specificity need to be established. This is even more imp or-

Table 1A Empirical bruxism diagnostic criteria for the use of the dental clinician (for cautionary remarks regarding validation and for additional information, see text) Abnormal tooth wear due to abrasion. For a method to assess the severity and progression of occlusal wear, see Johansson et al. [40]; Dental injury (e.g. tooth or restoration fracture / failure; tooth hypermobility); Hyperkeratotic lesions on the mucous membranes of cheeks (rims), tongue (impressions), or lips (impressions); Hypertrophy on voluntary contraction of the masseter or temporal is muscles; Pain, tenderness, fatigue, or stiffness in the facial or masticatory muscles; Temporomandibular joint problems; Sounds associated with bruxism, usually reported by a bed partner.

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tant since the validity of the relationship between bruxism and masticatory muscle pain [28] and of tooth wear [29] have been challenged. Furthermore, observations regarding tooth wear facets or muscle hypertrophy are descriptive and very subjective. The suggestion that hyperkeratotic lesions on oral mucous membranes and tongue indentations are indicative of clenching [30] also needs further support. An important characteristic that complicates bruxism studies is that the disorder shows a high night-to-night variability [2]. Consequently, further validation of and consensus on diagnostic criteria are needed. For the sleep disorders clinician, the ASDA [14] suggested the following criteria «a) and (b) are considered to be the minimal criteria): (a) tooth grinding or clenching during sleep; (b) abnormal tooth wear and/or sounds associated with bruxism and/or jaw muscle discomfort (not further defined; e.g. pain or fatigue); (c) presence of jaw muscle activity during sleep and absence of associated epileptic activity (see Concomitant disorders) as monitored polysomnographically; and (d) absence of medical or psychiatric disorders producing abnormal sleep movements (e.g. sleeprelated epilepsy). Other sleep disorders may be concurrently (e.g. obstructive sleep apnea). Additional information for the sleep disorders clinician is presented in Table lB. Additionally, the ASDA formulated severity and duration criteria. The severity criteria are as follows: (a) mild: occurs occasionally; no dental injury or psychosocial impairment; (b) moderate: occurs nightly; mild psychosocial impairment; and (c) severe: occurs nightly; dental injury; temporomandibular disorders; and moderate to severe psychosocial impairment. The duration criteria are: (a) acute: less than 7 days; (b) subacute: between 7 days and 1 month; and (c) chronic: more than 1 month. Although these criteria seem logical and applicable to the clinical setting, none has been validated so far. Therefore, the ASDA diagnostic criterion 'presence of jaw muscle activity during sleep' was tested against polysomnographic observations in a controlled study [31]. The sensitivity and specificity of the number of bruxism episodes

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Table lB Suggested bruxism diagnostic criteria for the use of the sleep disorders clinician (for cautionary remarks regarding validation and for additional information, see text): Absence of medical and psychiatric disorders that produce abnormal sleep movements (e.g. sleep-related epilepsy); - More than four bruxism episodes or more than 25 bruxism bursts per hour of sleep (thresholds established for research purposes); - Bruxism may be scored as follows, using audio and video recordings in parallel with a polysomnographic recording: - Bruxism burst: EMG activity with an amplitude of at least 20% of maximum voluntary contraction and a duration of at least 0.25 s. If burst duration is less than 0.25 s, then the activity is considered a fragmentary myoclonic contraction; - Phasic episode: at least three bursts, repetitive at a frequency of approximately 1 Hz and with burst durations between 0.25 and 2.0 s; - Tonic episode: a burst lasting more than 2.0 s; -- Mixed episode: a combination of phasic and tonic characteristics with interburst intervals shorter than 3.0 s. If an interburst interval is longer than 3.0 s, a new episode starts following the interval; --- Non-bruxism EMG activities (e.g. fragmentary myoclonus, coughing, face rubbing, and alternate opening and closing of the mouth) should be identified.

-

per night of sleep were estimated at 72% and 94%, respectively, if at least two episodes were

associated with grinding sounds. In order to discriminate bruxers from asymptomatic subjects for research purposes, thresholds of four bruxism episodes and 25 bruxism bursts per hour of sleep were used. It is, however, important to note that there are no standardized criteria for polysomnographic analyses of bruxism motor activity. In the recent literature, masticatory muscle activity is usually scored as bruxism if muscle activity levels are over 20-40% of maximum voluntary contraction, if at least three bursts of muscle activity are present for phasic (rhythmic) classifications, and if sustained activity is maintained more than 2 s for tonic events [13,32,33]. 5. Measurement techniques Numerous techniques are currently used for the evaluation of bruxism; they all have their

specific applications and limitations. They include measures of: (a) occlusal tooth wear, e.g. on Bruxcore Plates [34] or on study casts [35,36]; (b) interarch pressure or number of occlusal contacts, e.g. with the Oral Sensor (Anderson-Fox Co., USA; [37]); (c) masticatory muscle activity in the natural (home) environment using ambulatory systems [34,38-41]; (d) masticatory muscle activity in a sleep laboratory in parallel with audio and video monitoring [13]; and (e) other concomitant variables, such as changes in heart or respiratory rates [26,42-45]. The advantages and disadvantages of various medical recording techniques for sleep or movement disorders are discussed in two excellent reviews [46,47]. Ideally, the validation of a certain measurement technique should be performed in combination with clinical examinations and electromyographic (sleep laboratory or natural environment) recordings. 6. Concomitant disorders Bruxism can occur with a variety of sleep disorders, such as sleep apnea, restless legs syndrome (RLS), periodic limb movements during sleep (PLMS), jaw myoclonus, and grunting [12-14,20,25,45,48]' The appearance of these motor manifestations may be a consequence of a pathology or may be secondary to the induction of an arousal that is also frequently associated with bruxism [14,43-45,49]. It has been suggested that K-a complexes, EEG components indicative of arousal [50], may have a positive effect on the appearance of rhythmic motor manifestations (e.g. PLMS) and on the autonomic nervous system (e.g. increase in heart and respiratory rates). Rhythmic masticatory muscle activation (e.g. bruxism) may follow as a tertiary event. In over 75% of episodes of jaw motor activation, such a temporal sequence was observed indeed [51]. The association between RLS and bruxism was recently surveyed in 2019 Canadians. It was shown that about 10% of tooth grinders also had RLS, and at least 15% of the subjects with RLS also had bruxism [20]. Okeson et a1. [45] noted that in approximately 60% of cases, bruxism events were associated with leg muscle activity during sleep.

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The ASDA recommendation that epilepsy should be ruled out before diagnosing an abnormal sleep-related oromandibular motor activity needs to be discussed, because this association is very rare. It should be stressed that the placement of EEG electrodes in the vicinity of the temporalis muscle can produce artifacts resembling epileptic spiking. Indeed, it has been reported that facial and masticatory muscles can contaminate the EEG [52,53]. Bruxism can also occur in the presence of psychiatric and neurological disorders, such as tics, oral tardive dyskinesia, oromandibular dystonia (Meige's syndrome), coma, cerebrovascular accident, cerebellar hemorrhage, mental retardation, and sexual abuse [2,10,12,25,54-58]. Moreover, bruxism has been observed to occur in systemic disorders, such as Whipple's disease, in encephalopathy, and III alcohol abuse [2,10,25,56,59]. Stress, a condition that is endemic in the general population, often is cited to exacerbate bruxism [2,11,25,48]. However, Goulet et al. [3] demonstrated only a weak association between reported life stress and bruxism ('Y < 0.38). Moreover, Pierce et al. [41] found no overall relationship between EMG measures and self-reported stress in bruxers. Hence, this issue needs further clarification in future studies.

also noted with bruxism and RMMAs [13,20,27,32,43,45]. Furthermore, bruxism was noted to occur with sleep stage shifts [42-44). All of these observations are consistent with the hypothesis that sleep bruxism is part of an arousal response. According to the ASDA glossary of terms used in sleep disorders medicine [50], such a response is characterized by: (a) an abrupt sleep stage change to a lighter stage or wakefulness; (b) an increased EMG activity; (c) an increased heart rate; and (d) the presence of body movements. An argument favoring the arousal response hypothesis is derived from the 'cyclic alternating pattern' of arousal noted each 20-40 s [67]. This has been described as a periodic phenomenon of autonomic, motor, and cerebellar autoregulatory mechanisms [68]. Such oscillations have been observed for respiration, heart rate, and EEG waves in normal subjects. They are present in patients with apnea and RLS/PLMS as well [67-70). Similar oscillations were noted in the recurrence of bruxism episodes [71]. Even if this 20-40 s rhythm is not the only trigger for jaw muscle events, it may represent one factor that influences the probability that an episode of motor activation, such as apnea, PLMS, or bruxism, occurs along with an arousal response.

7. Pathophysiology

At present, there is no cure for bruxism. However, several treatment strategies can be used to control its adverse effects [48,61,72,73]. These strategies, which will be described below in more detail, include: patient education, behavior modification, physical therapy, occlusal therapy, pharmacotherapy, and orthopedic appliance therapy. An overview is presented in Table 2. The success of any treatment depends on patient motivation, cooperation, and compliance. Hence, the clinician should explain the nature of the problem, treatment options, and prognosis to the patient. Behavior modification strategies should be applied if a more structured approach is indicated. Among others, life-style counseling, hypnosis, and biofeedback may be considered [11]. This latter strategy, an EMG technique with a 'feedback

Rhythmic masticatory muscle actlvltIes (RMMAs) can be observed during the sleep of both

bruxers and asymptomatic subjects [31,43,60), Furthermore, diagnosed subjects do not brux every night [2,43,61] and bruxism tends to decrease with age [20]. Bruxism may therefore be considered as normal motor behavior in which certain factors, like disease [10,54,55,57,59], stress [2,3,11,41,62], personality [11,63-66], alcohol [25], and medication [15,25], have strengthened and increased normal jaw muscle activity. An increase in heart and respiratory rates and the presence of cortical EEG components in association with bruxism have been described above (see Measurement techniques and Concomitant disorders). The presence of body movements was

8. Management strategies

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Table 2 Overview of the management strategies that have been described in the literature to control the adverse effects of bruxism. For indication, contraindication, risks, side effects, and scientific support, see text -

-

-

Behavioral interventions: - Patient education (e.g. explanation of etiology, treatment options, and prognosis); - Behavior modification (e.g. life-style counseling, hypnosis, and biofeedback); ._.- Physiotherapy (e.g. rhythmic exercises, moist heat, and massage). Dental interventions: - Orthopedic appliance therapy (e.g. bite guard, occlusal stabilization splint). - Occlusal adjustments (e.g. equilibration, prosthodontics); 1 Pharmacological interventions: 2 - Benzodiazepines (diazepam); - Muscle relaxants (methocarbamoO.

1 Controversial 2 For

type of intervention (see text). short-term management of acute conditions only.

loop' to give patients more information about their muscle activities, has been studied extensively for the last two decades [63,74-76]. Although biofeedback was reported to reduce the duration of bruxism episodes [77], probably through its influences on a hypothetical bruxism generator [15], these findings have been contradicted by another investigation [76]. In addition, most biofeedback systems use sound to manage bruxism for both awake and sleep states. Although these tones may be very useful during the day, they may induce sleep disturbances, manifestations of arousal, or, even worse, bruxism itself [44,78]. Further, when applying biofeedback, the clinician must establish a threshold of EMG activity above which bruxism will be detected. However, in the absence of a good description of EMG characteristics and their variability in the normal population, and without a detailed insight into the effects of gender, age, and morphology on the surface EMG [79,80], the establishment of such a threshold remains an arbitrary procedure. Finally, it has been demonstrated that without a more general stress-management program, biofeedback provides temporary relief only [11].

By means of physical therapy procedures, like light rhythmic exercises, moist heat, and massage [81], relief of the pain that may concur with bruxism (see Introduction) can be obtained [2]. Another widely discussed approach is occlusal equilibration. Although it is still a topic of interest [82], its efficacy on bruxism has not been demonstrated in controlled clinical trials [83]. Therefore, occlusal equilibration is not recommended if iatrogenic occlusal factors are absent. Pharmacologic treatment has been used to treat bruxism and its symptoms. Several medicines, like the benzodiazepine diazepam (e.g. Valium®) and the muscle relaxant methocarbamol (Robaxacet®), have been reported to suppress bruxism motor activity [84,85]. However, none of these substances are recommended for the longterm treatment of the disorder because of the risk of dependence, the production of numerous side effects, and the absence of supportive data from controlled trials. The effects on bruxism of another popular muscle relaxant, cyclobenzaprine (Flexeril ®), used typically for fibromyalgia, are unknown [86-88]. Substances known to increase 5-HT transmission in the central nervous system, like tricyclic antidepressants (TeAs), were proposed as an interesting possibility for treating severe bruxism occurring in REM sleep [32]. Although this has been suggested by others as well [4,72], their use is not recommended because of the absence of any scientifically-sound evidence that supports its efficacy in the treatment of bruxism or any other oro mandibular movement disorder. Another serotonin-related substance, the 5-RT precursor Ltrytophan, has been tested for the treatment of bruxism, but no effect was shown in a controlled study [89]. Opioids are motor suppressant, and their efficacy for other sleep movements disorders, such as PLMS, is well-documented [90-92]. However, their use for bruxism is not recommended because of the risk of abuse and addiction. Only one short and incomplete report has stated that morphine had no effect when used in bruxism [93]. In the late sixties and early seventies, dopamine (DA)-related medicines, such as amphetamine and

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the catecholamine precursor L-dopa, were reported to exacerbate bruxism [94,95]. However, evidence for this statement was based only on case reports dealing with chronic use of these substances. An alternative hypothesis would be that bruxism accompanies the disorder treated with L-dopa (e.g. Parkinson's disease). Hence, the disorder, not the L-dopa, may exacerbate the bruxism. In addition, unpublished clinical observations on patients presenting both PLMS and bruxism showed that administration of L-dopa, which may be used to treat PLMS without marked side effects [91,92], had a beneficial effect on both disorders. Interestingly, it has recently been demonstrated in a controlled study that acute administration of L-dopa exerts an attenuating effect on bruxism: a reduction of 26.4% in the number of bruxism episodes per hour of sleep was found [96]. However, the use of L-dopa for the treatment of bruxism is not recommended because of its potential long-term side-effects, like insomnia and motor fluctuations. Further research is needed to assess the clinical implications of the long-term administration of L-dopa and other dopaminergic agents. In order to determine whether L-dopa exerts its central effect via 'D1-like' or 'D2-like' receptors [97], a neuro-imaging study focussing on striatal D2 receptor binding in bruxers is currently going on in our laboratory. In a preliminary analysis of four bruxers and four matched controls, we noted that bruxers had a lower D2 receptor binding [98]. If this observation can be confirmed in a larger subject sample, this might indicate that striatal D2 receptor down-regulation is involved in the pathophysiology of bruxism. In summary, none of the substances mentioned above are, at this point, recommended for the long-term treatment of bruxism. There are hardly any controlled studies to support their efficacy, and all may produce side effects. The scientific basis for the use of medicines in the management of orofacial pain and temporomandibular disorders, either as adjunctive to other strategies or as the primary treatment, is discussed in a recent review by Dionne [99]. Probably the best current treatment modality in the management of bruxism is the individually

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fabricated and adjusted orthopedic appliance, a removable device which fits between the maxillary and mandibular teeth. It is thought to reduce tooth damage and abnormal muscle activity, and to correct adverse oral habits [34,100-102]. There are several possible splint designs, varying from a hard acrylic occlusal stabilization splint to a soft polyvinyl bite guard. Guidelines on how to make such devices can be found in two extensive overviews [103,104]. The soft bite guard has been suggested as a simple technique for use in bruxers. However, it has been shown to increase rather than decrease bruxism-related muscle activity [101]. In addition, polyvinyl is not very durable. The hard occlusal stabilization splint (Fig. lA, B), on the other hand, is a more durable alternative. This device, which is usually made to fit on the maxillary arch, is individually adjusted to create stable and simultaneous occlusal contacts on all opposing teeth. It is constructed with only a minimal increase in vertical dimension (approximately 2 mm as measured between the first molars) and it occludes in centric relation, i.e., a position of comfortable mandibular closure [105]. Although the occlusal stabilization splint is probably the most effective type for decreasing bruxism-related muscle activity, it is not effective in 20% of patients [101]. In addition, a non-compliance of 21 % has been reported for splint therapy, owing to a reluctance to wear an orthopedic appliance at night [106]. Paradoxically, muscle activity is not always reduced by a splint [107]; it even increased in 20% of patients [108]. This latter effect may have resulted from stress induced by lack of adaptation to an oral appliance or from a positive sensory feedback response induced by an object between the teeth [109,110]. Nonetheless, although an occlusal stabilization splint may not actually prevent bruxism, it may help to reduce its symptoms. 9. Conclusion Bruxism is a common phenomenon. With a prevalence of 6-20% in the general population, it deserves full attention of clinicians who treat patients with musculoskeletal disorders. Both dental and polysomnographic criteria should be

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a

b

Fig. 1. (a) Example of an individually fabricated and adjusted orthopedic appliance: the hard occlusal stabilization splint (palatal view). The ball clasps are needed to obtain an optimal retention, whereas the extension of the acrylic resin into the palatal area warrants the rigidity and strength of the device. (b) The occlusal stabilization splint in the mouth.

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used for a multidisciplinary diagnosis of the disorder. Since the pathophysiology of bruxism is still unclear, there is no real cure for the disorder to date. Probably the best current treatment modality is the occlusal stabilization splint. However, there is very limited research to support the efficacy of any behavioral, dental, or pharmacological intervention.

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Acknowledgements

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This work was supported by the Canadian Medical Research Council (CMRC) and the Fonds de la Recherche en Sante du Quebec. F. Lobbezoo is a CMRC post-doctoral fellow.

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