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Principles for the management of bruxism*

Journal of Oral Rehabilitation 2008 35; 509–523 Review ArticlePrinciples for the management of bruxism* F . L O B B E Z O O * , J . VAN DER Z A A G * , M . K . A . VAN S E L M S * , H . L . H A M B U R G E R † &M . N A E I J E * *Department of Oral Function, Academic Centre for Dentistry Amsterdam (ACTA) and †Departments of Neurology andClinical Neurophysiology, and Amsterdam Center for Sleep-Wake Disorders, Slotervaart General Hospital, Amsterdam, The Netherlands SUMMARY The management of bruxism has been the treatment of bruxism, while in the preceding decade subject of a large number of studies. A PubMed (1987–1996), only approximately 5% of the studies search, using relevant MeSH terms, yielded a total of dealt with the pharmacological management of 177 papers that were published over the past bruxism. Unfortunately, a vast majority of the 135 40 years. Of these papers, 135 were used for the papers have a too low level of evidence. Only 13% of present review. Apparently, research into bruxism the studies used a randomized clinical trial design, management is sensitive to fashion. Interest in and even these trials do not yet provide clinicians studying the role of occlusal interventions and oral with strong, evidence-based recommendations for splints in the treatment of bruxism remained more the treatment of bruxism. Hence, there is a vast or less constant over the years: between 1966 and need for well-designed studies. Clinicians should be 2007, approximately 40–60% of the papers dealt aware of this striking paucity of evidence regarding with this subject. The percentage of papers that management of bruxism.
dealt with behavioural approaches, on the other hand, declined from >60% in the first 2 decades approaches, biofeedback, oral appliances, occlusion, (1966–1986) to only slightly >10% in the most recent medication, nutrition, study design, review decade (1997–2007). In the latter period, >40% of the papers studied the role of various medicines in the Accepted for publication 22 December 2007 are frequently mentioned in relation to bruxism.
Further, it has been shown that bruxism is part of a Bruxism is an oral movement disorder that is charac- sleep arousal response. In addition, bruxism appears to terized by grinding or clenching of the teeth. The be modulated centrally by various neurotransmitters.
disorder may occur during sleep as well as during Finally, pathophysiological factors like smoking, dis- wakefulness, and has an estimated prevalence in the eases, trauma, genetics and the intake of alcohol, general adult population of approximately 8–10% (1).
caffeine, illicit drugs and medications may be involved The aetiology of bruxism has a multifactorial nature.
in the aetiology of bruxism (1–3).
In the past, peripheral factors like occlusal discrepancies Bruxism should be diagnosed along multiple axes, and deviations in orofacial anatomy have been consid- viz. questionnaires, an oral history taking (including a ered the main causative factors for bruxism. Nowadays, bed partner's report of grinding sounds), an extra-oral such factors are known to play only a minor role, if any.
and intra-oral inspection for clinical signs of bruxism, Recent focus is more on central factors. Psychosocial and, in some cases, an electromyographic (EMG) factors like stress and certain personality characteristics recording of the activity of the masticatory muscles oreven a polysomnographic (PSG) recording of thesleeping patient. Any single one of these diagnostic *Based on a lecture given at the JOR Summer School 2007 sponsoredby Blackwell Munksgaard and Medotech.
tools should not be used in isolation, because patients ª 2008 The Authors. Journal compilation ª 2008 Blackwell Publishing Ltd may not be aware of the presence of bruxism, the The remaining 135 papers, which were published clinical signs of bruxism may reflect a problem in the between 1966 and 2007, show that research on bruxism past rather than one in the present, and EMG and PSG treatment is sensitive to fashion. Interest in studying the only give a random indication of a disorder that role of occlusal interventions and oral splints in the fluctuates over time (1, 3, 4).
treatment of bruxism remained more or less constant A host of dental problems have been ascribed to over the years: during the entire period, approximately bruxism, such as attrition (i.e. mechanical wear, 40–60% of the papers dealt with this subject. The resulting from parafunction, and limited to the con- percentage of papers that dealt with behavioural tacting surfaces of the teeth), hypertrophied mastica- approaches, on the other hand, declined from >60% in tory muscles, fractures ⁄ failures of restorations or dental the first 2 decades (1966–1986) to only slightly >10% in implants, headache and pain in the masticatory system the most recent decade (1997–2007). In the latter period, (temporomandibular disorder pain; TMD pain) (1, 5, 6).
>40% of the papers studied the role of various medicines Treatment of bruxism is indicated when the disorder in the treatment of bruxism, while in the preceding causes any one of these possible consequences. Unfor- decade (1987–1996), only approximately 5% of the tunately, there is a striking paucity of high-quality studies dealt with the pharmacological management of evidence regarding management of bruxism. Here, bruxism. These time trends are illustrated in Fig. 1.
a focused overview is given of the various occlusal, The type of material represented by the included papers was classified according to the PubMed Publi- approaches for bruxism. To demonstrate the complete- cation Types as an indication of the scientific strength ness of the review, the details of the literature search of the papers. Figure 2 shows the percentage distribu- strategy used are also provided.
A literature search was performed on 28 June 2007, using the National Library of Medicine's Medical Subject Headings (MeSH) Database and PubMed. MED- LINE was searched with the following query: ‘Brux- ism ⁄ therapy' or ‘Bruxism ⁄ drug therapy' or ‘Bruxism ⁄surgery' or ‘Bruxism ⁄ prevention and control' or ‘Brux- ism ⁄ rehabilitation', restricted to ‘Major Topic headings only' (MAJR) and using ‘English' and ‘Human' assearch limits. This strategy yielded 177 papers, 29 of them being reviews. Of the 29 review papers, nine were used for the present paper for the additional value of Fig. 1. Time trends in bruxism treatment. Percentage of papers, their reasoning. Five papers could not be traced by the published in the three specified periods, which deal with occlusal, institutional library, while a total of 17 papers were behavioural, or pharmacological interventions of bruxism.
omitted for various reasons. For example, six of thesepapers dealt with the repair of tooth surface loss caused by bruxism; not with the management of the disorderitself. The overview of the literature given here is therefore primarily based on 135 papers (177 papers, Case reports
minus 20 excluded reviews, minus five untraceable papers, minus 17 omitted papers). The overview is Letters to the Editor
supplemented with 15 papers that did not show up in the literature search, but that were nevertheless deemed important for the completeness of the over-view. These papers were traced using the reference lists Fig. 2. Percentage distribution of the publication types within the of already included papers.
set of included papers.
ª 2008 The Authors. Journal compilation ª 2008 Blackwell Publishing Ltd tion of the publication types within the set of 135 maximal voluntary clenching cannot be interpreted in included papers. Clearly, a vast majority of the 135 terms of bruxism.
papers have a low level of evidence. Only 13% of the A number of letters to the editor and case reports studies used a randomized clinical trial design, and even have been published with the objective of presenting most of these were more designed as experimental trials convincing descriptions of the efficacy of occlusal than as true clinical trials. In addition, it is not always interventions in the management of bruxism, by means clear whether bruxism during wakefulness, sleep of either occlusal equilibration (10) or occlusal reha- bruxism, or both were studied. Further, the use of bilitation with composite resin materials (11). In 1973, indirect or equivocally defined outcome measures for the however, Stephens (12) expressed his awareness of the quantification of bruxism is commonly encountered in lack of science in this domain full of controversies and the set of included papers. Publication type, bruxism suggested that occlusal adjustment is indicated only as type(s) and outcome measures are therefore part of this part of a periodontal treatment plan when trauma from review as to indicate quality of the evidence.
occlusion is present – a suggestion that was generallyfollowed by periodontists, especially in combinationwith the use of occlusal splints (13). More recently, in Occlusal approaches several letters to the editor, serious concerns and doubts Two categories of occlusal management strategies for have been expressed regarding occlusal interventions in bruxism can be distinguished: ‘true' occlusal interven- adult bruxers (14, 15) as well as in young bruxers with tions and occlusal appliances.
a mixed dentition (16). Of all authors, Greene et al. (17)are the most explicit by stating that occlusal adjustment‘… further mutilate[s] the dentition beyond what the ‘True' occlusal interventions bruxism itself has performed. This is a classical example This category, that includes approaches like occlusal of misuse of an irreversible procedure with no evidence equilibration, occlusal rehabilitation and orthodontic of its therapeutic value'.
treatment that is aimed at ‘achieving harmonious As opposed to the afore-mentioned ‘low-quality relationships between occluding surfaces', still gives evidence' prescriptions, comparative studies, letters rise to a great deal of controversies among dental and case reports, only one study did use a randomized clinicians and researchers. Protagonists usually claim clinical trial (RCT) design (18). In that study, the success of such approaches on the basis of their own effectiveness of an orthodontic technique (viz. buccal clinical experience. In the literature, however, no high- separators) in relieving bruxism activity was evaluated, quality evidence that supports the use of these irre- and no differences between the active treatment and versible techniques can be found: most of the papers on control conditions were observed. In a letter to the that subject are prescriptions (i.e. sets of statements, editor regarding this publication, the developer of the directories, or principles that describe an individual's buccal separator technique failed to provide new, approach to a clinical problem), comparative (single- convincing evidence in favour of his technique (19).
cohort) studies, letters to the editor and case reports. As In short, there is no support in the literature for the an example of a prescription, Butler (7) described an use of ‘true' occlusal interventions like equilibration, occlusal adjustment procedure for the treatment of rehabilitation and orthodontic alignment in the man- bruxism, amongst others, however, without a proper agement of bruxism. In view of the current insights into theoretical basis. Similarly, Frumker (8) formulated a the aetiology of bruxism, viz. that the disorder is mainly set of principles for a successful occlusal treatment, on regulated centrally – not peripherally (2, 20), future the basis of an unfounded idea that the better the research on this category of management strategies for occlusal anatomy and function, the easier the bruxers bruxism seems redundant.
‘relieve tension in the masticatory and associatedmusculature'. In an experimental comparative study, Occlusal appliances Holmgren and Sheikholeslam (9) tried to substantiatethe effects of occlusal adjustment on the myo-electrical The second category of occlusal management strategies activity of the jaw-closing muscles. However, their for bruxism contains the frequently used occlusal brief, daytime EMG recordings of postural activity and appliances. According to an article by John Sedgwick ª 2008 The Authors. Journal compilation ª 2008 Blackwell Publishing Ltd in Newsweek of 4 December 1995, approximately masseter muscle activity during sleep was found for 3Æ6 million ‘mouth guards' are being manufactured in the NTI splint as compared with a ‘regular' hard the USA on an annual basis. This represents a total cost occlusal splint, no evidence for the NTI splint's long- of at least $1 billion per year, indicating that insight term efficacy or safety is available so far. Finally, the into the efficacy of such appliances is important not fourth prescription describes the scientifically unsup- only from a dental point of view, but also from an ported concept of the pre-fabricated and chair-side economic one.
adjustable ‘Bruxism ‘S' Splint' that can be used in As for occlusal equilibration and orthodontic treat- combination with active orthodontic treatment (41).
ment, a vast majority of the scientific papers that deal More research is needed to assess the efficacy and with the role of occlusal splints in the treatment of safety of such unconventional, chair-side solutions bruxism are prescriptions, case reports, comparative before their application in dental practice can be studies and case–control studies. Most prescriptions describe clinical and technical procedures for the The case reports that deal with occlusal splints in the manufacture of various types of splints. These splints management of bruxism usually describe success in have different names [e.g. occlusal bite guard (modi- extreme and ⁄ or special-category patients. Bodenham fied), bruxism appliance, bite plate, night guard (42) successfully treated an athlete for sports-related (daytime) clenching by means of a ‘bite guard' (hard appearances and properties, but in essence most of acrylic-resin splint) in the lower jaw, while Jones (43) them are hard acrylic-resin stabilization appliances, successfully treated a 5-year-old girl with sleep bruxism mostly worn in the upper jaw (21–31). When a hard and related headache by means of a hard maxillary occlusal splint is intolerable for the patient, Taddey (32) splint – a treatment that must obviously have an suggests the use of a thin plastic shell like the one used as-short-as-possible duration, as to prevent gross dis- to apply home bleaching solutions. He claims that this ruption of the orofacial growth and development. Two solution works through a mechanism related to bio- case reports describe the application of bimaxillary soft feedback (see below); however, no evidence for the splints for heavy bruxers (44, 45). This solution efficacy of plastic shells in the treatment of bruxism is reportedly has the advantage of grinding sound reduc- provided. Three more prescriptions describe the man- tion. Its durability, however, can be questioned. An ufacture of soft-resin bruxism appliances (33–35).
interesting case is described by Cassisi et al. (46). Using a Although the concept of soft splints is appealing, hard longitudinal design, these authors showed that the splints are generally preferred over soft splints for number of EMG bruxism events per hour of sleep practical reasons (e.g. soft splints are more difficult to reduced in their 35-year-old female bruxer when a adjust than hard ones), to prevent inadvertent tooth hard occlusal splint or a palatal (non-occlusal) splint movements, and because hard splints are suggested to was worn as compared with a no-splint condition. On be more effective in reducing bruxism activity than soft the basis of their case study, the authors suggest that splints (36).
more research is needed using groups of bruxism Four prescriptions describe splints that do not patients and a proper study design.
require a contribution of a dental laboratory. The first Several studies assessed the efficacy of occlusal splints one describes an ‘in-office' procedure for the manu- in groups of bruxism patients, using a comparative, facture of a regular hard acrylic-resin bruxism device single-cohort ‘pre-treatment – post-treatment' design that reduces the delay in starting a bruxism treatment, and ⁄ or a case–control design. Although these are not because no dental laboratory is involved (37). A similar the strongest designs to assess the efficacy of treatment prescription describes the chair-side manufacture of a modalities (for that purpose, RCT with long-term composite splint (38). The third prescription describes evaluations are required), such studies are frequently the chair-side adjustment of the so-called ‘Nociceptive performed and the conclusions of these studies are Trigeminal Inhibition (NTI) Clenching Suppression stronger – and thus more valuable – than those of case System' – a small anterior splint that is supposed to reports. In an early study by Clark et al. (47), it was be effective, amongst others, in the management of shown that occlusal splint treatment resulted in a bruxism (39). Although in a randomized crossover decrease in nocturnal EMG activities in about half of trial by Baad-Hansen et al. (40) an inhibition in the patients, while in about a quarter of the patients, no ª 2008 The Authors. Journal compilation ª 2008 Blackwell Publishing Ltd change or – in the remaining quarter – even an increase of their 86 study participants. Again, the use of in EMG activity was observed. Using nocturnal EMG indirect bruxism measures renders this study difficult recordings as well, Hiyama et al. (48) found a significant to interpret unequivocally. In contrast to the findings reduction in bruxism activity while wearing an occlusal of the above-described comparative and case–control splint in all of their six study participants. An interesting studies, Sheikholeslam et al. (54) and Yap (55) found single-cohort study was performed by Okeson (36). He no effects of the occlusal splint on active nocturnal compared, in a group of ten bruxers, the efficacy of bruxism. However, these studies used awareness of hard versus soft occlusal splints. Both types of splints bruxism behaviour (54) and wear facets on the were worn by each of the ten participants, using a fixed occlusal splint (55), in combination with indirect order. It was shown that while the hard splint reduced clinical measures as outcome variables, which also nocturnal EMG activity in eight of 10 bruxers, the soft renders these studies inconclusive.
splint yielded an increase in bruxism activity in half of Several studies used the ‘higher quality' clinical trial the bruxers and a decrease in only one of the remaining design, although randomization to assign patients to five participants. This suggests that hard splints are test or control treatments ⁄ conditions (i.e. the ‘true' more effective in reducing bruxism activity than soft RCT design) was employed in a few studies only. Shiau splints. Nevertheless, the use of soft splints is still (56) observed that splint therapy did not change the common, at least in general dental practices in Sweden, length of the so-called silent period (an EMG charac- despite the lack of scientific support for their efficacy teristic that was believed to be related to bruxism, thus and effectiveness (49).
representing an indirect measure for that condition), A couple of studies used indirect measures for nor were there any differences in length of the silent bruxism, which render these studies difficult to inter- period between treated and untreated bruxers. Nagels pret in terms of occlusal splints being effective in the et al. (57) were mainly interested in the possible effects management of bruxism. Mejias and Mehta (50) of an occlusal splint on sleep quality in bruxers assessed the individual responses of bruxers to splint compared with normal volunteers, which turned out therapy. They found that their five participants all to be absent. Unfortunately, no indication is given reacted favourably to the treatment, as assessed by the regarding the effects of the splint on the bruxism wear of a special bruxism monitoring device [‘Brux- behaviour itself. This study thereby falls outside the core'; see Koyano (4)] that consists of differently main scope of this overview. Using a cross-over design coloured plastic layers – an assessment technique that and nocturnal EMG activity as an outcome measure, is easy to use but may lead to difficult-to-interpret Rugh et al. (58) did not observe any differences in outcomes because of the questionable paradigm that efficacy in the treatment of sleep bruxers between two bruxism and wear are fully related, and because of the different types of hard occlusal splints, viz. one with fact that the device itself may interfere with the canine guidance and another one with first molar bruxism behaviour. Using EMG recordings, Hamada guidance: in their eight participants, both splint types et al. (51) observed significant reductions in the yielded variable outcomes that more or less resembled masticatory muscle activity of bruxers. The post- those described by Clark et al. (47) (see above). Hach- treatment values were similar to those of healthy mann et al. (59) demonstrated in a small-scale study control subjects. In this study, however, the EMG that occlusal splints are effective in the treatment of measures were taken from voluntary daytime record- bruxism in 3- to 5-year-old children: untreated brux- ings, where direct EMG assessments of the actual ing children displayed increased wear facets, which bruxism behaviour are to be preferred. Also Moses were not observed in the treated group. Their conclu- (52) used daytime EMG measures to assess the sion that splints are thus efficient against bruxism is, restraining effect of his so-called Passivator appliance however, premature because the bruxism behaviour on bruxism. Consequently, this study is difficult to itself was not assessed, but only one of its possible interpret as well. Using indirect clinical measures of bruxism only (e.g. dental and musculoskeletal pain Two recent studies did use a ‘true' RCT design. Using complaints), Yustin et al. (53) found mandibular polysomnographic recordings, Dube´ et al. (60) and Van occlusal devices to be effective in the treatment of der Zaag et al. (61) compared the efficacy of a hard bruxism and of its associated pain complaints in most occlusal splint versus a palatal control device [i.e. a ª 2008 The Authors. Journal compilation ª 2008 Blackwell Publishing Ltd ‘placebo splint', which is actually inactive in bruxers as (68, 69). Future research should focus on developing long as it is kept thin (62)] in the treatment of sleep criteria for the clinical decision to use (or not to use) an bruxism. While Dube´ et al. (60) concluded that at two occlusal splint in an individual bruxism patient.
weeks, both devices reduce muscle activity associatedwith bruxism, Van der Zaag et al. (61) did not observe Behavioural approaches significant effects for either of the devices after fourweeks of usage. The combination of the results of both A wide variety of behavioural approaches have been studies corroborates the suggestion by Harada et al. (63) tried in the management of bruxism. Here, the most that oral appliances have only a transient effect on widely studied one of these approaches, viz. biofeed- (EMG-determined) sleep bruxism as measured over a back, will be reviewed first. In a subsequent section, the 6-week period. On the longer term, Ommerborn et al.
remaining behavioural techniques will be dealt with.
(64) observed a reduction in bruxism activity after12 weeks of occlusal splint therapy that continued into a 6-months follow-up. However, although these latterauthors used a strong (RCT) study design, they did not Biofeedback uses the paradigm that bruxers can quantify bruxism activity with EMG or polysomnogra- ‘unlearn' their behaviour when a stimulus makes them phy. Rather, they used the ‘Bruxcore' bruxism moni- aware of their adverse jaw muscle activities (‘aversive toring device, which has several disadvantages (see conditioning'). This technique has been applied for above). This makes their results difficult to interpret bruxism during wakefulness as well as for sleep brux- unequivocally. Interestingly, Van der Zaag et al. (61) ism. While awake, patients can be trained to control observed large differences between individual sleep their jaw muscle activities through auditory or visual bruxism patients. Some of them indeed showed a feedback from a surface EMG. For sleep bruxism, decrease in bruxism activity, while others showed no auditory, electrical, vibratory and even taste stimuli change or even an increase, which again is in line with can be used for feedback.
the findings of Clark et al. (47). The reasons for thesedifferences are as yet unclear.
Bruxism during wakefulness One of the early publica- Landry et al. (65) performed a short-term RCT to the tions on the use of biofeedback in the management of efficacy of mandibular advancement devices (MAD; bruxism during wakefulness is a prescription by a bimaxillary appliance that is indicated for the man- Mittelman (70). He described an EMG technique that agement of snoring and sleep apnea) when compared provides the daytime clencher with auditory feedback with that of ‘regular' maxillary occlusal splints. They from his ⁄ her muscle activity, ‘telling the degree of observed only a moderate reduction in polysomno- muscle activity or relaxation that is taking place.' The graphically established sleep bruxism with the occlusal subtitle of Mittelman's paper (‘It can be administered splint in situ, but a large decrease in bruxism activity easily and inexpensively in any dental office') sug- when the MAD was worn – regardless of the amount of gests that the technique is ready for broad applica- protrusion of the appliance. The authors could not tion. A similar suggestion is given in the review readily explain this result, but they hypothesized, articles by Cannistraci (71) and Rubeling (72). Shul- amongst others, that the fact that approximately two- man (73) used a flat occlusal splint for biofeedback.
thirds of their study sample reported localized pain with The splint was inserted in the explicit understanding the MAD in situ may be responsible for the observed that the appliance serves to remind the daytime decrease. After all, it has been reported that in the bruxer of adverse tooth contacts (i.e. contacts other presence of pain, bruxism activity may reduce consid- than those involved in chewing and swallowing). In erably (6, 66, 67).
the author's hands, an immediate success of approx- Given the contradictory results of the above-de- imately 50% was obtained. Kramer (74) applied a scribed studies and the scarcity of RCT on the efficacy of special kind of biofeedback to manage the daytime occlusal splints in the management of bruxism, it is bruxism problem of an 8-year-old boy with learning prudent to limit the use of oral splints in the manage- difficulties: whenever a bruxism event started, the ment of bruxism to the prevention or limitation of boy's teacher pressed her finger firmly against the dental damage that is possibly caused by the disorder boy's jaw for a few seconds. The intervention was ª 2008 The Authors. Journal compilation ª 2008 Blackwell Publishing Ltd successful in approximately 2 weeks and during the mustard, ginger, garlic, etc.) and embedded in a simple dental appliance. On the basis of a single case, the remained at a low level. The author suggested that author claimed long-term success. In most of the case this approach should be implemented with special reports, a sound blast was applied as the aversive populations in educational settings. This approach stimulus (82–87), although in one case study, this resembles the one used by Blount et al. (75), who technique failed to be effective (88). The sound successfully treated two profoundly retarded adult stimulus is supposed to actually wake up the patient, bruxers for their condition with ‘contingent icing', i.e.
who is then supposed to switch off the sound and brief applications of ice to the facial area whenever resume his ⁄ her sleep. The awakenings are a major bruxism occurred. Likewise, Rudrud and Halaszyn disadvantage of such approaches, because sleep dis- (76) used contingent massage to combat daytime ruption may lead to serious side effects like excessive bruxism. Unfortunately, strong scientific evidence for daytime sleepiness (89). Even more subtle techniques, the efficacy of any of these afore-described diurnal like the bruxism-contingent vibratory feedback system biofeedback approaches is lacking.
of Watanabe et al. (90) and the jaw-opening reflex In a comparative study by Manns et al. (77), the feedback system that was recently developed by Jadidi apparently successful application of auditory feedback et al. (91) that do not induce substantial sleep distur- from surface EMG activity was shown in 33 daytime bance, according to the authors, might still cause bruxers with myofascial pain. The study design, how- significant changes in sleep architecture that yield ever, precludes strong conclusions to be drawn from long-term adverse reactions like daytime sleepiness this study. Using a RCT design, Treacy (78) showed (89). This concern should be taken into consideration significant jaw-closing muscle activity decreases after a when evaluating new biofeedback devices for the 4-month treatment period with a muscle activity management of sleep bruxism.
awareness training program compared with an active An alternative approach was followed by Small (92), control treatment and a sham treatment. Although this who used daytime biofeedback sessions in combination finding supports the efficacy of this type of biofeedback with an occlusal splint for night-time use to combat the in the management of diurnal bruxism, no long-term sleep bruxism problem of a 36-year-old woman. A sim- results are given. This urges dentists to remain reserved ilar approach was followed by Cornellier et al. (93) in when applying this technique, especially because four adult bruxers. Just like the taste and sound blast another RCT failed to show significant decreases in methods, this approach also yielded positive (long- masticatory muscle EMG levels as a result of either a term) outcomes, with no sleep disruption as possible biofeedback training program or a control treatment side effect. Despite this advantage, Small (92) indicated (79). Hence, more research is needed to assess the that his case report is at best suggestive and proposed efficacy of biofeedback in the management of bruxism better, controlled studies to test the efficacy of his during wakefulness.
approach. Obviously, this holds true for all case reportsindicated and summarized here.
Sleep bruxism For the use of biofeedback in the Over the years, several comparative studies have management of sleep bruxism, Cherasia and Parks been published in which the efficacy of biofeedback on (80) published a prescription. Their technique used sleep bruxism was evaluated. Audible tones derived contingent arousal from sleep with actual awakenings.
from EMG recordings caused a significant reduction in Although the authors are aware of the lack of sleep bruxism activities in all of nine bruxers compared validation of their technique, they stated that its with control nights during which the biofeedback potential effectiveness, ease of use and lack of risk device was worn with an inactive bruxism warning warrant its consideration. So far, nine case reports, system (94). Similar findings, with longer evaluation representing a total of 13 patients, were published in periods of up to three months, were reported by Clark which some type of biofeedback was used to control et al. (95) and Hudzinski and Walters (96). Pierce and sleep bruxism. Nissani (81) used a taste stimulus to Gale (97) also found positive effects of nocturnal awaken the patient. This stimulus was caused by the biofeedback (viz. a contingent, aversive tone), but bruxism-related rupture of capsules, filled with an reported these effects to be transient during a 6-month aversive substance (agreed upon with the patient, e.g.
follow-up period. Nishigawa et al. (98) used contingent ª 2008 The Authors. Journal compilation ª 2008 Blackwell Publishing Ltd electrical lip stimulation to combat sleep bruxism, review, this author used three cases to illustrate the which turned out to be a promising technique for usefulness of this technique in the management of temporarily suppressing the disorder. However, the bruxism, as do several other authors (104, 105). Where long-term effects remain to be determined, and the these cases lack sufficient strength in terms of scientific above-described concern regarding the risk of sleep evidence, Clarke and Reynolds (106) wrote an abstract disruption and subsequent daytime sleepiness should in which they concluded on the basis of a stronger be assessed for this technique as well. Clearly, the study design (viz. a case–control study) and by using comparative study design of the papers that are sum- nocturnal EMG recordings that hypnotherapy provided marized in this paragraph precludes strong scientific profound relief from problems related to nocturnal conclusions to be drawn. To that end, better controlled bruxism. These results were later published as a full- studies are needed. In the only controlled clinical trial length paper, but now as a single-cohort study and with on the efficacy of nocturnal biofeedback, whenever a the addition of long-term effects as assessed with self- bruxism event exceeded a preset electromyographic report (107). The conclusion remained the same and threshold, an audible tone indeed yielded a better even appeared to be applicable to the follow-up period treatment outcome than a no-treatment control condi- of 4–36 months. The authors, however, were fully tion (99). Unfortunately, only short-term (2-months) aware of the limitations of their study and suggested results are given, but not the longer-term results, which some improvements to increase the strength of the are needed for a proper assessment of the efficacy and safety of any treatment modality.
Various relaxation techniques have been described in In short, despite the considerable amount of atten- relation to the management of bruxism. Relaxation, tion that researchers devoted to biofeedback [see also including meditation, is supposed to produce a sense of the review by Cassisi et al.(100)], there are serious self-esteem and control over one's body (102). Pear doubts whether this is actually an effective treatment (102) as well as other authors [e.g. Cannistraci and for bruxism, especially in the long-term. Further, the Friedrich (108)] described relaxation and meditation as possible consequences of the frequent arousals, like part of a holistic approach, which means that awareness excessive daytime sleepiness, need further attention and ‘wellness' of the whole body is being promoted.
before this technique can be applied for the safe However, no information whatsoever can be found in treatment of patients with bruxism.
the literature regarding the efficacy of this approach inthe treatment of bruxism. Only a comparative study byRestrepo et al. (109) provided slightly stronger evidence Other behavioural approaches for the positive effect of relaxation in 3- to 6-year-old Other behavioural approaches that have been described children who suffer from bruxism. A drawback of that in the literature for the management of bruxism study, however, is the use of indirect measures for include psychoanalysis, autosuggestion, hypnosis, pro- bruxism, which hampers an unequivocal interpretation gressive relaxation, meditation, self-monitoring, sleep of the outcome.
hygiene, habit reversal ⁄ habit retraining and massed Specifically for diurnal bruxism, self-monitoring – or practice. In the oldest review article that was found ‘habit awareness' – has been suggested as an appropri- with the present literature search strategy, Olkinuora ate therapy. According to Rosen (110), bruxers gain (101) described various psychiatric treatment tech- control of daytime clenching using a self-monitoring niques for bruxism, such as psychoanalysis and auto- procedure, which simply means that every time the patient notes the occurrence of clenching activity, this technique helps the bruxer become aware of the habit, event is jotted down in a diary or entered in some kind even while asleep, by giving him ⁄ her the autosugges- of counting device. This approach would finally lead to tion ‘I'll wake up if I gnash my teeth' before falling asleep.
a decrease in diurnal bruxism activity. Unfortunately, Unfortunately, this intriguing approach, which has Rosen's paper is a case report and lacks scientific been reviewed briefly by others as well (102), lacks For nocturnal bruxism, a specific approach has been Another approach, hypnosis, was reviewed more suggested, namely sleep hygiene measures (111). The than three decades ago by Goldberg (103). On top of his objective of measures like ‘avoid stimulants (e.g.
ª 2008 The Authors. Journal compilation ª 2008 Blackwell Publishing Ltd caffeine, nicotine) for several hours before bedtime' and sound scientific basis: most studies so far are case ‘maintain a regular sleep schedule' is to promote better reports, prescriptions and comparative studies. More sleep. Amongst others, better sleep means that more well-designed research is thus needed on the use of time is being spent in the deeper sleep stages and that these approaches in the management of bruxism.
less arousals from sleep occur. As bruxism mainlyoccurs in the lighter sleep stages and in relation to arousals (1), bruxism will probably decrease. However,as yet, no well-designed studies on this behavioural The use of medication in the management of bruxism treatment modality have been published.
has been studied increasingly over the past decades.
Behavioural techniques like habit reversal ⁄ habit Most studies so far are case reports, but for several retraining, and massed practice have all in common medicines RCT have been performed. An extensive that the adverse behaviour, i.e. bruxism, is actively review on the relationship between drugs and bruxism being combated. During habit reversal, a competing was published by Winocur et al. (121).
activity opposite to the bruxism behaviour, but involv- One of the oldest reports on a pharmacological ing the same muscles, is being taught to the bruxers approach for bruxism is the one published by Chasins (e.g. opening the mouth). Two papers, describing a total (122). He concluded that the short-term administration of five cases, claimed success for this technique, of the muscle relaxant methocarbamol yielded ‘good although good-quality evidence is lacking (112, 113).
control and improvement of the bruxism habit' of Zeldow (114) published a prescription of a similar approximately 40 bruxers compared with an equally technique, which he calls ‘habit retraining': the sized group of untreated bruxers. Besides the fact that replacement of a bad habit with a good one. As the the study design does not meet the current standard of good habit was maintaining a free-way space, it is an RCT, bruxism was assessed solely on the basis of the obvious that ‘habit retraining' is actually a variation of patients' reports. This makes the study difficult to ‘habit reversal'.
interpret. In a more recent, well-designed RCT, it was Especially during the late sixties and early seventies shown that sleep bruxism did improve with the of the past century, massed practice therapy for frequently prescribed, non-specific muscle relaxant bruxism was studied relatively widely. This behavio- clonazepam (a benzodiazepine), although the mainte- ural technique contains exaggerating the bruxism- nance of its therapeutic efficacy, its long-term tolera- related muscle activities, thereby making the habit bility and its risk of addiction need further attention punitive rather than rewarding. The first paper about this technique was a case report by Ayer and Gale Another drug that affects muscle function, by exert- (115). These authors suggested that (self-reported) ing a paralytic effect through an inhibition of acetyl- bruxism may be eliminated by massed practice ther- choline release at the neuromuscular junction, is apy. Comparative studies by the same authors came to botulinum toxin. So far, its application in the manage- the same conclusion (116, 117). They even put ment of bruxism is mainly described in case reports.
forward a theoretical model to explain the purported Without exception, these reports claimed success of efficacy of massed practice (118). Also, Vasta and botulinum toxin in decreasing (clinically assessed) Wortman (119) described the successful application of bruxism activity, especially in severe cases with massed practice therapy in the treatment of a single co-morbidities like coma (124), brain injury (125, bruxer, in whom bruxism activity was assessed objec- 126), amphetamine abuse (127), Huntington's disease tively by means of an automated time-sampling (128) and autism (129). Tan and Jankovic (130) procedure. Heller and Forgione (120), on the other reported the results of botulinum toxin injections in hand, did not observe any significant reductions in 18 bruxers. In only one of their patients, (transient) bruxism behaviour in their comparative study that dysphagia occurred as an adverse reaction. They con- used the wear of the ‘Bruxcore' bruxism monitoring cluded that this drug can be administered as a safe and device to assess bruxism activity (see above: Occlusal effective treatment for severe bruxers. They also stated, however, that this treatment modality should be In short, the value of the above-described behavio- confined to patients who are refractory to other ural approaches is questionable, because they all lack a (conventional) treatments, and that placebo-controlled ª 2008 The Authors. Journal compilation ª 2008 Blackwell Publishing Ltd studies are needed before evidence-based recommen- treatment of sleep bruxism, two RCT have been dations can be given.
performed. Unfortunately, low doses (25 mg per night) Several studies have been performed to assess the of amitriptyline turned out to be ineffective in the effects of serotonergic and dopaminergic medicines in management of sleep bruxism (142, 143), although the treatment of sleep bruxism. In a placebo-controlled some individual study participants clearly responded to RCT, bruxism-related nocturnal EMG activity was not the medication (144).
influenced by the serotonin precursor L-tryptophan For two sympatholytic medicines, experimental RCT (131). In contrast to that negative finding, a placebo- have been performed. Huynh et al. (145) found no controlled sleep laboratory RCT showed that the effects of the non-selective adrenergic beta-blocker catecholamine precursor L-dopa exerted a modest, propranolol on sleep bruxism, despite the positive attenuating effect on sleep bruxism (132). Likewise, response to this drug in two cases of antipsychotic- sleep bruxism activity was reduced by the administra- induced bruxism (146). The selective alpha-2 agonist tion of low doses of the dopamine D1 ⁄ D2 receptor clonidine, on the other hand, does seem a promising agonist pergolide in a severe bruxism case (133). The medicine for the management of sleep bruxism, dopamine D2 receptor agonist bromocriptine, on the although further safety assessments are still required other hand, did not cause an exacerbation or reduction because severe morning hypotension was noted in in sleep bruxism motor activity (134), although a report approximately 20% of the participants (145). Taking of two single-patient clinical trials yielded promising the above-described evidence together, it can be con- results for that drug (135). The effects of serotonin- cluded that although some pharmacological approaches related and dopamine-related drugs on bruxism there- for bruxism seem promising, they all need further fore remain unclear.
efficacy and safety assessments before clinical recom- For the use of anticonvulsant drugs in the treatment mendations can be made.
of bruxism, only case reports are available. Gabapentinwas successfully applied for the treatment of a 50-year- Miscellaneous approaches old man who suffered from bruxism, induced byvenlafaxine (an antidepressant; see below) (136).
Six papers describe management strategies for bruxism Likewise, self-reported bruxism was successfully man- that do not readily fit either one of the above-used aged with tiagabine in four of five cases described by categories of occlusal, behavioural, or pharmacological Kast (137). Unfortunately, no RCT are available to approaches. Five of them are related to physical assess the efficacy and safety of anticonvulsant drugs in therapy, while one is related to a surgical procedure the management of bruxism.
in the oral region. Ackerman (147) described his Antidepressant drugs may exert deviating effects on approach of instructing the patient with bruxism to bruxism: either they exacerbate the condition (selective develop his ⁄ her jaw-opening muscles. The objective is serotonin reuptake inhibitors, SSRI) or they are inert in ‘to develop the depressor muscles so that they will be as their effects (amitriptyline). While Stein et al. (138) strong or as firm as the elevator muscles. Then, they reported a decrease in nocturnal bruxism in two bruxers as a possible consequence of the use of the expressed the hope that by adopting this philosophy, SSRI paroxetine and citalopram, most papers reported future efforts to eliminate bruxism would be more bruxism to be induced by SSRI [reviewed in detail by successful. Also Quinn (148, 149) suggested the use of Lobbezoo et al. (139)]. Bostwick and Jaffee (140) physical rehabilitation techniques (viz. isokinetic exer- described four cases of sertraline-induced bruxism, cises) for depressor muscle strengthening. According to which were successfully treated with the serotonin 1A this author, such exercises will assist in, amongst receptor agonist buspirone. Two similar cases were others, correcting bruxism. Knutson (150) claimed a successfully managed with dosage manipulation by rapid and complete recovery of chronic sleep bruxism Ranjan et al. (141). These authors argued that such is a after upper cervical vectored manipulation of a 6-year- better approach than using buspirone as an antidote.
old child. Unfortunately, the level of evidence of the Obviously, only better-designed studies can provide us above-summarized prescriptions and case reports, all of with strong scientific evidence. For the efficacy assess- which used some sort of physical therapy to combat ment of the tricyclic antidepressant amitriptyline in the bruxism, is low. Even the positive results of a controlled ª 2008 The Authors. Journal compilation ª 2008 Blackwell Publishing Ltd trial, in which the buccinators muscles were trained by ing the lowest NNT and the largest ES. However, given means of a special device, viz. the Pro-Fono Facial the adverse reactions of these treatments (see above), Exerciser, are inconclusive because of the ambiguous the occlusal splint (60, 61) and clonazepam (123) quantification of the bruxism activities (151).
seemed to be acceptable (short-term) alternatives.
DiFrancesco et al. (152) reported the results of a However, Huynh et al. (153) stressed that further comparative study on a group of children with longitudinal, large-sample size RCT are needed before sleep-disordered breathing and bruxism, of whom a evidence-based recommendations can be given.
significant proportion ceased to report bruxism after In the absence of definitive evidence, bruxism can adenotonsillectomy. Apart from the fact that the scien- best be managed following the so-called ‘triple-P' tific strength of this paper is relatively low, the authors approach: Plates, Pep talk and Pills. ‘Plates' are occlusal failed to provide the readers with a plausible (i.e. non- appliances, most commonly of the hard acrylic resin occlusal) explanation for their finding, which might occlusal stabilization splint type. These appliances very well be coincidental.
probably function more like protectors of the remain-ing teeth rather than that they actually diminish thebruxism behaviour. ‘Pep talk' stands for counselling, a Conclusions and recommendations behavioural approach that includes addressing the From the above, it can be gathered that a vast patient's awareness of the movement disorder, relax- majority of the 135 papers that constitute the basis ation and lifestyle and sleep hygiene instructions.
of this review are more or less inconclusive: only 13% Albeit of unproven efficacy, these approaches can be of them used an appropriate RCT study design.
applied safely in bruxism patients. ‘Pills' represents Comparative studies, case report and prescriptions pharmacological interventions with centrally acting are the most commonly used study designs in this drugs such as benzodiazepines. As long as definitive literature search. Clinicians should be aware of this evidence is missing, the use of medicines in the striking paucity of evidence regarding the manage- treatment of bruxism should be confined to short ment of bruxism. They should also know that now- periods and to severe cases in which occlusal appli- adays, new management strategies for bruxism are ances and counselling were ineffective. Such should being proposed by commercial companies in the be performed in close collaboration with medical absence of any scientific proof for their efficacy and safety. Hence, there is a vast need for well-designed The triple-P approach reflects the current insight into studies on the management of bruxism.
the aetiology of bruxism, that is considered to be mainly Huynh et al. (153) used most of the above-described, regulated centrally; not peripherally (2). The approach well-designed RCTs to assess the number needed to also stresses that whenever bruxism treatment is treat (NNT, the number of patients who must be treated indicated, the disorder should be assessed by a multi- before the outcome can be expected to occur; the lower disciplinary team that includes dentists, psychologists the NNT, the more beneficial the treatment) and the and medical specialists. This important notion should effect size (ES, the magnitude of the effect of a not only be recognized by the dental discipline itself, treatment relative to a placebo condition; the higher but also by the other disciplines that are involved in this the ES, the more beneficial the treatment) for the team concept [e.g. psychology (154)].
various management strategies for sleep bruxism. Theyincluded three oral appliance studies and seven phar- macological studies in their analyses; all of them areincluded in the present review [Oral appliances: Dube´ 1. Lavigne GJ, Manzini C, Kato T. Sleep bruxism. In: Kryger M, et al. (60); Van der Zaag et al. (61); Landry et al. (65).
Roth T, Dement WC, eds. Principles and Practice of Sleep Medicine. Philadelphia, PA: Elsevier Saunders, 2005:946–959.
Pharmacological treatments: Etzel et al. (131); Lobbe- 2. Lobbezoo F, van der Zaag J, Naeije M. Bruxism: its multiple zoo et al. (132); Mohamed et al. (142); Lavigne et al.
causes and its effects on dental implants. An updated review.
(134); Raigrodski et al. (143); Saletu et al. (123); Huynh J Oral Rehabil. 2006;33:293–300.
et al. (145)]. Of these treatments, the mandibular 3. Lavigne GJ, Khoury S, Abe S, Yamaguchi T, Raphael K.
advancement device (65) and clonidine (145) seemed Bruxism physiopathology: what do we learn from sleep to be the most promising treatment approaches, yield- studies? J Oral Rehabil. 2008;35:476–494.
ª 2008 The Authors. Journal compilation ª 2008 Blackwell Publishing Ltd 4. Koyano K. Assessment of bruxism in the clinic. J Oral 30. Nassif NJ, al-Ghamdi KS. Managing bruxism and temporo- mandibular disorders using a centric relation occlusal device.
5. Johansson A, Johansson A-K, Omar R, Carlsson GE. Reha- Compend Contin Educ Dent. 1999;20:1071–1074, 1076, bilitation of the worn dentition. J Oral Rehabil. 2008;35:548– 31. Cowie RR. The clinical use of night guards: occlusal objec- 6. Svensson P, Jadidi F, Arima T, Baad-Hansen L Relationships tives. Dent Today. 2004;23:112, 114–115.
between craniofacial pain and bruxism. J Oral Rehabil.
32. Taddey JJ. Problems and solutions. TMD patients who are gaggers. Cranio. 1995;13:68.
7. Butler JH. Occlusal adjustment. Dent Dig. 1970;76:422–426.
33. Anthony TH. Soft thermoplastics in bruxism appliances.
8. Frumker SC. Occlusion and muscle tension. Basal Facts.
Trends Tech Contemp Dent Lab. 1995;12:32–36.
34. Grozev L, Michailov T. Treatment of bruxism and bruxo- 9. Holmgren K, Sheikholeslam A. Occlusal adjustment and mania (clinically tested). Folia Med (Plovdiv). 1999;41:147– myoelectric activity of the jaw elevator muscles in patients with nocturnal bruxism and craniomandibular disorders.
35. Kalman L. Occlusal appliances: a new material. Dent Today.
Scand J Dent Res. 1994;102:238–243.
10. Leon SP. The source of the problem. Dent Today. 2003;22:12.
36. Okeson JP. The effects of hard and soft occlusal splints on 11. Ford RT, Douglas W. The use of composite resin for creating nocturnal bruxism. J Am Dent Assoc. 1987;114:788–791.
anterior guidance during occlusal therapy. Quintessence Int.
37. Austin D, Attanasio R. A procedure for making a bruxism device in the office. J Prosthet Dent. 1991;66:266–269.
12. Stephens RG. Occlusal adjustment in periodontal therapy.
38. Leib AM. The occlusal bite splint – a noninvasive therapy for J Can Dent Assoc (Tor). 1973;39:332–337.
occlusal habits and temporomandibular disorders. Compend 13. Lester M, Baer PN. Survey of current therapy: bruxism Contin Educ Dent. 1996;17:1081–1084, 1086, 1088.
splints. Periodontal Case Rep. 1989;11:23–24.
39. Boyd JP. Improving TMD treatment and protecting restor- 14. Lalonde B. Occlusal splints. J Am Dent Assoc. 1996;127:554, ative dentistry. Dent Today. 1998;17:144.
40. Baad-Hansen L, Jadidi F, Castrillon E, Thomsen PB, Svens- 15. Wessberg G. Bruxism and the bite. Hawaii Dent J. 2001;32:4.
son P. Effect of a nociceptive trigeminal inhibitory splint on 16. Harnick DJ. Treating bruxism and clenching. J Am Dent electromyographic activity in jaw closing muscles during sleep. J Oral Rehabil. 2007;34:105–111.
17. Greene CS, Klasser GD, Epstein JB. ‘Observations' ques- 41. Sullivan TC. A new occlusal splint for treating bruxism and tioned. J Am Dent Assoc. 2005;136:852–853.
TMD during orthodontic therapy. J Clin Orthod. 2001;35:142– 18. Abraham J, Pierce C, Rinchuse D, Zullo T. Assessment of buccal separators in the relief of bruxist activity associated with 42. Bodenham RS. A bite guard for athletic training. A case myofascial pain-dysfunction. Angle Orthod. 1992;62:177– report. Br Dent J. 1970;129:85–86.
43. Jones CM. Chronic headache and nocturnal bruxism in a 19. Mintz AH. Acute TMJ versus chronic TMJ. Angle Orthod.
5-year-old child treated with an occlusal splint. Int J Paediatr 20. Lobbezoo F, Naeije M. Bruxism is mainly regulated centrally, 44. Thorp PD. An appliance to be worn at night for the heavy not peripherally. J Oral Rehabil. 2001;28:1085–1091.
tooth grinder. Dent Tech. 1975;28:144–145.
21. Allen DL. Accurate occlusal bite guards. Periodontics.
45. Maeda Y, Ikuzawa M, Mitani T, Matsuda S. Bimaxillary soft splints for unconscious hard-clenching patients: a clinical 22. Courant P. Use of removable acrylic splints in general report. J Prosthet Dent. 2001;85:342–344.
practice. J Can Dent Assoc (Tor). 1967;33:494–501.
46. Cassisi JE, McGlynn FD, Mahan PE. Occlusal splint effects on 23. Greenwald AS. The bruxism appliance and its varied appli- nocturnal bruxing: an emerging paradigm and some early cation: outline of procedure. N Y J Dent. 1968;38:443.
results. Cranio. 1987;5:64–68.
24. Askinas SW. Fabrication of an occlusal splint. J Prosthet 47. Clark GT, Beemsterboer PL, Solberg WK, Rugh JD. Nocturnal electromyographic evaluation of myofascial pain dysfunction 25. Glazebrook P. An equilibrated bite plate. Probe (Lond).
in patients undergoing occlusal splint therapy. J Am Dent 26. Gabriele P. A double night guard retainer. N Y State Dent 48. Hiyama S, Ono T, Ishiwata Y, Kato Y, Kuroda T. First night J. 1986;52:30–31.
effect of an interocclusal appliance on nocturnal masticatory 27. Ordene NM. A modified bruxism appliance. N Y State Dent muscle activity. J Oral Rehabil. 2003;30:139–145.
J. 1989;55:40–41.
49. Lindfors E, Magnusson T, Tegelberg A. Interocclusal appli- 28. Perel ML. Parafunctional habits, nightguards, and root form ances – indications and clinical routines in general dental implants. Implant Dent. 1994;3:261–263.
practice in Sweden. Swed Dent J. 2006;30:123–134.
29. Davis CR. Maintaining immediate posterior disclusion on an 50. Mejias JE, Mehta NR. Subjective and objective evaluation of occlusal splint for patient with severe bruxism habit. J Pros- bruxing patients undergoing short-term splint therapy.
thet Dent. 1996;75:338–339.
J Oral Rehabil. 1982;9:279–289.
ª 2008 The Authors. Journal compilation ª 2008 Blackwell Publishing Ltd 51. Hamada T, Kotani H, Kawazoe Y, Yamada S. Effect of 66. Lavigne GJ, Rompre´ PH, Montplaisir JY, Lobbezoo F.
occlusal splints on the EMG activity of masseter and Motor activity in sleep bruxism with concomitant jaw temporal muscles in bruxism with clinical symptoms. J Oral muscle pain: a retrospective pilot study. Eur J Oral Sci.
52. Moses AJ. Analysis of a functional appliance. CDS Rev.
67. Arima T, Arendt-Nielsen L, Svensson P. Effect of jaw muscle pain and soreness evoked by capsaicin before sleep on 53. Yustin D, Neff P, Rieger MR, Hurst T. Characterization of 86 orofacial motor activity during sleep. J Orofac Pain.
bruxing patients with long-term study of their management with occlusal devices and other forms of therapy. J Orofac 68. Dao TT, Lavigne GJ. Oral splints: the crutches for temporo- mandibular disorders and bruxism? Crit Rev Oral Biol Med.
54. Sheikholeslam A, Holmgren K, Riise C. Therapeutic effects of the plane occlusal splint on signs and symptoms of cranio- 69. Attanasio R. Bruxism and intraoral orthotics. Tex Dent mandibular disorders in patients with nocturnal bruxism.
J Oral Rehabil. 1993;20:473–482.
70. Mittelman J. Biofeedback: new answer to dental pain. It can 55. Yap AU. Effects of stabilization appliances on nocturnal be administered easily and inexpensively in any dental parafunctional activities in patients with and without signs of office. Dent Manage. 1976;16:21–22, 26–27.
temporomandibular disorders. J Oral Rehabil. 1998;25:64– 71. Cannistraci AJ. A method to control bruxism: biofeedback- assisted relaxation therapy. J Am Soc Prev Dent. 1976;6:12– 56. Shiau YY. The effect of the bite plane splint on the mandibular reposition in bruxers. Taiwan Yi Xue Hui Za 72. Rubeling RR Jr. Treating patients through biofeedback therapy. Dent Stud. 1979;57:57–62.
57. Nagels G, Okkerse W, Braem M, Van Bogaert PP, De Deyn B, 73. Shulman J. Teaching patients how to stop bruxing habits.
Poirrier R et al. Decreased amount of slow wave sleep in J Am Dent Assoc. 2001;132:1275–1277.
nocturnal bruxism is not improved by dental splint therapy.
74. Kramer JJ. Aversive control of bruxism in a mentally Acta Neurol Belg. 2001;101:152–159.
retarded child: a case study. Psychol Rep. 1981;49:815–818.
58. Rugh JD, Graham GS, Smith JC, Ohrbach RK. Effects of 75. Blount RL, Drabman RS, Wilson N, Stewart D. Reducing canine versus molar occlusal splint guidance on nocturnal severe diurnal bruxism in two profoundly retarded females.
bruxism and craniomandibular symptomatology. J Cranio- J Appl Behav Anal. 1982;15:565–571.
mandib Disord. 1989;3:203–210.
76. Rudrud E, Halaszyn J. Reduction of bruxism by contingent 59. Hachmann A, Martins EA, Araujo FB, Nunes R. Efficacy massage. Spec Care Dentist. 1981;1:122–124.
of the nocturnal bite plate in the control of bruxism for 77. Manns A, Miralles R, Adrian H. The application of audiosti- 3 to 5 year old children. J Clin Pediatr Dent. 1999;24:9– mulation and electromyographic biofeedback to bruxism and myofascial pain-dysfunction syndrome. Oral Surg Oral Med 60. Dube C, Rompre PH, Manzini C, Guitard F, De Grandmont P, Oral Pathol. 1981;52:247–252.
Lavigne GJ. Quantitative polygraphic controlled study on 78. Treacy K. Awareness ⁄ relaxation training and transcutaneous efficacy and safety of oral splint devices in tooth-grinding electrical neural stimulation in the treatment of bruxism.
subjects. J Dent Res. 2004;83:398–403.
J Oral Rehabil. 1999;26:280–287.
61. Van der Zaag J, Lobbezoo F, Wicks DJ, Visscher CM, 79. Wieselmann-Penkner K, Janda M, Lorenzoni M, Polansky R.
Hamburger HL, Naeije M. Controlled assessment of the A comparison of the muscular relaxation effect of TENS and efficacy of occlusal stabilization splints on sleep bruxism.
EMG-biofeedback in patients with bruxism. J Oral Rehabil.
J Orofac Pain. 2005;19:151–158.
62. Hasegawa K, Okamoto M, Nishigawa G, Oki K, Minagi S. The 80. Cherasia M, Parks L. Suggestions for use of behavioral design of non-occlusal intraoral appliances on hard palate measures in treating bruxism. Psychol Rep. 1986;58:719– and their effect on masseter muscle activity during sleep.
81. Nissani M. Can taste aversion prevent bruxism? Appl 63. Harada T, Ichiki R, Tsukiyama Y, Koyano K. The effect of oral Psychophysiol Biofeedback. 2000;25:43–54.
splint devices on sleep bruxism: a 6-week observation with 82. Heller RF, Strang HR. Controlling bruxism through automated an ambulatory electromyographic recording device. J Oral aversive conditioning. Behav Res Ther. 1973;11:327–329.
83. Funch DP, Gale EN. Factors associated with nocturnal 64. Ommerborn MA, Schneider C, Giraki M, Schafer R, Hand- bruxism and its treatment. J Behav Med. 1980;3:385–397.
schel J, Franz M et al. Effects of an occlusal splint compared 84. Moss RA, Hammer D, Adams HE, Jenkins JO, Thompson K, with cognitive-behavioral treatment on sleep bruxism activ- Haber J. A more efficient biofeedback procedure for the ity. Eur J Oral Sci. 2007;115:7–14.
treatment of nocturnal bruxism. J Oral Rehabil. 1982;9:125– 65. Landry ML, Rompre PH, Manzini C, Guitard F, De Grand- mont P, Lavigne GJ. Reduction of sleep bruxism using a 85. Feehan M, Marsh N. The reduction of bruxism using mandibular advancement device: an experimental controlled contingent EMG audible biofeedback: a case study. J Behav study. Int J Prosthodont. 2006;19:549–556.
Ther Exp Psychiatry. 1989;20:179–183.
ª 2008 The Authors. Journal compilation ª 2008 Blackwell Publishing Ltd 86. Watson TS. Effectiveness of arousal and arousal plus over- 105. LaCrosse MB. Understanding change: five-year follow-up of correction to reduce nocturnal bruxism. J Behav Ther Exp brief hypnotic treatment of chronic bruxism. Am J Clin 87. Foster PS. Use of the Calmset 3 biofeedback ⁄ relaxation 106. Clarke JH, Reynolds PJ. Hypnosis for treatment of nocturnal system in the assessment and treatment of chronic nocturnal bruxism. J Dent Res. 1989;68:402.
bruxism. Appl Psychophysiol Biofeedback. 2004;29:141– 107. Clarke JH, Reynolds PJ. Suggestive hypnotherapy for noctur- nal bruxism: a pilot study. Am J Clin Hypn. 1991;33:248–253.
88. Piccione A, Coates TJ, George JM, Rosenthal D, Karzmark P.
108. Cannistraci AJ, Friedrich JA. A multidimensional approach Nocturnal biofeedback for nocturnal bruxism. Biofeedback to bruxism and TMD. N Y State Dent J. 1987;53:31–34.
Self Regul. 1982;7:405–419.
109. Restrepo CC, Alvarez E, Jaramillo C, Velez C, Valencia I.
89. Roehrs T, Carskadon MA, Dement WC, Roth T. Daytime Effects of psychological techniques on bruxism in children sleepiness and alertness. In: Kryger M, Roth T, Dement WC, with primary teeth. J Oral Rehabil. 2001;28:354–360.
eds. Principles and Practice of Sleep Medicine. Philadelphia, 110. Rosen JC. Self-monitoring in the treatment of diurnal PA: Elsevier Saunders, 2005:39–50.
bruxism. J Behav Ther Exp Psychiatry. 1981;12:347–350.
90. Watanabe T, Baba K, Yamagata K, Ohyama T, Clark GT.
111. Morin CM. Psychological and behavioral treatments for A vibratory stimulation-based inhibition system for nocturnal primary insomnia. In: Kryger M, Roth T, Dement WC, eds.
bruxism: a clinical report. J Prosthet Dent. 2001;85:233–235.
Principles and Practice of Sleep Medicine. Philadelphia, PA: 91. Jadidi F, Castrillon E, Svensson P. Effect of conditioning Elsevier Saunders, 2005:726–737.
electrical stimuli on temporalis electromyographic activity 112. Rosenbaum MS, Ayllon T. Treating bruxism with the habit- during sleep. J Oral Rehabil. 2008;35:171–183.
reversal technique. Behav Res Ther. 1981;19:87–96.
92. Small MM. Treatment of nocturnal bruxism: a case study.
113. Blore D. Grinding down. Nurs Times. 1995;91:46–47.
Biol Psychol. 1978;6:235–236.
114. Zeldow LL. Treating clenching and bruxing by habit change.
93. Cornellier V, Keenan DM, Wisser K. The effects of EMG J Am Dent Assoc. 1976;93:31–33.
biofeedback training upon nocturnal and diurnal bruxing 115. Ayer WA, Gale EN. Extinction of bruxism by massed practice responses. Int J Orofacial Myology. 1982;8:11–15.
therapy. Report of case. J Can Dent Assoc (Tor). 1969;35:492– 94. Kardachi BJ, Clarke NG. The use of biofeedback to control bruxism. J Periodontol. 1977;48:639–642.
116. Ayer WA, Levin MP. Elimination of tooth grinding habits by 95. Clark GT, Beemstervoer P, Rugh JD. The treatment of massed practice therapy. J Periodontol. 1973;44:569–571.
nocturnal bruxism using contingent EMG feedback with an 117. Ayer WA. Massed practice exercises for the elimination of arousal task. Behav Res Ther. 1981;19:451–455.
tooth-grinding habits. Behav Res Ther. 1976;14:163–164.
96. Hudzinski LG, Walters PJ. Use of a portable electromyogram 118. Ayer WA, Levin MP. Theoretical basis and application of integrator and biofeedback unit in the treatment of chronic massed practice exercises for the elimination of tooth nocturnal bruxism. J Prosthet Dent. 1987;58:698–701.
grinding habits. J Periodontol. 1975;46:306–308.
97. Pierce CJ, Gale EN. A comparison of different treatments for 119. Vasta R, Wortman HA. Nocturnal bruxism treated by massed nocturnal bruxism. J Dent Res. 1988;67:597–601.
negative practice. A case study. Behav Modif. 1988;12:618– 98. Nishigawa K, Kondo K, Takeuchi H, Clark GT. Contingent electrical lip stimulation for sleep bruxism: a pilot study.
120. Heller RF, Forgione AG. An evaluation of bruxism control: J Prosthet Dent. 2003;89:412–417.
massed negative practice and automated relaxation training.
99. Casas JM, Beemsterboer P, Clark GT. A comparison of stress- J Dent Res. 1975;54:1120–1123.
reduction behavioral counseling and contingent nocturnal 121. Winocur E, Gavish A, Voikovitch M, Emodi-Perlman A, Eli I.
EMG feedback for the treatment of bruxism. Behav Res Ther.
Drugs and bruxism: a critical review. J Orofac Pain.
100. Cassisi JE, McGlynn FD, Belles DR. EMG-activated feedback 122. Chasins AI. Methocarbamal (robaxin) as an adjunct in the alarms for the treatment of nocturnal bruxism: current status treatment of bruxism. J Dent Med. 1959;14:166–170.
and future directions. Biofeedback Self Regul. 1987;12:13–30.
123. Saletu A, Parapatics S, Saletu B, Anderer P, Prause W, Putz H 101. Olkinuora M. A review of the literature on, and a discussion et al. On the pharmacotherapy of sleep bruxism: placebo- of studies of bruxism and its psychogenesis and some new controlled polysomnographic and psychometric studies with 124. Van Zandijcke M, Marchau MM. Treatment of bruxism with 102. Pear JH. Holistic care concepts, bruxism and necrotizing botulinum toxin injections. J Neurol Neurosurg Psychiatry.
ulcerative gingivitis. Dent Hyg (Chic). 1982;56:24–29.
103. Goldberg G. The psychological, physiological and hypnotic 125. Ivanhoe CB, Lai JM, Francisco GE. Bruxism after brain approach to bruxism in the treatment of periodontal disease.
injury: successful treatment with botulinum toxin-A. Arch J Am Soc Psychosom Dent Med. 1973;20:75–91.
Phys Med Rehabil. 1997;78:1272–1273.
104. Somer E. Hypnotherapy in the treatment of the chronic 126. Pidcock FS, Wise JM, Christensen JR. Treatment of severe nocturnal use of a dental splint prescribed for bruxism. Int J post-traumatic bruxism with botulinum toxin-A: case report.
Clin Exp Hypn. 1991;39:145–154.
J Oral Maxillofac Surg. 2002;60:115–117.
ª 2008 The Authors. Journal compilation ª 2008 Blackwell Publishing Ltd 127. See SJ, Tan EK. Severe amphethamine-induced bruxism: 142. Mohamed SE, Christensen LV, Penchas J. A randomized treatment with botulinum toxin. Acta Neurol Scand.
double-blind clinical trial of the effect of amitriptyline on nocturnal masseteric motor activity (sleep bruxism). Cranio.
128. Nash MC, Ferrell RB, Lombardo MA, Williams RB. Treat- ment of bruxism in Huntington's disease with botulinum 143. Raigrodski AJ, Christensen LV, Mohamed SE, Gardiner DM.
toxin. J Neuropsychiatry Clin Neurosci. 2004;16:381–382.
The effect of four-week administration of amitriptyline on 129. Monroy PG, Da Fonseca MA. The use of botulinum toxin-a sleep bruxism. A double-blind crossover clinical study.
in the treatment of severe bruxism in a patient with autism: a case report. Spec Care Dentist. 2006;26:37–39.
144. Melis M. Dr. Melis comments on Raigrodski, et al.'s article in 130. Tan EK, Jankovic J. Treating severe bruxism with botulinum the January 2001 issue of Cranio. Cranio. 2001;19:149.
toxin. J Am Dent Assoc. 2000;131:211–216.
145. Huynh N, Lavigne GJ, Lanfranchi PA, Montplaisir JY, 131. Etzel KR, Stockstill JW, Rugh JD, Fisher JG. Tryptophan De Champlain J. The effect of 2 sympatholytic medications supplementation for nocturnal bruxism: report of negative – propranolol and clonidine on sleep bruxism: experimental results. J Craniomandib Disord. 1991;5:115–120.
randomized controlled studies. Sleep. 2006;29:307–316.
132. Lobbezoo F, Lavigne GJ, Tanguay R, Montplaisir JY. The 146. Amir I, Hermesh H, Gavish A. Bruxism secondary to effect of catecholamine precursor L-dopa on sleep bruxism: a antipsychotic drug exposure: a positive response to propran- controlled clinical trial. Mov Disord. 1997;12:73–78.
olol. Clin Neuropharmacol. 1997;20:86–89.
133. Van der Zaag J, Lobbezoo F, van der Avoort PGGL, Wicks DJ, 147. Ackerman JB. A new approach to the treatment of bruxism Hamburger HL, Naeije M. Effects of pergolide on severe sleep and bruxomania. NY State Dent J. 1966;32:259–261.
bruxism in a patient experiencing oral implant failure. J Oral 148. Quinn JH. Mandibular exercises to control bruxism and deviation problems. Cranio. 1995;13:30–34.
134. Lavigne GJ, Soucy JP, Lobbezoo F, Manzini C, Blanchet PJ, 149. Quinn JH. Treating bruxism and clenching. J Am Dent Montplaisir JY. Double-blind, crossover, placebo-controlled trial of bromocriptine in patients with sleep bruxism. Clin 150. Knutson GA. Vectored upper cervical manipulation for chronic sleep bruxism, headache, and cervical spine pain in 135. Lobbezoo F, Soucy JP, Hartman NG, Montplaisir JY, Lavigne a child. J Manipulative Physiol Ther. 2003;26:E16.
GJ. Effects of the D2 receptor agonist bromocriptine on sleep 151. Jardini RS, Ruiz LS, Moyses MA. Electromyographic bruxism: report of two single-patient clinical trials. J Dent analysis of the masseter and buccinator muscles with the 136. Brown ES, Hong SC. Antidepressant-induced bruxism suc- cessfully treated with gabapentin. J Am Dent Assoc.
152. DiFrancesco RC, Junqueira PA, Trezza PM, De Faria ME, Frizzarini R, Zerati FE. Improvement of bruxism after T & A 137. Kast RE. Tiagabine may reduce bruxism and associated tempo- surgery. Int J Pediatr Otorhinolaryngol. 2004;68:441–445.
romandibular joint pain. Anesth Prog. 2005;52:102–104.
153. Huynh NT, Rompre PH, Montplaisir JY, Manzini C, Okura K, 138. Stein DJ, Van Greunen G, Niehaus D. Can bruxism respond to Lavigne GJ. Comparison of various treatments for sleep serotonin reuptake inhibitors? J Clin Psychiatry. 1998;59:133.
bruxism using determinants of number needed to treat and 139. Lobbezoo F, van Denderen RJA, Verheij JGC, Naeije M.
effect size. Int J Prosthodont. 2006;19:435–441.
Reports of SSRI-associated bruxism in the family physician's 154. Billups AJ. Mouthguards, nightguards, palliatives and col- office. J Orofac Pain. 2001;15:340–346.
laboration. Va Dent J. 1992;69:19–21.
140. Bostwick JM, Jaffee MS. Buspirone as an antidote to SSRI- induced bruxism in 4 cases. J Clin Psychiatry. 1999;60:857– Correspondence: Dr Frank Lobbezoo, Department of Oral Function, 141. Ranjan S, Chandra PS, Prabhu S. Antidepressant-induced Academic Centre for Dentistry Amsterdam (ACTA), Louwesweg 1, bruxism: need for buspirone? Int J Neuropsychopharmacol.
1066 EA Amsterdam, The Netherlands.
ª 2008 The Authors. Journal compilation ª 2008 Blackwell Publishing Ltd



DE JOHN WEBSTER TEATRODEFONDO La Duquesa de Malfi Terror y miseria en La duquesa de Malfi El autor. Webster, el poeta de los mataderos Los personajes: Animales y siluetas Reflexiones para una puesta en escena EL ESPACIO ESCÉNICO. Los hilos de la vida INTERÉS DEL ESPECTÁCULO TEATRO DE FONDO: RECORRIDO

Volume: 2, Issue: 1 April 2015 Twin Deficit Hypothesis: A Case of Pakistan Farrah Yasmin The Women University, Multan Pakistan Abstract: The prime motive of this study is to scrutinize the twin deficit for annual time series data over the period 1990-2010 for Pakistan. Twin deficit hypothesis expressed that an expansion in budget deficit will ground for rise in current account deficit. To diagnose affiliation amongst couple of variables, applied Unit root test (ADF-test), Johansen cointegration technique, Impulse response function and Granger causality test. The Granger causality demonstrate that the causality direction travel from current account deficit to budget deficit. When current account deficit occurs it leads to budget deficit. So the finding proves that there is a positive connection among both variables. Investigations are most reliable for Pakistan economy. Finally, this study confirms the rapport amid current account deficit and budget deficit. Keywords: Budget deficit, Current account deficit, Pakistan