Oral Splints the Crutches of TMD and Bruxism

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Critical Reviews in Oral Biology & Medicine

DOI: 10.1177/10454411980090030701 1998; 9; 345 Crit. Rev. Oral Biol. Med.

T.T. Dao and GJ Lavigne Oral Splints: the Crutches for Temporomandibular Disorders and Bruxism?

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ORAL SPLINTS: THE CRUTCHESFOR TEMPOROMANDIBULAR DISORDERS AND BRUXISM?T.T.T. DaoFaculty of Dentistry, University of Toronto, 124 Edward Street, Toronto, Ontario, (anada M5G 1 G6; (raniofacial Pain Research Unit at the Mount Sinai Hospital, Toronto

G.J. LavigneFaculte de M6decine Dentaire, Universite de Montr6al; (entre de Recherche en Sciences Neurologiques, DNpartement de Physiologie, Faculte de M6decine, Universit6 de Montr6al, (entred'Etude du Sommeil, D6partement de Psychiatrie, H6pital du Sacr6-Coeur, Montreal

ABSTRACT: Despite the extensive use of oral splints in the treatment of temporomandibular disorders (TMD) and bruxism,their mechanisms of action remain controversial. Various hypotheses have been proposed to explain their apparent efficacy(i.e., true therapeutic value), including the repositioning of the condyle and/or the articular disc, reduction in the electromyo-graphic activity of the masticatory muscles, modification of the patient's "harmful" oral behavior, and changes in the patient'socclusion. Following a comprehensive review of the literature, it is concluded that any of these theories is either poor or incon-sistent, while the issue of true efficacy for oral splints remains unsettled. However, the results of a controlled clinical trial lendsupport to the effectiveness (i.e., the patient's appreciation of the positive changes which are perceived to have occurred dur-ing the trial) of the stabilizing splint in the control of myofascial pain. In light of the data supporting their effectiveness butnot their efficacy, oral splints should be used as an adjunct for pain management rather than a definitive treatment. For sleepbruxism, it is prudent to limit their use as a habit management aid and to prevent/limit dental damage potentially induced bythe disorder. Future research should study the natural history and etiologies of TMD and bruxism, so that specific treatmentsfor these disorders can be developed.

Key words. Oral splints, temporomandibular disorders, bruxism, myofascial pain, disc displacement disorders.

(I) IntroductionAmong the treatments provided for temporomandibu-

lar disorders (TMD), intra-oral dental appliances,whether with full or partial occlusal coverage, andreferred to in this paper as oral splints, have been repeat-edly reported as being the most widely adopted choice.Introduced by Karolyi in 1901 (see Ramfjord and Ash,1994) for the treatment of bruxism, it is striking to seethe versatility of their current applications. Other thantheir use in the prevention of dental injuries and oralsoft-tissue trauma potentially induced by bruxism,sports, cheek biting (Walker and Rogers, 1992), and elec-troconvulsive therapy (Minneman, 1995), oral splints ofvarious designs have been prescribed in the manage-ment of diverse disorders including: (a) motor disorderssuch as Parkinson's disease (Durham et al., 1993) and oraltardive dyskinesia (Kai et al., 1994); (b) sleep disorderssuch as snoring (George, 1993) and sleep apnea (George,1993; Athanasiou et al., 1994; Lowe, 1994; Yoshida, 1994;Osseiran, 1995); (c) sensitive teeth related to chronicsinusitis (Dawson, 1974); (d) various headaches, from thetension-type to migraine (Ouayle et al., 1990; Lamey andSteele, 1996); and (e) all subgroups of TMD, e.g., myofas-cial pain, disc displacement disorders, and the arthri-tides (Table 1).

It is also surprising to see the wide acceptance oforal splints and their "multi-purpose usage", while littleis known about the mechanisms by which they exert theireffect. For the TMD, a survey of 10,000 members of theAmerican Dental Association identified oral splints asbeing, by far, the treatment most commonly used by bothgeneral practitioners and dental specialists (Glass et al.,1991, 1993). It is estimated that over three million splintsare provided to the American population every year, withan approximate cost of $990 million per year (i.e., 2.91% ofall 1990 US dental care dollars; Pierce et al., 1995). Thepopularity of oral splints has also extended throughoutthe five continents, as indicated by the various publica-tion languages found in the literature through a Medlinesearch, and the numerous names given to differentdesigns of splints (Table 2). Although their use as pro-tective devices is well-accepted, the benefits associatedwith their use in the management of motor disorders areat best anecdotal, and their true therapeutic value in thetreatment of TMD has not been established beyonddoubt. The aim of this paper is to review the proposedmechanisms by which oral splints exert their effects, andto assess the quality of the evidence supporting the effi-cacy of oral splints in the treatment of bruxism and thethree subgroups of TMD (Dworkin and LeResche, 1992).

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TABLE 1

Applications of Oral SplintsTemporomandibular disorders

Myofascial painDisc displacement disordersArthritides of the temporomandibular joints

Other pain disordersHeadaches/migraine

Motor and sleep disordersSleep bruxismSleep apneaParkinson's diseaseOral tardive dyskinesia

Occlusal rehabilitationOrthodonticsPeriodonticsProsthodonticsPhantom bite

Others (Prevention of tissue trauma, habits)Diurnal bruxismSportsCheek or fingernail bitingElectroconvulsive therapyLip commissure burnEsophageal refluxSinusitis

(11) Myofascial Pain (MFP) and Oral SplintsIn this section, we will review the literature pertaining tosplint therapy for myofascial pain of the masticatorymuscles. Since the subclassification of MFP becameavailable only in 1992 (Dworkin and LeResche), and ourreview will include the literature published before then,we will include in this section the available evidence onthe use of oral splints in the treatment of pain in TMDpatients. The literature dealing with the use of splints fordisc displacement disorders and the arthritides will bediscussed separately below. The comprehensiveness ofeach review section will vary according to the extent ofliterature published in each field.

(A) PHYSIOLOGICAL MECHANISMS PROPOSEDThere are several assumptions which underlie the world-wide acceptance of oral splints in the treatment ofmyofascial or TMD pain (Table 3). In the following, weshall discuss the limitations associated with each ofthese assumptions.

(a) Change in the vertical dimension of occlusionAccording to some early reports (Block, 1947;Christensen, 1970), oral splints contribute to the reduc-tion of "abnormal muscle activity" and pain by restoringthe patient's original vertical dimension of occlusion

TABLE 2

Synonyms for Oral Splints Used in theTreatment of Temporomandibular Disordersand Bruxism

Anterior deprogramming splintAnterior positioning splintAnterior repositioning splintBite splintBuccal separatorDisclusion splintDistal push splintFlat occlusal splintHawley splintHerbst splintHydrostatic splintLevandoski splintMandibular advancing repositioning splintMandibular orthopedic repositioning applianceMandibular repositioning splintMichigan occlusal splintMuscle deprogramming splintNight guardOcclusal correcting splintOcclusal disengagement splintOrthopedic interocclusal appliancePain release splintPivoting applianceProtrusive positionersStabilization splint

(VDO) which has been reduced by tooth wear or loss ofposterior teeth. This belief may have been influenced byCosten's hypothesis that facial pain and the accompany-ing auditory symptoms may be caused by a loss in theVDO, a subsequent posterior displacement of thecondyles and compression of the auriculo-temporalnerve (Costen, 1934). We now know that this hypothesisis not supported by studies which show the lack of con-tiguity between these anatomical structures (Shapiroand Truex, 1943; Sicher, 1948; Zimmerman, 1951). On theother hand, it is also important to note that the averagesplint thickness (8.1 mm), which appears to be the mostefficient in producing a rapid improvement in the symp-toms (Manns et al., 1983), exceeds by far the usualamount of vertical increase one wishes to restore in mostpatients. Furthermore, although an immediate decreasein the electromyographic (EMG) activity of the jaw eleva-tor muscles has been observed at various VDO augmen-tations obtained with splints (Manns et al., 1983), thereare no data pointing to the persistence of this effect inlong-term users of splints. More importantly, a decreasein EMG following a raised VDO does not necessarilyimply that a loss of VDO would induce pathological EMGincreases.

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TABLE 3

Mechanisms Proposed for Oral SplintEfficacy/Effectiveness

Myofascial painChange in the vertical dimension of occlusionRepositioning of the temporomandibular jointsDecrease in the level of muscle activityReducing bruxismRemoval of occlusal interferencesEnhancing the patient's cognitive awareness

Disc displacement disorders"Recapturing" the disc'Unloading" the joints

Arthritis/arthralgia"Unloading" the joints

Sleep bruxismRemoval of occlusal interferencesChange in muscle activityModification of patient's habits

(b) Repositioning of the temporomandibular jointsAnother theory stipulates that the success achieved withoral splints is due to the repositioning of the displacedtemporomandibular joint (TMJ) in a more "therapeutic"or "concentric position" within the temporal fossae(Weinberg, 1972, 1979, 1983a,b; Weinberg and Lager,1980), thus improving the maxillo-mandibular relation-ship and eliminating the muscle imbalance and its resul-tant pain. This concept is based on the measurement ofthe joint spaces between the projected surface of thecondyle and the radiological border of the temporal fos-sae and is therefore associated with several pitfalls. First,it does not address the large variability of condylar posi-tions found in both the general asymptomatic (Pullingeret al., 1985) and patient population (Brand et al., 1989).Second, it does not account for the significant errors anddistortions inherent in the projection of a three-dimen-sional joint complex on the flat surface of a radiograph.This is particularly important, since the variations in thecondylar position as observed on radiographs may sim-ply reflect the variations of the shape of the osseouscomponents of the same joint from its medial to its lat-eral aspects (Eckerdal and Lundberg, 1979; Blaschke andBlaschke, 1981; Dumas et al., 1986). Third, it does not takeinto consideration the variation in the thickness of thesoft-tissue components which is not reflected on con-ventional radiographs but which contributes to the lackof uniformity of the joint space (Hatcher et al., 1986).Finally, as discussed below, the belief that an "abnormalmuscle activity" or "muscle imbalance" could be thecause of muscle pain has been questioned (Lund andWidmer, 1989; Lund et al., 1989, 1991, 1993).

(c) Decrease in the level of muscle activityThe apparent effect of oral splints has been assumed tobe related to a decrease in muscle activity (Lobbezoo etal., 1993; Visser et al., 1995). Their efficacy was furtherattributed to a reduced EMG in the temporalis muscleswhich appear to present greater changes as comparedwith the masseter muscles (Lobbezoo et al., 1993).Although a decrease in EMG signals in the jaw-closingmuscles has been repeatedly reported in most of thestudies on splints (Dahlstrom and Carlsson, 1984;Dahlstrom and Haraldson, 1985; Dahlstrom et al., 1985;Holmgren et al., 1985; Graham and Rugh, 1988; Naeijeand Hansson, 1992; Lobbezoo et al., 1993; Visser et al.,1995), the data are still contradictory, and the availableevidence suggests that the degree to which this phe-nomenon was related to the clinical remission of MFPsymptoms remains unsettled. Besides the few studieswhich show a concomitant reduction of EMG activity andpatients' pain reports, these reports were not collectedunder blind conditions (Dahlstrom and Haraldson, 1985;Visser et al., 1995), and some experiments were done inasymptomatic subjects (Dahlstrom et al., 1985; Grahamand Rugh, 1988; Lobbezoo et al., 1993), while other inves-tigations have simply yielded opposing results: anincrease in EMG activity (Wood and Tobias, 1984).Contrasting results have also been obtained within thesame study (Visser et al., 1995), where it was shown thatafter a short-term use of a splint (3 to 6 wks), the EMGactivity decreased in 15 out of 35 patients, but increasedin four others and remained unchanged in the rest of thesample population. Similarly, it was reported in anotherstudy (Holmgren et al., 1985) that 15 min after the inser-tion of an occlusal splint, the postural activity of the tem-poral muscles decreased in 52%, but increased in 22%,and remained unchanged in 26% of the patients.Comparable results were obtained for nocturnal activityof the masseter muscles: The EMG levels decreased in52%, increased in 20%, and remained unchanged in 28%of the patients (Clark et al., 1979). These effects may betransitory, since it has been reported that at two to fourweeks after treatment, the activity of the temporalis mus-cle during clenching on the splint was comparable withthat measured without the splint, while the massetermuscle did not display any significant changes (Naeijeand Hansson, 1992). The between-study variability couldbe due to various reasons, including the differences inthe clinical protocols adopted during the experiment(e.g., data recording with or without the splint, at rest orduring function, period of time after splint insertion, dif-ferent splint thickness), or the heterogeneity of thepatient group (e.g., presence or absence of pain, brux-ism). Nevertheless, together with the presence of diversesubgroups of patients in the same study displaying con-trasting responses to splint usage, these data indicatethat the overall EMG response to splint therapy and its

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biological significance are not well-understood and stillwarrant further investigation.

(d) Reducing bruxism in relation to TMD

It is often believed that oral splints contribute to the suc-cess of TMD management by reducing bruxing activity.This belief is based on the assumptions that bruxism is acontributing or causative factor for TMD (Ramfjord andAsh, 1983; Mongini, 1984; Okeson, 1985; Rugh andHarlan, 1988; Dawson, 1989). However, these assump-tions have been questioned (Clark and Adler, 1985;Lobbezoo and Lavigne, 1997). In fact, although signifi-cant correlations between parafunction and dysfunctionhave been reported through epidemiological surveys(Egermark-Eriksson et al., 1981; Nilner, 1983; Allen et al.,1990; Magnusson et al., 1993; Widmalm et al., 1995), theassociation of two events in time does not prove causa-tion (Spilker, 1991), and the temporal sequence of causeand effect cannot be established on the basis of cross-sectional studies (Locker and Slade, 1988). Furthermore,the association does not make epidemiologic sense,since bruxism is more prevalent in children and decreas-es in adulthood, while the prevalence of TMD is low inchildren and older people, and peaks between the agesof 18 and 45 (Lobbezoo and Lavigne, 1997).

It is also important to note that most of the splintstudies were focused on sleep bruxism, and did not dif-ferentiate between the clenching (or tonic) and grinding(phasic or rhythmic) forms of the disorder, althoughclenching, which occurs mainly during the daytime, hasbeen reported to be associated with higher risk for jawpain (Goulet et al., 1993, 1994, 1995). On the other hand,many patients with sleep bruxism have no masticatorymuscle pain at all (Clark and Sakai, 1990; Dao et al.,1994b; Lund, 1995), and sleep bruxers tend to have theirhighest pain in the morning, while myofascial painpatients have their worst pain in the evening (Dao et al.,1994b). This suggests that sleep bruxism and myofascialpain may be two different entities. Recent data also sug-gest that jaw pain and motor activity in sleep bruxismmay not always be positively correlated, since sleepbruxers with pain had fewer bruxing episodes per hourthan those who did not report any pain (Lavigne et al.,1997).

If the available data do not substantiate either theassumption that bruxism is the cause of TMD or thebelief that pain levels are proportional to the amount ofmotor activity, attempting to reduce bruxism with an oralsplint to treat TMD may not be a viable option at thispoint. This is even more true since the ability of oralsplints to decrease bruxism has not been established, asreviewed in a separate section below.

(e) Removal of occlusal interferencesPerhaps the most popular theory on the mechanism of

action of oral splints proposed by the dental professionwould be the one which postulates that occlusal splintsare effective because they reduce the amount of toothcontact, alter the periodontal proprioceptive input to thecentral nervous system (Ramfjord and Ash, 1971; Yustinet al., 1993), and provide the patient with an "interferencefree" or "ideal occlusal scheme" (Posselt, 1968; Ramfjordand Ash, 1971, 1994; Timm and Ash, 1977). Therefore,whether oral splints provide full or partial coverage ofthe teeth, they would "prevent disturbing influences tothe neuromuscular system from occlusal contacts onmandibular closure and movements" (Ramfjord and Ash,1971; Timm and Ash, 1977). However, this assumption isbased mostly on EMG studies comparing the muscleactivity before and during the wear of oral splints, andthe limitation of that evidence has already been dis-cussed. Moreover, the concept that these interferencescan induce abnormal muscle activity and subsequentpain (Clayton, 1995) is contradicted by the body of evi-dence which refutes the second part of the equation, i.e.,the role of muscle hyperactivity as the cause for muscu-lar pain (Lund and Widmer, 1989; Lund et al., 1989, 1991,1993). It is also important to keep in mind that toothcontact occurs only during a very limited part of the day.If we rely on early studies showing that the estimatedtooth contact time during a day was 17.5 minutes in anormal subject (Graf, 1969), and the mean difference oftooth contact time during sleep between bruxers andnon-bruxers was about 9 minutes (Kydd and Daly, 1985),the estimated total contact time would approximate only26.5 minutes/day, i.e., about 1.8% of the 24-hour cycle.Furthermore, although various studies have shown thatexperimentally induced sensory feedback le.g., pain(Lund, 1995); heavy pressure on teeth (Lavigne et al.,1987)1 from the orofacial region can influence themandibular reflexes, the level of muscle activity(Sunakawa et al., 1993), and the position of the mandible(Obrez et al., 1993), there is no evidence to support thebelief that routine tooth contact can exert the sameeffect. Besides, it is difficult to attribute the clinical suc-cess of oral splints to the changes in occlusion, since adecrease in pain intensity and an improvement in painrelief scores have also been obtained with the use ofnon-occluding splints, i.e., those which do not cover theteeth and leave the occlusion unmodified (Greene andLaskin, 1972; Rubinoff et al., 1987; Dao et al., 1994a; Feineand Lavigne, 1995).

(B) BEHAVIORAL MECHANISMS:THE COGNITIVE AWARENESS THEORY

According to this theory, the presence of the splint as aforeign object in the mouth would likely change the oraltactile stimuli, decrease the oral volume and space forthe tongue, and make the patients conscious about theposition and potentially harmful use of their jaw (Greene

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and Laskin, 1972; Rugh and Robbins, 1982). Although itseems reasonable to suppose that this increased aware-ness would influence the patients' learning to alter orreduce their harmful behavior and therefore contributeto the overall success of the intervention (Rugh andSolberg, 1979; Rugh, 1991), this concept still needs to beproven.

(C) CLINICAL EFFICACY/EFFECTIVENESSAlthough the mechanism of action of oral splints has notbeen elucidated, the acceptance of this treatmentmodality remains overwhelming. This faith in splint ther-apy may have been reinforced by nearly five decades ofhigh clinical success rates achieved with splints alone,whether inserted into the maxillary or mandibular arch-es, or combined with other therapies (Zarb andThompson, 1970; Greene and Laskin, 1972; Carraro andCaffesse, 1978; Dahlstrom et al., 1982; Okeson et al., 1982,1983, Clark, 1984, 1988; Uriegas et al., 1985; Clark et al.,1988; Suvinen and Reade, 1989; Tsuga et al., 1989;Wilkinson et al., 1992; Carlson et al., 1993; Turk et al., 1993;Gray et al., 1994; Long, 1995; Visser et al., 1995). The ques-tion that may arise is not so much whether patients'improvements can be obtained with splints, but ratherhow much of the reported improvements reflect the effi-cacy, i.e., true therapeutic value of these oral devices, andhow much may be due to other factors such as the nat-ural course of the disorder, the placebo effect, the doc-tor-patient relationship, and/or other undetermined con-founding elements. While a reliable answer would begiven by the results of randomized controlled clinical tri-als (RCTs), most of the studies cited above did not followmany of the contemporary fundamental principles ofclinical trials (Spilker, 1991), and the overall quality ofthe design of RCTs in the TMD field published before1994 has been reported to be below acceptable levels(Antczak-Bouckoms, 1995). Furthermore, in the absenceof a control group (Okeson et al., 1982; Tsuga et al., 1989;Wilkinson et al., 1992), and in light of the evidence show-ing the cyclical fluctuation of MFP symptoms over time(Dworkin et al., 1991; Hampf, 1992; Dao et al., 1995a,b;Huggins et al., 1996), it is not possible to determinewhether the decrease in pain observed in the study rep-resented the specific outcome of the treatment or thenatural progression of the condition toward a more qui-escent phase. As well, it is likely that the positive resultscould be due, in part, to the placebo effect which is oftenassociated with the treatment of MFP, and which hasbeen observed in 30-64% of the patients (Greene andLaskin, 1971, 1972, 1983; Goodman et al., 1976). One canalso argue that the patients' desire to please or gratifytheir clinician may have accounted for the favorable datawhich were not collected under blind conditions (Greeneand Laskin, 1972; Okeson et al., 1982; Clark et al., 1988;Suvinen and Reade, 1989; Tsuga et al., 1989; List et al.,

1992; Wilkinson et al., 1992; Turk et al., 1993; Visser et al.,1995).

If appropriate care has not been given to the controlfor bias during an evaluation process which relies almostexclusively on patients' subjective reports, it is reason-able to conclude that the efficacy of oral splints has notbeen established beyond doubt. To address this issue,we have designed a randomized, controlled, and blindclinical trial to assess the efficacy of this treatmentapproach. The results of the study have been published(Dao et al., 1994a). In summary, MFP patients were ran-domly allocated to three groups: a passive control group,in which patients had a stabilizing maxillary splint only30 minutes at each of their seven visits over an 11-weekperiod; an active control group, in which patients wore apalatal splint 24 hrs/day except for oral hygiene and atmealtimes, but the splint did not change the patients'occlusion; and a treatment group, in which patients worea maxillary stabilizing splint 24 hrs/day except duringoral hygiene and at mealtimes. Our data show a signifi-cant decrease of patients' reports of pain intensity andpain unpleasantness in all three groups of patients after11 weeks of treatment, both at rest and after a chewingtest, but there were no significant differences betweengroups. If the between-group differences observed at theend of the study were used to calculate the sample sizeneeded to fulfill statistical criteria for demonstrating sig-nificant differences, 750 and 240 patients would need tobe recruited for pain intensity and pain unpleasantness,respectively. As discussed previously, if such a large pop-ulation is needed to prove that the small differencesbetween the efficacy of the splint and that of the placeboare real, it is prudent to assume that the therapeuticcomponent of that therapy is negligible.

Our data cast doubt on the therapeutic value (effica-cy) of oral splints in the treatment of MFP, and they alsosuggest that the decrease in pain during the trial was notdue to changes in the patients' occlusion. In light ofthese results, any phase II therapy where permanentocclusion-changing procedures are used to maintain themaxillo-mandibular relationship obtained with the splintis totally unjustified.

Soft resilient splints are also commonly used in themanagement of MFP, although they provide mixedresults. While their short-term efficacy in reducing painhas been reported in several case reports (Verban, 1986;Wright, 1988; Ahlin, 1991; Bledsoe, 1991; Williams, 1991)and studies (Harkins et al., 1988; Wright et al., 1995),aggravation of the symptoms has been observed in somepatients (Nevarro et al., 1985; Harkins et al., 1988).Concerns have also been raised regarding the effects ofthese appliances on the changes in occlusal contacts(Singh and Berry, 1985; Harkins et al., 1988), and patients'complaints about splint bulkiness have been reported(Harkins et al., 1988; Wright et al, 1995). The data from a

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recent randomized controlled clinical trial in MFPpatients suggest that the patients' satisfaction and com-fort, as well as a decrease in clenching, can be obtainedequally with soft and hard splints (Huggins et al., 1997).However, there was no report regarding their effect onother cardinal symptoms, such as pain and/or muscletenderness.

If the efficacy of oral splints for the treatment of MFPis questionable, the question arises as whether weshould still prescribe oral splints to manage this disor-der. Before we reach a conclusion, it is necessary to con-sider some related issues which may affect that decision.When one is treating a musculoskeletal pain of unknownorigin, trying to cure the condition, i.e., to remove itscause, is simply an absurd exercise. Perhaps the best wecan hope for is an improvement of the patient's own per-ception of his/her condition and quality of life. In thisregard, our data show that the quality of life improvedsignificantly in all three of the previously discussedpatient groups. Moreover, patients who wore either thepalatal or stabilizing splint reported significantly morepain relief than those who did not have the appliancebetween their appointments (Feine and Lavigne, 1995).However, although the report of pain relief reflects theeffectiveness of the therapy (i.e., the patient's apprecia-tion of the positive changes which are perceived to haveoccurred during the trial), pain relief is a poor estimateof treatment efficacy, because that outcome measure isbased on the memory of pain, and the validity of retro-spective reports including the memory of pain has beenquestioned (Feine et al., 1992; Schwarz and Sudman,1994). Thus, given the self-limiting nature of MFP, theimportance of the placebo effect associated with oralsplints, and the non-invasive nature of this approach(when they are not followed by occlusal therapy), oralsplints appear to fulfill the following patients' generalexpectations from health care services, i.e., (1) to be aliveas long as possible; (2) to be functioning normally; (3) tobe free of pain and other physical, psychological, orsocial symptoms; (4) to be free of iatrogenic problemsfrom the treatment regimen; and (5) to remain solvent(White, 1967; Fries et al., 1980; Fries, 1983, 1991). In theabsence of any other forms of therapy with a provengreater curative value (Chapman, 1991; Clark et al., 1995),and in light of the data supporting their effectiveness butnot their efficacy, we conclude that oral splints shouldstill be used as an adjunct to patient management, butonly until the etiology of MFP is elucidated and a morespecific treatment regimen for this condition is developed.

(III) Disc Displacement Disordersand Oral Splints

The displacement of the TMJ disc from its textbook-likeposition, between the mandibular condyle and the tem-

poral eminence, to an anterior and medial or lateralposition was first identified by Annandale in 1887. Discdisplacement disorders are now classified into the fol-lowing subtypes (Dworkin and LeResche, 1992):

(1) Disc displacement with reduction (DDR): The discis displaced from its original position between thecondyle and the eminence to an anterior and medial orlateral position, but reduces on full opening, usuallyresulting in a noise.

(2) Disc displacement without reduction (DDWR),with limited opening: a condition in which the disc is dis-placed from its original position between the condyleand the eminence to an anterior and medial or lateralposition, associated with limited mandibular opening.

(3) Disc displacement without reduction, withoutlimited opening: same as #2 but not associated with lim-ited mandibular opening.

Although surgical repositioning or resection of thearticular disc was among the first treatments proposedfor disc displacement disorders, more conservative ther-apies using oral splints started to gain popularity in the1970's. Whether they were resilient or hard, adapted tomaxillary or mandibular teeth, designed as a stabilizingappliance or a jaw repositioner device, oral splints pre-scribed for disc displacement disorders often wereintended to have a common goal: to "recapture" the dis-placed disk, and thereby eliminate the clinical problemsthat are thought to be caused by its dislocation (e.g.,pain, limited mandibular movements, and joint sounds;Anderson et al., 1985). It was further believed that anyimprovement in joint noises, pain, and mandibularmotion obtained with splint therapy would occur as theresult of disc recapturing (Anderson et al., 1985; Le Belland Kirveskari, 1985) and/or joint "unloading" (Israel,1994; Moncayo, 1994). Upon remission of the clinicalsymptoms, the splint was supposed to be graduallyadjusted to "walk the disk back" to allow the mandible toreturn to its original position. If this did not work out,permanent alterations of the dentition with orthodon-tics, prosthodontics, or orthognathic surgery were rec-ommended as "phase II", to maintain the new therapeu-tic maxillo-mandibular relationship obtained with thesplint (Haden, 1983; Anderson et al., 1985; Lundh et al.,1985; Tallents et al., 1990; Lew, 1992). This entireapproach to recapturing and stabilizing TMJ disks mayhave been motivated by the belief that disc displace-ment (DD), which often starts as "a clicking jaw", couldbe a progressive disorder if left untreated. Many author-ities postulated that DD can lead to increased risks ofdeveloping pain (Brooke and Grainger, 1988), impairedmobility (e.g., "closed lock"; Dolwick, 1995), and degen-erative joint diseases (see Milam, 1995). In the followingparagraphs, we will review the few mechanisms pro-posed for oral splints in the treatment of DD and therisks and benefits associated with their use, in the con-

):

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text of the natural progression and long-term prognosisof these disorders.

(A) PHYSIOLOGICAL MECHANISMS

(a) "Recapturing" the disc with the stabilizing splintThe stabilizing splint described earlier for MFP has alsobeen widely used in the treatment of DD. The data on itsability to reposition the disc are still very sparse, and theavailable evidence suggests that disc recapturing doesnot occur in conjunction with the use of stabilizingsplints. Using magnetic resonance imaging (MRI) to visu-alize the disc before and after 3-4 months of treatment of10 DDWR patients with stabilizing splints, it was foundthat the disc remained anteriorly displaced anddeformed, and its relationship with the condyle wasunchanged (Choi et al., 1994). This is consistent with thedata of another MRI pilot splint study showing that theimproved jaw movements and pain remission in threepatients after a three-month treatment period occurredwithout any sign of disc recapturing (Chen et al., 1995). Asreviewed below, these data are similar to those reportedfor anterior repositioning splints.

(b) "Recapturing" the discwith the anterior repositioning splint

As their name indicates, anterior repositioning splints(ARSplint) are designed to maintain the jaw in a protru-sive position, in an attempt to "decompress the jointstructures" (Scapino, 1983), allow the anteriorly dis-placed disk to regain its "normal" relationship with thecondyle head and the articular fossae, and allow for"healing of the elongated posterior disk attachment"(Dolwick and Riggs, 1983). To ensure a proper alignmentof the "disc-condyle complex", various imaging methodshave been used to visualize the position of the disc dur-ing the fabrication of the ARSplints, including arthrogra-phy (Manzione et al., 1984; Tallents et al., 1985) and mag-netic resonance imaging (Cohen and MacAfee, 1994;Moritz et al., 1995). However, the consistency and pre-dictability of these appliances in repositioning the dischave been questioned. In an MRI study involving 18patients and 30 clicking joints treated with the Sved-typesplint, Kirk (1991) reported that disc repositioningoccurred in only three joints. Similarly, Manco andMessing (1986) found that 41.8% of the discs evaluatedwith direct sagittal computed tomography were not repo-sitioned after ARSplint therapy. Manzione et al. (1984)reported that 46% of the patients with painful DD treatedwith ARSplints still had anterior DD. In another studyusing MRI before and immediately after an average ofnine months' treatment with an ARSplint, disc reposi-tioning was observed in 96% of the 26 fully reducingdiscs, but not in the seven partially reducing and the 14non-reducing discs (Simmons and Gibbs, 1995).

(c) Unloading the jointsIt has been suggested that overloading the TMJ cancause DD (Moncayo, 1994) and degenerative arthritis,and that oral splints work by decompressing the joints(Israel, 1994). This may have been based on the beliefthat the mandibular opening induced by the splint thick-ness would be accompanied by an increase in the jointspace and a decrease in the loading forces exerted on thearticular surfaces of the TMI. While direct evidence sup-porting this assumption is not available, TMJ unloadinghas been assessed indirectly through various methods.

Using a static mechanical model based on vectoranalysis to estimate the clenching forces transmitted tothe TM), dos Santos and his colleagues concluded thatthe insertion of a stabilizing splint tends to decrease thepressure in the joints, while the use of an ARSplint tendsto increase the pressure in the joint structures (dosSantos et al., 1988). However, this model has never beenvalidated in vivo in dynamic conditions.

The forces exerted on the TMJs have also been esti-mated in a clinical study using a jaw-tracking device topredict the condylar movements induced by clenchingtasks (Ito et al., 1986). Since the condylar movements werenot significant during clenching on either the stabilizingor the ARSplint, it was inferred that the forces were main-ly directed to the molars, and decompressive effects atthe TM) level were induced by use of the splints. However,it is important to note that the condylar movements wereestimated from an arbitrary point in the condyle that doesnot reflect the loading articular surfaces of the TMJs.Furthermore, neither of these studies takes into accountthe possible changes in the position of the disc relative tothe TM) during the jaw movements, although this mayalso influence the magnitude of the joint loading.

Another approach involved the measurement ofintra-articular pressure at the posterior slope of the emi-nence in the upper compartment of the TM) (Nitzan,1994). Besides the lack of data showing the validity andreliability of this technique in assessing intra-articularfluid pressure, such measurements do not provide directinformation regarding the loading of the articular sur-faces of the TM). More recently, Kukobi et al. (1997) usedtomograms of the TMJ and measured the joint space dur-ing maximum teeth intercuspation and clenching on twotypes of splints. The stabilizing splint did not induce anysignificant increase in joint space, and there was a signif-icant reduction in the anterior joint space associated withthe ARSplint; this suggests that these splints do notunload the TMJ.

It appears from the reviewed literature that oralsplints do not generally enable clinicians to repositionthe articular disc, or to decompress the joint structures.In successful cases of disc repositioning, follow-up dataare still lacking, and the long-term outcomes of thisaggressive treatment approach still need to be assessed.

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(B) CLINICAL EFFICACY/EFFECTIVENESS

(a) Stabilizing splints in the treatmentof disc displacement disorders

Stabilizing splints have been reported, in uncon-trolled studies, to be effective in decreasing pain andjoint noises, and in improving the range of mandibularmotion (Choi et al., 1994; Chen et al., 1995; Linde et al.,1995). However, in controlled (but non-blinded) studiescomparing the outcome of stabilizing splints with that ofa control group, although the overall improvement inpain, joint sounds, and maximal opening was noticeable,no significant differences could be found between thegroups (Lundh et al., 1988, 1992; Sato et al., 1995). Whilethis lack of between-group differences could be due tothe small sample sizes, it is also possible that the paral-lel improvement in the non-treated group simply reflect-ed the natural course of the disorder. This is supportedby reports that the symptoms associated with DDR orDDWR appear to improve over time without treatment(Pedersen and Hansen, 1987; Lundh et al., 1992; Sato etal., 1995). For instance, without treatment, pain has beenreported to decrease in 36% of the patients diagnosedwith DDWR after one year (Lundh et al., 1992).Interestingly, these authors also found a higher inci-dence of symptoms worsening in the treatment group ascompared with the control group. Similarly, the datafrom another study have showed that 41.9% of thepatients with DDWR who refused any treatment had asignificant increase in mouth opening and decrease inpain after one year, although joint noises remainedunchanged (Sato et al., 1995). Taken together, these datashow that not only is the ability of stabilizing splints torecapture the articular disc doubtful, but also, the clini-cal efficacy in the treatment of DD remains to be proven.

Stabilizing splints have also been compared withtheir counterpart, the ARSplint. The results of an uncon-trolled study (Anderson et al., 1985) and those of a con-trolled but non-blinded study (Lundh et al., 1985) sug-gested that the ARSplint provided more improvementsthan the stabilizing one. However, it is important to notethat the less-than-optimal design of these studies castsdoubt on any inference about the true therapeutic valueof the treatment approaches evaluated. Furthermore, theavailable data indicate that the efficacy of the ARSplint inthe treatment of DD has also not been establishedbeyond doubt. The quality of the evidence supportingthe clinical efficacy of ARSplints and the extent to whichthe improvements in the symptoms are correlated tochanges in the disc position will be discussed below.

(b) Anterior repositioning splintsin the treatment of disc displacement disorders

Pain relief and/or improvement of mandibular range ofmotion have been reported in most of the DD treatment

studies that we have reviewed so far, whether or not theposition of the disc was assessed by imaging techniques.However, the extent to which these positive resultsreflect the true benefit obtained with the ARSplintremains to be determined, since these studies failed toobserve many of the rules of clinical trials that are nowconsidered as critical if the validity of the results is to beensured (Spilker, 1991). For instance, because of theabsence of a control group, several studies (Le Bell andKirveskari, 1985; Chen et al., 1995; Simmons and Gibbs,1995) would be better qualified as case series, whichoften include potential biases and tend to be positivewith respect to treatment outcome (DeRouen, 1995). Instudies where a control group was included, patients'subjective reports, such as pain, were not collectedunder blind conditions (Lundh et al., 1985, 1988; Tallentset al., 1990). Furthermore, whether these results weremainly due to splint treatment or to group allocationbias cannot be determined, since patients were not ran-domized into treatment groups (Tallents et al., 1990).

On the other hand, when objective signs such asjoint noises were used as a measure of treatment out-come, the success rates were much lower, and relapserates were alarmingly high: From 40 to 50% of patientswho received ARSplints still experienced joint noises at1 to 3 yrs post-treatment (Le Bell and Kirveskari, 1985;Tallents et al., 1990). Furthermore, as discussed earlier,with the use of imaging techniques such as magnetic res-onance imaging (MRI), computed tomography, andarthrography to visualize the position of the disc, it wasoften found that the perceived clinical success was notassociated with a recaptured disc. For instance, in anMRI study involving 30 clicking joints treated with theSved-type splint, it was reported that although jointnoises were eliminated in 27 joints, disc repositioningoccurred in only three joints (Kirk, 1991). Similarly,Manco and Messing (1986) found that even though jointnoises were eliminated, 41.8% of the discs evaluatedwith direct sagittal computed tomography were not repo-sitioned after ARSplint therapy.

Taken together, these data suggest that subjectivereports of improvements following ARSplint therapy donot generally occur as the result of disc recapturing.Furthermore, the specificity of joint sounds as a sign ofDD or as an outcome variable to measure the success ofsplint therapy for DD may be questioned, since displaceddiscs visualized with arthrography in the absence of jointsounds have also been reported (Roberts et al., 1986). Itis interesting to note that the absence of changes in theposition of displaced discs in the presence of positiveclinical outcome has also been reported in studies usingother treatment modalities such as the stabilizing splint,as discussed above, or following successful arthroscopicsurgery (Gabler et al., 1989).

These data further suggest that the symptoms asso-

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ciated with DD do not always occur as a result of a dis-placed disc. In light of these results, the "Phase II" con-cept of therapy-where irreversible alterations of thedentition with occlusal equilibration, prosthodontics,orthodontics, or orthognathic surgery are performed tostabilize the recaptured disc-becomes totally unjusti-fied. This is even more true considering the frequentreturn of signs and symptoms of DD after/during post-splint extensive oral reconstruction: For example, thedisc was displaced again in 33% of the patients after 6months' treatment with mandibular repositioning onlays(Westesson and Lundh, 1988), while joint noisesrecurred in 43% during or soon after the completion ofmajor prosthodontic treatment (Moloney and Howard,1986). In patients who received orthodontic intervention,500o experienced a return in joint sounds, and in 35%,pain recurred during the treatment (Moloney andHoward, 1986). These high relapse rates inspire cautionagainst the use of invasive therapies.

The literature on the use of a soft oral splint in thetreatment of DD is more limited. Favorable results suchas a decrease in pain and joint noises have been report-ed following 20 days of continuous use of a soft splint (24hrs/day; Harkins et al., 1988). However, the validity ofthese data is questionable, since they were not collectedunder blind conditions, and patients were not random-ized into treatment groups. Furthermore, there are con-cerns that the use of soft splints may be associated withocclusal changes (Singh and Berry, 1985; Harkins et al.,1988).

Taken together, the available data indicate that,although oral splints have been repeatedly reported tobe effective in improving the range of mandibular motionand in decreasing pain and joint noises associated withDD, these results need to be confirmed with well-designed clinical trials. Furthermore, the belief that thedisc can be either consistently recaptured or predictablystabilized by oral splints is not supported by any of theimaging studies reviewed so far. If the clinical improve-ments observed in DD patients are not associated withapparent changes in the disc position, it becomes evi-dent that disc repositioning should not constitute theultimate objective of the splint. Moreover, in view of thequestionable benefits and the potential harmful effectsassociated with ARSplints (i.e., uncontrolled tooth move-ments; Brown et al., 1994), and the expense and invasive-ness of so-called "Phase II" therapy, we conclude thatthese approaches appear unacceptable in either theshort- or long-term treatment of DD.

Our conclusion is further supported by the body ofevidence suggesting that DD is unlikely to be a progres-sive disorder in the majority of patients. For instance, ithas been reported that 40% of the patients who had onlycounseling for DD were symptom-free after 8-15 years(Pedersen and Hansen, 1987); the condition was consid-

ered unchanged in 50%, and was aggravated in 7% of thepatients. A three-year follow-up of 70 patients with DDRwhose symptoms relapsed after splint treatmentrevealed that reciprocal clicking remained unchanged in71% of the patients and disappeared in 29% (Lundh et al.,1987). Only 9% developed locking. Similar data wereobtained by Greene and Laskin (1988) through a tele-phone survey of 203 patients who presented with painfulclicking joints and were treated with conservativeapproaches from 1 to 15 years earlier: Thirty percentreported that the joint noises had disappeared, 33%reported improvement, and 36% reported no change.Only 1% reported that their condition had become worse.When De Leeuw et al. (1994) compared the findings in 99patients with clinical signs of DD before and 30 yearsafter non-surgical and non-repositioning treatment, theyfound that the degree of mouth-opening remained stable(and acceptable) in patients with DDR, but increased sig-nificantly in the majority of patients with DDWR. Theprevalence of joint clicking remained unchanged in bothgroups. The generally favorable prognosis observed dur-ing the natural course of DD speaks against the use ofany splint therapy associated with potential iatrogenicsequellae.

(IV) Oral Splints in theManagement of Bruxism

(A) PHYSIOLOGICAL MECHANISMAmong the applications of oral splints, their use as aprotective device against the potential dental and periodon-tal damage induced by sleep bruxism is perhaps the leastcontested, while information about daytime bruxism isstill lacking. However, the concept that oral splints canbe used to treat bruxism by removing the occlusal inter-ferences that are thought to trigger bruxing activity(Ramfjord, 1961; Krogh-Poulsen and Olsson, 1966;Schaerer et al., 1967; Kawazoe et al., 1980; Sheikholeslamet al., 1986) is no longer tenable. It has been shown thatocclusal adjustments do not stop sleep bruxism (Baileyand Rugh, 1980), and that experimentally placed deflec-tive occlusal contacts reduce rather than enhance masti-catory muscle activity during sleep (Rugh et al., 1984).Furthermore, epidemiological data indicate that bruxersand control subjects cannot be distinguished on thebasis of their morphological occlusal characteristics(Greene and Marbach, 1982).

Currently, there are no reliable data to support theetiologic role of occlusion in bruxism, and instead theavailable evidence tends to favor a central nervous sys-tem and behavioral involvement rather than a specificperipheral cause. A recent review on the epidemiologyand pathophysiology of sleep bruxism reveals that thisdisorder can occur in the presence of various psychiatric,neurological, and systemic disorders (Lavigne and

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Montplaisir, 1995). Sleep bruxism may be associatedwith the autonomic arousal response, or result frominteractions between the limbic and motor systems(Lavigne and Montplaisir, 1995). There is also emergingevidence suggesting that some neurotransmitters maybe implicated in the pathophysiology of sleep bruxism(Lobbezoo et al., 1997). Other reported exacerbating fac-tors include stress, drugs or alcohol, disease, and per-sonality (Lavigne and Montplaisir, 1995).

In light of these data, it is no longer reasonable toaccept occlusion as the cause of bruxism. Therefore, thehypothesis that oral splints work by removing occlusalinterferences becomes questionable, and in addition,the efficacy of oral splints in decreasing bruxing activityis also debatable, as reviewed below.

(B) CLINICAL EFFICACY/EFFECTIVENESSSeveral studies have reported that the use of oral splintswas associated with a decrease in nocturnal EMG activi-ty in the masticatory muscles (Ramfjord, 1961; Fuchs,1975; Rugh and Solberg, 1975; Solberg et al., 1975;Kawazoe et al., 1980; Hamada et at., 1982; Sheikholeslamet at., 1986; Pierce and Gale, 1988; Kurland, 1993). Thiseffect appeared to be transient, since the EMG valuesreturned to baseline levels when the treatment was with-drawn (Rugh and Solberg, 1975; Solberg et al., 1975; Clarket al., 1979; Sheikholeslam et al., 1986; Pierce and Gale,1988). The decrease in the EMG data was interpreted asbeing the result of a reduction in bruxism activity, withthe return to their original values perceived as a resump-tion of the parafunctional activity. These inferences arenot supported by the evidence that we shall reviewbelow. First, the majority of these early studies relied onthe average EMG scores rather than on any measures ofthe frequency, intensity, and duration of the rhythmic jawactivity (including EMG, audio, or video signals) that arenow considered critical in the evaluation of sleep brux-ism (Lavigne et al., 1996). Second, we cannot rule out thepossibility that the observed decrease in the EMG activ-ity during the treatment and its post-treatment increasecould reflect the non-specific and transient responses ofthe jaw elevator muscles to the changes in the VDOobtained with the splints (Dahlstrom and Carlsson, 1984;Dahlstrom and Haraldson, 1985; Dahlstrom et al., 1985;Holmgren et al., 1985; Graham and Rugh, 1988; Naeijeand Hansson, 1992; Lobbezoo et al., 1993; Visser et al.,1995; see section on MFP, above). Third, opposite resultshave also been reported. Within the same study, Okeson(1987) found no significant change in the EMG activity intwo out of ten of the patients who had a hard maxillarysplint and in four out of ten of those who wore a soft one.More importantly, five out of the ten patients who hadthe soft splint showed a significant increase in the EMGscores. Similarly, when the effects of canine vs. molarguidance on hard splints were compared in bruxers, it

was found that both splints decreased the nightly EMGmasseter values in three subjects, but increased thesescores in three other subjects (Rugh et at., 1989). Otherresearchers simply reported that the occlusal splints donot stop sleep bruxism (Gentz, 1972; Kydd and Daly,1985; Holmgren et at., 1993). A noticeable increase inclenching and bruxing in some patients wearing the softresilient appliances has also been reported (Harkins etat., 1988). These contrasting data suggest that the sleepbruxers' EMG responses to splint therapy are not pre-dictable. Furthermore, since occlusion is no longerregarded as an important etiopathologic variable insleep bruxism, the use of "occlusal" splints should bereconsidered as a more limited treatment modality. Theycan potentially be useful as habit management aids, andthey definitely can protect the dental/periodontal struc-tures against some of the adverse effects of prolongedhyper-loading. Again, the "post-splint Phase 11 therapy"for bruxism where extensive occlusal rehabilitation isadvocated for more permanent results (Yustin et al., 1993)becomes unjustifiable.

(V) The ArthritidesThe literature pertaining to the use of oral splints in themanagement of the arthritides is very sparse and mostlyanecdotal. For osteoarthritis of the TMJ, oral splints mayhave been adopted following the belief that functionalloading, which is thought to be caused by the loss ofmolar support or to occur during mastication or bruxism,may play a role in the cause and progression of the dis-order (Kopp and Carlsson, 1988). In patients withrheumatoid arthritis who present with a destruction ofthe condyle and a consequent rapid progression of thedentition toward an open bite, oral splints have alsobeen used to provide a temporary stabilization of theocclusion before proceeding with a permanent prosthet-ic rehabilitation or occlusal adjustment (Kopp, 1994).Whatever the rationale proposed to support the use oforal appliances, it would be presumptuous to pretendthat we could treat these degenerative, connective tis-sue, and/or autoimmune disorders with a simpleocclusal approach. Moreover, it is important to note thatno specific study has ever been conducted to assesseither their efficacy or their effectiveness in the treat-ment of the arthritides affecting the TMJ. It is thus pru-dent at this time to restrict the use of oral splints as anadjunct to the palliative management of the symptomsassociated with these conditions.

(VI) ConclusionDespite the nearly universal prescription of oral splintsin the treatment of TMDs or bruxism, the quality of theevidence supporting the mechanisms of action suggest-ed for their presumed efficacy is still questionable. Thisis not surprising, since their efficacy itself remains

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unestablished, and the rationale underlying each of themechanisms proposed is based on unsubstantiatedhypothetical etiologies. Although the prospect for curingTMDs and/or bruxism, or trying to eliminate theirunknown cause, remains an unrealistic expectation, itstill can be argued that improving the patient's percep-tion of well-being, or changing harmful habits throughthe judicious application of a non-invasive and cost-effi-cient management strategy (such as the use of stabiliz-ing splints), may represent an acceptable alternative.This strategy also may be justifiable in light of the evi-dence showing that painful TMD can undermine thepatient's quality of life significantly (Reisine and Weber,1989; Dao et al., 1994a,b) and cause substantial psycho-logical distress (Turk and Rudy, 1990; Von Korff et al.,1992). However, the limitations of this approach shouldbe acknowledged by practitioners so that faulty extrapo-lations from the treatment outcome and the unfounded"Phase 11 therapy" can be avoided. If we recognize thatthe apparent improvements observed in most of thestudies on oral splints could be due to the non-specificeffects of treatment (i.e, placebo, doctor-patient rela-tionship), or the natural cyclic evolution of the condition,also referred to as the regression toward the mean(Whitney and Von Korff, 1992), then we must concludethat oral splints can be used only as an adjunct to TMDpain patient management, until the natural history andthe etiologies of TMDs are elucidated, and more specifictreatments for these conditions are developed. For brux-ism, as mentioned earlier, it is prudent to limit the use oforal splints for habit management and to prevent/limitthe dental damage potentially induced by the disorder.In summary, it is critical to keep in mind that oral splintsdo not cure, but they may contribute to the patient'swell-being just like crutches, which are useful as a non-specific "healing aid" during a patient's orthopedic reha-bilitation phase, but which are not regarded as a prima-ry or definitive treatment modality.

AcknowledgmentsThe authors thank Drs. A Charbonneau, J.S Feine, and I.P. Lund fortheir contributions in earlier clinical trials. G.I. Lavigne is presentlysupported by the Medical Research Council of Canada and the Fondsde la Recherche en Sante du Quebec.

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