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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.
REFERENCESAhlin IH (1991). Clinical application of remoldable
appli-
ances for craniomandibular disorder. Cranio Clin Int1 65-79.
Allen ID, Rivera-Morales WC, Zwemer ID (1990). Theoccurrence of
temporomandibular disorder symp-toms in healthy young adults with
and without evi-dence of bruxism. Cranio 8:312-318.
Anderson GC, Schulte JK, Goodkind RI (1985).
Comparative study of two treatment methods forinternal
derangement of the temporomandibularjoint. I Prosthet Dent
53:392-397.
Annandale T (1887). Displacement of the inter-articularcartilage
of the lower jaw, and its treatment by opera-tion. Lancet 1:41
1.
Antczak-Bouckoms A (1995). Reaction papers to chapters12 and 13.
In: Temporomandibular disorders andrelated pain conditions. Sessle
BJ, Bryant PS, DionneRA, editors. Seattle: IASP Press, pp.
237-245.
Athanasiou AE, Papadopoulos MA, Mazaheri M,Lagoudakis M (1994).
Cephalometric evaluation ofpharynx, soft palate, adenoid tissue,
tongue, andhyoid bone following the use of a mandibular
reposi-tioning appliance in obstructive sleep apnea patients.Int J
Adult Orthod Orthognath Surg 9:273-283.
Bailey IO, Rugh JD (1980). Effect of occlusal adjustmenton
bruxism as monitored by nocturnal EMG record-ings (abstract). I
Dent Res 59:317.
Blaschke DD, Blaschke T] (1981). Normal TMJ bony rela-tionships
in centric occlusion. J Dent Res 60:98-104.
Bledsoe S (1991). Selection, application and manage-ment of
temporomandibular disorders: a post-treat-ment comparison between
patients from a universityclinic and from private practice. Cranio
Clin Int 1: 13-38.
Block LS (1947). Diagnosis and treatment of distur-bances of the
temporomandibular joint, especially inrelation to vertical
dimension. J Am Dent Assoc 34:253-260.
Brand JW, Whinery IG Ir, Anderson QN, Keenan KM(1989). The
effects of temporomandibular joint inter-nal derangement and
degenerative joint disease ontomographic and arthrotomographic
images. OralSurg Oral Med Oral Pathol 67:220-223.
Brooke RI, Grainger RM (1988). Long-term prognosis for
theclicking jaw. Oral Surg Oral Med Oral Pathol 65:668-670.
Brown DT, Gaudet EL, Phillips C (1994). Changes in ver-tical
tooth position and face height related to long-term anterior
repositioning splint therapy. Cranio12:19-22.
Carlson N, Moline D, Huber L, Jacobson 1 (1993).Comparison of
muscle activity between conventionaland neuromuscular splints. J
Prosthet Dent 70:39-43.
Carraro IJ, Caffesse RG (1978). Effect of occlusal splintson TMJ
symptomatology. J Prosthet Dent 40:563-566.
Chapman CE (1991). Can the use of physical modalitiesfor pain
control be rationalized by research evidence?Can J Physiol
Pharmacol 69:704-712.
Chen CW, Boulton IL, Gage JP (1995). Effects of splinttherapy in
TMI dysfunction: a study using magneticresonance imaging. Aust Dent
J 40.71-78.
Choi BH, Yoo IH, Lee WY (1994). Comparison of magnet-ic
resonance imaging before and after nonsurgicaltreatment of closed
lock. Oral Surg Oral Med Oral Pathol78:301-305.
9(3)345361998 Cri Re Ora Bil Me 35355Crit Rev Oral Biol
Med9(3):345-361 11998)
by on August 28, 2009 http://cro.sagepub.comDownloaded from
http://cro.sagepub.com
-
Christensen 1 (1970). Effect of occlusion-raising proce-dures on
the chewing system. Dent Pract 20:233-238.
Clark GT (1984). A critical evaluation of orthopedic
inter-occlusal appliance therapy: design, theory, and over-all
effectiveness. J Am Dent Assoc 108:359-364.
Clark GT (1988). Interocclusal appliance therapy. In: Atextbook
of occlusion. Mohl ND, Zarb GA, CarlssonGE, Rugh ID, editors.
Chicago: Quintessence, pp. 271-284.
Clark GT, Adler RC (1985). A critical evaluation of
occlusaltherapy: occlusal adjustment procedures. J Am DentAssoc
110:743-750.
Clark GT, Sakai S (1990). Masticatory muscle hyperactivi-ty and
muscle pain. Adv Pain Res Ther 17:201-212.
Clark GT, Beemsterboer PL, Solberg WK, Rugh ID (1979).Nocturnal
electromyographic evaluation of myofas-cial pain dysfunction in
patients undergoing occlusalsplint therapy. I Am Dent Assoc
99:607-611.
Clark GT, Lanham F, Flack VF (1988). Treatment outcomeresults
for consecutive TMJ clinic patients. JCraniomandib Disord
2:87-95.
Clark GT, Choi J, Browne PA (1995). The efficacy of physi-cal
medicine treatment, including occlusal appli-ances, for a
population with temporomandibular dis-orders. In: Temporomandibular
disorders and relatedpain conditions. Sessle BJ, Bryant PS, Dionne
RA, edi-tors. Seattle: IASP Press, pp. 375-397.
Clayton JA (1995). Occlusion and prosthodontics. DentClin North
Am 39:313-333.
Cohen SG, MacAfee KA (1994). The use of magnetic res-onance
imaging to determine splint position in themanagement of internal
derangements of the tem-poromandibular joint. Cranio
12:167-171.
Costen lB (1934). A syndrome of ear and sinus symptomsdependent
upon disturbed function of temporo-mandibular-joint. Ann Otol
Rhinol Laryngol 43:1-15.
Dahlstrom L, Carlsson SG (1984). Treatment of mandibu-lar
dysfunction: the clinical usefulness of biofeedbackin relation to
splint therapy. J Oral Rehabil 11:277-284.
Dahlstrom L, Haraldson T (1985). Bite plates and stabi-lization
splints in mandibular dysfunction. A clinicaland electromyographic
comparison. Acta OdontolScand 43:109-114.
Dahlstrom L, Carlsson GE, Carlsson SG (1982).Comparison of
effects of electromyographic biofeed-back and occlusal splint
therapy on mandibular dys-function. Scand I Dent Res
90:151-156.
Dahlstrom L, Haraldson T, Janson ST (1985).Comparative
electromyographic study of bite platesand stabilization splints.
Scand J Dent Res 93:262-268.
Dao TTT, Lavigne GC, Charbonneau A, Feine IS, Lund IP(1994a).
The efficacy of oral splints in the treatment ofmyofascial pain of
the jaw muscles: a controlled clin-ical trial. Pain 56:85-94.
Dao TTT, Lund IP, Lavigne GC (1 994b). Comparison of pain
and quality of life in bruxers and patients withmyofascial pain
of the masticatory muscles. I OrofacPain 8:350-356.
Dao TTT, Lund JP, Lavigne GC (1995a). How effective
issumatriptan in relieving myofascial pain of the masti-catory
muscles? (abstract). I Dent Res 74:223.
Dao TTT, Lund JP, Remillard G, Lavigne GC (1995b). Ismyofascial
pain of the temporal muscles relieved byoral sumatriptan? A
cross-over pilot study. Pain62:241-244.
Dawson PE (1974). Evaluation, diagnosis and treatmentof occlusal
problems. 1st ed. St. Louis: C.V. Mosby.
Dawson PE (1989). Evaluation, diagnosis and treatmentof occlusal
problems. 2nd ed. St. Louis: C.V. Mosby.
de Leeuw R, Boering G, Stegenga B, De Bont LG (1994).Clinical
signs of TMI osteoarthrosis and internalderangement 30 years after
nonsurgical treatment. IOrofac Pain 8:18-24.
DeRouen TA (1995). Statistical and methodologicalissues in
temporomandibular disorder research. In:Temporomandibular disorders
and related pain con-ditions. Sessle BJ, Bryant PS, Dionne RA,
editors.Seattle: IASP Press, pp. 459-465.
Dolwick MF (1995). Temporomandibular joint disk dis-placement:
clinical perspectives. In:Temporomandibular disorders and related
pain con-ditions, Progress in pain research and management.Sessle
BJ, Bryant PS, Dionne RA, editors. Seattle: IASPPress, pp.
79-87.
Dolwick MF, Riggs RR (1983). Diagnosis and treatment ofinternal
derangements of the temporomandibularjoint. Dent Clin North Am
27:561-572.
dos Santos J, Suzuki H, Ash MM (1988). Mechanicalanalysis of the
equilibrium of occlusal splints. IProsthet Dent 59:346-352.
Dumas AL, Moaddab MB, Homayoun NH, McDonough J(1986). A
three-dimensional developmental measure-ment of the
temporomandibular joints. Cranio 4:23-35.
Durham TM, Hodges ED, Henry MJ, Geasland J, Straub P(1993).
Management of orofacial manifestations ofParkinson's disease with
splint therapy: a case report.Spec Care Dentist 13:155-158.
Dworkin SF, LeResche L (1992). Research diagnostic cri-teria for
temporomandibular disorders: review, crite-ria, examinations and
specifications, critique. JCraniomandib Disord Facial Oral Pain
6:301-355.
Dworkin SF, LeResche L, Von Korff M, Dicker B, SommersE,
Truelove E (1991). Constant, remitted, and cyclicpain patterns in
TMD: three-year follow-up (abstract).J Dent Res 70:441.
Eckerdal 0, Lundberg M (1979). Temporomandibular jointrelations
as revealed by conventional radiographictechniques. Dentomaxillofac
Radiol 8:65-70.
Egermark-Eriksson 1, Carlsson GE, Ingervall B (1981).
356 Grit Rev Oral Biol Med (1998)356 Crit Rev Oral Biol Med
9(3):345-361 (1998) by on August 28, 2009
http://cro.sagepub.comDownloaded from
http://cro.sagepub.com
-
Prevalence of mandibular dysfunction and orofacialparafunction
in 7-, 11 -, 15-year-old Swedish children.Eur I Orthodont
3:163-172.
Feine JS, Lavigne Gl (1995). Assessment of treatment effi-cacy
for chronic orofacial pain. In: Brain and oral func-tions. Morimoto
T, Masuya T, Takada K, editors.Amsterdam: Elsevier, pp.
257-264.
Feine IS, Lavigne GI, Dao TTT, deGrandmont P,Charbonneau A, Lund
IP (1992). Retrospective psy-chometric reports are poor estimates
of treatmentsuccess. Controlled Clin Trials 13:433.
Fries IF (1983). Toward an understanding of patient out-come
measurement. Arthrit Rheum 26:697-704.
Fries IF (1991). The hierarchy of quality-of-life assess-ment,
the health assessment questionnaire (HAQ),and issues mandating
development of a toxicityindex. Controlled Clin Trials 12(Suppl):
106S-1 17S.
Fries JF, Spitz P, Kraines RG, Holman HR (1980).Measurement of
patient outcome in arthritis. ArthritRheum 23:137-145.
Fuchs P (1975). The muscular activity of the chewingapparatus
during night sleep. I Oral Rehabil 2:35-48.
Gabler MJ, Greene CS, Palacios E, Perry HT (1989). Effectof
arthroscopic temporomandibular joint surgery onarticular disc
position. I Orofac Pain 3:191-202.
Gentz R (11972). Apparatus for recording bruxism duringsleep.
Swed Dent 1 65:327-342.
George PT (1993). Treatment of snoring and obstructivesleep
apnea with a dental device. Gen Dent 41:294-298.
Glass EG, McGlynn FD, Glaros AG (1991). A survey oftreatments
for myofascial pain dysfunction. Cranio9: 165- 168.
Glass EG, Glaros AG, McGlynn FD (1993). Myofascial
paindysfunction: treatments used by ADA members.Cranio 11
25-29.
Goodman P, Greene CS, Laskin DM (1976). Response ofpatients with
myofascial pain-dysfunction syndrometo mock equilibration. I Am
Dent Assoc 92:755-758.
Goulet JP, Lund IP, Montplaisir I, Lavigne G (1993).
Dailyclenching, nocturnal bruxism, and stress and theirassociation
with TMD symptoms. I Orofac Pain 7:120.
Goulet JP, Montplaisir 1, Lund JP, Lavigne G (1994).Relations
entre les habitudes parafonctionnelles, lestress, et les symptomes
temporomandibulaires. In:9e Colloque de l'Association
InternationaleFrancophone de Recherche Odontologique
(AIFRO).Simard-Savoie S, editor. Montreal: Meridien, pp.
139-144.
Goulet IP, Lavigne GI, Lund JP (1995). law pain preva-lence
among French-speaking Canadians in Quebecand related symptoms of
temporomandibular disor-ders. I Dent Res 74:1738-1744.
Graf H (1969). Bruxism. Dent Clin North Am 13:659-665.Graham GS,
Rugh JD (1988). Maxillary splint occlusal
guidance patterns and electromyographic activity of
the jaw-closing muscles. I Prosthet Dent 59:73-77.Gray RI,
Quayle AA, Hall CA, Schofield MA (1994).
Physiotherapy in the treatment of temporomandibu-lar joint
disorders: a comparative study of four treat-ment methods. Br Dent
1 176:257-261.
Greene CS, Laskin DM (1971). Meprobamate therapy forthe
myofascial pain-dysfunction (MPD) syndrome: adouble-blind
evaluation. I Am Dent Assoc 82:587-590.
Greene CS, Laskin DM (1972). Splint therapy for themyofascial
pain-dysfunction (MPD) syndrome: a com-parative study. J Am Dent
Assoc 84:624-628.
Greene CS, Laskin DM (1983). Long-term evaluation oftreatment
for myofascial pain-dysfunction syndrome:a comparative analysis. I
Am Dent Assoc 107:235-238.
Greene CS, Laskin DM (1988). Long-term status of TMJclicking in
patients with myofascial pain and dysfunc-tion. J Am Dent Assoc
117:461-465.
Greene CS, Marbach 11 (1982). Epidemiologic studies
ofmandibular-dysfunction: A critical review. J ProsthetDent
48:184-190.
Haden JL (1983). Occlusal finalization following TMJ ther-apy. I
Craniomandib Pract 1: 15-19.
Hamada T, Kotani H, Kawazoe Y, Yamada S (1982). Effectof
occlusal splints on the EMG activity of masseterand temporal
muscles in bruxism with clinical symp-toms. I Oral Rehabil
9:119-123.
Hampf G (1992). A new clinical approach to the treat-ment of
temporomandibular dysfunction and orofa-cial dysesthesia: natural
history and comparisonswith similar chronic pain conditions. I
CraniomandibDisord 6:56-63.
Harkins S, Marteney IL, Cueva 0, Cueva L (1988).Applications of
soft occlusal splints in patients suf-fering from clicking
temporomandibular joints. ICraniomandib Pract 6:71-76.
Hatcher DC, Blom RI, Baker CG (1986).Temporomandibular joint
spatial relationships.Osseous and soft tissues. I Prosthet Dent
56:344-353.
Holmgren K, Sheikholeslam A, Riise C (1985). An
elec-tromyographic study of the immediate effect of anocclusal
splint on the postural activity of the anteriortemporal and
masseter muscles in different bodypositions with and without visual
input. I Oral Rehabil12:483-490.
Holmgren K, Sheikholeslam A, Riise C (1993). Effect of
afull-arch maxillary occlusal splint on parafunctionalactivity
during sleep in patients with nocturnal brux-ism and signs and
symptoms of craniomandibulardisorders. I Prosthet Dent
69:293-297.
Huggins KH, Dworkin SF, LeResche L, Truelove E (1996).Five-year
course for temporomandibular disordersusing RDC/TMD (abstract). I
Dent Res 75:352.
Huggins KH, Truelove EL, Dworkin S, LeResche L,Sommers E,
Schubert M (1997). Randomized clinicaltrial (RCT) of a soft splint
for TMD (abstract). I Dent Res
9(3(345-361 (1998) Crit Rev Oral Biol Med357
Crit Rev Oral Biol Med 3579(3):345-361 (1998) by on August 28,
2009 http://cro.sagepub.comDownloaded from
http://cro.sagepub.com
-
76:389.Israel HA (1994). Current concepts in the surgical
man-
agement of temporomandibular joint disorders. l OralMaxillofac
Surg 52:289-294.
Ito T, Gibbs CH, Marguelles-Bonnet R, Lupkiewicz SM,Young HM,
Lundeen HC, et al. (1986). Loading on thetemporomandibular joint
with five occlusal condi-tions. J Prosthet Dent 56:478-484.
Kai S, Kai H, Tashiro H (1994). Tardive dyskinesia affect-ed by
occlusal treatment-a case report. Cranio12:199-203.
Kawazoe Y, Kotani H, Hamada T, Yamada S (1980). Effectof
occlusal-splints on the electromyographic activi-ties of masseter
muscles during maximum clenchingin patients with
myofascial-pain-dysfunction-syn-drome. I Prosthet Dent
43:578-580.
Kirk WS Jr (1991). Magnetic resonance imaging andtomographic
evaluation of occlusal appliance treat-ment for advanced internal
derangement of the tem-poromandibular joint. J Oral Maxillofac Surg
49:9-12.
Kopp S (1994). Rheumatoid arthritis. In:Temporomandibular joint
and masticatory muscledisorders. Zarb GA, Carlsson GE, Sessle BI,
Mohl ND,editors. Copenhagen: Munksgaard, pp. 346-355.
Kopp S, Carlsson GE (1988). The temporomandibularjoint: problems
related to occlusal function. In: Atextbook of occlusion. Mohl ND,
Zarb GA, CarlssonGE, Rugh JD, editors. Chicago: Quintessence, pp.
235-248.
Krogh-Poulsen WE, Olsson A (1966). Occlusal dishar-monies and
dysfunction of the stomatognathic sys-tem. Dent Clin North Am
10:627-635.
Kuboki T, Azuma Y, Orsini MG, Hirooka T, Yatani H,Yamashita A
(1997). The effect of occlusal appliancesand clenching on the
temporomandibular jointspace. J Orofac Pain 11:67-77.
Kurland P (1993). Night-grinding (letter). Br Dent J 174:55.Kydd
WL, Daly C (1985). Duration of nocturnal tooth con-
tacts during bruxing. J Prosthet Dent 53:717-72 1.Lamey PJ,
Steele JG (1996). Migraine: the effect of acrylic
appliance design on clinical response. Br Dent J180:137-140.
Lavigne GJ, Montplaisir I (1995). Bruxism.
Epidemiology,diagnosis, pathophysiology and pharmacology.
In:Orofacial pain and temporomandibular disorders.Fricton JR,
Dubner R, editors. New York: Raven Press,pp. 387-404.
Lavigne G, Kim JS, Valiquette C, Lund JP (1987). Evidencethat
periodontal pressoreceptors provide positivefeedback to jaw closing
muscles during mastication. INeurophysiol 58:342-358.
Lavigne GJ, Rompre PH, Montplaisir JY (1996). Sleepbruxism:
validity of clinical research diagnostic crite-ria in a controlled
polysomnographic study. J Dent Res75: 546-552.
Lavigne GI, Rompre PH, Montplaisir IY, Lobbezoo F(1997). Motor
activity in sleep bruxism with concomi-tant jaw muscle pain. A
retrospective pilot study. EurJ Oral Sci 105:92-95.
Le Bell Y, Kirveskari P (1985). Treatment of reciprocalclicking
of the temporomandibular joint using amandibular repositioning
splint and occlusal adjust-ment. Proc Finn Dent Soc 81:251-255.
Lew KK (1992). Orthodontic finalization following thera-py with
an anterior repositioning splint. Int J AdultOrthodont Orthognath
Surg 7:251-263.
Linde C, Isacsson G, lonsson BG (1995). Outcome of 6-week
treatment with transcutaneous electric nervestimulation compared
with splint on symptomatictemporomandibular joint disk displacement
withoutreduction. Acta Odontol Scand 53:92-98.
List T, Helkimo M, Andersson S, Carlsson GE (1992).Acupuncture
and occlusal splint therapy in the treat-ment of craniomandibular
disorders. Part 1. A com-parative study. Swed Dent 1
16:125-141.
Lobbezoo F, Lavigne Gl (1997). Do bruxism and tem-poromandibular
disorders have a cause-and-effectrelationship? I Orofac Pain
11:15-23.
Lobbezoo F, van der Glas HW, van Kampen FM, BosmanF (1993). The
effect of an occlusal stabilization splintand the mode of visual
feedback on the activity bal-ance between jaw-elevator muscles
during isometriccontraction. I Dent Res 72:876-882.
Lobbezoo F, Lavigne GJ, Tanguay R, Montplaisir JY (1997).The
effect of catecholamine precursor L-dopa onsleep bruxism: a
controlled clinical trial. MovementDisord 12:73-78.
Locker D, Slade G (1988). Prevalence of symptoms asso-ciated
with temporomandibular disorders in aCanadian population. Community
Dent Oral Epidemiol16:310-313.
Long JH Jr (1995). Interocclusal splint designed to
reducetenderness in lateral pterygoid and other muscles
ofmastication. I Prosthet Dent 73:316-318.
Lowe AA (1994). Dental appliances for the treatment ofsnoring
and obstructive sleep apnea. In: Principlesand practice of sleep
medicine. Kryger MH, Roth T,Dement WC, editors. Philadelphia:
Saunders, pp. 722-735.
Lund IP (1995). Pain and the control of muscles. Adv PainRes
Ther 21:103-1 15.
Lund IP, Widmer CG (1989). An evaluation of the use ofsurface
electromyography in the diagnosis, documen-tation and treatment of
dental patients. J CraniomandibDisord Facial Oral Pain
3:125-137.
Lund JP, Widmer CG, Schwartz G (1989). What is the linkbetween
myofascial pain and dysfunction? In: EMG ofjaw reflexes in man. Van
Steenberghe D, De Latt A,editors. Leuven: Leuven University Press,
pp. 427-444.
Lund JP, Donga R, Widmer CG, Stohler CS (1991). The
358~~~~~~~~~ ~GrtRvOa ()3531(98358 Crit Rev Oral Biol Med
9(3):345-361 (1998) by on August 28, 2009
http://cro.sagepub.comDownloaded from
http://cro.sagepub.com
-
pain adaptation model: a discussion of the relation-ship between
chronic musculoskeletal pain andmotor activity. Can J Physiol
Pharmacol 69:683-694.
Lund JP, Stohler CS, Widmer CG (1993). The relationshipbetween
pain and muscle activity in fibromyalgia andsimilar conditions. In
Progress in fibromyalgia andmyofascial pain. Voeroy H, Merskey H,
editors.Amsterdam: Elsevier, pp. 311-327.
Lundh H, Westesson PL, Kopp S, Tillstrom B (1985).Anterior
repositioning splint in the treatment of tem-poromandibular joints
with reciprocal clicking: com-parison with a flat occlusal splint
and an untreatedcontrol group. Oral Surg Oral Med Oral Pathol
60:131-1 36.
Lundh H, Westesson PL, Kopp S (1987). A three-year fol-low-up of
patients with reciprocal temporomandibu-lar joint clicking. Oral
Surg Oral Med Oral Pathol 63:530-533.
Lundh H, Westesson PL, Jisander S, Eriksson L
(1988).Disk-repositioning onlays in the treatment of
tem-poromandibular joint disk displacement: comparisonwith a flat
occlusal splint and with no treatment. OralSurg Oral Med Oral
Pathol 66:155-162.
Lundh H, Westesson PL, Eriksson L, Brooks SL
(1992).Temporomandibular joint disk displacement withoutreduction.
Treatment with flat occlusal splint versusno treatment. Oral Surg
Oral Med Oral Pathol 73:655-658.
Magnusson T, Carlsson GE, Egermark 1 (1993). Changesin
subjective symptoms of craniomandibular disor-ders in children and
adolescents during a 10-yearperiod. J Orofac Pain 7:76-82.
Manco LG, Messing SG (1986). Splint therapy evaluationwith
direct sagittal computed tomography. Oral Surg61 5-1 1.
Manns A, Miralles R, Santander H, Valdivia J (1983).Influence of
the vertical dimension of occlusion in thetreatment of myofascial
pain-dysfunction syndrome. IProsthet Dent 50:700-709.
Manzione JV, Tallents R, Katzberg RW, Oster C, Miller TL(1984)
Arthrographically guided splint therapy forrecapturing the
temporomandibular joint meniscus.Oral Sura Oral Med Oral Pathol
57:235-240.
Milam SB (1995). Articular disk displacements anddegenerative
temporomandibular joint disease. In:Temporomandibular disorders and
related pain con-ditions. Progress in pain research and
management.Sessle BI, Bryant PS, Dionne RA, editors. Seattle:
IASPPress, pp. 89-112.
Minneman SA (1995). A history of oral protection for theECT
patient past, present, and future. Convulsive Ther11:94-103.
Moloney F, Howard IA (1986). Internal derangements ofthe
temporomandibular joint. III. Anterior reposition-ing splint
therapy. Aust Dent J 31:30-39.
Moncayo S (1994). Biomechanics of pivoting appliances.
I Orofac Pain 8:190-196.Mongini F (1984). The stomatognathic
system. Chicago:
Quintessence.Moritz M, Behr M, Held P, Dammer R, Niederdellmann
H
(1995). Comparative study of results of electronicaxiography
with results of magnetic resonance imag-ing including MRI-assisted
splint therapy. ActaStomatol Belg 92:35-38.
Naeije M, Hansson TL (1992). Short-term effect of stabi-lization
appliance on masticatory muscle activity inmyogenous
craniomandibular disorder patients.Craniomandib Disord Facial Oral
Pain 5:245-250.
Nevarro E, Barghi N, Rey R (1985). Clinical evaluation
ofmaxillary hard and resilient occlusal splints(abstract). J Dent
Res 64:3 13.
Nilner M (1983). Relationships between oral parafunc-tions and
functional disturbances and diseases of thestomatognathic system
among children aged 7-14years. Acta Odontol Scand 41:167-172.
Nitzan DW (1994). lntraarticular pressure in the function-ing
human temporomandibular joint and its alter-ation by uniform
elevation of the occlusal plane. IOral Maxillofac Surg
52:671-679.
Obrez A, Zhang X, Stohler CS (1993). The effect of exper-imental
muscle pain on mandibular range of motion(abstract). J Dent Res
72:372.
Okeson IP (1985). Fundamentals of occlusion and
tem-poromandibular disorders. St. Louis: C.V. Mosby.
Okeson IP (1987). The effect of soft and hard occlusalsplints on
nocturnal bruxism. J Am Dent Assoc 1 14:788-791.
Okeson JP, Kemper JT, Moody PM (1982). A study of theuse of
occlusal-splints in the treatment of acutechronic patients with
craniomandibular-disorders. JProsthet Dent 48:708-712.
Okeson JP, Moody PM, Kemper JT, Haley JV (1983).Evaluation of
occlusal splint therapy and relaxationprocedures in patients with
temporomandibular dis-orders. I Am Dent Assoc 107:420-424.
Osseiran HS (1995). Treating obstructive sleep apnea:can an
intraoral prosthesis help? I Am Dent Assoc126:461-466.
Pedersen A, Hansen H1 (1987). Long-term evaluation of211
patients with internal derangement of the tem-poromandibular joint.
Community Dent Oral Epidemiol15:344-347.
Pierce CI, Gale EN (1988). A comparison of differenttreatments
for nocturnal bruxism. I Dent Res 67:597-601.
Pierce CI, Weyant RI, Block HM, Nemir DC (1995). Dentalsplint
prescription patterns: a survey. J Am Dent Assoc126:248-254.
Posselt U (1968). Physiology of occlusion and rehabilita-tion.
Oxford: Blackwell Scientific Publications.
Pullinger A, Hollender L, Solberg WK, Petersson A
9)3) 345 361 (1998) Crit Rev Oral Biol Med 3599(3) 345-361 1998)
Crit Rev Oral Biol Med 359 by on August 28, 2009
http://cro.sagepub.comDownloaded from
http://cro.sagepub.com
-
(1985). A tomographic study of mandibular condyleposition in an
asymptomatic population. I ProsthetDent 53:706-713.
Quayle AA, Gray RJ, Metcalfe RI, Guthrie E, Wastell D(1990).
Soft occlusal splint therapy in the treatment ofmigraine and other
headaches. I Dent 18:123-129.
Ramfiord SP (1961). Bruxism, a clinical and electromyo-graphic
study. I Am Dent Assoc 62:21-44.
Ramfjord SP, Ash MM (1971). Occlusion. 2nd ed.Philadelphia: W.B.
Saunders.
Ramfjord S, Ash MM (1983). Occlusion. 3rd ed.Philadelphia: W.B.
Saunders.
Ramfjord SP, Ash MM (1994). Reflections on theMichigan occlusal
splint. I Oral Rehabil 21:491-500.
Reisine ST, Weber J (1989). The effects of temporo-mandibular
joint disorders on patient's quality of life.Community Dent Hlth
6:257-270.
Roberts CA, Tallents RH, Katzberg RW, Sanchez-Woodworth RE,
Manzione IV, Espeland MA, et al.(1986). Clinical and arthrographic
evaluation of tem-poromandibular joint sounds. Oral Surg Oral Med
OralPathol 62:373-376.
Rubinoff MS, Gross A, McCall WD (1987). Conventionaland
nonoccluding splint therapy compared forpatients with myofascial
pain dysfunction syndrome.Gen Dent Nov-Dec:502-506.
Rugh JD (1991). Behavioral therapy for temporomandibu-lar
disorders. Curr Opin Dent 1:497-502.
Rugh JD, Harlan 1 (1988). Nocturnal bruxism and
tem-poromandibular disorders. Adv Neurol 49:329-341.
Rugh ID, Robbins 1W (1982). Oral habit disorders. In:Behavioral
aspects in dentistry. Ingersoll BD, editor.New York:
Appleton-Century-Crofts, pp. 179-202.
Rugh ID, Solberg WK (1975). Electromyographic studiesof bruxist
behavior before and during treatment. CADent Assoc J 43:56-59.
Rugh JD, Solberg WK (1979). Psychological implicationsin
temporomandibular pain and dysfunction. In:Temporomandibular joint.
Function and dysfunction.Zarb G, Carlsson G, editors.
Copenhagen:Munksgaard, pp. 239-268.
Rugh ID, Barghi N, Drago CI (1984). Experimentalocclusal
discrepancies and nocturnal bruxism. IProsthet Dent 51:548-553.
Rugh ID, Graham GS, Smith IC, Ohrbach RK (1989).Effects of
canine versus molar occlusal splint guid-ance on nocturnal bruxism
and craniomandibularsymptomatology. J Craniomandib Disord Facial
Oral Pain3:203-210.
Sato S, Kawamura H, Motegi K (1995). Management ofnonreducing
temporomandibular joint disk displace-ment. Evaluation of three
treatments. Oral Surg OralMed Oral Pathol Oral Radiol Endod
80:384-388.
Scapino RP (1983). Histopathology associated with mal-position
of the human temporomandibular joint disc.
Oral Surg Oral Med Oral Pathol 55:382-397.Schaerer P, Stallard
RE, Zander HA (1967). Occlusal inter-
ferences and mastication: an electromyographicstudy. I Prosthet
Dent 17:438-449.
Schwarz N, Sudman S (1994). Autobiographical memoryand the
validity of retrospective reports. New York:Springer-Verlag.
Shapiro HH, Truex RC (1943). The temporomandibularjoint and the
auditory function. I Am Dent Assoc30:1147-1168.
Sheikholeslam A, Holmgren K, Riise C (1986). A clinicaland
electromyographic study of the long-term effectsof an
occlusal-splint on the temporal and massetermuscles in patients
with functional disorders andnocturnal bruxism. I Oral Rehabil
13:137-145.
Sicher H (1948). Temporomandibular articulation inmandibular
overclosure. I Am Dent Assoc 36:131 -139.
Simmons HC, Gibbs SI (1995). Recapture of temporo-mandibular
joint disks using anterior repositioningappliances: an MRI study.
Cranio 13:227-237.
Singh BP, Berry DC (1985). Occlusal changes followinguse of soft
occlusal splints. J Prosthet Dent 54:711-715.
Solberg WK, Clark GT, Rugh ID (1975). Nocturnal
elec-tromyographic evaluation of bruxism patients under-going
short-term splint therapy. J Oral Rehabil 2:215-223.
Spilker B (1991). Guide to clinical trials. New York:
RavenPress.
Sunakawa M, Chiang CY, Kwan CL, Hu JW, Sessle BI(1993).
Increased jaw electromyographic activityinduced by applications of
inflammatory irritant to rattooth pulp (abstract). In:
Abstracts-7th WorldCongress on Pain. International Association for
theStudy of Pain, editor. Seattle: IASP Publications, p.543.
Suvinen T, Reade P (1989). Prognostic features of value inthe
management of temporomandibular joint pain-dysfunction syndrome by
occlusal splint therapy. IProsthet Dent 61:355-361.
Tallents RH, Katzberg RW, Miller TL, Manzione IV, Oster C(1985).
Arthrographically assisted splint therapy. JProsthet Dent
53:235-238.
Tallents RH, Katzberg RW, Macher DI, Roberts CA (1990).Use of
protrusive splint therapy in anterior disk dis-placement of the
temporomandibular joint: a 1- to 3-year follow-up. J Prosthet Dent
63:336-341.
Timm TA, Ash MM (1977). The occlusal bite plane splint.An
adjunct to orthodontic treatment. J Clin Orthod11:383-390.
Tsuga K, Akagawa Y, Sakaguchi R, Tsuru H (1989). Ashort-term
evaluation of the effectiveness of stabi-lization-type occlusal
splint therapy for specific symp-toms of temporomandibular joint
dysfunction syn-drome. J Prosthet Dent 61:610-61 3.
Turk DC, Rudy TE (1990). The robustness of an empirical-
360 Crit Rev Oral Biol Med9(3)345-361 (1998)
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