Critical Reviews in Oral Biology & Medicine

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Oral Splints: the Crutches for Temporomandibular Disorders and Bruxism?

T.T. Dao and GJ Lavigne
Crit. Rev. Oral Biol. Med. 1998; 9; 345
DOI: 10.1177/10454411980090030701
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ORAL SPLINTS: THE CRUTCHES

FOR TEMPOROMANDIBULAR DISORDERS AND BRUXISM?
T.T.T. Dao
Faculty 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. Lavigne
Faculte de M6decine Dentaire, Universite de Montr6al; (entre de Recherche en Sciences Neurologiques, DNpartement de Physiologie, Faculte de M6decine, Universit6 de Montr6al, (entre
d'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 electromyographic activity of the masticatory muscles, modification of the patient's "harmful" oral behavior, and changes in the patient's
occlusion. Following a comprehensive review of the literature, it is concluded that any of these theories is either poor or inconsistent, while the issue of true efficacy for oral splints remains unsettled. However, the results of a controlled clinical trial lend
support to the effectiveness (i.e., the patient's appreciation of the positive changes which are perceived to have occurred during the trial) of the stabilizing splint in the control of myofascial pain. In light of the data supporting their effectiveness but
not their efficacy, oral splints should be used as an adjunct for pain management rather than a definitive treatment. For sleep
bruxism, it is prudent to limit their use as a habit management aid and to prevent/limit dental damage potentially induced by
the disorder. Future research should study the natural history and etiologies of TMD and bruxism, so that specific treatments
for these disorders can be developed.
Key words. Oral splints, temporomandibular disorders, bruxism, myofascial pain, disc displacement disorders.

(I) Introduction
Among the treatments provided for temporomandibular disorders (TMD), intra-oral dental appliances,
whether with full or partial occlusal coverage, and
referred to in this paper as oral splints, have been repeatedly 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 see
the versatility of their current applications. Other than
their use in the prevention of dental injuries and oral
soft-tissue trauma potentially induced by bruxism,
sports, cheek biting (Walker and Rogers, 1992), and electroconvulsive therapy (Minneman, 1995), oral splints of
various designs have been prescribed in the management of diverse disorders including: (a) motor disorders
such as Parkinson's disease (Durham et al., 1993) and oral
tardive dyskinesia (Kai et al., 1994); (b) sleep disorders
such as snoring (George, 1993) and sleep apnea (George,
1993; Athanasiou et al., 1994; Lowe, 1994; Yoshida, 1994;
Osseiran, 1995); (c) sensitive teeth related to chronic
sinusitis (Dawson, 1974); (d) various headaches, from the
tension-type to migraine (Ouayle et al., 1990; Lamey and
Steele, 1996); and (e) all subgroups of TMD, e.g., myofascial pain, disc displacement disorders, and the arthritides (Table 1).

It is also surprising to see the wide acceptance of

oral splints and their "multi-purpose usage", while little
is known about the mechanisms by which they exert their
effect. For the TMD, a survey of 10,000 members of the
American Dental Association identified oral splints as
being, by far, the treatment most commonly used by both
general practitioners and dental specialists (Glass et al.,
1991, 1993). It is estimated that over three million splints
are provided to the American population every year, with
an approximate cost of $990 million per year (i.e., 2.91% of
all 1990 US dental care dollars; Pierce et al., 1995). The
popularity of oral splints has also extended throughout
the five continents, as indicated by the various publication languages found in the literature through a Medline
search, and the numerous names given to different
designs of splints (Table 2). Although their use as protective devices is well-accepted, the benefits associated
with their use in the management of motor disorders are
at best anecdotal, and their true therapeutic value in the
treatment of TMD has not been established beyond
doubt. The aim of this paper is to review the proposed
mechanisms by which oral splints exert their effects, and
to assess the quality of the evidence supporting the efficacy of oral splints in the treatment of bruxism and the
three subgroups of TMD (Dworkin and LeResche, 1992).
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TABLE 2
Synonyms for Oral Splints Used in the
Treatment of Temporomandibular Disorders
and Bruxism
Anterior deprogramming splint
Anterior positioning splint

TABLE 1
Applications of Oral Splints
Temporomandibular disorders
Myofascial pain
Disc displacement disorders
Arthritides of the temporomandibular joints
Other pain disorders
Headaches/migraine
Motor and sleep disorders
Sleep bruxism
Sleep apnea
Parkinson's disease
Oral tardive dyskinesia
Occlusal rehabilitation
Orthodontics
Periodontics
Prosthodontics
Phantom bite
Others (Prevention of tissue trauma, habits)
Diurnal bruxism
Sports
Cheek or fingernail biting
Electroconvulsive therapy
Lip commissure burn
Esophageal reflux
Sinusitis

Anterior repositioning splint

Bite splint
Buccal separator

Disclusion splint
Distal push splint
Flat occlusal splint
Hawley splint
Herbst splint
Hydrostatic splint
Levandoski splint
Mandibular advancing repositioning splint
Mandibular orthopedic repositioning appliance
Mandibular repositioning splint
Michigan occlusal splint
Muscle deprogramming splint
Night guard
Occlusal correcting splint
Occlusal disengagement splint
Orthopedic interocclusal appliance
Pain release splint
Pivoting appliance
Protrusive positioners

Stabilization splint

(11) Myofascial Pain (MFP) and Oral Splints

In this section, we will review the literature pertaining to
splint therapy for myofascial pain of the masticatory
muscles. Since the subclassification of MFP became
available only in 1992 (Dworkin and LeResche), and our
review will include the literature published before then,
we will include in this section the available evidence on
the use of oral splints in the treatment of pain in TMD
patients. The literature dealing with the use of splints for
disc displacement disorders and the arthritides will be
discussed separately below. The comprehensiveness of
each review section will vary according to the extent of
literature published in each field.

(A) PHYSIOLOGICAL MECHANISMS PROPOSED

There are several assumptions which underlie the worldwide acceptance of oral splints in the treatment of
myofascial or TMD pain (Table 3). In the following, we
shall discuss the limitations associated with each of
these assumptions.

(a) Change in the vertical dimension of occlusion

According to some early reports (Block, 1947;
Christensen, 1970), oral splints contribute to the reduction of "abnormal muscle activity" and pain by restoring
the patient's original vertical dimension of occlusion

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(VDO) which has been reduced by tooth wear or loss of

posterior teeth. This belief may have been influenced by
Costen's hypothesis that facial pain and the accompanying auditory symptoms may be caused by a loss in the
VDO, a subsequent posterior displacement of the
condyles and compression of the auriculo-temporal
nerve (Costen, 1934). We now know that this hypothesis
is not supported by studies which show the lack of contiguity between these anatomical structures (Shapiro
and Truex, 1943; Sicher, 1948; Zimmerman, 1951). On the
other hand, it is also important to note that the average
splint thickness (8.1 mm), which appears to be the most
efficient in producing a rapid improvement in the symptoms (Manns et al., 1983), exceeds by far the usual
amount of vertical increase one wishes to restore in most
patients. Furthermore, although an immediate decrease
in the electromyographic (EMG) activity of the jaw elevator muscles has been observed at various VDO augmentations obtained with splints (Manns et al., 1983), there
are no data pointing to the persistence of this effect in
long-term users of splints. More importantly, a decrease
in EMG following a raised VDO does not necessarily
imply that a loss of VDO would induce pathological EMG
increases.

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TABLE 3
Mechanisms Proposed for Oral Splint
Efficacy/Effectiveness

(c) Decrease in the level of muscle activity

The apparent effect of oral splints has been assumed to
be related to a decrease in muscle activity (Lobbezoo et
al., 1993; Visser et al., 1995). Their efficacy was further
attributed to a reduced EMG in the temporalis muscles
which appear to present greater changes as compared

Myofascial pain
Change in the vertical dimension of occlusion
Repositioning of the temporomandibular joints
Decrease in the level of muscle activity
Reducing bruxism
Removal of occlusal interferences
Enhancing the patient's cognitive awareness
Disc displacement disorders
"Recapturing" the disc
'Unloading" the joints
Arthritis/arthralgia
"Unloading" the joints
Sleep bruxism
Removal of occlusal interferences
Change in muscle activity
Modification of patient's habits

with the masseter muscles (Lobbezoo et al., 1993).

Although a decrease in EMG signals in the jaw-closing
muscles has been repeatedly reported in most of the
studies on splints (Dahlstrom and Carlsson, 1984;
Dahlstrom and Haraldson, 1985; Dahlstrom et al., 1985;
Holmgren et al., 1985; Graham and Rugh, 1988; Naeije
and Hansson, 1992; Lobbezoo et al., 1993; Visser et al.,
1995), the data are still contradictory, and the available
evidence suggests that the degree to which this phenomenon was related to the clinical remission of MFP
symptoms remains unsettled. Besides the few studies
which show a concomitant reduction of EMG activity and
patients' pain reports, these reports were not collected
under blind conditions (Dahlstrom and Haraldson, 1985;
Visser et al., 1995), and some experiments were done in
asymptomatic subjects (Dahlstrom et al., 1985; Graham
and Rugh, 1988; Lobbezoo et al., 1993), while other investigations have simply yielded opposing results: an
increase in EMG activity (Wood and Tobias, 1984).
Contrasting results have also been obtained within the
same study (Visser et al., 1995), where it was shown that
after a short-term use of a splint (3 to 6 wks), the EMG
activity decreased in 15 out of 35 patients, but increased
in four others and remained unchanged in the rest of the
sample population. Similarly, it was reported in another
study (Holmgren et al., 1985) that 15 min after the insertion of an occlusal splint, the postural activity of the temporal muscles decreased in 52%, but increased in 22%,
and remained unchanged in 26% of the patients.
Comparable results were obtained for nocturnal activity
of the masseter muscles: The EMG levels decreased in
52%, increased in 20%, and remained unchanged in 28%
of the patients (Clark et al., 1979). These effects may be
transitory, since it has been reported that at two to four
weeks after treatment, the activity of the temporalis muscle during clenching on the splint was comparable with
that measured without the splint, while the masseter
muscle did not display any significant changes (Naeije
and Hansson, 1992). The between-study variability could
be due to various reasons, including the differences in
the clinical protocols adopted during the experiment
(e.g., data recording with or without the splint, at rest or
during function, period of time after splint insertion, different splint thickness), or the heterogeneity of the
patient group (e.g., presence or absence of pain, bruxism). Nevertheless, together with the presence of diverse
subgroups of patients in the same study displaying contrasting responses to splint usage, these data indicate
that the overall EMG response to splint therapy and its

(b) Repositioning of the temporomandibular joints

Another theory stipulates that the success achieved with
oral splints is due to the repositioning of the displaced
temporomandibular 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 relationship and eliminating the muscle imbalance and its resultant pain. This concept is based on the measurement of
the joint spaces between the projected surface of the
condyle and the radiological border of the temporal fossae and is therefore associated with several pitfalls. First,
it does not address the large variability of condylar positions found in both the general asymptomatic (Pullinger
et al., 1985) and patient population (Brand et al., 1989).
Second, it does not account for the significant errors and
distortions inherent in the projection of a three-dimensional joint complex on the flat surface of a radiograph.
This is particularly important, since the variations in the
condylar position as observed on radiographs may simply reflect the variations of the shape of the osseous
components of the same joint from its medial to its lateral aspects (Eckerdal and Lundberg, 1979; Blaschke and
Blaschke, 1981; Dumas et al., 1986). Third, it does not take
into consideration the variation in the thickness of the
soft-tissue components which is not reflected on conventional radiographs but which contributes to the lack
of uniformity of the joint space (Hatcher et al., 1986).
Finally, as discussed below, the belief that an "abnormal
muscle activity" or "muscle imbalance" could be the
cause of muscle pain has been questioned (Lund and
Widmer, 1989; Lund et al., 1989, 1991, 1993).
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biological significance are not well-understood and still

warrant further investigation.
(d) Reducing bruxism in relation to TMD
It is often believed that oral splints contribute to the success of TMD management by reducing bruxing activity.
This belief is based on the assumptions that bruxism is a
contributing or causative factor for TMD (Ramfjord and
Ash, 1983; Mongini, 1984; Okeson, 1985; Rugh and
Harlan, 1988; Dawson, 1989). However, these assumptions have been questioned (Clark and Adler, 1985;
Lobbezoo and Lavigne, 1997). In fact, although significant correlations between parafunction and dysfunction
have been reported through epidemiological surveys
(Egermark-Eriksson et al., 1981; Nilner, 1983; Allen et al.,
1990; Magnusson et al., 1993; Widmalm et al., 1995), the
association of two events in time does not prove causation (Spilker, 1991), and the temporal sequence of cause
and effect cannot be established on the basis of crosssectional studies (Locker and Slade, 1988). Furthermore,
the association does not make epidemiologic sense,
since bruxism is more prevalent in children and decreases in adulthood, while the prevalence of TMD is low in
children and older people, and peaks between the ages
of 18 and 45 (Lobbezoo and Lavigne, 1997).
It is also important to note that most of the splint
studies were focused on sleep bruxism, and did not differentiate between the clenching (or tonic) and grinding
(phasic or rhythmic) forms of the disorder, although
clenching, which occurs mainly during the daytime, has
been reported to be associated with higher risk for jaw
pain (Goulet et al., 1993, 1994, 1995). On the other hand,
many patients with sleep bruxism have no masticatory
muscle pain at all (Clark and Sakai, 1990; Dao et al.,
1994b; Lund, 1995), and sleep bruxers tend to have their
highest pain in the morning, while myofascial pain
patients have their worst pain in the evening (Dao et al.,
1994b). This suggests that sleep bruxism and myofascial
pain may be two different entities. Recent data also suggest that jaw pain and motor activity in sleep bruxism
may not always be positively correlated, since sleep
bruxers with pain had fewer bruxing episodes per hour
than those who did not report any pain (Lavigne et al.,
1997).
If the available data do not substantiate either the
assumption that bruxism is the cause of TMD or the
belief that pain levels are proportional to the amount of
motor activity, attempting to reduce bruxism with an oral
splint to treat TMD may not be a viable option at this
point. This is even more true since the ability of oral
splints to decrease bruxism has not been established, as
reviewed in a separate section below.

(e) Removal of occlusal interferences

Perhaps the most popular theory on the mechanism of
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action of oral splints proposed by the dental profession

would be the one which postulates that occlusal splints
are effective because they reduce the amount of tooth
contact, alter the periodontal proprioceptive input to the
central nervous system (Ramfjord and Ash, 1971; Yustin
et al., 1993), and provide the patient with an "interference
free" or "ideal occlusal scheme" (Posselt, 1968; Ramfjord
and Ash, 1971, 1994; Timm and Ash, 1977). Therefore,
whether oral splints provide full or partial coverage of
the teeth, they would "prevent disturbing influences to
the neuromuscular system from occlusal contacts on
mandibular closure and movements" (Ramfjord and Ash,
1971; Timm and Ash, 1977). However, this assumption is
based mostly on EMG studies comparing the muscle
activity before and during the wear of oral splints, and
the limitation of that evidence has already been discussed. Moreover, the concept that these interferences
can induce abnormal muscle activity and subsequent
pain (Clayton, 1995) is contradicted by the body of evidence which refutes the second part of the equation, i.e.,
the role of muscle hyperactivity as the cause for muscular pain (Lund and Widmer, 1989; Lund et al., 1989, 1991,
1993). It is also important to keep in mind that tooth
contact occurs only during a very limited part of the day.
If we rely on early studies showing that the estimated
tooth contact time during a day was 17.5 minutes in a
normal subject (Graf, 1969), and the mean difference of
tooth contact time during sleep between bruxers and
non-bruxers was about 9 minutes (Kydd and Daly, 1985),
the estimated total contact time would approximate only
26.5 minutes/day, i.e., about 1.8% of the 24-hour cycle.
Furthermore, although various studies have shown that
experimentally induced sensory feedback le.g., pain
(Lund, 1995); heavy pressure on teeth (Lavigne et al.,
1987)1 from the orofacial region can influence the
mandibular 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 the
belief that routine tooth contact can exert the same
effect. Besides, it is difficult to attribute the clinical success of oral splints to the changes in occlusion, since a
decrease in pain intensity and an improvement in pain
relief scores have also been obtained with the use of
non-occluding splints, i.e., those which do not cover the
teeth and leave the occlusion unmodified (Greene and
Laskin, 1972; Rubinoff et al., 1987; Dao et al., 1994a; Feine
and Lavigne, 1995).

(B) BEHAVIORAL MECHANISMS:

THE COGNITIVE AWARENESS THEORY
According to this theory, the presence of the splint as a
foreign object in the mouth would likely change the oral
tactile stimuli, decrease the oral volume and space for
the tongue, and make the patients conscious about the
position and potentially harmful use of their jaw (Greene

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and Laskin, 1972; Rugh and Robbins, 1982). Although it

seems reasonable to suppose that this increased awareness would influence the patients' learning to alter or
reduce their harmful behavior and therefore contribute
to the overall success of the intervention (Rugh and
Solberg, 1979; Rugh, 1991), this concept still needs to be
proven.

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

1995).
If appropriate care has not been given to the control
for bias during an evaluation process which relies almost
exclusively on patients' subjective reports, it is reasonable to conclude that the efficacy of oral splints has not
been established beyond doubt. To address this issue,
we have designed a randomized, controlled, and blind
clinical trial to assess the efficacy of this treatment
approach. The results of the study have been published
(Dao et al., 1994a). In summary, MFP patients were randomly allocated to three groups: a passive control group,
in which patients had a stabilizing maxillary splint only
30 minutes at each of their seven visits over an 11-week
period; an active control group, in which patients wore a
palatal splint 24 hrs/day except for oral hygiene and at
mealtimes, but the splint did not change the patients'
occlusion; and a treatment group, in which patients wore
a maxillary stabilizing splint 24 hrs/day except during
oral hygiene and at mealtimes. Our data show a signifi-

(C) CLINICAL EFFICACY/EFFECTIVENESS

Although the mechanism of action of oral splints has not
been elucidated, the acceptance of this treatment
modality remains overwhelming. This faith in splint therapy may have been reinforced by nearly five decades of
high clinical success rates achieved with splints alone,
whether inserted into the maxillary or mandibular arches, or combined with other therapies (Zarb and
Thompson, 1970; Greene and Laskin, 1972; Carraro and
Caffesse, 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 question that may arise is not so much whether patients'
improvements can be obtained with splints, but rather
how much of the reported improvements reflect the efficacy, i.e., true therapeutic value of these oral devices, and
how much may be due to other factors such as the natural course of the disorder, the placebo effect, the doctor-patient relationship, and/or other undetermined confounding elements. While a reliable answer would be
given by the results of randomized controlled clinical trials (RCTs), most of the studies cited above did not follow
many of the contemporary fundamental principles of
clinical trials (Spilker, 1991), and the overall quality of
the design of RCTs in the TMD field published before
1994 has been reported to be below acceptable levels
(Antczak-Bouckoms, 1995). Furthermore, in the absence
of a control group (Okeson et al., 1982; Tsuga et al., 1989;
Wilkinson et al., 1992), and in light of the evidence showing 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 determine
whether the decrease in pain observed in the study represented the specific outcome of the treatment or the
natural progression of the condition toward a more quiescent phase. As well, it is likely that the positive results
could be due, in part, to the placebo effect which is often
associated with the treatment of MFP, and which has
been observed in 30-64% of the patients (Greene and
Laskin, 1971, 1972, 1983; Goodman et al., 1976). One can
also argue that the patients' desire to please or gratify
their clinician may have accounted for the favorable data
which were not collected under blind conditions (Greene
and Laskin, 1972; Okeson et al., 1982; Clark et al., 1988;
Suvinen and Reade, 1989; Tsuga et al., 1989; List et al.,
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cant decrease of

patients' reports of pain intensity and

pain unpleasantness in all three groups of patients after

11 weeks of treatment, both at rest and after a chewing
test, but there were no significant differences between
groups. If the between-group differences observed at the
end of the study were used to calculate the sample size
needed to fulfill statistical criteria for demonstrating significant differences, 750 and 240 patients would need to
be recruited for pain intensity and pain unpleasantness,
respectively. As discussed previously, if such a large population is needed to prove that the small differences
between the efficacy of the splint and that of the placebo
are real, it is prudent to assume that the therapeutic
component of that therapy is negligible.
Our data cast doubt on the therapeutic value (efficacy) of oral splints in the treatment of MFP, and they also
suggest that the decrease in pain during the trial was not
due to changes in the patients' occlusion. In light of
these results, any phase II therapy where permanent
occlusion-changing procedures are used to maintain the
maxillo-mandibular relationship obtained with the splint
is totally unjustified.
Soft resilient splints are also commonly used in the
management of MFP, although they provide mixed
results. While their short-term efficacy in reducing pain
has 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 some
patients (Nevarro et al., 1985; Harkins et al., 1988).
Concerns have also been raised regarding the effects of
these 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
rlBo

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recent randomized controlled clinical trial in MFP

patients suggest that the patients' satisfaction and comfort, as well as a decrease in clenching, can be obtained
equally with soft and hard splints (Huggins et al., 1997).
However, there was no report regarding their effect on
other cardinal symptoms, such as pain and/or muscle
tenderness.
If the efficacy of oral splints for the treatment of MFP
is questionable, the question arises as whether we
should still prescribe oral splints to manage this disorder. Before we reach a conclusion, it is necessary to consider some related issues which may affect that decision.
When one is treating a musculoskeletal pain of unknown
origin, trying to cure the condition, i.e., to remove its
cause, is simply an absurd exercise. Perhaps the best we
can hope for is an improvement of the patient's own perception of his/her condition and quality of life. In this
regard, our data show that the quality of life improved
significantly in all three of the previously discussed
patient groups. Moreover, patients who wore either the
palatal or stabilizing splint reported significantly more
pain relief than those who did not have the appliance
between their appointments (Feine and Lavigne, 1995).
However, although the report of pain relief reflects the
effectiveness of the therapy (i.e., the patient's appreciation of the positive changes which are perceived to have
occurred during the trial), pain relief is a poor estimate
of treatment efficacy, because that outcome measure is
based on the memory of pain, and the validity of retrospective reports including the memory of pain has been
questioned (Feine et al., 1992; Schwarz and Sudman,
1994). Thus, given the self-limiting nature of MFP, the
importance of the placebo effect associated with oral
splints, and the non-invasive nature of this approach
(when they are not followed by occlusal therapy), oral
splints appear to fulfill the following patients' general
expectations from health care services, i.e., (1) to be alive
as long as possible; (2) to be functioning normally; (3) to
be free of pain and other physical, psychological, or
social symptoms; (4) to be free of iatrogenic problems
from the treatment regimen; and (5) to remain solvent
(White, 1967; Fries et al., 1980; Fries, 1983, 1991). In the
absence of any other forms of therapy with a proven
greater curative value (Chapman, 1991; Clark et al., 1995),
and in light of the data supporting their effectiveness but
not their efficacy, we conclude that oral splints should
still be used as an adjunct to patient management, but
only until the etiology of MFP is elucidated and a more
specific treatment regimen for this condition is developed.

(III) Disc Displacement Disorders

and Oral Splints
The displacement of the TMJ disc from its textbook-like
position, between the mandibular condyle and the tem-

350

poral eminence, to an anterior and medial or lateral

position was first identified by Annandale in 1887. Disc
displacement disorders are now classified into the following subtypes (Dworkin and LeResche, 1992):
(1) Disc displacement with reduction (DDR): The disc
is displaced from its original position between the
condyle and the eminence to an anterior and medial or
lateral position, but reduces on full opening, usually
resulting in a noise.
(2) Disc displacement without reduction (DDWR),
with limited opening: a condition in which the disc is displaced from its original position between the condyle
and the eminence to an anterior and medial or lateral
position, associated with limited mandibular opening.
(3) Disc displacement without reduction, without
limited opening: same as #2 but not associated with limited mandibular opening.
Although surgical repositioning or resection of the
articular disc was among the first treatments proposed
for disc displacement disorders, more conservative therapies using oral splints started to gain popularity in the
1970's. Whether they were resilient or hard, adapted to
maxillary or mandibular teeth, designed as a stabilizing
appliance or a jaw repositioner device, oral splints prescribed for disc displacement disorders often were
intended to have a common goal: to "recapture" the displaced disk, and thereby eliminate the clinical problems
that 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 any
improvement in joint noises, pain, and mandibular
motion obtained with splint therapy would occur as the
result of disc recapturing (Anderson et al., 1985; Le Bell
and Kirveskari, 1985) and/or joint "unloading" (Israel,
1994; Moncayo, 1994). Upon remission of the clinical
symptoms, the splint was supposed to be gradually
adjusted to "walk the disk back" to allow the mandible to
return to its original position. If this did not work out,
permanent alterations of the dentition with orthodontics, prosthodontics, or orthognathic surgery were recommended as "phase II", to maintain the new therapeutic maxillo-mandibular relationship obtained with the
splint (Haden, 1983; Anderson et al., 1985; Lundh et al.,
1985; Tallents et al., 1990; Lew, 1992). This entire
approach to recapturing and stabilizing TMJ disks may
have been motivated by the belief that disc displacement (DD), which often starts as "a clicking jaw", could
be a progressive disorder if left untreated. Many authorities postulated that DD can lead to increased risks of
developing pain (Brooke and Grainger, 1988), impaired
mobility (e.g., "closed lock"; Dolwick, 1995), and degenerative joint diseases (see Milam, 1995). In the following
paragraphs, we will review the few mechanisms proposed for oral splints in the treatment of DD and the
risks and benefits associated with their use, in the con):

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text of the natural progression and long-term prognosis

of these disorders.

(c) Unloading the joints

It has been suggested that overloading the TMJ can
cause DD (Moncayo, 1994) and degenerative arthritis,
and that oral splints work by decompressing the joints
(Israel, 1994). This may have been based on the belief
that the mandibular opening induced by the splint thickness would be accompanied by an increase in the joint
space and a decrease in the loading forces exerted on the
articular surfaces of the TMI. While direct evidence supporting this assumption is not available, TMJ unloading
has been assessed indirectly through various methods.
Using a static mechanical model based on vector
analysis to estimate the clenching forces transmitted to
the TM), dos Santos and his colleagues concluded that
the insertion of a stabilizing splint tends to decrease the
pressure in the joints, while the use of an ARSplint tends
to increase the pressure in the joint structures (dos
Santos et al., 1988). However, this model has never been
validated in vivo in dynamic conditions.
The forces exerted on the TMJs have also been estimated in a clinical study using a jaw-tracking device to
predict the condylar movements induced by clenching
tasks (Ito et al., 1986). Since the condylar movements were
not significant during clenching on either the stabilizing
or the ARSplint, it was inferred that the forces were mainly directed to the molars, and decompressive effects at
the TM) level were induced by use of the splints. However,
it is important to note that the condylar movements were
estimated from an arbitrary point in the condyle that does
not reflect the loading articular surfaces of the TMJs.
Furthermore, neither of these studies takes into account
the possible changes in the position of the disc relative to
the TM) during the jaw movements, although this may
also influence the magnitude of the joint loading.
Another approach involved the measurement of
intra-articular pressure at the posterior slope of the eminence in the upper compartment of the TM) (Nitzan,
1994). Besides the lack of data showing the validity and
reliability of this technique in assessing intra-articular

(A) PHYSIOLOGICAL MECHANISMS

(a) "Recapturing" the disc with the stabilizing splint
The stabilizing splint described earlier for MFP has also
been widely used in the treatment of DD. The data on its
ability to reposition the disc are still very sparse, and the
available evidence suggests that disc recapturing does
not occur in conjunction with the use of stabilizing
splints. Using magnetic resonance imaging (MRI) to visualize the disc before and after 3-4 months of treatment of
10 DDWR patients with stabilizing splints, it was found
that the disc remained anteriorly displaced and
deformed, and its relationship with the condyle was
unchanged (Choi et al., 1994). This is consistent with the
data of another MRI pilot splint study showing that the
improved jaw movements and pain remission in three
patients after a three-month treatment period occurred
without any sign of disc recapturing (Chen et al., 1995). As
reviewed below, these data are similar to those reported
for anterior repositioning splints.

(b) "Recapturing" the disc

with the anterior repositioning splint
As their name indicates, anterior repositioning splints
(ARSplint) are designed to maintain the jaw in a protrusive position, in an attempt to "decompress the joint
structures" (Scapino, 1983), allow the anteriorly displaced disk to regain its "normal" relationship with the
condyle head and the articular fossae, and allow for
"healing of the elongated posterior disk attachment"
(Dolwick and Riggs, 1983). To ensure a proper alignment
of the "disc-condyle complex", various imaging methods
have been used to visualize the position of the disc during the fabrication of the ARSplints, including arthrography (Manzione et al., 1984; Tallents et al., 1985) and magnetic resonance imaging (Cohen and MacAfee, 1994;
Moritz et al., 1995). However, the consistency and predictability of these appliances in repositioning the disc
have been questioned. In an MRI study involving 18
patients and 30 clicking joints treated with the Sved-type
splint, Kirk (1991) reported that disc repositioning
occurred in only three joints. Similarly, Manco and
Messing (1986) found that 41.8% of the discs evaluated
with direct sagittal computed tomography were not repositioned after ARSplint therapy. Manzione et al. (1984)
reported that 46% of the patients with painful DD treated
with ARSplints still had anterior DD. In another study
using MRI before and immediately after an average of
nine months' treatment with an ARSplint, disc repositioning was observed in 96% of the 26 fully reducing
discs, but not in the seven partially reducing and the 14
non-reducing discs (Simmons and Gibbs, 1995).
9(3 34

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9(3)-.345-361 (1998)

Gri Re

fluid pressure, such measurements do not provide direct

information regarding the loading of the articular surfaces of the TM). More recently, Kukobi et al. (1997) used
tomograms of the TMJ and measured the joint space during maximum teeth intercuspation and clenching on two
types of splints. The stabilizing splint did not induce any
significant increase in joint space, and there was a significant reduction in the anterior joint space associated with
the ARSplint; this suggests that these splints do not
unload the TMJ.
It appears from the reviewed literature that oral
splints do not generally enable clinicians to reposition
the articular disc, or to decompress the joint structures.
In successful cases of disc repositioning, follow-up data
are still lacking, and the long-term outcomes of this
aggressive treatment approach still need to be assessed.
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(B) CLINICAL EFFICACY/EFFECTIVENESS

(a) Stabilizing splints in the treatment
of disc displacement disorders
Stabilizing splints have been reported, in uncontrolled studies, to be effective in decreasing pain and
joint noises, and in improving the range of mandibular
motion (Choi et al., 1994; Chen et al., 1995; Linde et al.,
1995). However, in controlled (but non-blinded) studies
comparing the outcome of stabilizing splints with that of
a control group, although the overall improvement in
pain, joint sounds, and maximal opening was noticeable,
no significant differences could be found between the
groups (Lundh et al., 1988, 1992; Sato et al., 1995). While
this lack of between-group differences could be due to
the small sample sizes, it is also possible that the parallel improvement in the non-treated group simply reflected the natural course of the disorder. This is supported
by reports that the symptoms associated with DDR or
DDWR appear to improve over time without treatment
(Pedersen and Hansen, 1987; Lundh et al., 1992; Sato et
al., 1995). For instance, without treatment, pain has been
reported to decrease in 36% of the patients diagnosed
with DDWR after one year (Lundh et al., 1992).
Interestingly, these authors also found a higher incidence of symptoms worsening in the treatment group as
compared with the control group. Similarly, the data
from another study have showed that 41.9% of the
patients with DDWR who refused any treatment had a
significant increase in mouth opening and decrease in
pain after one year, although joint noises remained
unchanged (Sato et al., 1995). Taken together, these data
show that not only is the ability of stabilizing splints to
recapture the articular disc doubtful, but also, the clinical efficacy in the treatment of DD remains to be proven.
Stabilizing splints have also been compared with
their counterpart, the ARSplint. The results of an uncontrolled study (Anderson et al., 1985) and those of a controlled but non-blinded study (Lundh et al., 1985) suggested that the ARSplint provided more improvements
than the stabilizing one. However, it is important to note
that the less-than-optimal design of these studies casts
doubt on any inference about the true therapeutic value
of the treatment approaches evaluated. Furthermore, the
available data indicate that the efficacy of the ARSplint in
the treatment of DD has also not been established
beyond doubt. The quality of the evidence supporting
the clinical efficacy of ARSplints and the extent to which
the improvements in the symptoms are correlated to
changes in the disc position will be discussed below.
(b) Anterior repositioning splints
in the treatment of disc displacement disorders
Pain relief and/or improvement of mandibular range of
motion have been reported in most of the DD treatment
352

studies that we have reviewed so far, whether or not the

position of the disc was assessed by imaging techniques.
However, the extent to which these positive results
reflect the true benefit obtained with the ARSplint
remains to be determined, since these studies failed to
observe many of the rules of clinical trials that are now
considered as critical if the validity of the results is to be
ensured (Spilker, 1991). For instance, because of the
absence of a control group, several studies (Le Bell and
Kirveskari, 1985; Chen et al., 1995; Simmons and Gibbs,
1995) would be better qualified as case series, which
often include potential biases and tend to be positive
with respect to treatment outcome (DeRouen, 1995). In
studies where a control group was included, patients'
subjective reports, such as pain, were not collected
under blind conditions (Lundh et al., 1985, 1988; Tallents
et al., 1990). Furthermore, whether these results were
mainly due to splint treatment or to group allocation
bias cannot be determined, since patients were not randomized into treatment groups (Tallents et al., 1990).
On the other hand, when objective signs such as
joint noises were used as a measure of treatment outcome, the success rates were much lower, and relapse
rates were alarmingly high: From 40 to 50% of patients
who received ARSplints still experienced joint noises at
1 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 resonance imaging (MRI), computed tomography, and
arthrography to visualize the position of the disc, it was
often found that the perceived clinical success was not
associated with a recaptured disc. For instance, in an
MRI study involving 30 clicking joints treated with the
Sved-type splint, it was reported that although joint
noises were eliminated in 27 joints, disc repositioning
occurred in only three joints (Kirk, 1991). Similarly,
Manco and Messing (1986) found that even though joint
noises were eliminated, 41.8% of the discs evaluated
with direct sagittal computed tomography were not repositioned after ARSplint therapy.
Taken together, these data suggest that subjective
reports of improvements following ARSplint therapy do
not generally occur as the result of disc recapturing.
Furthermore, the specificity of joint sounds as a sign of
DD or as an outcome variable to measure the success of
splint therapy for DD may be questioned, since displaced
discs visualized with arthrography in the absence of joint
sounds have also been reported (Roberts et al., 1986). It
is interesting to note that the absence of changes in the
position of displaced discs in the presence of positive
clinical outcome has also been reported in studies using
other treatment modalities such as the stabilizing splint,
as discussed above, or following successful arthroscopic
surgery (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 displaced disc. In light of these results, the "Phase II" concept of therapy-where irreversible alterations of the
dentition with occlusal equilibration, prosthodontics,
orthodontics, or orthognathic surgery are performed to
stabilize the recaptured disc-becomes totally unjustified. This is even more true considering the frequent
return of signs and symptoms of DD after/during postsplint extensive oral reconstruction: For example, the
disc was displaced again in 33% of the patients after 6
months' treatment with mandibular repositioning onlays
(Westesson and Lundh, 1988), while joint noises
recurred in 43% during or soon after the completion of
major 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 and
Howard, 1986). These high relapse rates inspire caution
against the use of invasive therapies.
The literature on the use of a soft oral splint in the
treatment of DD is more limited. Favorable results such
as a decrease in pain and joint noises have been reported following 20 days of continuous use of a soft splint (24
hrs/day; Harkins et al., 1988). However, the validity of
these data is questionable, since they were not collected
under blind conditions, and patients were not randomized into treatment groups. Furthermore, there are concerns that the use of soft splints may be associated with
occlusal changes (Singh and Berry, 1985; Harkins et al.,
1988).
Taken together, the available data indicate that,
although oral splints have been repeatedly reported to
be effective in improving the range of mandibular motion
and in decreasing pain and joint noises associated with
DD, these results need to be confirmed with welldesigned clinical trials. Furthermore, the belief that the
disc can be either consistently recaptured or predictably
stabilized by oral splints is not supported by any of the
imaging studies reviewed so far. If the clinical improvements observed in DD patients are not associated with
apparent changes in the disc position, it becomes evident that disc repositioning should not constitute the
ultimate objective of the splint. Moreover, in view of the
questionable benefits and the potential harmful effects
associated with ARSplints (i.e., uncontrolled tooth movements; Brown et al., 1994), and the expense and invasiveness of so-called "Phase II" therapy, we conclude that
these approaches appear unacceptable in either the
short- or long-term treatment of DD.
Our conclusion is further supported by the body of
evidence suggesting that DD is unlikely to be a progressive disorder in the majority of patients. For instance, it
has been reported that 40% of the patients who had only
counseling for DD were symptom-free after 8-15 years
(Pedersen and Hansen, 1987); the condition was consid1998)
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ered unchanged in 50%, and was aggravated in 7% of the

patients. A three-year follow-up of 70 patients with DDR
whose symptoms relapsed after splint treatment
revealed that reciprocal clicking remained unchanged in
71% of the patients and disappeared in 29% (Lundh et al.,
1987). Only 9% developed locking. Similar data were
obtained by Greene and Laskin (1988) through a telephone survey of 203 patients who presented with painful
clicking joints and were treated with conservative
approaches from 1 to 15 years earlier: Thirty percent
reported 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 99
patients with clinical signs of DD before and 30 years
after non-surgical and non-repositioning treatment, they
found that the degree of mouth-opening remained stable
(and acceptable) in patients with DDR, but increased significantly in the majority of patients with DDWR. The
prevalence of joint clicking remained unchanged in both
groups. The generally favorable prognosis observed during the natural course of DD speaks against the use of
any splint therapy associated with potential iatrogenic
sequellae.

(IV) Oral Splints in the

Management of Bruxism
(A) PHYSIOLOGICAL MECHANISM
Among the applications of oral splints, their use as a
protective device against the potential dental and periodontal damage induced by sleep bruxism is perhaps the least
contested, while information about daytime bruxism is
still lacking. However, the concept that oral splints can
be used to treat bruxism by removing the occlusal interferences that are thought to trigger bruxing activity
(Ramfjord, 1961; Krogh-Poulsen and Olsson, 1966;
Schaerer et al., 1967; Kawazoe et al., 1980; Sheikholeslam
et al., 1986) is no longer tenable. It has been shown that
occlusal adjustments do not stop sleep bruxism (Bailey
and Rugh, 1980), and that experimentally placed deflective occlusal contacts reduce rather than enhance masticatory muscle activity during sleep (Rugh et al., 1984).
Furthermore, epidemiological data indicate that bruxers
and control subjects cannot be distinguished on the
basis of their morphological occlusal characteristics
(Greene and Marbach, 1982).
Currently, there are no reliable data to support the
etiologic role of occlusion in bruxism, and instead the
available evidence tends to favor a central nervous system and behavioral involvement rather than a specific
peripheral cause. A recent review on the epidemiology
and pathophysiology of sleep bruxism reveals that this
disorder can occur in the presence of various psychiatric,
neurological, and systemic disorders (Lavigne and

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Montplaisir, 1995). Sleep bruxism may be associated

with the autonomic arousal response, or result from
interactions between the limbic and motor systems
(Lavigne and Montplaisir, 1995). There is also emerging
evidence suggesting that some neurotransmitters may
be implicated in the pathophysiology of sleep bruxism
(Lobbezoo et al., 1997). Other reported exacerbating factors include stress, drugs or alcohol, disease, and personality (Lavigne and Montplaisir, 1995).
In light of these data, it is no longer reasonable to
accept occlusion as the cause of bruxism. Therefore, the
hypothesis that oral splints work by removing occlusal
interferences becomes questionable, and in addition,
the efficacy of oral splints in decreasing bruxing activity
is also debatable, as reviewed below.

(B) CLINICAL EFFICACY/EFFECTIVENESS

Several studies have reported that the use of oral splints
was associated with a decrease in nocturnal EMG activity in the masticatory muscles (Ramfjord, 1961; Fuchs,
1975; Rugh and Solberg, 1975; Solberg et al., 1975;
Kawazoe et al., 1980; Hamada et at., 1982; Sheikholeslam
et at., 1986; Pierce and Gale, 1988; Kurland, 1993). This
effect appeared to be transient, since the EMG values
returned to baseline levels when the treatment was withdrawn (Rugh and Solberg, 1975; Solberg et al., 1975; Clark
et al., 1979; Sheikholeslam et al., 1986; Pierce and Gale,
1988). The decrease in the EMG data was interpreted as
being the result of a reduction in bruxism activity, with
the return to their original values perceived as a resumption of the parafunctional activity. These inferences are
not supported by the evidence that we shall review
below. First, the majority of these early studies relied on
the average EMG scores rather than on any measures of
the frequency, intensity, and duration of the rhythmic jaw
activity (including EMG, audio, or video signals) that are
now considered critical in the evaluation of sleep bruxism (Lavigne et al., 1996). Second, we cannot rule out the
possibility that the observed decrease in the EMG activity during the treatment and its post-treatment increase
could reflect the non-specific and transient responses of
the jaw elevator muscles to the changes in the VDO
obtained with the splints (Dahlstrom and Carlsson, 1984;
Dahlstrom and Haraldson, 1985; Dahlstrom et al., 1985;
Holmgren et al., 1985; Graham and Rugh, 1988; Naeije
and Hansson, 1992; Lobbezoo et al., 1993; Visser et al.,
1995; see section on MFP, above). Third, opposite results
have also been reported. Within the same study, Okeson
(1987) found no significant change in the EMG activity in
two out of ten of the patients who had a hard maxillary
splint and in four out of ten of those who wore a soft one.
More importantly, five out of the ten patients who had
the soft splint showed a significant increase in the EMG
scores. Similarly, when the effects of canine vs. molar
guidance on hard splints were compared in bruxers, it
354

found that both splints decreased the nightly EMG

subjects, but increased these
scores in three other subjects (Rugh et at., 1989). Other
researchers simply reported that the occlusal splints do
not stop sleep bruxism (Gentz, 1972; Kydd and Daly,
1985; Holmgren et at., 1993). A noticeable increase in
clenching and bruxing in some patients wearing the soft
resilient appliances has also been reported (Harkins et
at., 1988). These contrasting data suggest that the sleep
bruxers' EMG responses to splint therapy are not predictable. Furthermore, since occlusion is no longer
regarded as an important etiopathologic variable in
sleep bruxism, the use of "occlusal" splints should be
reconsidered as a more limited treatment modality. They
can potentially be useful as habit management aids, and
they definitely can protect the dental/periodontal structures against some of the adverse effects of prolonged
hyper-loading. Again, the "post-splint Phase 11 therapy"
for bruxism where extensive occlusal rehabilitation is
advocated for more permanent results (Yustin et al., 1993)
becomes unjustifiable.
was

masseter values in three

(V) The Art hritides

The literature pertaining to the use of oral splints in the
management of the arthritides is very sparse and mostly
anecdotal. For osteoarthritis of the TMJ, oral splints may
have been adopted following the belief that functional
loading, which is thought to be caused by the loss of
molar support or to occur during mastication or bruxism,
may play a role in the cause and progression of the disorder (Kopp and Carlsson, 1988). In patients with
rheumatoid arthritis who present with a destruction of
the condyle and a consequent rapid progression of the
dentition toward an open bite, oral splints have also
been used to provide a temporary stabilization of the
occlusion before proceeding with a permanent prosthetic rehabilitation or occlusal adjustment (Kopp, 1994).
Whatever the rationale proposed to support the use of
oral appliances, it would be presumptuous to pretend
that we could treat these degenerative, connective tissue, and/or autoimmune disorders with a simple
occlusal approach. Moreover, it is important to note that
no specific study has ever been conducted to assess
either their efficacy or their effectiveness in the treatment of the arthritides affecting the TMJ. It is thus prudent at this time to restrict the use of oral splints as an
adjunct to the palliative management of the symptoms
associated with these conditions.

(VI) Conclusion
Despite the nearly universal prescription of oral splints
in the treatment of TMDs or bruxism, the quality of the
evidence supporting the mechanisms of action suggested for their presumed efficacy is still questionable. This
is not surprising, since their efficacy itself remains

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unestablished, and the rationale underlying each of the

mechanisms proposed is based on unsubstantiated
hypothetical etiologies. Although the prospect for curing
TMDs and/or bruxism, or trying to eliminate their
unknown cause, remains an unrealistic expectation, it
still can be argued that improving the patient's perception of well-being, or changing harmful habits through
the judicious application of a non-invasive and cost-efficient management strategy (such as the use of stabilizing splints), may represent an acceptable alternative.
This strategy also may be justifiable in light of the evidence showing that painful TMD can undermine the
patient's quality of life significantly (Reisine and Weber,
1989; Dao et al., 1994a,b) and cause substantial psychological distress (Turk and Rudy, 1990; Von Korff et al.,
1992). However, the limitations of this approach should
be acknowledged by practitioners so that faulty extrapolations from the treatment outcome and the unfounded
"Phase 11 therapy" can be avoided. If we recognize that
the apparent improvements observed in most of the
studies on oral splints could be due to the non-specific
effects of treatment (i.e, placebo, doctor-patient relationship), 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 conclude
that oral splints can be used only as an adjunct to TMD
pain patient management, until the natural history and
the etiologies of TMDs are elucidated, and more specific
treatments for these conditions are developed. For bruxism, as mentioned earlier, it is prudent to limit the use of
oral splints for habit management and to prevent/limit
the dental damage potentially induced by the disorder.
In summary, it is critical to keep in mind that oral splints
do not cure, but they may contribute to the patient's
well-being just like crutches, which are useful as a nonspecific "healing aid" during a patient's orthopedic rehabilitation phase, but which are not regarded as a primary or definitive treatment modality.

Acknowledgments
The authors thank Drs. A Charbonneau, J.S Feine, and I.P. Lund for
their contributions in earlier clinical trials. G.I. Lavigne is presently
supported by the Medical Research Council of Canada and the Fonds
de la Recherche en Sante du Quebec.

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