INTRODUCTION

T
he oral device known as the occlusal splint (OS) is frequently used in the
management of sleep bruxism (SB) to protect teeth from damage (e.g.,
wear or fracture) resulting from forceful jaw muscle contractions or to
reduce concomitant orofacial pain, if present (Pierce et al., 1995; Okeson,
2003). However, the efficacy of the OS in reducing jaw muscle activity
remains controversial. Some studies reported a reduction in SB motor
activity (electromyographic [EMG] recording) when comparisons were
made with recordings from the baseline night, whereas others showed no
effect (Solberg et al., 1975; Okeson, 1987; Rugh et al., 1989; Okkerse et al.,
2002; Sjholm et al., 2002). It should be noted that these studies did not
include a palatal-control device (PCD), which covers the palatal area
without protecting the tooth. The absence of a PCD prevents any conclusion
that occlusal tooth coverage explains OS action. The use of a PCD, in a
limited number of SB subjects, was reported to reduce or have no effect on
SB motor activity (Cassisi et al., 1987; Hiyama et al., 2003).
SB is a parasomnia, an excessive motor activity with tooth-grinding,
that intrudes upon a subject's otherwise normal sleep (Thorpy, 1997;
Lobbezoo and Naeije, 2001). Evidence from recent controlled studies
suggests that most SB episodes are secondary to a cascade of physiological
events related to sleep arousal (Okura et al., 1996; Macaluso et al., 1998;
Kato et al., 2001, 2003). The predominant sequence is as follows: a transient
(3-10 sec) brain and heart activation, a rise in muscle tone of jaw openers-
suprahyoid muscles, then rhythmic contractions of jaw-closer muscles with
occasional tooth-grinding. The incidence of sleep arousals in SB subjects is
within the normal range ( 14 arousals/hr of sleep) (Mathur and Douglas,
1995; Boselli et al., 1998; Lavigne et al., 2001a). However, SB episodes
associated with sleep arousals are characterized by a rapid onset of
tachycardia and an important rise in electroencephalographic or
electromyographic activities (Kato et al., 2001). The influences of OS on
sleep arousal are unknown.
Sleep apnea (i.e., cessation of breathing in sleep with hypoxemia and
risk of hypertension, daytime sleepiness) is a health hazard found twice as
often in the general population reporting tooth-grinding than in the normal
population (Krieger, 2000; Ohayon et al., 2001). The safety of using OS in
subjects with SB and sleep apnea needs to be assessed. In a recent
preliminary study, it was noticed that, out of 10 subjects with a clear
diagnosis of sleep apnea, the use of OS aggravated respiratory disturbances
(e.g., from a lower to a more severe diagnostic category) in four of them
(Gagnon et al., 2004). However, it was reported by others that OS had no
effect on the mean index of respiratory disturbances per hour of sleep. Since
individual subject variation was not shown in these studies, we do not know
if some of them had an aggravation (Sjholm et al., 1994; Mehta et al.,
2001; Gotsopoulos et al., 2002).
The objective of the present study was to assess, by the use of a short-
ABSTRACT
The efficacy of occlusal splints in diminishing
muscle activity and tooth-grinding damage
remains controversial. The objective of this study
was to compare the efficacy and safety of an
occlusal splint (OS) vs. a palatal control device
(PCD). Nine subjects with sleep bruxism (SB)
participated in this randomized study. Sleep
laboratory recordings were made on the second
night to establish baseline data. Patients then wore
each of the splints in the sleep laboratory for
recording nights three and four, two weeks apart,
according to a crossover design. A statistically
significant reduction in the number of SB episodes
per hour (decrease of 41%, p = 0.05) and SB
bursts per hour (decrease of 40%, p < 0.05) was
observed with the two devices. Both oral devices
also showed 50% fewer episodes with grinding
noise (p = 0.06). No difference was observed
between the devices. Moreover, no changes in
respiratory variables were observed. Both devices
reduced muscle activity associated with SB.
KEY WORDS: sleep bruxism, tooth grinding, bite
splint, randomized controlled study.
Received May 14, 2003; Last revision November 26, 2003;
Accepted March 2, 2004
Quantitative Polygraphic
Controlled Study on Efficacy
and Safety of Oral Splint Devices
in Tooth-grinding Subjects
C. Dub
1,2
, P.H. Rompr
1,2
,
C. Manzini
1,2
, F. Guitard
1,2
,
P. de Grandmont
1
, and G.J. Lavigne
1
*
,2
1
Dpartement de Restauration, Prosthodontics Postgraduate
Program, Facult de mdecine dentaire, Universit de
Montral, C.P. 6128, Succursale Centre-ville, Montral
(Qubec) H3C 3J7, Canada; and
2
Centre d' tude du
sommeil, Hpital du Sacr-Cur de Montral, Canada;
*corresponding author, Gilles.Lavigne@Umontreal.ca
J Dent Res 83(5):398-403, 2004
RESEARCH REPORTS
Clinical
398
J Dent Res 83(5) 2004 Splint Devices in Sleep Tooth-grinders 399
term controlled-random design,
whether OS reduced SB motor
activity, influenced sleep variables
(e.g., duration and quality of sleep,
number of arousals), and are safe
with regard to respiratory
parameters (e.g., apnea/hypopnea,
snoring) in young healthy SB
subjects.
MATERIALS & METHODS
Population
Five young women and four men
(mean age
+
SEM, 23.7
+
0.9 yrs;
range, 20-29 yrs) with a history of
tooth grinding were selected for this
study. All participants signed a
consent form and received financial
compensation for inconvenience
related to the study. The institutional
ethics committee approved the study.
Subjects were recruited by
referrals from clinicians and by
advertising on the University
campus. A history of tooth-grinding
events occurring 3 times or more a
week, as reported by the patient's sleep partner over the preceding
6 mos, was the main criterion for selection (Lavigne et al., 1996;
Thorpy, 1997; Lobbezoo et al., 2001). The presence of tooth wear
ranging from class 2 through class 4 (Johansson et al., 1993) on at
least 3 occlusal surfaces and/or masseter muscle hypertrophy upon
voluntary clenching and/or symptoms of morning orofacial jaw
muscle fatigue were also noted when all subjects were examined.
To be eligible to participate in the study, SB subjects were
required to be between 18 and 45 years of age, have a good
comprehension of French, be able to sign a consent form, and
agree to spend at least 4 nights at the sleep research laboratory.
The first night was for habituation and was not included in the
statistical analysis. The second night was used to record jaw
muscle activity and tooth-grinding sounds to establish baseline
levels and to rule out other sleep disorders. At least 4 phasic (3
muscle contractions at a frequency of 1 Hz) or mixed (phasic and
tonic contractions) episodes of SB per hour of sleep with 2 audible
tooth-grinding events per night had to be present to confirm a
subject's eligibility to participate in the study (Lavigne et al.,
2001a,b). During baseline recording, patients who showed signs of
other sleep disorderssuch as periodic leg movements during
sleep (> 10 events per hour of sleep), electroencephalographic
(EEG) epileptiform activity, sleep apnea (> 5 apnea or hypopnea
events per hour of sleep)and snoring were excluded. Also
excluded were patients reporting pain, those who had been treated
with any type of oral device in the preceding 6 mos, those wearing
a partial denture, missing more than 2 posterior teeth (third molars
excluded), presenting gross malocclusion, or taking medication or
alcohol on a regular basis. Finally, a negative history of medical,
neurological, motor, or psychiatric disorders was required for
subjects to be included in the study.
Experimental Procedure and Occlusal Splint Fabrication
This crossover study evaluated two oral devices (Fig. 1): a hard
acrylic U-shaped occlusal splint and a palatal device (e.g., not
interfering with the occlusion in any mandibular movements). The
OS was used as the treatment and the PCD as the active control.
The technician scoring sleep and oromandibular activity data was
blind to the type of device used.
Maxillary and mandibular arch impressions were made with
alginate, and models were cast in artificial stone. The centric tooth
relation was taken with a blue wax waffle. A face bow was used to
mount the models on a semi-adjustable articulator. The two oral
devices were made on the maxillary models and then inserted and
adjusted. The OS was adjusted in centric relation with the use of a
32-m articulation paper. Only the points corresponding to contact
between the lower buccal cusp and the splint were preserved. We
adjusted lateral guidance and protrusion by eliminating any contact
other than with the canine in lateral or incisor in anterior-posterior
mandibular movements. The OS was 1-2 mm thick over the incisor
tooth area. The PCD was adjusted for maximum tooth
intercuspation, and any tooth contact upon mandibular movement
was eliminated (Fig. 1). The same operator (CD) provided the
treatments, and each patient was given the same instructions. To
prevent bias toward the design of the oral devices, and since most
subjects expected tooth protection, subjects were told that both
splints had been reported to be beneficial and that one of the study
goals was to test the efficacy and comfort of both devices. This
"goal" was reinforced with a questionnaire given at the end of the
night and another at the end of the study assessing sleep quality,
oral device comfort, preference, and efficacy.
The first night of sleep laboratory recording was for
habituation. The second night was used for sleep disorders
diagnosis and to establish baseline data. A computer-generated
sequence then randomly assigned which of the two oral devices
was to be worn first by each patient. Patients were given two
weeks to get used to the splint. The subjects then spent a third
night at the laboratory, wearing their first splint, for the collection
Figure 1. Photographs of the occlusal splint (a,b) and palatal control device (c,d) on model and in
mouth, respectively.
400 Dub et al. J Dent Res 83(5) 2004
of polygraphic data. The second splint was given on the next
morning and was worn by the subject for two weeks. Further
laboratory recordings were made on the fourth night, with subjects
wearing their second splint. Patient compliance was checked on an
irregular basis by a 'phone call to the patient to ensure that he/she
was using the oral device as requested.
Polysomnographic Recordings and Scored Variables
Sleep recordings were made on each of the 4 nights from 10:30
p.m. to 7:00 a.m. The setting of the recordings has been described
elsewhere (Lavigne et al., 1996; Lobbezoo et al., 1997). In
summary, the following surface electrodes were used: 2
electroencephalograms (C
3
A
2
, O
2
A
1
), one electrocardiogram
(EKG) and bilateral electro-oculograms (EOGs), and
electromyograms (EMGs) from the masseter, sternocleidomastoid,
anterior tibialis, and one site for chin/suprahyoid activities. Data
were collected and amplified with a sampling rate of 128 Hz and
kept for further scoring with the use of sleep recording and scoring
software (Harmonie, Stellate System, Montral, Canada). Audio
and video signals were recorded in parallel. Information on sleep
quality, total duration, efficiency, percentages of stage duration,
number of micro-arousals per hour, number of awakenings per
hour, and sleep latency was calculated. Moreover, the frequency of
SB episodes per hour of sleep, the number of bruxism bursts per
hour, and the number of episodes with sounds were estimated. A
detailed analysis of SB muscle activity was also performed for the
right masseter. For each SB episode, the total episode duration,
number of bursts, number of bursts/sec, mean amplitude of the
bursts (RMS calculation), sum of burst duration, mean burst
duration, and mean interval between bursts were calculated
(Lavigne et al., 1997). The sleep scoring was done according to the
standard criteria of Rechtschaffen and Kales (1968), and the final
diagnosis of SB was made according to previously published
criteria (Lavigne et al., 1996).
Respiratory function was assessed by nasal airflow measures
through a thermistor sensor (Thermocouple, Protech, Woodville,
WA, USA) and a thoracic and abdominal belt. The number of
apnea-hypopnea events per hour of sleep was computed. The
presence of swallowing events was estimated indirectly with the
use of video signals and laryngeal movements as recorded over the
thyroid cartilage with a piezoelectric sensor (Opti-Flex, Newlife
Technologies, Midlothian, VA, USA). This method is a valid and
non-invasive technique currently used in sleep medicine
(Miyawaki et al., 2003). An index of the number of swallowing
events per hour was computed based on data from the piezoelectric
sensor.
Statistical Analysis
We used repeated-measures ANOVA to evaluate treatment effects.
The baseline data were then compared with data from either the
occlusal or palatal nights by paired comparisons. Friedman two-
way ANOVA followed by Wilcoxon signed-ranks tests for paired
comparisons were used when the data distribution was not normal.
We performed sign tests to evaluate whether subjects did or did not
improve with the splints.
RESULTS
The influence of the oral
devices on sleep variables
was that both reduced the
percentage of time that
subjects spent in deep
non-REM sleep (stages 3
and 4, Table). However,
simple contrast analysis
revealed trends only
when baseline recordings
were compared with
those with OS (14.9% to
10.6%; p = 0.057) and
PCD (14.9% to 11.0%; p
= 0.085). Although the
duration of stages 3 and 4
was slightly lower during
the nights with oral
devices, no other sleep
variables (e.g., efficiency,
sleep latency, incidence
of micro-arousals or
awakenings) differed
among the 3 recorded
conditions. The presence
of the splints did not
induce an increase in the
respiratory variables,
apnea and hypopnea
index, which remained
low for the whole study.
A non-statistically signif-
Table. Sleep and Bruxism Variables (means
+
SEM) during Baseline, OS, and PCD Nights
p Values
Variable Baseline (B) OS PCD overall B-OS B-PCD
Sleep
% Stage 1 4.2
+
0.7 6.7
+
1.3 6.4
+
1.5 0.17 0.12 0.13
% Stage 2 56.9
+
2.1 60.2
+
1.9 57.9
+
1.7 0.41 0.25 0.73
% Stages 3 & 4 14.9
+
2.4 10.6
+
1.6 11.0
+
1.9 0.038 0.057 0.085
% REM 24.0
+
2.1 21.4
+
2.6 24.7
+
2.0 0.40 0.34 0.81
Sleep efficiency % 95.8
+
1.5 93.3
+
2.7 95.7
+
1.4 0.54 0.44 0.99
Sleep latency (min)
a
8.3 [1.0-69.3] 4.3 [0.7-25.3] 3.7 [0.7-32.0] 0.37 0.44 0.52
Micro-arousals/hr 9.7
+
2.1 8.0
+
1.9 7.6
+
1.7 0.50 0.38 0.37
Awakenings/hr 3.1
+
0.8 3.8
+
1.0 3.4
+
1.1 0.62 0.40 0.52
Apnea + hypopnea/hr
a
0.4 [0.0-3.8] 0.8 [0.1-2.3] 0.4 [0.0-2.7] 0.92 1.00 0.89
Swallowing/hr 7.3
+
1.4 12.2
+
3.4 8.8
+
2.4 0.15 0.12 0.40
Bruxism
Overnight
Episodes/hr
a
6.3 [3.7-10.5] 3.7 [0.2-8.2] 3.7 [2.8-7.9] 0.016 0.051 0.051
Episodes with noise 22.1
+
4.9 10.9
+
3.9 10.0
+
4.1 0.057 0.058 0.054
Bursts/hr 48.4
+
5.7 26.4
+
6.6 28.2
+
5.6 0.026 0.048 0.046
% Episodes in stages 1 & 2 80.7
+
3.4 77.7
+
10.2 83.3
+
4.7 0.80 0.78 0.63
Within an episode
Total episode duration (sec) 18.1
+
2.1 18.6
+
2.1 17.0
+
1.4 0.82 0.87 0.66
Bursts 6.4
+
0.3 4.6
+
0.5 4.4
+
0.5 0.007 0.02 0.003
Bursts/sec 0.44
+
0.09 0.24
+
0.01 0.25
+
0.01 0.027 0.067 0.060
Burst amplitude (V) 26.0
+
2.7 31.1
+
4.7 27.5
+
1.5 0.48 0.33 0.62
Total burst duration (sec) 6.8
+
0.5 5.6
+
0.4 5.1
+
0.3 0.002 0.019 0.004
Mean burst duration (sec) 1.6
+
0.2 2.0
+
0.3 1.8
+
0.2 0.18 0.10 0.093
Interval between bursts (sec) 0.65
+
0.08 0.93
+
0.06 0.91
+
0.04 0.018 0.063 0.018
a
Median [min-max].
J Dent Res 83(5) 2004 Splint Devices in Sleep Tooth-grinders 401
icant increase in the number of
swallowing events per hour was
observed with the OS (67%; p =
0.12).
The median number of SB
episodes per hour of sleep was
lower compared with the baseline
(Table, Fig. 2a) when OS and PCD
were used (41% reduction; p =
0.051). This result occurred in eight
of the nine SB subjects (Fig. 3; sign
test, p = 0.04). The number of SB
episodes with tooth-grinding
sounds was decreased by 51% and
55% with OS and PCD,
respectively (Table, Fig. 2b; p
<
0.058). This result occurred in six
of nine SB subjects with OS and
eight of nine with PCD (p < 0.04). The number of muscle
contractions (bursts per hour of sleep) was significantly lower
with both oral devices (Table, Fig. 2c; OS = reduction of 45%,
p < 0.05, and PCD = reduction of 42%, p < 0.05). A decrease in
bursts per hour of sleep was observed for seven out of nine SB
subjects with OS and eight out of nine with PCD. A detailed
analysis of each SB episode showed that while episode duration
did not change (p = 0.82), there were fewer bursts within
episodes with both the OS (reduction of 28%; p = 0.02) and the
PCD (reduction of 31%; p = 0.003) compared with baseline
data. Bruxism burst amplitude was not changed, regardless of
whether splints were used (p = 0.48). Interestingly, the interval
between bursts was increased with both splints (40% increase;
p
<
0.06).
At the end of study, when we asked subjects which oral
device they preferred, all subjects found that the PCD was more
comfortable to use, but most felt that the OS offered the best
tooth protection (71%). When asked, no patients reported
mouth dryness during the night or in the morning. Patients
were also asked to rate the comfort of the splints on a VAS
scale. Interestingly, patients rated both splints as equally
comfortable (OS, 79.3
+
4.7 mm/100; PCD, 77.8
+
8.1
mm/100; p = 0.84). During a telephone interview made one
year after the end of the study, five of seven (two had moved to
another country) were still using the device; four preferred the
OS and one the PCD.
DISCUSSION
This study gives support for the use of an oral device to reduce
SB motor activity. More importantly, it shows that oral devices
(with or without tooth coverage) reduced jaw muscle activity in
SB subjects. Although a similar frequency of sleep arousals
was noted across sleep conditions, most EMG variables were
significantly reduced with the use of both devices.
Interestingly, in our young SB subjects, there was no obvious
exacerbation of sleep respiratory variables with OS and PCD.
The present study has obvious limitations that require
caution to be exercised when the data are interpreted. First, all
SB subjects were young and were tooth grinders (not
clenchers); they may then not represent SB in the general
population. Second, the subjects were also very motivated to
participate in the study, since their dentists had recommended
an occlusal splint and their sleep partner was complaining of
tooth-grinding sounds. Motivation may be a potential bias.
There might be a deceptive bias regarding oral device design,
since the PCD did not offer tooth protection. To prevent this,
we clearly explained that both designs had been used in a
previous study and that both were suggested to be effective.
Third, the period of habituation to each oral device was short (2
wks), which may have prevented us from observing long-term
influence. Interestingly, other studies have reported that OS
induce a reduction in oromotor activity that persists up to 6 mos
(Sheikholeslam et al., 1986; Pierce and Gale, 1988). Fourth, the
OS used in the present study was made for the maxilla. A study
design with OS made on the mandible may have given different
results. Fifth, the sample size of the study was small, although a
sufficient statistical power was obtained for most important
outcomes (e.g., SB oromotor variables). The power was low
only to show a statistical difference for the swallowing-
laryngeal movement. For this variable, a sample size of 25
subjects would have been needed for the difference greater than
Figure 2. Comparison among baseline (B), occlusal splint (OS), and palatal control device (PCD) nights
for the number of (a) bruxism episodes per hour, (b) episodes with tooth-grinding noise, and (c) bursts
per hour. Median is shown for episodes/hr, since the data distribution was not normal; otherwise,
means
+
SEM are shown (nine subjects). * p
<
0.05 when compared with baseline value (details in
Table).
Figure 3. Individual data distribution for the number of bruxism
episodes per hr for baseline (B), occlusal splint (OS), and palatal control
device (PCD) nights. The median is circled. A decrease more important
than night-to-night variability (25%) was observed for six and five
patients, respectively, when occlusal splint and palatal control device
nights were compared with the baseline night.
402 Dub et al. J Dent Res 83(5) 2004
60% between the baseline and OS night to reach a power of
80% at an alpha level of 0.05. Regarding the sleep respiratory
disturbance index, even with low power we felt comfortable
with the observed result, since the difference (0.4 vs. 0.8) is
well below the diagnostic criteria of 5 apnea and hypopnea
episodes per hour of sleep (Krieger, 2000).
In our study, although SB subjects had similar sleep
efficiency, with or without oral devices, the nights with the OS
and PCD showed that stages 3 and 4 (so-called "restorative
sleep") were nearly 1/3 shorter (trend only). This is contrary to
another report showing that OS has no influence on slow-wave
activity (SWA: a measure that is similar to stages 3 and 4)
(Nagels et al., 2001). Since our study was short-term, it could
be possible that, with time, the duration of stages 3 and 4 with
oral devices tends to normalize toward values usually observed
in young normal sleepers (17-21%) (Boselli et al., 1998;
Landolt and Borbely, 2001).
The most interesting finding of this study is that the use of
oral devices in SB subjects reduces the frequency of SB
oromotor events and tooth-grinding-related activities. Only one
patient showed an exacerbation of SB with the OS. This was
not unexpected, since others have found that nearly 20% of SB
patients had more muscle contractions with such oral devices
(Clark et al., 1979). SB is an exaggerated muscular response
(e.g., frequency and amplitude) in ongoing "usual sleep arousal
response" in otherwise normal sleeper (Okura et al., 1996;
Macaluso et al., 1998; Kato et al., 2001, 2003; Lavigne et al.,
2001a, 2002). We have found in this study, as well as in a
previous one, that the frequency of sleep arousals in these
young SB subjects remains within the range observed in normal
subjects (<14 arousals/hr of sleep) (Mathur and Douglas, 1995;
Boselli et al., 1998). However, the use of an oral device could
then reduce the strength of sleep arousal reaction in preventing
excessive muscle activation, an hypothesis currently under
investigation in our laboratory. We recently suggested that SB
activity may contribute to the recovery of airway patency in
sleep (Lavigne et al., 2003). It could then be possible that the
palatal thickness ( 1 mm) of an oral device modifies tongue
position during sleep. This obviously needs more attention,
since, during the light sleep of normal young subjects, the
posterior displacement of the tongue and soft palate contributes
to reduced airway patency (Trudo et al., 1998). The common
rationale for the use of OS is to prevent tooth damage from SB-
tooth-grinding, and since both devices reduced the oromotor
activity, the mechanism of action is to be further investigated.
ACKNOWLEDGMENTS
This study was supported by Canadian Institutes of Health
Research and Qubec FRSQ grants. We also thank A. Petersen
and F. Blanger for editing this paper and Dr. Y. Gagnon for
his clinical expertise.
REFERENCES
Boselli M, Parrino L, Smerieri A, Terzano MG (1998). Effect of age
on EEG arousals in normal sleep. Sleep 21:351-357.
Cassisi JE, McGlynn FD, Mahan PE (1987). Occlusal splint effects on
nocturnal bruxing: an emerging paradigm and some early results.
Cranio 5:64-68.
Clark GT, Beemsterboer PL, Solberg WK, Rugh JD (1979). Nocturnal
electromyographic evaluation of myofascial pain dysfunction in
patients undergoing occlusal splint therapy. J Am Dent Assoc
99:607-611.
Gagnon Y, Mayer P, Morisson F, Rompr PH, Lavigne GJ (2004).
Aggravation of sleep apnea by the use of occlusal splint in apneic
patients: a pilot study. Int J Prosthodont (in press).
Gotsopoulos H, Chen C, Qian J, Cistulli PA (2002). Oral appliance
therapy improves symptoms in obstructive sleep apnea: a
randomized, controlled trial. Am J Respir Crit Care Med 166:743-
748.
Hiyama S, Ono T, Ishiwata Y, Kato Y, Kuroda T (2003). First night
effect of an interocclusal appliance on nocturnal masticatory
muscle activity. J Oral Rehabil 30:139-145.
Johansson A, Haraldson T, Omar R, Kiliaridis S, Carlsson GE (1993).
A system for assessing the severity and progression of occlusal
tooth wear. J Oral Rehabil 20:125-131.
Kato T, Rompr PH, Montplaisir JY, Sessle BJ, Lavigne GJ (2001).
Sleep bruxism: an oromotor activity secondary to micro-arousal. J
Dent Res 80:1940-1944.
Kato T, Montplaisir JY, Guitard F, Sessle BJ, Lund JP, Lavigne GJ
(2003). Evidence that experimentally induced sleep bruxism is a
consequence of transient arousal. J Dent Res 82:284-288.
Krieger J (2000). Respiratory physiology: breathing in normal
subjects. In: Principles and practice of sleep medicine. 3rd ed.
Kryger MH, Roth T, Dement WC, editors. Philadelphia: Saunders,
pp. 229-241.
Landolt HP, Borbely AA (2001). Age-dependent changes in sleep EEG
topography. Clin Neurophysiol 112:369-377.
Lavigne GJ, Rompr PH, Montplaisir J (1996). Sleep bruxism: validity
of clinical research diagnostic criteria in a controlled
polysomnographic study. J Dent Res 75:546-552.
Lavigne GJ, Rompr PH, Montplaisir JY, Lobbezoo F (1997). Motor
activity in sleep bruxism with concomitant jaw muscle pain. A
retrospective pilot study. Eur J Oral Sci 105:92-95.
Lavigne GJ, Rompr PH, Poirier G, Huard H, Kato T, Montplaisir JY
(2001a). Rhythmic masticatory muscle activity during sleep in
humans. J Dent Res 80:443-448.
Lavigne GJ, Guitard F, Rompr PH, Montplaisir JY (2001b).
Variability in sleep bruxism activity over time. J Sleep Res
103:237-244.
Lavigne GJ, Rompr PH, Guitard F, Sessle BJ, Kato T, Montplaisir JY
(2002). Lower number of K-complexes and K-alphas in sleep
bruxism: a controlled quantitative study. Clin Neurophysiol
113:686-693.
Lavigne GJ, Kato T, Kolta A, Sessle BJ (2003). Neurobiological
mechanisms involved in sleep bruxism. Crit Rev Oral Biol Med
14:30-46.
Lobbezoo F, Naeije M (2001). A reliability study of clinical tooth wear
measurements. J Prosthet Dent 86:597-602.
Lobbezoo F, Lavigne GJ, Tanguay R, Montplaisir JY (1997). The
effect of catecholamine precursor L-dopa on sleep bruxism: a
controlled clinical trial. Mov Disord 12:73-78.
Macaluso GM, Guerra P, Di Giovanni G, Boselli M, Parrino L,
Terzano MG (1998). Sleep bruxism is a disorder related to
periodic arousals during sleep. J Dent Res 77:565-573.
Mathur R, Douglas NJ (1995). Frequency of EEG arousals from
nocturnal sleep in normal subjects. Sleep 18:330-333.
Mehta A, Qian J, Petocz P, Darendeliler MA, Cistulli PA (2001). A
randomized, controlled study of a mandibular advancement splint
for obstructive sleep apnea. Am J Respir Crit Care Med 163:1457-
1461.
Miyawaki S, Lavigne GJ, Mayer P, Guitard F, Montplaisir JY, Kato T
J Dent Res 83(5) 2004 Splint Devices in Sleep Tooth-grinders 403
(2003). Association between sleep bruxism, swallowing-related
laryngeal movement, and sleep positions. Sleep 26:461-465.
Nagels G, Okkerse W, Braem M, Van Bogaert PP, De Deyn B, Poirrier
R, et al. (2001). Decreased amount of slow wave sleep in
nocturnal bruxism is not improved by dental splint therapy. Acta
Neurol Belg 101:152-159.
Ohayon MM, Li KK, Guilleminault C (2001). Risk factors for sleep
bruxism in the general population. Chest 119:53-61.
Okeson JP (1987). The effects of hard and soft occlusal splints on
nocturnal bruxism. J Am Dent Assoc 114:788-791.
Okeson JP (2003). Management of temporomandibular disorders and
occlusion. 5th ed. St. Louis: Mosby, p. 428.
Okkerse W, Brebels A, De Deyn PP, Nagels G, De Deyn B, Van
Bogaert PP, et al. (2002). Influence of a bite-plane according to
Jeanmonod, on bruxism activity during sleep. J Oral Rehabil
29:980-985.
Okura K, Makano M, Bando E, Kondo K, Takeuchi H, Nishigawa K,
et al. (1996). Analysis of biological signals during sleep associated
bruxism. J Jpn Soc Stomatognath Funct 3:83-93.
Pierce CJ, Gale EN (1988). A comparison of different treatments for
nocturnal bruxism. J Dent Res 67:597-601.
Pierce CJ, Chrisman K, Bennett ME, Close JM (1995). Stress,
anticipatory stress, and psychologic measures related to sleep
bruxism. J Orofac Pain 9:51-56.
Rechtschaffen A, Kales A, editors (1968). A manual of standardized
terminology, techniques and scoring techniques for sleep stages of
human subjects. Los Angeles: Brain Research Institute.
Rugh JD, Graham GS, Smith JC, Ohrbach RK (1989). Effects of
canine versus molar occlusal splint guidance on nocturnal bruxism
and craniomandibular symptomatology. J Craniomandib Disord
3:203-210.
Sheikholeslam A, Holmgren K, Riise C (1986). A clinical and
electromyographic study of the long-term effects of an occlusal
splint on the temporal and masseter muscles in patients with
functional disorders and nocturnal bruxism. J Oral Rehabil
13:137-145.
Sjholm TT, Polo OJ, Rauhala ER, Vuoriluoto J, Helenius HY (1994).
Mandibular advancement with dental appliances in obstructive
sleep apnoea. J Oral Rehabil 21:595-603.
Sjholm T, Lehtinen I, Polo O (2002). The effect of mouth guard on
masseter muscle activity during sleep. J Sleep Res 11(Suppl
1):209-210.
Solberg WK, Clark GT, Rugh JD (1975). Nocturnal electromyographic
evaluation of bruxism patients undergoing short term splint
therapy. J Oral Rehabil 2:215-223.
Thorpy MJ, editor (1997). International classification of sleep
disorders: diagnostic and coding manual, revised. Rochester, MN:
Allen Press, pp. 182-185.
Trudo FJ, Gefter WB, Welch KC, Gupta KB, Maislin G, Schwab RJ
(1998). State-related changes in upper airway caliber and
surrounding soft-tissue structures in normal subjects. Am J Respir
Crit Care Med 158:1259-1270.