Archives of Oral Biology (2006) xxx, xxxxxx

www.intl.elsevierhealth.com/journals/arob

Sleep bruxism and temporomandibular disorder:

Clinical and polysomnographic evaluation
Cinara Maria Camparis a,*, Gilberto Formigoni b,
Manoel Jacobsen Teixeira c, Lia Rita Azeredo Bittencourt d,
Sergio Tufik d, Jose Tadeu Tesseroli de Siqueira e

a
Araraquara School of Dentistry, Sao Paulo State University (UNESP), Brazil
b
Otorhinolaryngology Division, Hospital das Clnicas, Medical School,
University of Sao Paulo (USP), Brazil
c
Interdisciplinar Pain Center, Functional Neurosurgery Division, Hospital das Clnicas,
Medical School, University of Sao Paulo (USP), Brazil
d
Sleep Institute, Paulista Medical School, Federal University of Sao Paulo (UNIFESP), Brazil
e
Orofacial Pain Clinic, Dentistry Division, Hospital das Clnicas, Medical School,
University of Sao Paulo (USP), Brazil

Accepted 1 March 2006

KEYWORDS Summary
Bruxism;
Sleep; Objective: To seek better understanding of chronic musculoskeletal facial pain and
Facial pain; its relation to sleep bruxism, by comparing patients with sleep bruxism, with and
Temporomandibular without temporomandibular disorder.
disorders; Design: Forty sleep bruxism patients were evaluated according to the Research
Myofascial pain Diagnostic Criteria for Temporomandibular Disorders: group A20 patients with
myofascial pain, 3 men, 17 women; average age 32.7 yr; mean duration of pain
4.37 yr; group B20 without myofascial pain, 5 men, 15 women; average age 30.8 yr.
Sleep and bruxism were evaluated in one-night polysomnography.
Results: There were no statistically significant differences for bruxism and sleep
variables of the two groups: number of bursts and bruxism episodes per hour,
amplitude and duration of bruxism episodes, sleep efficiency and latency, percentage
of non-REM and REM sleep, respiratory events, periodic limb movements, and micro-
arousals.

Presentation at a meeting: preliminary findings of this paper were presented at the 17th European Sleep Research Society Congress,
Prague, 59 October 2004.
* Corresponding author at: Rua Humaita, 1680, 14801-903 Araraquara, SP, Brazil. Tel.: +55 16 33016406; fax: +55 16 33016406.
E-mail address: cinara@foar.unesp.br (C.M. Camparis).

00039969/$ see front matter # 2006 Published by Elsevier Ltd.

doi:10.1016/j.archoralbio.2006.03.002

AOB-1716; No of Pages 8
2 C.M. Camparis et al.
Conclusions: The polysomnographic characteristics of patients with sleep bruxism,
with and without orofacial pain, are similar. More studies are necessary to clarify the
reasons why some sleep bruxism patients develop chronic myofascial pain, and others
do not.
# 2006 Published by Elsevier Ltd.
Introduction
Orofacial pain is a common complaint in medical and
dental practice, thus their scope with regard to
orofacial pain includes the diagnosis and treatment
of disorders affecting the entire head and neck.
Temporomandibular disorders (TMDs) encompass
a range of conditions associated with pain and
dysfunction of the head and neck region. Diagnosis
continues to be made in a descriptive manner on the
basis of presenting signs and symptoms, which may
occur in different combinations and degrees. Epi-
demiological studies have provided a general insight
into the role of some local and systemic factors in
the onset and perpetuation of TMD, but they remain
controversial. The form in which these factors act in
each subject to cause a TMD is still not defined.1
Bruxism is considered to be the combination of
parafunctional clenching and grinding activities,
exerted both during sleep and while awake, because
both phenomena are not adequately differentiated
in most scientific articles. Most of the data regarding
the etiology of bruxism come from studies of sleep-
related bruxism and taking all the evidence
together, bruxism appears to be regulated mainly
centrally, not peripherally.2
Up to now, repetitive activities or microtraumas,
like sleep bruxism, are considered to be important
factors in the onset and perpetuation of pain in TMD,
alternatively muscle fatigue is considered to be one
of the causes of pain associated with TMD.3 It has
been demonstrated that significant levels of post-
exercise muscle soreness can be elicited in the
masticatory system of healthy subjects, by standar-
dised grinding movements.4
Although different studies have examined the
association between bruxism and TMD symptoms,
the findings are not conclusive and their inter-rela-
tionship is still far from being explained. It has been
suggested that bruxism is a cause, or a risk factor, of
myofascial pain of the masticatory muscles. The
pain associated with bruxism is not a mandatory
finding: many subjects who appear to brux nightly
have no masticatory muscle pain. This implies that
the degree of specificity of the association bruxism-
TMD is low, which reduces the probability of estab-
lishing a valid cause-effect relationship.5
The present study was designed to seek a better
understanding of chronic musculoskeletal facial
pain and its relation to the sleep bruxism, by com-
paring the bruxism and sleep characteristics of two
samples of subjects with long-standing sleep brux-
ism, with and without chronic facial pain com-
plaints.
Materials and methods
Forty consecutive patients (32 women and 8 men)
were selected according to the report that they
frequently presented with tooth grinding sounds
during sleep, confirmed by a roommate or family
member. The selected patients were divided into
two groups according the presence or absence of
orofacial pain as the main complaint:
I. group A: bruxism with TMD (n = 20) and
II. group B: bruxism without TMD (n = 20).
A standardised diagnostic protocol was applied to
all patients equally by the same trained dentist. It
consisted of a systematic evaluation of cervical,
cranial, facial, dental and other oral structures
according the following diagnostic instruments or
exams:
1. Preliminary interview, to detail: (a) the chief
complaint, (b) the general pain characteristics
when it was the chief complaint (location, inten-
sity, quality, duration, time of pain worsening,
aggravating and alleviating factors) and (c) the
medical history.
2. The Portuguese version of the Research Diagnos-
tic Criteria for Temporomandibular Disorders
(RDC/TMD).6,7
3. Polysomnographic recording (PSG) to confirm the
presence of sleep bruxism, analyse the sleep
architecture and the presence of sleep disorders,
which included: electroencephalogram (EEG),
bilateral electro-oculograms (EOG), electrocar-
diogram (ECG), oronasal airflow analyser, pulse
oximeter, chest-wall movement register and
electromyograms (EMG) of chin/suprahyoid,
bilateral masseter and anterior tibialis muscles.
One all-night polysomnographic recording was
made for each subject, in a sound-attenuated
and temperature-controlled room. Audio and
video recordings were made simultaneously.
Sleep bruxism and temporomandibular disorder
Before sleep recordings, each patient performed
series of five tasks of two seconds duration, to
allow signal recognition and calibration of EMG:
voluntary clenching (maximal intercuspal occlu-
sion), lateral and protrusive jaw movements,
swallowing, and coughing. Three levels of volun-
tary contractions were executed: at maximum
(100%), moderate (50%) and light (20%)
levels. Before the PSG the patients also answered
a brief questionnaire about the presence of pain
during the day and in the morning after, and
about the presence of pain during the night.
Data analysis
All EMG potentials of right masseter activity with
amplitude of at least 20% of the maximum voluntary
contractions were retained for analysis.8,9 EMG
events were defined and scored according to three
different types of episodes: phasic (rhythmic), tonic
(sustained), or mixed (both phasic and tonic).8 A
phasic episode corresponds to at least three EMG
bursts of 0.252.0 s duration, separated by two
inter-burst intervals. A tonic episode corresponds
to an EMG burst lasting more than 2.0 s. The total
number of bruxism episodes and bursts were
expressed as an index per hour of sleep as well as
in bursts per episode. The percentage of bruxism
episodes with micro-arousals, the total duration of
bruxism episodes(s), the percentage of bruxism epi-
sodes in each sleep stage and the mean bruxism
episodes amplitude (mV) were also calculated. The
polysomnographic diagnostic cut-off criteria for
sleep bruxism were: (1) more than four bruxism
episodes per hour, (2) more than six bruxism bursts
per episode and/or 25 bruxism bursts per hour of
sleep, and (3) at least two episodes with grinding
sounds.9 Sleep parameters were scored in 30 s
epochs according to a standard method.10
The statistical analyses were performed using x2-
test (Fishers exact test for low expected frequency)
to measure differences in proportions between the
two compared groups. The analysed qualitative
variables were obtained from the RDC/TMD self-
Table 1 Sample demographic data
Demographic data Group A
Mean age (min. max.) 32.7 (2254)
Women n (%) 17 (85.0)
Men n (%) 3 (15.0)
Total n (%) 20 (100.0)
a
MannWhitney test.
b
Fishers exact test.
3
report, RDC/TMD axis I and II levels of depression
and non-specific physical symptoms. The Mann
Whitney test was used to compare age and the
quantitative variables of bruxism and sleep between
the two groups. The data were analysed using the
SPSS 11.0 for Windows program.
Exclusion criteria
The exclusion criteria were: use of drugs (psycho-
tropic, antidepressant, antianxiety, anticonvulsive
and analgesic), lack of posterior occlusal support,
the use of an occlusal splint or to be undergoing
orthodontic treatment, and fibromyalgia.
All the patients gave informed consent to proce-
dures approved by the Ethics Committee of the
Medical School.
Results
The ages ranged from 17 to 54 yr (mean
36.1  11.3 yr). Twenty patients (17 women and 3
men) related orofacial pain as their main complaint
(group A), and 20 patients (15 women and 5 men) did
not report any type of orofacial pain as their main
complaint (group B). There was no statistically sig-
nificant difference between the mean age ( p = 0.55)
and the gender ( p = 0.47) of the two groups (Table 1).
RDC/TMD self-reported symptoms, axis I
and II diagnosis (Table 2)
The self-reported RDC/TMD characteristics showed
the presence of diurnal tooth grinding/clenching,
uncomfortable bite and morning jaw pain/stiffness
in both groups. The morning jaw pain/stiffness
presented higher prevalence in the group A
( p = 0.0113). According the RDC/TMD axis I diagno-
sis, the group A presented myofascial pain (100.0%),
disc displacement (10.0%) and arthralgia (85.0%).
For group A, the frequencies of depression was
15.0%: normal, 55.0%: moderate and 30.0%: severe,
and for group B, 50.0%: normal, 35.0%: moderate
Group B p Values
30.8 (1754) 0.4083 a
15 (75.0) 0.6950 b
5 (25.0)
20 (100.0)
4 C.M. Camparis et al.
Table 2 General characteristics of the sample according the RDC/TMD axis I and II
Variables
Diurnal tooth grinding/clenching n (%)
Uncomfortable/unusual bite n (%)
Morning facial fatigue/pain n (%)
Myofascial pain n (%)
TMJ click n (%)
Arthralgia n (%)
Limitations related to mandibular functioning
Depression n (%)
Non-specific physical symptoms n (%)
a
x2-test.
b
MannWhitney test.
and 15.0%: severe. For non-specific physical symp-
toms, the diagnoses for group A were 5.0%: normal,
45.0%: moderate and 50.0%: severe, and for group B,
55.0%: normal, 35.0%: moderate and 10.0%: severe.
There was statistically significant difference
between groups A and B for non-specific physical
symptoms scale ( p = 0.001) and limitations related
to mandibular functioning ( p = 0.001) but there was
no significance for depression levels. For the statis-
tics of depression and non-specific physical symp-
toms the observed frequencies of moderate and
severe levels were added.
Headache and body pain with reference to
the last month before PSG (RDC/TMD
questionnaire)
All patients of group A (100%) and 12 patients of
group B (60%) presented headache complaint with
reference to the last month before the PSG record-
ing ( p = 0.0016). In the group A, 90% reported low
back pain and, in the group B, 55% ( p = 0.0336). The
complaint of general muscle soreness was reported
by 90% of group A and 70% of group B ( p = 0.1175).
Presence of pain during the day before
and the PSG night
Seventeen of the 20 patients of group A (85%) pre-
sented facial pain complaint during the day before
the polysomnographic recording and nine (45%)
related mild or moderate pain during the night, in
the vertebral column or head. The patients of group
B did not present pain during the day before the
polysomonographic recording, but six of them (30%)
related mild discomfort in the vertebral column
during the night.
Group A facial pain characteristics
For group A, pain duration ranged from 1 to 10 yr
(mean 4.37 yr, median 4.00 yr) and the intensity of
Group A (n = 20) Group B (n = 20) p Values
13 (65.0) 10 (50.0) 0.5224
11 (55.0) 5 (25.0) 0.1066
15 (75.0) 6 (30.0) 0.0113 a
20 (100.0) 0 (0.0)
14 (70.0) 6 (30.0) 0.0269 a
17 (85.0) 0 (0.0)
0.25 0.06 0.0010 b
17 (85%) 10 (50%) 0.0958
19 (95%) 9 (45%) 0.0010 a
pain (VAS) at the moment of clinical evaluation
ranged from 3 to 10 (mean 4.69). The pain char-
acteristics were: bilateral location (95.0%) and
tightness/pressure quality (70.0%). The time when
pain occurred or worsened was the morning period
for 65.0% of group A patients and the complaint of
frontotemporal headache was present in 65.0% in
the last six months ( p = 0.001).
Sleep self-report with reference to the
last month before PSG (RDC/TMD
questionnaire)
Fifteen per cent of the patients of group A did not
relate any trouble with falling asleep, whereas 85%
did. In group B, 55% did not and 45% did relate
trouble with falling asleep ( p = 0.0203). In group
A, 90% related restless or disturbed sleep, whereas
10% did not (n = 2). For group B, 60% related restless
or disturbed sleep and 40% did not ( p = 0.0679).
Sleep variables (Table 3)
The analysed sleep variables were: latency, effi-
ciency, REM latency, percentage of stages 14,
and REM sleep, number per hour and duration of
micro-arousals, periodic limb movements and
obstructive sleep apnea. All patients presented
normal sleep parameters10,2022 and no statistically
significant differences were found between the two
groups for all these variables. Signs of alteration in
the sleep efficiency (<85%) occurred in five patients
of group A and five of group B. The sleep efficiency
corresponds to the sleep time in relation to time in
bed and its reduction may be occur as a function of
an increased latency or number of micro-arousals.20
Bruxism variables (Table 4)
All patients submitted to PSG recording presented
rhythmic masticatory muscle activity during sleep
and were included in the diagnostic criteria for sleep
Sleep bruxism and temporomandibular disorder 5

Table 3 Means and standard deviations for sleep variables

Variables Group A (n = 20) Group B (n = 20) p Values a
Mean S.D. Mean S.D.
Total sleep time (min) 397.2 61.9 382.9 50.2 0.1420
NREM sleep latency (min) 16.5 13.0 16.8 14.2 0.9031
REM latency (min) 104.7 52.5 114.5 56.9 0.4093
Sleep efficiency (%) 88.0 11.8 89.1 8.3 0.8498
Stage 1 (%) 2.6 1.4 2.3 1.0 0.4242
Stage 2 (%) 57.2 7.3 56.9 8.2 0.8817
Stage 3 (%) 3.2 0.7 3.7 2.3 0.6747
Stage 4 (%) 17.9 6.8 17.2 5.6 0.6948
REM sleep (%) 19.1 5.3 20.0 4.9 0.4734
Periodic leg movements (n/h) 0.6 0.7 1.0 0.9 0.1242
Obstructive sleep apnea (n/h) 0.8 0.6 1.1 0.7 0.2647
Micro-arousals (n/h) 10.0 3.8 11.7 6.4 0.2615
Duration of micro-arousals (s) 7.6 1.7 9.3 3.1 0.5876
a
MannWhitney test.

Table 4 Means and standard deviations for bruxism variables

Variables Group A (n = 20) Group B (n = 20) p Values a
Mean S.D. Mean S.D.
Number of episodes/h 6.2 2.2 8.0 3.9 0.1016
Number of bursts/h 25.0 10.8 32.5 32.6 0.5075
Number of bursts/episode 3.7 1.6 3.8 1.6 0.9352
Total duration of episodes (s) 323.5 144.1 450.4 389.8 0.2977
Episodes in stage 1(%) 4.5 4.0 2.6 3.4 0.0943
Episodes in stage 2 (%) 64.8 12.8 68.6 14.0 0.5338
Episodes in stages 3 and 4 (%) 7.5 5.9 9.4 9.0 0.6161
Episodes in REM sleep (%) 23.2 12.8 19.9 13.0 0.3104
Episodes with micro-arousals (%) 84.9 9.5 85.7 18.5 0.2444
Maximum voluntary contraction (mV) 243.9 125.8 281.1 177.7 0.8181
EMG amplitude (mV) 143.9 49.4 158.1 78.8 0.8711
a
MannWhitney test.

bruxism proposed by Lavigne et al.9 According these
criteria the diagnosis can be correctly predicted in
81.3% of controls and 83.3% of bruxers. The present
study also used the amplitude criteria of Sjoholm
et al.8 which establishes phasic, tonic and mixed
episodes of muscle contraction with at least 20% of
the amplitude of the maximum voluntary contrac-
tion, that aim to discard oral motor activities, such
as coughing, deglutition and talking while sleeping,
which could be confused with bruxism in the EMG.
The audiovisual register of the patient during sleep
also helps to identify oral motor activities not
related to bruxism.
Sleep bruxism was analysed through the following
variables: number of episodes per hour of sleep,
number of bursts per hour of sleep, number of bursts
per episode, total duration of episodes, percentage
of episodes in stages 14 and REM sleep, percentage
of episodes with micro-arousals, maximum volun-
tary contraction and amplitude of bruxism episodes.
No statistically significant differences were found
between the two groups for all these variables, but
the patients with pain presented 6.2 episodes per
hour of sleep and, those without pain, 8.0 episodes,
that is to say, 20% more episodes than those with
pain. The percentage of bruxism episodes in each
sleep stage was statistically equal for the two groups
and the highest percentage occurred in stage 2.
Discussion
In the clinical evaluation, only patients that report
frequent and long-standing sleep bruxism, con-
firmed by room-mate or family member were
selected. The patients were selected consecutively
and paired by gender and age to obtain a more
uniform sample of patients (Table 1), whose sleep
bruxism was confirmed by polysomnography. RDC/
TMD allowed the two groups to be differentiated for
the presence or absence of TMD. The criterion for
chronic pain was based on the International Associa-
6 C.M. Camparis et al.
tion for the Study of Pain (IASP) definition: pain
without apparent biological value that has persisted
beyond the normal tissue healing time, which
usually takes 3 months.11
According to the RDC/TMD axis I, the chronic
orofacial pain (mean duration of 4.37 yr) of the
patients in group A was diagnosed as myofascial pain
and arthralgia, diagnostic sub-groups of TMD. The
RDC/TMD axis II showed that patients with TMD pre-
sented higher non-specific physical symptom scores
( p = 0.0001) and higher frequency of moderate and
severe depression, although not statistically signifi-
cant (Table 2). Considering the questions of the RDC/
TMD questionnaire, higher frequency of complaints
of headache and low back pain could be observed in
the patients of group A than those of group B. More-
over, patients of group A presented higher frequency
of diseases or comorbidities, mentioned in the med-
ical history at the preliminary interview.
The results of this study showed clinical charac-
teristics of sleep bruxism patients with TMD (group
A) to be compatible with previous studies:1215
bilateral facial pain, frontotemporal headache,
with time of worsening being in the morning and
the commonest pain quality being tightness/pres-
sure. The morning pain/stiffness may be a post-
exercise muscle soreness and a clinical sign of mas-
ticatory muscle activity during sleep.16 In a recent
longitudinal case study,17 data of recorded nights
showed that variations in nocturnal masticatory
muscle activity did not contribute to variations in
morning jaw muscle pain, which was related to the
evening jaw muscle pain, that was explained by
daytime clenching. This study enhances the impor-
tance of daytime clenching and stress events in the
maintenance of pain. However, the present study
showed the frequency of daytime clenching self-
report was similar for both groups and a higher
frequency of morning pain/stiffness in group A
(Table 2).
At present, it is not clear why some patients with
sleep bruxism develop chronic myofascial pain and
others, like the patients in group B, do not. Some
patients in group B (30.0%), even without any facial
pain complaint, reported morning fatigue or pain,
but did not develop chronic myofascial pain. Persis-
tent and chronic pain conditions are associated with
prolonged functional changes in the nervous system,
commonly referred to as central sensitisation.18
Thus, in chronic pain patients, factors like central
sensitisation, neuroplasticity, dysfunction of the
inhibitory neural descendent system and psycho-
social abnormalities may be present. Diffusion and
amplification of persistent deep pain, such as TMD,
may be also the result of an increase in endogenous
descending facilitation.19
In the present study, one-night polysomnography
was carried for each patient, whose results were
analysed the next day to verify the possibility of
undesired effects having occurred and check
whether another night would be necessary. All the
patients presented normal sleep parameters20 and
did not present sleep disorders21,22 and it was not
considered necessary to perform a second night of
examination. The effect of the different environ-
ment and the devices used in the PSG, such as the
discomfort of the electrodes, the limitation of
movements and the potential psychological conse-
quences due to the patient being observed and
evaluated has been mentioned in literature. Some
authors performed one night polysomnography and,
depending on the quality of sleep observed and the
presence of sleep disorders, the exam would be
repeated or considered as being representative of
the patient.2327 Others recommend two nights of
examination and consider the results of the second
night, the results of the first night being discarded
and considered as serving to habituate the
patient.2832
Considering the presence of pain and the quality
of sleep, one knows that painful conditions interfere
with sleep and that the intrinsic sleep disorders also
contribute to the pain experience. It would appear
therefore, that there is a reciprocal relation
between quality of sleep and pain and the control
of sleep quality may influence the control of painful
conditions.33 Patients with chronic pain report poor
quality of sleep, therefore they take longer to fall
asleep and have slow waves of sleep broken up by
the intrusion of alpha waves. However, there is still
no explanation for sleep pattern alterations of
patients with chronic pain. It would appear that
as the painful stimuli increase in intensity and dura-
tion, the consequences could range from slightly
disturbed sleep to the accentuated loss of sleep
time. Studies demonstrate that serotonin plays an
important role in the modulation of pain during vigil
and during sleep.34 In the present study, no signifi-
cant differences were found for the sleep variables,
in spite of group A being comprised of patients with
chronic myofascial pain. However, the RDC/TMD
questionnaire showed that patients of both groups
presented complaints about trouble with falling
asleep and restless or disturbed sleep, with higher
frequency in group A.
Considering the bruxism variables (Table 4), no
statistically significant difference was found
between the two groups and a percentage of about
85% of bruxism episodes were related to micro-
arousals. Although the nature of the relation
between micro-arousals and motor activity is
unknown, it is possible that sleep bruxism may be
Sleep bruxism and temporomandibular disorder
associated with imbalance of the influences that
maintain sleep, through transitory increase of the
induced activity of micro-arousals. Kato et al.35
observed that a clear sequence of cortical and
autonomic-cardiac activation precedes the mandib-
ular motor activity in the patients with bruxism and
suggested that sleep bruxism is a powerful motor
manifestation secondary to the micro-arousals.
Recently, sleep bruxism was incorporated to the
International Classification of Sleep Disorders
(2005)36 as a sleep related movement disorder
instead of a parasomnia.
Although not statistically significant, in the pre-
sent study patients without pain presented 20% more
bruxism episodes than those with pain. The influence
of pain in the bruxism pattern was studied in patients
with non-myofascial pain, compared with subjects
without any facial pain and it was observed that the
patients with pain presented with 40% fewer bruxism
episodes, suggesting that pain decreases the number
of beginnings of bruxism episodes, but does not affect
their contents.29 The effect of the experimental pain
evoked by the injection of capsaicin into the mass-
eter muscles in subjects with bruxism, with and with-
out facial pain showed that muscle pain is associated
with less electromyographic activity of the muscles
during sleep.31
The results of the present study raise questions
about the belief that the presence or absence of
facial pain may be associated with higher or lower
frequency and amplitude and with the type of mus-
cle contraction of sleep bruxism episodes. The the-
ory of the vicious cycle myospasmpainmyospasm
has been used since the decade of 40 to explain the
etiology of chronic painful conditions, such as lom-
balgia, the chronic tension type headache and myo-
fascial pain and many authors have also used it to
explain the pathophysiology of TMD. The pain model
for TMD was therefore, based on two premises: that
muscle hyperactivity can lead to pain and pain leads
to tonic hyperactivity. The first would appear to be
true, therefore when the muscles are voluntarily
contracted for longer periods, the muscle fibers
start to present fatigue, but the second premise
is questionable. The pain adaptation model was
considered to be a way to relate persistent pain
to the associated motor signs and symptoms and as a
substitute for the hypothesis of the vicious cycle.
This model is based on the following postulates:
persistent pain has a general effect on the motor
system, including changes in facial expression and
corporal position and escape from physical work;
the activation of the nociceptores in one part of the
body inhibits the agonist motor neurons and facil-
itates the antagonists; the nociceptores of the skin,
teeth, conjunctive tissue, muscles and joints have
7
similar effect on the motor system. These changes
related to pain are considered adaptive, to prevent
futures damage and to allow tissue repair.16 In the
present research, this protective mechanism can be
observed in the patients of group A that presented a
higher index of limitations related to mandibular
functioning than group B. Sleep bruxism, as a motor
jaw activity, is perhaps also modulated by the influ-
ence of chronic pain on the motor system.29,37
Clinically, the results of the present study point
out the importance of the professional, who acts in
the control of chronic painful conditions, knowing
the pathophysiology of pain. In the case of patients
with bruxism and TMD, control of the symptoms
must not consider only the presence of muscle
hyperactivity as a pain maintaining factor, but also
the functional alterations of the central nervous
system. Thus, the management and control of
chronic pain must involve therapeutic options with
a local and central action mechanism.
References
1. Okeson JP, editor. Orofacial pain: guidelines for assessment,
diagnosis and management. Chicago: Quintessence; 1996.
2. Lobbezoo F, Naeije M. Bruxism is mainly regulated centrally,
not peripherally. J Oral Rehabil 2001;28:108591.
3. Okeson JP. Management of temporomandibular disorders
and occlusion. 4th ed. St. Louis: Mosby; 1998.
4. Arima T, Svensson P, Arendt-Nielsen L. Experimental grinding
in healthy subjects: a model for postexercise jaw muscle
soreness? J Orofac Pain 1999;13:10414.
5. Lobbezoo F, Lavigne GJ. Do bruxism and temporomandibular
disorders have a cause-and-effect relationship? J Orofac Pain
1997;11:1523.
6. Dworkin SF, LeResche L. Research diagnostic criteria for
temporomandibular disorders: review, criteria, examinations
an specifications, critique. J Craniomandib Disord 1992;6:
30155.
7. Kosminsky M, Lucena LBS, Siqueira JTT, Pereira Junior F, Goes
PSA. Cultural adaptation of the Research Diagnostic Criteria
for Temporomandibular Disorders: Axis II questionnaire. J
Bras Cln Odontol Int 2004;8:5161.
8. Sjoholm TT, Lehtinen I, Helenius H. Masseter muscle activity
in diagnosed sleep bruxists compared with non-symptomatic
controls. J Sleep Res 1995;4:4855.
9. Lavigne GJ, Rompre PH, Montplaisir JY. Sleep bruxism: valid-
ity of clinical research diagnostic criteria in a controlled
polysomnographic study. J Dent Res 1996;75:54652.
10. Rechtschaffen A, Kales A. A manual of standardized termi-
nology, techniques and scoring system for sleep stages of
human subjects. Los Angeles: Brain Research Institute/UCLA;
1968.
11. International Association for the Study of Pain. How preva-
lent is chronic pain? Pain Clin Updates 2003;9: 14.
12. Lobbezoo-Scholte AM, Lobbezoo F, Steenks MH, De Leeuw JRJ,
Bosman F. Diagnostic subgroups of craniomandibular disorders.
Part II. Symptom profiles. J Orofac Pain 1995;9:3743.
13. Dao TTT, Lund JP, Lavigne GJ. Comparison of pain and quality
of life in bruxers and patients with myofascial pain of the
masticatory muscles. J Orofac Pain 1994;8:3506.
8 C.M. Camparis et al.
14. Ciancaglini R, Gherlone EF, Radaelli G. The relationship of
bruxism with craniofacial pain and symptoms from the mas-
ticatory system in the adult population. J Oral Rehabil
2001;28:8428.
15. Kampe T, Tagdae T, Bader G, Edman G, Karlsson S. Reported
symptoms and clinical findings in a group with longstanding
bruxing behaviour. J Oral Rehabil 1997;24:5817.
16. Lund JP. Pain and the control of muscles. In: Fricton JR,
Dubner R, editors. Orofacial pain and temporomandibular
disorders. New York: Raven Press; 1995. p. 10315.
17. Van Selms MKA, Lobbezoo F, Wicks DJ, Hamburger E. Cranio-
mandibular pain, oral parafunctions, and psychological stress
in a longitudinal case study. J Oral Rehabil 2004;31:73845.
18. Sessle BJ. The neural basis of temporomandibular joint and
masticatory muscle pain. J Orofac Pain 1999;13:23845.
19. Ren K, Dubner R. Descending modulation in persistent pain:
an update. Pain 2002;100:16.
20. Carskadon MA, Rechtschaffen A. Monitoring and staging
human sleep. In: Kryger MH, Roth T, Dement WC, editors.
Principles and practice of sleep medicine. Philadelphia: W.B.
Saunders; 2000. p. 1197215.
21. American Academy of Sleep Medicine. Sleep-related breath-
ing disorders in adults: recommendation for syndrome defini-
tions and measurements techniques in clinical research.
Sleep 1999;22:66789.
22. American Sleep Disorders Association. Atlas Task Force
recording and scoring leg movements. Sleep 1993;16:749
59.
23. Reding GR, Zepelin H, Robinson JE, Zimmerman SO, Smith V.
Nocturnal teeth-grinding: all-night psychophysiologic stu-
dies. J Dent Res 1968;47:78697.
24. Ware JC, Rugh JD. Destructive bruxism: sleep stage relation-
ship. Sleep 1988;11:17281.
25. Okeson JP, Phillips BA, Berry DTR, Baldwin RM. Nocturnal
bruxing events: a report of normative data and cardiovas-
cular response. J Oral Rehabil 1994;21:62330.
26. Bader GG, Kampe T, Tagdae T. Body movements during sleep
in subjects with long-standing bruxing behavior. Int J
Prosthodont 2000;13:32733.
27. Sjoholm TT, Lowe AA, Miyamoto K, Fleetham JA, Ryan CF.
Sleep bruxism in patients with sleep-disordered breathing.
Arch Oral Biol 2000;45:88996.
28. Velly Miguel AM, Montplaisir J, Rompre PH, Lund JP, Lavigne
GJ. Bruxism and other orofacial movements during sleep. J
Craniomandib Disord 1992;6:7181.
29. Lavigne GJ, Rompre PH, Montplaisir JY, Lobbezoo F. Motor
activity in sleep bruxism with concomitant jaw muscle pain.
Eur J Oral Sci 1997;105:925.
30. Macaluso GM, Guerra P, Di Giovanni G, Boselli M, Parrino L,
Terzano MG. Sleep bruxism is a disorder related to periodic
arousals during sleep. J Dent Res 1998;77:56573.
31. Arima T, Arendt-Nielsen L, Svensson P. Effect of jaw muscle
pain and soreness evoked by capsaicin before sleep on oro-
facial motor activity during sleep. J Orofac Pain 2001;15:
24556.
32. Miyawaki S, Tanimoto Y, Araki Y, Katayama A, Fujii A, Takano-
Yamamoto T. Association between nocturnal bruxism and
gastroesophageal reflux. Sleep 2003;26:88892.
33. Moldofski H. Sleep and pain. Sleep Med Rev 2001;5:38798.
34. Foo H, Mason P. Brainstem modulation of pain during sleep
and waking. Sleep Med Rev 2003;7:14554.
35. Kato T, Montplaisir JY, Guitard F, Sessle BJ, Lund JP, Lavigne
GJ. Evidence that experimentally induced sleep bruxism is a
consequence of transient arousal. J Dent Res 2003;82:284
8.
36. American Academy of Sleep Medicine. The international
classification of sleep disorders. Diagnostic and coding man-
ual. 2nd ed. Westchester, Illinois: American Academy of
Sleep Medicine; 2005.
37. Lavigne GJ, Kato T, Kolta A, Sessle BJ. Neurobiological
mechanisms involved in sleep bruxism. Crit Rev Oral Biol
Med 2003;14:3046.