Movement Disorders
Vol. 17, Suppl. 2, 2002, pp. S67–S69
© 2002 Movement Disorder Society
Published by Wiley-Liss, Inc.
DOI 10.1002/mds.10064
Sleep Bruxism as a Motor Disorder
Antoon De Laat, MD, PhD,1 and Giudo M. Macaluso, MD2
1
Cluster Oral Physiology, Dept. Oral and Maxillo-Facial Surgery, School of Dentistry, Oral Pathology and Maxillo-Facial
Surgery, Catholic University of Leuven, Leuven, Belgium
2
Sezione di Odontostomatologia, Universita degli Studi di Parma, Parma, Italy
Bruxism, defined as parafunctional jaw muscle activ-
ity during the day or night, and characterized by clench-
ing or grinding the teeth, splinting the jaw muscles, or
rhythmic chewing-like empty mouth movements, has
been a major problem and challenge to dentistry. It may
cause severe wear, attrition, and abfraction of teeth, den-
tal pain (e.g., cracked tooth syndrome), overload of den-
tal implants and increased periodontal problems. Also
pain and dysfunction of the jaw system, collectively em-
braced under the term craniomandibular or temporoman-
dibular disorders, have been discussed in relation to
bruxism, but the evidence has been controversial.1 In
contrast to limb muscles, where eccentric muscle con-
traction leads to muscle pain, such exercise in jaw
muscles did not result in the occurrence of a vicious pain
cycle.2 In addition, most people exhibiting bruxist be-
haviour do not report pain, and those who do, complain
especially of pain in the morning.3 Recent studies, dis-
criminating between diurnal parafunctions and bruxism
during sleep, are more inclined to use the definition put
forward by the American Sleep Disorder Association4
defining bruxism as periodical, stereotyped movement
disorders of the teeth-jaw system, involving grinding and
clenching of the teeth during the night (sleep bruxism).
This sleep disorder is classified among the parasomnias.
Epidemiology and Diagnosis
Bruxism is reported by 6 to 20% of the population,5
also in children (14%), and decreases after the age of 50
years.6 Tooth clenching (and not tooth grinding) is re-
ported more often (22%) in women than in men.5 In
patients with temporomandibular disorders, the reported
frequency is 26 to 66%.7
The diagnosis of sleep bruxism is not easy. Self-report
Key words: sleep; bruxism; temporomandibular disorders; dopa-
mine D2 receptors; polysomnography; arousal; parasomnias
*Correspondence to: Antoon De Laat, School of Dentistry, K.U.
Leuven, Capucijnenvoer 7, B-3000 Leuven, Belgium.
E-mail: antoon_delaat@med.kuleuven.ac.be
S67
by the patient or the patient’s spouse is unreliable,
whereas studying dental wear intraorally or on dental
casts cannot trace when the wear occurred, nor discrimi-
nate between excessive wear and normal aging.8 The use
of electromyography is limited because it does not allow
discrimination between clenching and grinding, and can-
not exclude other activities such as cuffing, swallowing,
myoclonus, somniloqui, and tics, unless combined with
video and audio recording in the environment of a sleep
laboratory. By using this methodology, rhythmic masti-
catory muscle activities (RMMAs, characterised by
lower electromyographic (EMG) activity than in brux-
ism, and excluding tooth grinding) were observed in 56%
of the general sleep laboratory population,6 which in-
spired the hypothesis that bruxism may represent basi-
cally normal orofacial motor behaviour in which certain
factors increased the activity and pushed it into the
pathological range of jaw-muscle activity. Consequently,
the following polysomnographic cut-off criteria were
proposed: (1) at least 2 bruxism episodes with grinding
sounds, and (2) more than 4 bruxism episodes per hour of
sleep, and/or more than 25 bursts of bruxism per hour of
sleep, and/or more than 6 RMMA bursts per episode.9 By
using these criteria, the clinically established presence or
absence of bruxism was correctly predicted in 83% of
bruxers and 81% of asymptomatic control subjects.
Etiology
Most theories adhere to a multifactorial etiology of
bruxism10 and discriminate between peripheral factors
(anatomy, dental occlusion, receptor input), central (cen-
tral nervous system, CNS), and psychological factors.
Even if Ramfjord’s hypothesis, stating that interfer-
ences in the dental occlusion were an important etiologic
factor, were based on uncontrolled and questionable
electromyographic research, it has ruled the therapy for
bruxers for decades. Only more recently, clear evidence
has been produced indicating that the removal of occlu-
sal interferences did not influence bruxist behaviour and
that artificial interferences resulted in a decreased and
S68 A. DE LAAT AND G.M. MACALUSO

not increased EMG activity in 90% of the test subjects.10
In addition, the correlation between clinically diagnosed
bruxism and asymmetric condylar height or bizygomatic
and skull-width was shown wrong by Lobbezoo and col-
leagues,12 who could not find significant differences be-
tween bruxers and nonbruxers regarding 26 occlusal and
25 anatomical variables in a controlled study using poly-
somnographic diagnosis.
Sleep bruxism was studied in relation to sleep physi-
ology, suggesting that it is an arousal-related phenom-
enon. Recently, Macaluso and associates13 could dem-
onstrate the association between bruxism episodes and
an arousal response in non-rapid eye movement sleep
(see Fig. 1). These findings could suggest that transient
arousals of the central nervous system are the broader
physiological mechanism that hosts bruxism episodes.
Nevertheless, the sleep of bruxers is mostly normal, and
only subtle differences in sleep microstructure are pre-
sent when compared with control subjects.
Clinical and controlled experimental studies using
SPECT, elucidated the possible role of the central dopa-
minergic system in the pathophysiology of sleep brux-
ism. Lobbezoo and coworkers14 documented an abnor-
mal side imbalance in striatal D2 receptor expression in
bruxists, comparable to other movement disorders, e.g.,
spasmodic torticollis. Low-dose levodopa (L-dopa) or
bromocryptine decreased bruxis activity, whereas in-
creased bruxism has been associated by long-term use of
dopamine antagonists, of L-dopa in parkinsonism, and of
selective serotonin reuptake inhibitors.15 Other iatrogen-
ic forms of bruxism such as the use of ecstasy or nicotine
might be explained by the resulting increase in central
dopaminergic activity.16
Psychological factors such as stress, anxiety, and ag-
gression have been discussed frequently as an initiating
cofactor of bruxist behaviour. Even if these psychologi-
cal factors are difficult to evaluate, bruxists were char-
acterized as perfectionists and showed an increased ten-
dency for aggression and anxiety. Using the Minnesota
Multiphasic Personality Inventory or in studies using re-
ported stress,5 no or only weak correlations were re-
ported. A possible link between the previously men-
tioned peripheral factors and the central pathophysiologi-
cal hypotheses was re-inspired by recent animal
research; when bruxing rats were subjected to acute
changes in the relation between their incisor teeth (by

FIG. 1. Episodes of bruxism occurring during transient arousals (A). Note the presence of leg movements during the first episode. Upper traces ⳱
electroencephalography; EOG, electro-oculography; EMG, mentalis EMG; TEMP., MASS., and TIB ANT, EMG of the temporalis, masseter, and
tibialis anterior muscles left and right, respectively; O-N PNG, airflow; THOR PNG, thoracal pneumogram; EKG, heart rate.

Movement Disorders, Vol. 17, Suppl. 2, 2002

 SLEEP BRUXISM AS A MOTOR DISORDER
cutting them asymmetrically or covering them with an
acrylic cap), an asymmetry in the central dopaminergic 6.
system at the level of the basal ganglia could be ob-
served.17 In contrast, a previously mentioned asymmetry
7.
in D2-receptor expression could not be correlated to oc-
clusal variables in man.12,17 8.
CONCLUSION
9.
Sleep bruxism is considered an exaggerated manifes-
tation of an otherwise normal occurrence of rhythmic
masticatory muscle activity. Its cause is considered mul- 10.
tifactorial and peripheral factors (dental occlusion,
11.
anatomy of the jaw system) seem to play a minor role.
Similar to other parasomnias, sleep bruxism has typically 12.
been associated with arousals. In addition, there are in-
dications that modifications of the central dopaminergic
balance are involved, which support the major role of
central mechanisms in its pathophysiology. 13.
REFERENCES
14.
1. Lobbezoo F, Lavigne GJ. Do bruxism and temporomandibular
disorders have a cause-and-effect relationship? J Orofac Pain 1997;
11:15–23.
2. Svensson P. Pain mechanisms in myogenous temporomandibular 15.
disorders. Pain Forum 1997;6:158–165.
3. Dao TTT, Lund JP, Lavigne GJ. Comparison of pain and quality of
life in bruxers and patients with myofascial pain of the masticatory 16.
muscles. J Orofac Pain 1994;4:211–226.
4. Thorpy MJ. Parasomnias. In: Thorpy MJ, ed. International classi-
fication of sleep disorders: diagnostic and coding manual. Roch- 17.
ester, MN: Allen Press, 1990:142–185.
5. Goulet JP, Lund JP, Montplaisir JY. Daily clenching, nocturnal
S69
bruxism and their association with TMD symptoms [abstract].
J Orofac Pain 1996;10:120.
Lavigne GJ, Montplaisir JY. Bruxism: epidemiology, diagnosis,
pathophysiology and pharmacology. Adv Pain Res Therapy 1995;
21:387–404.
Carlsson GE, Leresche L. Epidemiology of temporomandibular
disorders. Prog Pain Res Management 1995;4:211–226.
Seligman DA, Pullinger AG. The degree to which dental attrition
in modern society is a function of age and of canine contact.
J Orofac Pain 1995;9:266–275.
Lavigne GJ, Rompré PH, Montplaisir JY. Sleep bruxism: validity
of clinical research diagnostic criteria in a controlled polysomno-
graphic study. J Dent Res 1996;75:546–552.
Rugh JD, Barghi N, Drago CJ. Experimental occlusal discrepan-
cies and nocturnal bruxism. J Prosthet Dent 1984;51:548–553.
Ramfjord SP. Bruxism, a clinical and electromyographic study.
J Am Dent Assoc 1961;62:21–44.
Lobbezoo F, Ianfrancesco C, Rompré PH, Soucy JP, Montplaisir
JY, Lavigne GJ. Associations between morphological measures
and neurochemical factors in patients with sleep-related oromotor
activities: an exploration. Proceedings Closed Meeting EACD,
1999.
Macaluso GM, Guerra P, Di Giovanni G, Boselli M, Parrino L,
Terzano MG. Sleep bruxism is a disorder related to periodic arous-
als during sleep. J Dent Res 1998;77:565–573.
Lobbezoo F, Soucy JP, Montplaisir JY, Lavigne GJ. Striatal D2
receptor binding in sleep bruxism: a controlled study with iodine-
123-iodobenzoamide and single photon emission computed to-
mography. J Dent Res 1996;75:1804–1810.
Lobbezoo F, Lavigne GJ, Tanguay R, Montplaisir JY. The effect of
the catecholamine precursor L-dopa on sleep bruxism: a controlled
clinical trial. Mov Disord 1997;12:73–78.
Lavigne GJ, Lobbezoo F, Rompré PH, Nielsen TA, Montplaisir
JY. Cigarette smoking as a risk or exacerbating factor for restless
leg syndrome and sleep bruxism. Sleep 1997;20:290–293.
Areso MP, Giralt MT, Sainz B, Prieto M, Garcia-Vallejo P, Gomez
FM. Occlusal disharmonies modulate central catecholaminergic
activity in the rat. J Dent Res 1999;78:1204–1213.
Movement Disorders, Vol. 17, Suppl. 2, 2002