Sleep Medicine Reviews, Vol. 4, No.

1, p 27–43, 2000
SLEEP
MEDICINE
reviews
REVIEW ARTICLE

Sleep bruxism; an overview of an

oromandibular sleep movement disorder
Gaby Bader1 and Gilles Lavigne2
1
Sleep Unit, Department of Clinical Neurophysiology, Institute of Clinical Neuroscience,
University of Gothenburg, Gothenburg, Sweden; 2(1) Centre d’étude sur le sommeil, Hopital
Sacré-Coeur and (2) Neuroscience Research Center, Faculté de Médecine Dentaire et de
Médecine, Université de Montréal, Montréal, Quebec H3C 3J7, Canada

Sleep bruxism (SB) is a stereotyped movement disorder characterized by grinding or clenching of the
teeth during sleep. The majority of the population will at some time during their lifetime grind or clench
their teeth. It becomes a pathological condition when the subject presents severe tooth damage or complains
of non-restorative sleep. The prevalence of SB is difficult to estimate, since quite often the subjects are
unaware of having the disorder. There is no gender difference. SB is more frequent in the younger
generation, with a decline over age. The symptom recognized in children can persist in adulthood. The
aetio-pathophysiology is still unclear. SB has been associated with tooth interference, psychosocial and
environmental factors, brain transmitters and basal ganglia dysfunction. Attempts have been made to
specify the personality traits of bruxers, reported to be greater anxiety or vulnerability to stress; however,
this is still controversial. SB subjects were observed to present vigilance–sleepiness and somatic problems.
However, they are generally good sleepers. Some authors reported SB during all sleep stages, others
observed the majority of bruxe episodes during light sleep and REM and often associated with arousal
transients. No abnormalities of the autonomic nervous system could be shown in awake SB subjects.
While some studies have shown an association between SB and PLM or breathing disorders, others did
not confirm this. There is no specific treatment for SB: each subject has to be individually evaluated
and treated. Three management alternatives are used: dental, pharmacological and psychobehavioural.
 2000 Harcourt Publishers Ltd

Key words: bruxism, sleep, teeth clenching, teeth grinding, parasomnia

Introduction

The term “la bruxomanie” was first introduced by Marie Pietkiewicz in 1907 [1]. It
was later adapted as “bruxism” to describe gnashing and grinding of the teeth occurring
without a functional purpose. This tooth movement is produced by rhythmic or
sustained–tonic contractions of the masseter and other jaw muscles; it usually occurs
without patient awareness. Bruxism can occur during wakefulness or sleep; the latter

Correspondence to be addressed to: G. Bader MD, PhD.∗ Sleep Unit, Department of Clinical
Neurophysiology, Institute of Clinical Neuroscience, University of Gothenburg, 413 45,
Gothenbourg, Sweden. Tel: 46 31 3421455. Fax: 46 31 821268. E-mail: baderg@mednet.gu.se

1087–0792/00/010027+17 $35.00/0  2000 Harcourt Publishers Ltd

28 G. Bader and G. Lavigne

is referred to as “nocturnal bruxism”. However, the term “sleep bruxism” (SB) is more
appropriate since grinding during daytime sleep can also develop.
Bruxism during daytime or wakefulness is commonly a semi-voluntary “clenching”
activity of the jaw, with usually no sound. During the night, the bruxe episodes are
accompanied by a loud involuntary grinding or tapping of the teeth. In this report we
will refer only to bruxism during sleep. Sleep bruxism is defined in the International
Classification of Sleep Disorders as “a stereotyped movement disorder characterized
by grinding or clenching of the teeth during sleep” [2]. It is classified as a parasomnia,
i.e. it is not a primary disorder of sleep, but a disorder intruding into or occurring
during sleep.

Epidemiology and prevalence

Bruxism is a very common condition, the majority of the population (85 to 90%) will,
at some time, grind or clench the teeth to some degree. Frequent teeth grinding is
present in about 5% [2] to 8% of adults [3], although some authors have even reported
higher figures [4]. It is difficult to assess the prevalence of SB: the estimates of
prevalence are usually based on questionnaires, and often the subjects are not aware
of having this disorder, especially when living alone—since no-one can report such
sounds during sleep.
Most often the disorder is first recognized by a dentist, since it can lead to abnormal
wear of teeth, temporomandibular dysfunction and pain. The disorder is also frequently
brought to the attention of the patient by a sleep partner, a roommate or a family
member disturbed by hearing the unpleasant, sometime repetitive, loud, grinding
tooth sounds. The patient may even seek medical help for atypical headache or jaw
pain upon morning arousal.
Since the presence of SB is variable over short periods [5], epidemiological data
should be interpreted cautiously. Moreover, epidemiological studies should take into
consideration that other oromotor activities could be misleading (e.g. tics, myoclonia,
chewing automatism, abnormal swallowing, sighs, smiling, etc.) [6]; up to 40% of jaw
muscle EMG recording is not specific to SB.

Gender

Conversely to daytime clenching reports, there is no gender difference in SB prevalence

[3, 4, 7]. However, studying bruxism in twins, Hublin et al. [8] reported a significant
gender difference in childhood and adult bruxism, women reporting slightly more
childhood bruxism than men.

Age

In healthy infants, the age of onset of SB is about 1 year of age, soon after the eruption
of the deciduous incisors [2]. Although children and young adults seem to be similarly
affected, the disorder is appearing more frequently in the younger population [9]. The
prevalence in children is between 14% to 20% [10, 11]. A decline is noted over age. In
 Sleep bruxism 29

adults aged 60 and over, only 3% are being aware of frequent grinding [3]. These data
in older populations have probably to be normalized for the high number of denture
wearers, since most dentures are made of plastic that prevents grinding sounds.

Course

Although there are few reports on the natural development of sleep bruxism—tooth
grinding, bruxism appears to be a persistent chronic disorder. Abe and Shimakawa
[10] reported that the symptom, when recognized in children, persisted in 35% of
them in adulthood. Hublin et al. [8] reviewing data of a twin cohort also showed that
grinding reports/awareness persisted in 86% of them in adulthood.

Aetio-pathophysiology

To our knowledge, in a normal healthy population with frequent grinding, there is no

report of a neuro-pathological lesion which could explain the disorder. In the literature,
SB and grinding have been associated with: (1) peripheral factors such as tooth
interference in dental occlusion; (2) psychosocial influences such as stress or anxiety;
(3) central causes involving brain neurotransmitters or basal ganglia [5, 12, 13].
Small anatomical abnormalities, such as rough cusp ends and malocclusion, have
been suggested to be predisposing factors; however, correction of these defects does
not necessarily lead to a disappearance of the disorder. The review of the role of
occlusion is well beyond the scope of this paper and the related debate is not yet
resolved [14–16].
Studies on monozygotic and dizygotic twin pairs [17, 18] have suggested that
genetics may play a role in the genesis and even the pattern of bruxism [8]. So far no
genetic marker has been found to explain the mode of transmission of SB, although a
child of bruxer parents is more likely to be affected than those of parents not presenting
bruxism [4, 7].
The environmental factors that affect gene expression and the familial and psycho-
social influences are unknown. These may be important since a correlation has been
often reported between anxiety, stress and SB. This will be discussed in the next clinical
section.
The putative influence of neurotransmitters, mainly dopamine (DA), in the genesis
of SB was first suggested from a case report of a Parkinson patient who was reported
to grind under L-dopa therapy [19]. A recent clinical trial, done in non-neurological
SB patients, revealed that L-dopa did not exacerbate SB but rather reduced its frequency
by almost 30% [20]. Moreover, since L-dopa is not a specific DA precursor, it remains
to be demonstrated if the other catecholamines such as adrenaline also modulate SB.
Regarding this point, it was recently suggested that propranolol, a beta adrenergic
blocker, reduces SB [21, 22]. Controlled trials are needed before reaching any conclusion
on the role of adrenergic-related substances, since the effect could be either central to
the motor system excitability, or peripheral in inducing behavioural–cardiovascular
relaxation. Serotonin is another neurotransmitter suggested to cause SB exacerbation;
selective re-uptake inhibitors such as fluoxetine and sertraline were associated with
grinding [23, 24].
30 G. Bader and G. Lavigne

Clinical features

Since bruxism is common in the general population, it can be considered almost as

normal behaviour. It is when the patient has severe tooth damage, the noise is sufficient
to disturb bed partners, sleep is disturbed or pain reported, that it becomes a
pathological condition.
Bruxism occurring while awake or asleep was clinically defined [16] as a para-
functional activity that includes teeth clenching, grinding, bracing and gnashing.
Common consensus is that teeth contact is a necessary condition for bruxism [1, 5,
25]. Consequently bruxing without tooth contact is probably not bruxism. Bruxism
activity is not confined to jaw muscle contraction and tooth contact, since cheek sucking
and tongue pressure against teeth are concomitant findings [26].

Personality traits

It is difficult to extract from the literature a clear characteristic behavioural pattern or

personality traits for SB subjects (SBs) since there is a lack of controlled studies. Some
authors reported that chronic bruxers are anxious, hyperactive [27, 28], aggressive [29]
“rigid . . . cautious . . . affected by feelings of inferiority, apprehensive . . .”, worriers
[30] and that they score high on “suspicious scale” [28].
Kampe et al. [31] studied, by means of a personality inventory, the personality traits
of a group of bruxers as compared to a normal population. They observed that these
subjects were more predisposed to anxiety, were more vulnerable to psychosomatic
disorders and were less socialized, these features being more accentuated in frequent
clenchers. They found strong positive correlations between muscular tension and
headache, tooth clenching, use of medication and painful jaw muscles.
Emotional factors such as anxiety, frustration, fear and emotional stress have all
been related to muscular hyperactivity [32, 33]. Thus sleep bruxism was suggested to
be closely related to emotional condition [34]. Psychological factors (e.g. anxiety) and
environmental stress have been suggested to play a role in promoting bruxism [35,
36]. However, in a study conducted in 100 adults with SB, using ambulatory EMG for
monitoring SB motor activity and ratings of daytime stress in parallel, it was not
possible to confirm a relation between stress report and bruxism recordings [37]; a
correlation was only found in eight of these subjects.
Moreover, Hartmann [38] stated that subjects with SB do not easily admit to
psychological problems related (or not) to life events. Life pressure may influence
sleep quality, prevent restorative sleep or be associated with a higher risk of sleep
arousals, Kampe et al. [31] reported that 69% of patients with bruxism, who clenched
and ground their teeth, thought that stress or anxiety was the cause of their bruxing
behaviour or aggravated the symptoms.

Vigilance/sleepiness and somatic problems

It has been suggested that SBs are more vigilant or motor responsive [39]. We recently
tested this suggestion with a vigilance reaction time test done during the daytime [40].
None of the polygraphic measures were significant in comparison to the ones of
 Sleep bruxism 31

matched controls (reaction time, EEG, EMG, heart rate), with the exception of “anxiety
ratings” towards the task and performance, which were rated much higher in SBs.
General motor restlessness, as well as daytime sleepiness, were reported to be more
common among bruxers [41]. In a recent study of 29 bruxers aged 23–68 years,
based on a questionnaire and clinical examination, Kampe et al. [31] reported “sleep
disturbances” in 72% of the subjects. In the study of Bader et al. [42], based on a
questionnaire submitted to 33 SB subjects, 80% reported that they were often “very
sleepy during the daytime”, and 68% sometimes struggled to stay awake. The majority
(66%) experienced during childhood daytime sleepiness.
In the study by Kampe et al. [31], 86% of the subjects reported pain. About 55% of
them complained of everyday discomfort, 21% once or twice a week. Aches in the
neck, back, throat or shoulders were reported by 69% and frequent headaches by 48%.
Headaches in the morning were reported by 65% of a group of 33 sleep bruxers, and
another 65% reported muscle tension disturbing sleep [42]. Other frequently reported
symptoms (>40%) were pain in the face or jaw, stiffness in the jaw in the morning,
temporomandibular joint (TMJ) sounds and chewing difficulty [31, 42, 43]. Subjects
also complained about frequent abdominal pain (77%) [42]. In the same study, libido
was decreased in 50% of the subjects, and 31% admitted having sexual problems.
Tinnitus has been suggested to be associated to craniomandibular disorders. In one
study, bruxism was reported by 39% of the tinnitus patients [44]; while the prevalence
of clenching was 23% and of grinding 19%; 6% of the patients reported both disorders.

Sleep and polysomnographic features

In general, most SBs are good sleepers [26, 41]; it is the sleep partners who have
disturbed sleep due to the tooth sounds.
Sleep is continuous and not found to be fragmented when scored according to
classical rules [26, 42]. Only a few authors report values of sleep efficiency in bruxism;
these were usually normal [26, 42, 45]. While Bader et al. [42] found prolonged REM
latencies, Boutros et al. [45] reported decreased latencies and percentages of REM. The
reasons behind these findings ranged from ageing to pathological conditions, but the
number of patients studied were very few.

Oromotor and bruxing activity

During sleep, in the absence of grinding, rhythmic activity in jaw muscles, similar to
the phasic pattern noted in SB in 58% of controlled asymptomatic subjects, was
frequently observed [46]; the mean index of rhythmic masticator muscle activity was
1.6 episodes per hour [46] while in SBs it was 5.4 [26]. This type of oromotor activity
corresponds to the chewing automatism previously noted by Gastaut et al. [47] and
Halasz [48], and is not correlated with tooth grinding.
In order to detect and study sleep bruxism, the standard polysomnogram has to
include additional EMG derivations; surface electrodes are placed over bilateral mas-
seter and temporal muscles, sometimes even on the frontal muscles; audio-video
recordings help to confirm the nature of the sounds (e.g. grinding, snoring etc.) and
the type of movements (e.g. sigh, swallowing, coughing, myoclonus, body rocking,
etc.).
The electrographic picture of a bruxism episode can vary from a sustained tonic
contraction to a phasic burst, with an increase in muscle potential (more than 20% of
32 G. Bader and G. Lavigne

the maximal voluntary activity awake) lasting 0.5 or more with an inter-movement
interval of more than 3 s [26, 42, 49]. These increases in muscle potential, to be clearly
identified as bruxism, have to be correlated to the loud “grinding sound” as noted
on-line by a vigilant technician or recorded for later analysis. There is no standard
criteria for reports of bruxe episodes; usually indices are used to give the total number
of episodes per hour of sleep.
C3 – A2

100 µV
C4 – A1

Rmass

Lmass

T3 – O1

Submental EMG

ECG

Micro

RTB

EOL

EOR

Flow

1s

Figure 1 Polysomnographic record during an episode of bruxism in a 25-year-old

man. Phasic burst. LMass: left masseter, RMass: right masseter, Micro: microphone,
ECG: electrocardiogram, RTB: right tibial, EOL: left eye, EOR: right eye, Flow: air flow.

Bader et al. [42] reported an average of 167 oro-facial episodes during the night; but
close to 40% of such episodes may not be specific to SB [6, 26]. The number of SB
episodes can be highly variable from night to night across a short time interval [5].
Usually the phasic activity dominates [26] although tonic activity was observed to
increase during the night (Bader et al. submitted 1998). Phillips et al. [50] reported that
bruxism is also affected by sleep position.

Sleep stage distribution of bruxe episodes

Some studies reported bruxism during all sleep stages with a majority during light
sleep and seldom during slow wave sleep (SWS) and wakefulness [12, 51]. More recent
 Sleep bruxism 33

studies have reported the majority of bruxe episodes during stages I and II [26, 41].
In an open study, SBs were scored mainly in stage II and in REM [42]. The subjects
were in an older age range (23–63 years) than in the other investigations.
The presence of SB in REM is a controversial issue. Only in an early report was SB
associated with REM sleep [52], which was later retracted [53]. However, age may not
be the sole factor explaining Bader’s findings [42] since a study done in 60–87-year-
old SB subjects revealed that only 8% of SB episodes occurred in REM [54]. Other
factors, such as presence of pain [42, 45] or scoring criteria, may explain the differences.
We found that bursts of bruxe are longer when occurring in deep sleep, and
significantly shorter in REM, as compared to stage II [42]; the significance of this
finding has still to be explained.
Ware and Rugh [49] suggested, in a retrospective study based on SB-EEG artefact
scorings, that grinding occurring in REM sleep is often associated with a severe tooth
destructive pattern. Again this needs to be revised for factors previously cited and for
their influences on sleep architecture, since it was recently noted that 60 to 80% of SB
episodes appeared in the so-called arousal active transient EEG phases, or CAP (cyclic
alternating pattern) [55, 56].
Another EEG parameter was associated with SB, the K-complex, a sign of arousal
[12]. A recent report showed that SBs had three times fewer K complexes than matched
controls and this with no further difference in spindle distribution [57], in contrast to
what was observed in patients with another sleep movement disorder, restless leg
movement (RLS) [58]. The significance of these findings is currently under review in
the perspective of the role of K-events as being part of a sleep “protective” mechanism
to preserve good and deep sleep. It has to be remembered that most studies have
showed that SB subjects have a good sleep quality [26, 41].

Shifts of sleep stage

According to reports comparing SB and controls, no major signs of sleep fragmentation
such as awakenings, major body movements or sleep stage shifts are noted in SB
macro-architecture [26, 41, 56, 59]. In contrast, Satoh and Harada [12] and Bader et al.
[42] observed, in open studies, that many bruxing episodes lead to a shift in sleep
stage, usually towards awakening or lighter sleep, suggesting that bruxism may be
part of an arousal phenomenon. The mean number of reported stage shifts was 70,
one third occurring within the first minute following a bruxing episode, while 15% of
bruxing episodes developed after a shift in sleep stage (Bader et al. submitted). Most
of the shifts developed when bruxism occurred during light sleep and REM, and very
seldom during SWS; the “shift-triggering” factor may be either too weak or partly
inhibited in SWS [42].

Alpha activity
We found that during the 10 s preceding the development of a bruxing episode,
especially when occurring during light sleep, the subjects developed short-term alpha
activity [42]. These micro-awakenings were also observed, although seldom, in deeper
sleep. These periods of alpha activity preceding bruxings were too short to be scored
as awakenings according to Rechtschaffen and Kales’ sleep staging criteria [60] based
on epoch lengths of 20–30 s. Such scorings resulted in a normal sleep structure whereas,
in reality, sleep was fragmented by repeated short arousals/awakenings, worsening
sleep quality and probably yielding to non-restorative night sleep. This hypothesis
should be confirmed in a controlled study including SBs with and without pain.
34 G. Bader and G. Lavigne

Alpha-delta
Bader et al. [42] observed alpha intrusion during deep sleep (alpha-delta) in 15% of
patients. This is usually seen in disorders that disrupt nocturnal sleep and, although
not specific to pain, is also a characteristic feature of the fibromyalgia syndrome [61].

Autonomic nervous activity

Patients with bruxism often report clinical symptoms related to the autonomic nervous
system. As an example, in a recent study of 33 patients [42], 38% of the subjects
complained about palpitations at night, and 77% of sweating at night. Blood pressure
was higher than normal in 19% of the subjects. Satoh and Harada [12] were the first
to report a vasoconstriction of the finger tip and skin potential changes as concomitant
responses with tooth grinding.
More specific changes in the autonomic activity have been described during sleep.
Tachycardia was a frequent occurrence with SB [12, 41, 59]. More precisely a 17% heart
rate increase was observed during bruxing events and this was seen to “precede” the
onset of the bruxe episode [59, 62]. Conversely, recent reports showed that the
development of tachycardia was not prior but “at the onset” of the burst, and perhaps
as a consequence of the bruxe episode [42]. With most SB episodes, tachycardia
persisted for 10 s and no secondary bradycardia was present. The concomitant related
decrease in the R-R interval might then reflect a generalized autonomic response to
arousal stimuli.
Another question relating to the autonomic nervous system was raised in the
literature: do SBs also present with abnormalities of the autonomic nervous system
while awake? Kronholm et al. [63] proposed an association between the level of daytime
sympathetic nervous activity and nocturnal motor activity, body movements being
associated with increased autonomic nervous lability. Sjöholm et al. [41] performed
autonomic tests during wakefulness in 11 SB patients and reported abnormalities in
64%. Some alterations in at least two variables reflecting the cardiovascular autonomic
function were observed: in the blood pressure regulation during the Valsalva manoeuvre
(fall in the systolic and even diastolic blood pressure) and in the biphasic heart rate
response during standing up. The authors suggested that an abnormality in the
sympathetic vasoconstriction function may be associated to bruxism, although no
direct comparison was made with age/gender matched controls. In order to verify
whether bruxers present any dysfunction of the autonomic nervous system during
wakefulness, autonomic tests were performed in 12 patients with well-defined bruxism
and in 19 “non-bruxer” controls (Bader et al. submitted). Continuous non-invasive
finger blood pressure and heart rate variability were measured at rest, in an orthostatic
test performed on a tilting table and following a stress stimulus. Changes in skin
resistance were recorded in response to arousal stimuli (galvanic skin response). Skin
blood flow was monitored continuously using laser Doppler flowmetry to evaluate
skin sympathetic vasomotor function through measurement of changes in skin blood
flow in the most superficial layers of the skin. None of the tests revealed a significant
difference between SB and controls. This is similar to a recent report that also excluded
a primary autonomic dysfunction in SB patients [64]. Sjöholm’s [41] study did not
support the idea of a disturbed autonomic function as a predisposing factor for sleep
bruxism. However, autonomic tests during wakefulness have some limitations: the
tests are performed during the day in a state where the responses can be influenced
by physiological conscious control and/or the emotional state of the subject.
 Sleep bruxism 35

Associated clinical symptoms

SB has been associated with other motor manifestations occurring during sleep such
as gross body movements, periodic limb movements and respiratory movements
related to sleep breathing disorders [6, 13, 38, 65, 66].

Body movement activity

About one third of SB episodes have been associated with body movements [41, 42,
51]. In an attempt to study whether patients with SB also have different motor activity
during sleep, sleep recordings of eight healthy subjects were compared with those of
11 bruxers (Bader et al. submitted). Motor activity was detected with sensor pads
placed under the mattress and movements were first grouped according to duration,
as scored with polygraphic traces and video recordings. As expected, movements of
short duration were associated with twitch and jerks, while signals of long duration
were correlated with longer movements such as major postural shifts.
SB patients had significantly more body movements during sleep, compared to
controls, especially movements of short duration, after about 4 h of sleep. An increase
in movement during sleep has previously been observed in normal subjects; the
maximal motility occurred mainly during the second half of the night [67, 68].
Since SB subjects present frequent micro-arousals [42, 56] and since movements are
often preceded by a shift of sleep stage, it is possible that the short movements
observed may also reflect the increased tendency for arousal in these patients. No
significant correlation was found between the occurrence of masseter activity and
body movements [42, 69].

Periodic limb movements (PLM)

Ware and Rugh [49] reported that between 75 and 85% of bruxism occurred in
association with EMG bursts in the anterior tibialis muscle. The association between
reported RLS-related PLM symptoms is only noted in approximately 10% of the tooth
grinders, while conversely 15 to 17% of RLS-related symptoms had also reported tooth
grinding [3, 70]. Moreover, the simultaneous occurrence of the PLM and SB was only
observed in one patient, out of over 33 SBs, although six of them complained about
intermittent RLS [42]. PLM and SB are probably two concomitant but independent
sleep movement disorders. Their simultaneous occurrence being coincidental and/or
often secondary to an arousal response known to facilitate any kind of motor activation,
such as apnoea, PLM or even bruxism.

Breathing disorders
Although some authors reported earlier that SB is associated to sleep apnoea [50, 66,
71], others found no marked breathing disorders, or pathological levels of oxygen
desaturations in SB patients [42]. In this later study, although 36% of 33 SBs self-
reported snoring, sleep recordings revealed sleep apnoea in only four patients. Thus
it has yet to be confirmed that patients with sleep apnoea are at higher risk of presenting
SB grinding.

Pain
Myalgia is reported by 20 to 30% of sleep bruxers and could either be due to the
intense use of jaw muscles inducing a “post-exercise” reaction [72], or to a less specific
condition similar to myofascial pain/fibromyalgia [61, 73].
36 G. Bader and G. Lavigne

The suggestion of a reaction, such as “post-exercise” pain, is based on data collected

in young and healthy SBs [26, 74]. These subjects were good sleepers. The ones who
complained of morning muscle pain presented a lower frequency of SB-related episodes
of bruxism. One explanation could be that a “protective mechanism” prevented the
overuse of jaw muscle [72, 74]. In the “non-pain” sleep bruxers it is possible, however,
that an adaptation mechanism had taken place since bruxism is frequent and chronic in
some of them.
The similarities between myofascial pain and myalgia complaint in the sample of sleep
bruxers in the study of Bader et al. [42] may look surprising at first. These were older and
more psychosomatic subjects than those investigated in Lavigne et al. [26, 74]; they
reported anxiety, tension, headache and orofacial pain, daytime sleepiness, diffuse body
and abdominal pain, poor sleep and some level of alpha-delta EEG intrusion [42]. Before
concluding that SB is an exacerbation or risk factor for myofascial pain/fibromyalgia,
a study is needed to assess the role of coincidental and/or concomitant confounding
variables (e.g. anxiety, presence of other sleep disorder episodes, etc.) and the specificity
of the findings compared with age-sex matched “asymptomatic sleep problem” controls.

Differential diagnosis

Bruxism should not be confused with other facial sleep movements such as swallowing,
coughing, grunting or alternating jaw opening–closing [6, 13, 75]. Continuous re-
cordings of sounds—which then have to be differentiated from snoring noise—or
careful reports by vigilant technicians on the type of sound heard are the best way to
identify SB, since the grinding noise of bruxers is characteristic.
The muscle potential increase, as recorded in the polysomnogram, must be differentiated
from (1) simple body or head movements; (2) myoclonus, which are periodic short muscle
contractions during sleep; (3) head-banging, rhythmic movements of the head—
occasionally occurring at a frequency of about 1 Hz which is within the frequency of bruxe
episodes; (4) other rhythmic oromandibular activities (e.g. sleep chewing automatism).

Treatment

No permanent resolution of oromotor activity has yet been demonstrated. The main
clinical interventions related to SB are directed towards tooth protection, in reducing
the grinding, towards relief of facial or temporal pain, and towards improving sleep
quality if this one is defective. Three types of management strategies are used: dental,
pharmacological and psychobehavioural.

Dental

Three types of dental treatments are suggested for SB. The first two are: (1) adjustment
of tooth bite, or occlusion; and (2) restoration of the tooth surfaces and contours (e.g. with
crowns, bridges and fillings in composites) and, in some patients, major orthodontic
treatment. These interventions are extensive and irreversible, consequently they are
not recommended in most cases [14, 16]. The third type is the use of either a soft
mouth guard–protector or a hard plastic bite splint (“plaque occlusale” or “gouttière”).
While these are widely used to protect teeth and control pain or temporomandibular
 Sleep bruxism 37

joint dysfunction, the true efficacy in reducing oromotor activities or sleep-related

arousals is still a matter of debate. Moreover, we noted that less than 20% of our
patients were still using these oral splints over a year, due to discomfort or for aesthetic
reasons. Caution is also suggested before prescribing these oral appliances since an
increase in oromotor activity has been noticed in some patients (more than 20%) with
both soft and hard oral devices [76, 77]. In addition, the mechanism of action of these
devices (e.g. placebo; behavioural habit corrector; sensory-motor alterations; etc.)
remains to be demonstrated.

Pharmacological

Several pharmacological agents have been used in treatments for SB management. The
ones reported to reduce SB are benzodiazepine (e.g. diazepam), muscle relaxant (e.g.
methocarbomol), catecholamine precursors such as L-dopa, and the beta adrenergic
antagonist propranolol [20–22, 78, 79]. So far only L-dopa has been tested in a controlled
design using polygraphic objective assessments [20]. Consequently other agents have to
be used with caution: benzodiazepines could be associated with pharmacodependance
and daytime drowsiness while adrenergic drugs could exacerbate some sleep-related
disorders such as REM disorder behaviour, apnoea and insomnia [80–83]. Serotonin-
related medication, such as low dose amitriptyline, was reported to have no effect on SB
[84]. Moreover, the serotonin selective re-uptake inhibitors (SSRI), such as fluoxetine and
sertraline, were associated with grinding and daytime clenching [23, 85]. Consequently,
clinicians should be aware of the possible exacerbation of SB-related motor activity in
patients treated with SSRI for conditions such as depression. Finally, botulinum toxin was
administered to some patients with severe masseter muscle hypertrophy [77, 86]; however,
both efficacy, on SB-related oromotor activity, and risk/benefit ratio are unknown.

Psychobehavioural

Relaxation, biofeedback training programmes and hypnosis were all cited in the
literature among psychobehavioural strategies in relation to SB, although several
questions have been raised on their efficacy for SB [88–90]. Most bruxers appeared
reluctant to comply to the routine related to these approaches. Self-care management
strategies are frequently suggested to patients, although no controlled study has
assessed their efficacy. Among such strategies, standard sleep hygiene should be
recommended: relaxation, avoidance of coffee or other psychostimulant substances in
the evening, no smoking—reported to be a risk factor for SB [74].
In conclusion, there is no specific treatment for SB. Each patient has to be individually
evaluated and treatment directed towards the most obvious factors associated with
SB, and aimed at preventing secondary dental complications. Since most patients do
not consider SB a problem, and since only a very low percentage of bruxers will need
treatment [5], patient education is mandatory if as clinicians we want to prevent tooth
damage, sleep grinding annoying sounds, facial pain or temporomandibular disorders.

Conclusions

Although reports on bruxism have been published since 1960, the aetiology and
pathophysiology of this disorder are still unclear. Are we dealing with one or many
38 G. Bader and G. Lavigne

entities; is there any difference—and clinical significance—between (1) nocturnal and

diurnal bruxism, (2) phasic or tonic contractions of the masseter muscles, (3) short and
long bursts, (4) bursts occurring e.g. in stage II or in REM sleep, (5) isolated bruxe
episodes and those associated with other sleep movement disorders or to pain?
Is SB an abnormal activity? It is indeed when it prevents restorative sleep, induces
pain and disturbs sleep. The answer becomes less certain when there is no grinding.
The mouth is normally active during sleep, with a possible function in the lubrication
of the oropharyngeal area since salivation and swallowing levels are usually very low
during sleep [91, 92]. The influence of age on SB is still unclear: i.e. is the lower
prevalence due to changes in lifestyle or biological variables (e.g. lower dopaminergic
receptor function)?
The most common sleep-related findings in SBs, in regard to the presence of oromotor
activity, is the non-specific rise in heart rate, the presence of alpha EEG activity that
should be assessed and compared to matched controls, the association of SB episodes
with body movements. These findings suggest that SB is a motor transient activity
that may be related to normal fluctuations in sleep. Satoh and Harada [12] also
concluded that tooth grinding, triggered by an abrupt lightening of sleep, is an
arousal reaction. This is further supported by the fact that SB episodes appear during
transient EEG changes, or CAP, the latter as being hypothesized to be part of brain
ongoing macro-oscillation that allows for heart rate or respiratory modulation during
sleep [93].

Research Agenda
1. Prospective, multicentre investigations—with parallel validation—on well-de-
fined and cultural homogeneous populations. Study of the incidence, prevalence,
sex distribution and age influence of the disorder. Multidisciplinary approach
with sleep specialists, dentists, psychologists, physiotherapists
2. Longitudinal studies to follow up the development of the disorder, especially
according to:
Differences between grinding (phasic) and clenching (tonic contractions)
Differences/interactions between day and night bruxism
Differences between isolated bruxism and those associated with pain or other
sleep movements
Research should be also aimed at studying:
The influences of peripheral and psychosocial factors
The role of the autonomic nervous system
Which patients are most likely to be responsive to therapy
Therapy development
Further questions of interest:
Is SB an abnormal motor activity, such as PLM, occurring during sleep in relation
(or not) to sleep homeostasis? Is daytime bruxism related more to social/behavioural
factors?
Are SB patients more tolerant to pain?
Can chronic bruxism induce localized neuropathies, due e.g. to micro-trauma, such
as the ones observed in extremities (people using vibrating instruments or submitted
to repetitive mechanical stresses)?
 Sleep bruxism 39

Practice Points
1. The presence or absence of daytime symptoms (e.g. hypersomnolence, pain, tooth
sensitivity etc.) can be indicative of the severity of sleep bruxism and are important
for making clinical decisions regarding diagnostic testing and treatment
2. Prioritize patients for extensive polysomnography with sound recording and
video-polygraphic monitoring to identify other sleep movements
Exclude sleep oro-facial movements other than SB
Exclude use of concomitant medication which could induce secondary bruxism,
e.g. L-dopa in Parkinson or SSRI in depression

Practice Points: Treatment

Treatment is non-specific—each patient has to be individually evaluated
Treatment has to be primarily directed towards the most obvious factors associated
with SB
Indications Aims of treatment
SB destroys sleep Protect sleep and prevent secondary dental
complications
Annoying grinding Relieve source of annoyance
sounds
SB induces pain Relieve pain
SB disturbs sleep Improve sleep quality
Type of treatment (isolated or combined)
Dental Oral comfort—oral appliances
Psychobehavioural Sleep hygiene, relaxation
Pharmacological Benzodiazepine, antidepressant (exclude SSRI),
muscle relaxant, catecholamine

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