Sl eep B r uxism

An Integrated Clinical View

Thomas Bornhardt, DDS, MSc*, Veronica Iturriaga, DDS, MSc, PhD

KEYWORDS
 Bruxism  Sleep bruxism  Obstructive sleep apnea  Gastroesophageal reflux  Sleep arousal

KEY POINTS
 Clinically, sleep bruxism presents mainly as teeth grinding associated with rhythmic masticatory
muscle activity.
 Sleep bruxism has a strong coexistence with sleep arousal, obstructive sleep apnea, gastroesoph-
ageal reflux, and the use or abuse of substances such as alcohol, coffee, tobacco, and some drugs.
 Currently, central pathophysiological factors are considered the most important in the development
of sleep bruxism, displacing peripheral factors.

BACKGROUND and may be a severe manifestation of this action.11

A cascade of physiologic events that make up the
Sleep bruxism (SB) is a masticatory muscle activity SB episode itself is described and includes (1)
during sleep, characterized as rhythmic (phasic) or autonomic-cardiac activation, 4 to 8 minutes
nonrhythmic (tonic) muscle contraction.1 In adults before RMMA/SB; (2) increase in electroencepha-
there is an estimated 8% SB prevalence,2,3 lographic (EEG) activity 4 seconds before RMMA/
whereas in the pediatric population it is 3.4% to SB; (3) tachycardia 1 second before RMMA/SB;
40.6%.4 As reported by the International Classifi- and (4) increase in muscle tone of the suprahyoid
cation of Sleep Disorders, 3rd edition (ICSD-3) of muscles 0.8 seconds before RMMA/SB.3,12 From
the American Academy of Sleep Medicine a clinical point of view, SB presents mainly as teeth
(AASM), SB is classified as a movement disorder grinding11,13 rather than clenching, the latter being
during sleep.5 However, in the latest international closely related to awake bruxism.12
consensus it is proposed that SB occurs in healthy Because there is no consensus regarding the
subjects, without a central movement disorder, or etiologic factors of SB, it is currently defined as a
with any other sleep disorder.1 Furthermore, it has multifactorial disease.3,14 Two types of risk factors
been proposed to consider SB as a condition or related to SB development have been described,
activity, rather than a disease or risk factor for oro- the peripheral risk factors (dental occlusion and
facial structures.1,6 Accordingly, and depending orofacial bone anatomy) and the central risk fac-
on its pathophysiology, SB could be classified as tors (pathophysiological and psychological). While
a risk factor, a protective factor, or an innocuous ruling out occlusal components as part of the SB
factor.1 etiology, central factors are currently considered
When considering a polysomnographic view to play a significant role.15,16 Likewise, primary
point, a rhythmic masticatory muscle activity psychological aspects and anxiety have for years
(RMMA) is seen as a motor manifestation of SB. been the subject of debate. This should, however,
Such RMMAs are also reported in 59.8% of sub- be considered carefully because an etiologic rela-
jects without SB.7 Nevertheless, 90% of subjects tionship has not yet been established.2,17–21 The
with SB present RMMA,8–10 and these events are aim of this article was to review the main and clin-
characterized by greater amplitude and frequency, ically relevant pathophysiological risk factors,
sleep.theclinics.com

Department of Integral Adult Care Dentistry, Temporomandibular Disorder and Orofacial Pain Program, Sleep
& Pain Research Group, Faculty of Dentistry, Universidad de La Frontera, Avenida Francisco Salazar 01145,
Temuco, Chile.
* Corresponding author.
E-mail address: [email protected]

Sleep Med Clin - (2021) -–-

https://doi.org/10.1016/j.jsmc.2021.02.010
1556-407X/21/Ó 2021 Elsevier Inc. All rights reserved.
2 Bornhardt & Iturriaga

related to SB in adults and their diagnostic and masseter muscles is generated; this is pro-
process. posed as a method to stabilize the mandibular po-
sition, prompting hyoid position, thus achieving
PATHOPHYSIOLOGICAL FACTORS better control of the UA lumen.33 These phenom-
ena would explain the increased UA lumen as a
Among the central and clinically important patho- result of the RMMA/SB episode,9 and the
physiological risk factors for SB recently identified, improvement of its permeability.
are phenomena related to sleep, gastroesopha- In reference to respiratory events (REs) and SB, it
geal pH/gastroesophageal reflux, and substance has been reported that approximately 80.5% of
use or abuse among others. RMMA/SB episodes occur on average 5 minutes
following REs, and analyzing the 30-seconds inter-
Phenomena Linked to Sleep
val, 86.8% occur between 0 and 10 seconds after
The most significant sleep-related phenomena the RE.31 Because most REs are associated with
that impact SB are sleep arousal (SA) and obstruc- OSA and with an SA, a common relationship with
tive sleep apnea (OSA). SAs are observed during SB is suspected.29,34 In this manner, rhythmic-
polysomnography and are defined as an abrupt type SB has been associated with SA phenomena,
shift of EEG frequency, including alpha, theta, particularly those generated after RE.29,35 It has
and/or frequencies greater than the 16 Herz (but been noted that an increase in the SA index related
not spindles) that lasts at least 3 seconds, with at to RE would increase the possibility of prompting an
least 10 seconds of stable sleep preceding the RMMA/SB event by 5%.30 Similarly, there could be
change. Rapid eye movement (REM) sleep re- a relationship between oxygen desaturation index
quires a concurrent increase in submental electro- and the presence of RMMA/SB.30 An increase of 1
myography (EMG) lasting at least 1 second.22 The point in the index of spontaneous SA per hour of
relationship between RMMA/SB events and SA sleep, would decrease the probability of RMMA/
was initially documented in the late 1960s,23,24 SB event by 11%.30 This coincides with the fact
the specific relationship, however, remains un- that an RMMA/SB episode could be triggered, in
clear.25 It has been remarked that the RMMA/SB contrast to mild and transient states of hypoxia,9,28
phenomenon may be secondary to SA in approxi- and that oxygen saturation values return to physio-
mately 79% of events and concomitant in 100% of logic levels, seconds after RMMA/SB.36 Reportedly,
these events.8,26 It has further been suggested 54.9% of RMMA/SB occurs after REs, whereas
that the episode of RMMA/SB could be part of a 25.5% precede them.31 Furthermore, a supine posi-
generalized arousal phenomenon.12 Experimental tion during sleep increases the probability of an RE,
induction of SA is able to generate an RMMA/SB and that position can also increase SB events.37
event, resulting in a response associated with Regarding the number of REs per hour of sleep,
teeth grinding in 7.5% of cases25 and is 7 times RMMA/SB episodes are mostly associated with
greater in subjects with SB in comparison with mild and moderate OSA.28,35 Fifty-four percent of
control subjects.25 Moreover and pending evalua- patients with mild OSA present RMMA/SB,
tion, studies agree that SA distribution that results whereas it has only been reported in 40% of mod-
in an RMMA/SB event is associated with A3 phase erate OSA.38 It is proposed that most RMMA/SB
in the cyclic alternating pattern.12,24,27 associated with OSA would be at the cutoff point
For its part, OSA is characterized by repetitive of 5.3 REs per hour of sleep, with a sensitivity of
episodes of complete (apnea) or partial (hypo- 0.533 and specificity 0.907.28 It was further
pnea) upper airway obstruction occurring during observed that 4 seconds before the RMMA/SB
sleep. These events often result in reduced blood episode, respiratory amplitude increased between
oxygen saturation and are usually terminated by 8% and 23%, which would then increase when the
brief SAs.5 Prevalence of SB in patients with suprahyoid muscle group was activated, reaching
OSA varies between 33.3% and 50.0%, where 60% to 82% amplitude. This would end with a res-
subjects with OSA have an odds ratio of 1.8 to pre- piratory amplitude increase of 108% to 206%,
sent RMMA/SB.28–31 It is proposed that the posi- whereas the episode of RMMA/SB itself is being
tion of the jaw can influence the upper airway carried out. There appears to be a clear need to
(UA) lumen, affecting its patency and the possibil- improve UA patency.39 Finally, in episodes of
ity of collapse during sleep. Position of the hyoid RMMA/SB associated with SA, the respiratory
bone is advanced and raised during mandibular amplitude is 11 times greater than when an iso-
closure, causing an increase/maintenance of the lated SA occurs.39 Although a direct cause has
UA patency.32 When presented with hypercapnia not yet been defined, the effect of some RMMA/
and the respiratory inspiratory threshold load, a SB seems to be related to respiratory require-
direct proportional activation of the genioglossus ments during sleep and SA distribution.
 Sleep Bruxism 3

Gastroesophageal pH and Gastroesophageal some substances, namely alcohol, coffee, to-

Reflux Disease bacco, and certain drugs. It has been reported
that subjects with SB have a higher intake of
The evidence suggests that gastroesophageal
alcohol before going to bed47 and also more SB
reflux disease (GERD) is related to development
events.48–51 Furthermore, coffee is one of the
of SA, dry mouth/digestive tract, greater number
most commonly used stimulating substances
of swallows, and a supine position.40 An important
worldwide, and it is frequently associated with
association between GERD and OSA has also
SB.48,50 Tobacco consumption is also strongly
been reported.41 SB prevalence is noted in
related to SB occurrence.47–49,51,52 Tobacco
73.7% of the patients with GERD,42 including
smokers have 5 times more SB episodes than
rhythmic episodes noted in 70% of the subjects
nonsmokers, considering that along with an
and nonrhythmic events in 10%.43 An odds ratio
increased use of tobacco, the probability of pre-
of 6.58 is estimated for the presence of SB in sub-
senting SB also increases.52 In contrast, the use
jects with GERD42; in long-term GERD cases, SB
of stimulants in patients with excessive daytime
is associated with severe dental wear.44,45
sleepiness associated with OSA, mainly caffeine
From an experimental point of view, a reduction
and nicotine, has frequently been reported and
of gastroesophageal (GE) pH causes an increase
may also increase SB association. In reference
in the frequency of EMG bursts, RMMA episodes,
to the use of drugs, the information is complex,
RMMA with tooth grinding, swallowing, and SA
due to methodological difficulties of the studies.53
events.46 Thus, the episode of RMMA/SB associ-
The use of antidepressants, barbiturates, and
ated with swallowing could result in GE pH in-
psychostimulant drugs has been associated with
crease.46 Swallowing activity is associated with
a higher risk of developing SB.53–55 The use of
the amount of saliva present in the mouth,
botulinum toxin appears to reduce SB events,
providing bicarbonate and the epidermal growth
although adverse reactions have been described
factor.40 However, the amount of saliva and swal-
at the mandibular bone level.51 Drugs such as clo-
lowing episodes decreases to one-tenth during
nazepam and clonidine have also been associ-
sleep versus wakefulness.40 Most swallows take
ated with fewer SB events. Nevertheless, there
place in N1-N2 stages of No REM sleep and some-
are severe adverse effects such as morning hypo-
times during REM sleep, the latter being related to
tension in the case of clonidine, or a high addic-
SA.10 In subjects with SB, these swallows increase
tion profile with clonazepam.51 The relationship
up to 7 times, especially in the N2 No REM stage.10
between these substances and SB is described
It has also been observed that the supine position
in greater detail in Table 1. Finally, illegal drugs
during sleep, is associated with a 70% increase in
were not considered in this review, however, the
RMMA/SB and swallowing. On the other hand, it
association with BS is difficult to determine due
has been reported that a rapid drop in GE pH to
to reporting bias.
4 to 5 can trigger an RMMA/SB episode in a statis-
tically significant manner; a pH of 4 or less in the Other Associated Factors
GE tract induces an RMMA/SB event in 100% of
cases.40 When proton pump inhibitors have been There is growing research that identifies certain
used, a 40% reduction in EMG, RMMA, and genetic factors that would predispose the devel-
RMMA bursts associated with tooth grinding is opment of SB. These include single nucleotide
observed.40,46 polymorphism (SNP) of HTR2A associated with
In light of the preceding, it is proposed that SB the serotonergic system and of DRD3 (SNP
and GERD share a common pathophysiological/ rs6280, C allele) in the dopaminergic system.56–58
etiologic mechanism42 in which buffering and In addition, a recent study observed that the
lubrication capacity of saliva would play an impor- HTR2A polymorphism rs2770304 could affect the
tant role.46 In addition, salivary secretion would be association between SB and OSA.58 Favorable
enhanced, as a result of periodontal mechanore- outcomes have also been reported as to the rela-
ceptor stimulation during the RMMA/SB.40 It is tion between SB and coactivations between the
possible that the acidification itself of the gastro- central nervous system and the autonomic ner-
esophageal pathway would activate visceral vagal vous system.21,31,59
inputs at the trigeminal mesencephalic nucleus
level, thus activating the masticatory muscles.45 DIAGNOSIS
The gold standard for SB diagnosis is polysom-
Substance Use or Abuse
nography with audio/video recording.13,60,61 How-
The evidence suggests a pathophysiological rela- ever, because it is not always easily accessible, a
tionship between SB and the consumption of clinical diagnosis is extremely important. The use
4 Bornhardt & Iturriaga

Table 1
Relation between substance use or abuse and sleep bruxism

Substance Relation with Sleep Bruxism (SB) Odds Ratio

Alcohol Binge drinking and heavy drinking are closely related 1.9
with SB development.
Coffee Drinking 8 cups of coffee per day is related to weekly SB 1.5–1.9
events.
Tobacco Tobacco use could double the likelihood of SB. 2.8
Heavy smokers have a greater probability of SB. 2.5
The use of smokeless tobacco is also associated with SB. 2.05
Drugs There is a relation between SB and use of the
following:
 Paroxetine 3.63
 Venlafaxine 2.28
 Duloxetine 2.16
 Methylphenidate 1.67
 Fluoxetine, sertraline, citalopram, escitalopram, and –
some barbiturates.
 Dopaminergic drugs (agonist and antagonist) pre- –
sent mixed results.
 The use of botulinum toxin A, buspirone, clonaze- –
pam, clonidine, and gabapentin could reduce SB
events.

of clinical diagnostic criteria proposed by ICSD-3 report of teeth grinding of at least 4 times per
is accepted and also recommended.62 These week associated with tooth wear shows a likeli-
criteria take into account as necessary and essen- hood ratio of 6 and a diagnostic odds ratio of
tial, the presence of regular or frequent tooth 13.6.62 In addition, the use of portable 4-channel
grinding, sounds occurring during sleep, associ- diagnostic devices is an alternative to the gold
ated with at least 1 or more of the following: (1) standard with acceptable validity,67 and is a prom-
abnormal tooth wear; (2) transient morning jaw ising area in the future.
muscle pain or fatigue; (3) temporary headache; Finally, progress of SB studies has led to new re-
or (4) jaw locking on awakening; all being consis- quirements and proposals that resulted in the
tent with reports of tooth grinding during sleep.5
It is important to consider that over time the
Box 1
perception of these criteria has varied. For Main sleep bruxism differential diagnosis for
instance, dental wear is currently considered a morning headaches
poor indicator of current SB, although it may be
an indicator of SB in the past.63 Given the high as- I. Primary headaches with circadian rhythm
sociation rate between GERD and dental wear,64 it II. Secondary headaches that occur on waking:
is important to exercise caution in the specific
Headache attributed to temporomandib-
diagnosis of tooth wear. It is also suggested that
ular disorders (11.7)a
SB events would not necessarily be a direct cause
of muscle pain.65 With regard to headaches in the Sleep apnea headache (10.1.4)a
temporal region, a temporomandibular disorder Medication overuse headache (8.2)a
should be considered first as a possible cause Headache attributed to substance with-
for the headaches.65,66 Hence, the morning head- drawal (8.3)a
ache is not only related to SB, there is also a vari-
Some headaches attributed to nonvascular
ety of headaches that could be related (Box 1). intracranial disorder (7)a
Currently, the agreement for SB clinical diagnostic
a
criteria is being evaluated via polysomnography, Headache Classification Committee of the Interna-
tional Headache Society (IHS) The International Classi-
where the report of teeth grinding at least once
fication of Headache Disorders, 3rd edition.
per week, associated with muscle pain or fatigue, Cephalalgia. 2018;38(1):1-211. doi:10.1177/
has a likelihood ratio of 6, a diagnostic odds ratio 0333102417738202.
of 13.5, and a specificity of 90%.62 Likewise, the
 Sleep Bruxism 5

Fig. 1. Proposed algorithm for clinical approach of SB.

development of an SB classification system based tooth grinding during sleep remains the main clin-
on the diagnostic method applied. This classifica- ical diagnostic criterion for SB.
tion includes possible SB (self-report of the sub- In conclusion, Fig. 1 proposes an algorithm to
ject), probable (clinical diagnosis with/without assist clinicians when SB is suspected, wherein
positive self-report), and definitive (instrumental the different central pathophysiological factors
diagnosis with or without self-report and/or posi- associated with SB are evaluated, allowing for an
tive clinical diagnosis).1 It should be noted that adequate diagnosis and individualized treatment
as regards this classification, the vast majority of program.
studies are based on probable SB. Definitive diag-
nosis of this disorder has improved in recent years CLINICS CARE POINTS
with the aid of polysomnography.

SUMMARY
 In adults the estimated prevalence of SB is 8%
Evidently, SB is of great concern to clinicians, re- and RMMA is its motor manifestation.
searchers, and patients. Therefore, in addition to
a significant increase in related research, the  RMMA/SB phenomenon may be secondary to
SA in approximately 79% of events and
concept of SB has also evolved.21 SA, OSA,
concomitant in 100% of these events.
gastroesophageal pH/GERD and the use or abuse
of certain substances have increasingly been cited  The RMMA/SB seems to be more related to
as important pathophysiological or concomitant mild OSA than moderate or severe OSA.
SB factors. It is worthwhile mentioning, that with  A reduction of GE pH causes an increase in the
adequate treatment of these disorders, a reduc- frequency of EMG bursts, RMMA episodes,
tion and/or full recovery has also been re- RMMA with tooth grinding, swallowing,
ported.46,68,69 Furthermore, clinical diagnosis is and SA events.
critical, given the difficulty of accessing a diag-  There is growing research identifying genetic
nostic gold standard. In this sense, the report of factors related to SB.
6 Bornhardt & Iturriaga

12. Lavigne GJ, Huynh N, Kato T, et al. Genesis of sleep

 The most agreement for SB clinical diagnostic
criteria were the report of tooth grinding at bruxism: motor and autonomic-cardiac interactions.
least once per week, associated with muscle Arch Oral Biol 2007;52(4):381–4.
pain or fatigue; and grinding of the teeth at 13. Lavigne GJ, Rompré PH, Montplaisir JY. Sleep
least 4 times per week associated with tooth bruxism: validity of clinical research diagnostic
wear. criteria in a controlled polysomnographic study.
 Tooth wear alone is not a good predictor of J Dent Res 1996;75(1):546–52.
current SB. 14. Castroflorio T, Bargellini A, Rossini G, et al. Sleep
bruxism and related risk factors in adults: a system-
atic literature review. Arch Oral Biol 2017;83:25–32.
15. Lobbezoo F, Naeije M. Bruxism is mainly regulated
DISCLOSURE
centrally, not peripherally. J Oral Rehabil 2001;
The authors have nothing to disclose. 28(12):1085–91.
16. Lobbezoo F, Ahlberg J, Manfredini D, et al. Are
bruxism and the bite causally related? J Oral Reha-
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