Narrative Review

Sleep bruxism
The past, the present, and the future—evolution of a
concept
Davis C. Thomas, BDS, DDS, MSD, MSc Med, MSc; Daniele Manfredini, DDS, MSc, PhD;
Jaimin Patel, BDS, MDS; Aaron George, BDS; Bindu Chanamolu, BDS, MS;
Priyanka Kodaganallur Pitchumani, BDS; Linda Sangalli, DDS, MS, PhD

ABSTRACT

Background. The concept of sleep bruxism (SB) has evolved exponentially over the past several
decades. Many theories and hypotheses have been proposed as to the definition, pathophysiology,
and management of SB, from the early 1960s through the present. The role of peripheral factors,
such as dental occlusion, in the pathogenesis of SB has been discarded.
Types of Studies Reviewed. The authors searched several electronic databases (ie, PubMed,
Google Scholar, Web of Science, Embase, and Ovid MEDLINE) for studies on bruxism. The search
was conducted from January 1961 through May 2023 and yielded 4,612 articles, of which 312 were
selected for comprehensive review after eliminating duplicates and nonfocused articles.
Results. There has been an evident progressive shift from the role of peripheral factors, such as
dental occlusion, to more central factors, such as the involvement of a central pattern generator as
well as the autonomic nervous system, in the genesis of bruxing movements. There is continued
robust interest in the dental community to elucidate the contributing factors involved in SB.
Conclusions and Practical Implications. The neurophysiology of SB appears to be leaning more
toward central rather than peripheral factors. There is increasing evidence of the role of the
autonomic nervous system, genetics, and comorbidities in the genesis of SB. The scientific literature
seems to refute the role of dental occlusion in the causation of bruxing movements. As per the
literature, there has been a paradigm shift in the definition and genesis of SB and its possible dental
implications and management, which also highlights the need for succinct scientific studies in this
regard.
Key Words. Bruxism; sleep; movement disorder; dental splints; tooth grinding; polysomnography.

JADA 2024:n(n):n-n
https://doi.org/10.1016/j.adaj.2023.12.004

T
he definition and concept of bruxism have evolved over the past several decades, leading to
2 separate entities—awake bruxism (AB) and sleep bruxism (SB). In the first article on
bruxism, published in JADA in 1961, Ramfjord1 surmised a few things that we are revisiting
in the context of the literature. Certain hypotheses that Ramfjord proposed, such as anger and
aggression are related to bruxism, may have some scientific basis. The 2013 international consensus
defined the repetitive masticatory muscle activity (RMMA) associated with SB, and described terms
such as mandibular thrusting and bracing.2 The International Classification of Sleep Disorders, Third
Edition (ICSD-3),3 from the American Academy of Sleep Medicine, adopted the term sleep-related
bruxism to indicate “a repetitive jaw-muscle activity characterized by clenching or grinding of the
teeth and/or by bracing or thrusting of the mandible.”4 The latest consensus article on bruxism
specifically defined 2 separate entities, that is, SB and AB.5 Furthermore, the possibility of a dif-
ference in the pathogenesis of SB vs AB is also becoming apparent. The Standardised Tool for the
Assessment of Bruxism is the latest development toward a successful protocol for assessment of Copyright ª 2023
American Dental
bruxism.6-8 The objective of our study was to comprehensively look at the available literature to
Association. All rights
conduct a narrative review of the evolution of the concept of SB. Many times, SB has been a reserved.

JADA n(n) n http://jada.ada.org n n 2024 1

 somewhat controversial topic. We aimed to bring some clarity based on the evolution of the
literature on this topic.

METHODS
We searched several electronic databases (ie, PubMed, Web of Science, Google Scholar, Scopus,
Embase, and Ovid MEDLINE) for published articles focused on bruxism. The period searched was
62 years, from January 1961 (when the first article on SB appeared in JADA1) through May 2023.
The key words in the search included, but were not limited to, bruxism, sleep-related bruxism, sleep
bruxism, awake bruxism, and tooth grinding. All articles selected were in the English language and
with access to the full-text version. All other articles were excluded.

Definition
SB is classified in ICSD-33 as a sleep-related movement disorder. The definitions proposed over time
are presented in Table 1 and the timeline of the evolution of these definitions is presented in
Figure 1.

Classification
Bruxism can be classified according to the etiology, circadian presentation, type, and frequency of
electromyography (EMG) activities, and the duration, severity, and frequency of EMG episodes18,19
(Table 2).

Etiology and etiopathology

The proposed etiology of SB is multifactorial24,33-36; the exact etiopathology of SB remains largely
unknown.28,37 A plethora of peripheral and central factors have been proposed. In the past, a
progressive shift from a peripheral view (eg, features of dental occlusion, such as interferences) to a
concept of more central control was generally accepted,33,38,39 thus conferring a key role of the
activation of the central nervous system in SB.21,38 The list of conditions associated with bruxism
has been growing in the literature, and a linear 1-to-1 correlation with multiple factors may not
exist in a biological model.40
One of the first cardinal articles on bruxism was published in JADA in 19611 and hypothesized
the etiology and management of bruxism. In the article, the author claimed that occlusal in-
terferences coupled with nervous tension initiated bruxism, that elimination of bruxism is possible
by means of occlusal adjustments, and that occlusion had to be adjusted to what was then believed
to be centric relation to achieve muscle balance in bruxers.1 This was probably one of the earlier
conceptual errors that led to a surmountable amount of confusion in the field of bruxism. As the
literature evolved, several factors were proposed as initiating and perpetuating bruxism. These
included, but were not limited to, peripheral factors,1,41-44 psychological factors,45-52 exogenous
ABBREVIATION KEY factors (eg, illicit drugs and prescription medications),53-56 genetic factors,30,57-59 systemic comor-
AAP: American Academy bidities,20,60 and cardiorespiratory-related sleep arousals.61 We will discuss these concepts and the
of Prosthodontics. up-to-date literature.
AASM: American Academy
of Sleep Medicine.
Peripheral Factors: Occlusion and Orofacial Anatomy
AB: Awake bruxism.
EMG: Electromyography. The older literature had proposed occlusal factors in the etiology of SB.1,62,63 Some authors
GPT: Glossary of considered discrepancies between various static and dynamic occlusal relationships as being
prosthodontic terms. responsible for the development of bruxism.33 Therefore, occlusal adjustments performed in an
ICSD: International
attempt to restore a balanced occlusion were thought to be the mainstay of bruxism management.1
Classification of Sleep
Disorders. However, these studies were found to have several methodological flaws, including lack of a control
ICSD-3: International group, use of indirect measures to detect bruxism, and probable erroneous simulations of bruxing
Classification of Sleep movements.33,64
Disorders, Third
Edition.
Subsequent evidence derived from stronger methodological studies has led to questions about the
OSA: Obstructive sleep direct influence of occlusal factors on modulating bruxism activity.33,39,65 It was observed that
apnea. bruxism was present equally in patients with and without occlusal interferences,66-68 occlusal ad-
PSG: Polysomnography. justments did not appreciably influence bruxism,69-72 and bruxers and nonbruxers did not differ in
RMMA: Rhythmic
terms of occlusion and cephalometric and dental variables.73,74 Some of these studies had a limited
masticatory muscle
activity. number of participants and, therefore, the results may not be extrapolated to a larger patient
SB: Sleep bruxism. population. The literature does not support the earlier notion that SB is somehow related to dental

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Table 1. Definition of bruxism according to various sources and consensus over time.*

YEAR SOURCE DEFINITION DESCRIPTION

1987 AAP† (GPT,‡ 5th edition)9 Grinding of teeth Parafunction

1990 AASM§ (ICSD{)10 Parasomnia Stereotyped movement disorder characterized by grinding or clenching
of the teeth during sleep

1997 AASM (ICSD, revised)11 Parasomnia Stereotyped movement disorder characterized by grinding or clenching
of the teeth during sleep

1999 AAP (GPT, 7th edition)12 Parafunctional grinding of teeth An oral habit consisting of involuntary rhythmic or spasmodic
nonfunctional gnashing, grinding, or clenching of teeth, in other than
chewing movements of the mandible, which may lead to occlusal
trauma

2005 AASM (ICSD, 2nd edition)13 Sleep-related movement disorder Oral activity characterized by grinding or clenching of the teeth during
sleep, which is generally accompanied by sleep arousals

2005 AAP (GPT, 8th edition)14 Parafunctional grinding of teeth Oral habit consisting of involuntary rhythmic or spasmodic nonfunctional
gnashing, grinding, or clenching of teeth, in other than chewing
movements of the mandible, which may lead to occlusal trauma

2008 American Academy of Parafunctional activity Diurnal or nocturnal parafunctional activity, including clenching, bracing,
Orofacial Pain15 gnashing, and grinding of the teeth

2013 International Medical and Repetitive masticatory Repetitive masticatory muscle activity, characterized by clenching or
Dental Consensus2 muscle activity grinding of the teeth or by bracing or thrusting of the mandible

2014 AASM (ICSD, 3rd edition)3 Sleep-related movement disorder Alternative names: nocturnal bruxism, nocturnal teeth grinding, tooth
clenching
Definition: repetitive jaw-muscle activity, clenching or grinding, bracing,
or thrusting of the mandible
Types: sleep bruxism, awake bruxism

2017 AAP (GPT, 9th edition)16 Parafunctional grinding of teeth Oral habit characterized by involuntary rhythmic or spasmodic
nonfunctional gnashing, grinding, or clenching of teeth

2018 International Medical and Dental Masticatory muscle activity Not a movement disorder in otherwise healthy individuals; a masticatory
Consensus5 muscle activity during sleep, characterized as rhythmic (phasic) or
nonrhythmic (tonic) activity

2022 International Classification of 7A83. Sleep-related bruxism, Repetitive, rhythmic jaw muscle contractions. This occurs during sleep.
Diseases, 11th revision17 sleep teeth grinding Can be tonic or phasic

* Priyanka Kodaganallur Pitchumani digitized the table. † AAP: American Academy of Prosthodontics. ‡ GPT: Glossary of prosthodontic terms. § AASM: American
Academy of Sleep Medicine. { ICSD: International Classification of Sleep Disorders.

AAP
International
(GPT, 8th edition13)
Consensus4
Parafunctional
Not a
grinding of teeth,
movement
oral habit
AAP International disorder in
(GPT, AASM AASM (ICSD, 2nd edition12) consensus2 otherwise
5th edition8) (ICSD, Sleep-related Repetitive healthy people,
Parafunctional revised10)10 movement masticatory masticatory
grinding of teeth 1990 Parasomnia 1999 disorder 2008 muscle activity 2014 muscle activity 2022

1987 AASM 1997 AAP 2005 American Academy 2013 AASM 2018 International
(ICSD) (GPT, 7th edition11) of Orofacial Pain14 (ICSD, 3rd edition3) Classification
Parasomnia Parafunctional Parafunctional Sleep-related of Diseases,
grinding of activity movement 11th revision16
teeth, oral disorders and Sleep-related
habit oral bruxism
parafunction

Figure 1. Timeline of the evolution of the definition of bruxism. AAP: American Academy of Prosthodontics. AASM: American Academy of Sleep
Medicine. GPT: Glossary of prosthodontic terms. ICSD: International Classification of Sleep Disorders. Linda Sangalli designed the figure. Linda Sangalli
and Priyanka Kodaganallur Pitchumani digitized the figure.

occlusion.5,75,76 Several other researchers have challenged the assumption that the presence of
tooth wear and occlusal attrition confirmed a diagnosis of bruxism77,78 or aided in determining its
severity.79 In a 2019 narrative review, researchers reported the association of tooth wear with SB

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Table 2. Criteria for various classifications of bruxism.*

CRITERIA CLASSIFICATION DESCRIPTION

Etiology3,18,20-23 Primary No identifiable cause or any associated medical problem
Secondary Secondary to medication or recreational drugs, parasomnias, sleep-related disorders or
movement disorders, or neurologic or psychiatric condition
Iatrogenic Treatment-induced

Circadian Manifestation5,18,20,24-27 Awake bruxism During wakefulness

Sleep bruxism During sleep

Type of RMMA† in SB‡,5,18,22,28 Tonic (sustained) 1 electromyography burst lasting > 2 s

Phasic (rhythmic) Brief, repetitive, muscle contractions; generally < 2 s
Mixed Phasic and tonic burst

Movement of the Mandible29-31 Static Teeth clenching or bracing

Dynamic Tooth grinding or thrusting in lateral or anteroposterior direction

Duration Acute 7 d
Subacute > 7 d-< 1 mo
Chronic  1 mo

Severity32 Mild Not every night, no evidence of dental injury, no psychosocial impairment
Moderate Nightly occurrence, mild psychosocial impairment
Severe Nightly occurrence; history of dental injury, temporomandibular disorder, or physical injury;
moderate or severe psychosocial impairment

Frequency of Electromyography Low frequency of RMMA Index§ is 2-4

Episodes20,21,28 RMMA
High frequency of RMMA Index is  4 or the Burst Index is  25
RMMA

Diagnostic Tool2,5 Possible SB Based on self-report, questionnaire, or anamnesis during clinical examination (transformed into
“positive self-report only” in 2018)
Probable SB Based on self-report and clinical inspection (transformed into “positive clinical inspection, with or
without a positive self-report” in 2018)
Definitive SB Based on self-report and clinical inspection and polysomnography (transformed into “positive
instrumental assessment, with or without a positive self-report and/or positive clinical inspection”
in 2018)

* Priyanka Kodaganallur Pitchumani digitized the table. † RMMA: Rhythmic masticatory muscle activity. ‡ SB: Sleep bruxism. § RMMA Index: No. of RMMA episodes per
hour of sleep.

and conditions such as dental sleep disorders, xerostomia, orofacial pain, and gastric reflux.80 In
short, the literature does not support that mechanistic peripheral factors form an etiologic foun-
dation for the development of SB.33,39

Psychological Factors
The role of stress in the development of bruxism was supported in the early literature; researchers found
that jaw-muscle activity and muscle tone were enhanced in bruxers during stressful periods.81-85
Researchers seemed to have confirmed such an association when bruxism was self-reported.45-52
Concepts such as stress sensitivity and their relation to SB have been examined in the literature.86-88
In EMG-based studies, researchers have questioned the causal relationship between stress and
SB.89,90 This may be due to possible multiple contributory factors or the adoption of diagnostic criteria
on the basis of the number of EMG episodes rather than their duration and muscle work, or a stress and
anxiety trait may be better correlated with muscle activity.91
Lack of proper diagnostic criteria may be one of several reasons for contradictory findings in these
studies.24,92,93 The possible factors include, but are not limited to, day-to-day and diurnal variations
in bruxism, presence or absence of pain,86 variability of screening and diagnostic tools,86,89 and
variability of criteria for identifying, defining, and classifying what stress means to patients.87,88 The
stress–bruxism relationship may be supported mostly by studies in which bruxism is clinically
diagnosed or self-reported,45-52 and EMG studies have yielded conflicting findings.86,89,90 Some of
the literature has referred to psychological distress.86 The psychological traits of bruxers include
higher vulnerability to anxiety, performance-oriented behaviors, aggressive and hyperactive traits,
and dysfunctional coping skills, among others.20,47,48,82,87,88,94-107 Nevertheless, contradicting
findings have been derived from other studies36,108,109 in which SB and psychological distress
were only weakly correlated during a 20-year observation period110 and bruxism was not

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correlated to stress during a 3-week period of recording.90 Some researchers have failed to reveal any
difference in psychological parameters between bruxers and nonbruxers with facial pain.33,111
Similarly, results of a systematic search revealed that psychological distress is correlated mostly to
AB and less to SB.86

Exogenous Factors
Pathophysiological exogenous factors that may contribute to SB include medication or illicit drugs,
caffeine, alcohol, and tobacco.28,33,112-115 Many of the studies lacked the desired quality of evidence
necessary to extrapolate the findings to clinical practice. In addition, there was no substantive evi-
dence of a cause-and-effect relationship between the medication and SB. Although in some of these
studies the researchers seemed to indicate an association between selective serotonin reuptake in-
hibitor and serotonin and norepinephrine reuptake inhibitor use and SB, some others refuted any such
relationship. Vitamin D deficiency and low dietary calcium intake were also associated with SB.116

Genetic Factors and Familial Predisposition

No specific gene has been identified to explain the genetic predisposition to bruxism.20,57 It is
possible that the genesis of SB may be attributed to a genetic polymorphism rather than a single
gene.28,57,59 Although a familial predilection for SB has been reported,20,32,117 monozygotic twins
appear more similar in terms of SB than dizygotic twins118; however, this association was not
confirmed in a similar study of a large cohort.119 Patients with HTR24 and HTR2A gene variants
are at a much higher risk of having SB.57,120 These genes code for certain serotonin receptors,57
which are responsible for circadian rhythm, arousal, and muscle tone control.120,121 Single nucle-
otide polymorphism of the telomerase reverse transcriptase also seems to influence the intensity of
SB.122 In contrast, researchers could not confirm any genetic factors in the etiology of bruxism.57,118
Researchers tracking the pedigree of 4 generations of a family reported a reasonably strong genetic
predilection.30

Comorbidities of SB
Systemic conditions
SB-associated systemic conditions include, but are not limited to, hypertension, metabolic and hor-
monal disturbances, Crohn disease, cardiovascular events, and peripheral arterial disease.61,123-125
Fluctuations in systolic blood pressure were found to be associated with SB,126-130 the magnitude
of which was found to be particularly influenced by arousals and body movements.126 Increased heart
rate variability that occurs with SB, secondary to enhanced sympathetic activity, leads to hypertension
and cardiovascular sequelae.61 A sympatholytic medication, such as clonidine, was found to prevent the
autonomic and motor activation of SB.131 An association between SB intensity and renalase con-
centration,132 diabetes,133 and autoimmune disorders (eg, systemic lupus erythematosus, rheumatoid
arthritis, Raynaud syndrome, and multiple sclerosis)60,134 has been reported. An association between
new-onset bruxism and trigeminal nerve injury has been proposed.135

Localized (tissue- and organ-specific)

Associations between SB and gastroesophageal reflux disease,80,136-142 higher body mass index,123
rhinitis and sinusitis,114 trauma,38 and obstructive sleep apnea143-147 (OSA) have been reported.

Miscellaneous
SB has been found to be associated with some neurodegenerative conditions (including Parkinson
disease, parkinsonism, Alzheimer disease, and dementia148-152), neurologic disorders (such as epi-
lepsy20), and sleep-related disorders (eg, insomnia, periodic limb movements, restless legs syndrome,
and rapid eye movement behavior disorder133,143,147,149,153). Although the literature supports an
association between SB and OSA,143-146 other comprehensive reviews have discredited a clear
relationship.146,154-157 Researchers have observed that morning chronotype was correlated with
greater protection against SB than evening chronotype,158 although this was not confirmed in
another study conducted on a cohort of dental students.159 Although a positive association was
found between temporomandibular disorders and SB when self-reported or detected clinically,160 no
conclusive association was found between SB and temporomandibular disorders in studies supported
by polysomnography (PSG) findings.161

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 Comorbidities of AB
According to a 2017 review, AB was present mostly in patients with hyperkinetic movement
disorders, such as Rett syndrome, Down syndrome, autistic spectrum disorders,148 and attention-
deficit hyperactivity disorder.162 AB is also considered to be a risk factor for development of
temporomandibular disorders,163,164 although a cause-and-effect relationship does not seem to be
supported in the literature.165 Other comorbidities include generalized anxiety disorder,166 de-
mentia,167 Huntington disease,168-170 and STXBP1 encephalopathy.171

Pathogenesis of SB
Neurochemicals
Neurotransmitters proposed in the pathogenesis of SB,32,120,172 especially those involved in motor
neuron activity control and sleep-wake regulation,28 include dopamine, serotonin, noradrenaline,
orexin, acetylcholine, and gamma-aminobutyric acid. The neurophysiology and motor pathways in
the generation of mandibular movements and SB are presented in Figure 2.

Dopamine
An imbalance in the direct and indirect pathways in the basal nuclei has been suggested in the
pathogenesis of SB.32,173-175 Structures such as the nigrostriatal projection within the basal nuclei
are part of this system.33,176 Although dopamine is not normally active during sleep, it is hy-
pothesized to be linked to sleep arousal activation.28,177 Administration of dopamine precursors,
such as l-DOPA, and D2 receptor agonists, has been proposed to inhibit bruxism episodes in the
short term.33,174,175 SB may occur secondary to dopaminergic medications.33,176,178,179

Serotonin
Serotonin has functions in arousal, circadian rhythm, breathing, and muscle tone.120 Treatment
with amitriptyline (a drug inhibiting the reuptake of serotonin at the postsynaptic cleft) and
tryptophan (a precursor of serotonin) have not been reported to influence bruxism activity; how-
ever, the use of selective serotonin reuptake inhibitors and serotonin and norepinephrine reuptake
inhibitors seems to increase clenching and grinding in susceptible people.32,55,180-199 Many of these

Cerebral motor cortex

Thalamus
Putamen
Globus pallidus externa
Globus pallidus interna
Subthalamus

Substantia nigra (pars compacta)

Midbrain

Mesencephalic trigeminal nucleus

Reticular formation (shaded area)

Motor nucleus of trigeminal nerve

Pons

Foramen ovale
Proprioceptive afferents

Medulla
Proposed central pattern generator
of sleep bruxism in brainstem?
Fibers of masseter
Stretch receptors of periodontal
ligament and jaw elevating muscles

Figure 2. Proposed neurophysiology of normal mandibular movements and sleep bruxism (diagram not to scale). Figure courtesy of Dr. Jaimin Patel.

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studies may not have the desired level of evidence and, therefore, the findings may not be
extrapolated to clinical practice.

Norepinephrine
Norepinephrine has been implicated in the pathogenesis of SB by virtue of its role in the sympathetic-
cardiac activation seen within sleep arousals.28 This is supported by evidence that adrenergic agonists,
such as clonidine, reduce RMMA episodes by 60%. Moreover, it is also involved in the shift from non–
rapid eye movement sleep to rapid eye movement sleep, when SB episodes may occur.28,200

Other Neurotransmitters
Other neurotransmitters, such as gamma-aminobutyric acid, orexin, and cholecystokinin, may in-
fluence RMMA during sleep28 due to their role in cardiac and respiratory activation, sleep in-
duction, and maintenance.22 We could not find literature supporting the definitive roles of these
neurotransmitters in the genesis or perpetuation of SB movements.

Autonomic Arousal Response

SB has been found to be associated with arousals from sleep.28 Most RMMAs are reported to occur
concomitant with an arousal response.201,202 Arousals are accompanied by various physiological
responses, including increases in heart rate and muscle activity, peripheral vasoconstriction, change
in respiratory activity, appearance of K complexes in the electroencephalogram, and body
movements.33,86,172,201,203 SB, RMMA, and sleep arousals are accompanied by increased sympa-
thetic and brainstem activity.32,37,172,203,204 Sleep-related arousal has been proposed as a trigger for
jaw-opener muscle activity.201 Finally, approximately 4 seconds after the arousal, episodes of SB and
RMMA are detected on an EMG recording, with or without subsequent swallowing.20 The role of
sympathetic activation in SB was also confirmed indirectly via a reduction in RMMA in bruxers
after administration of clonidine.32,205

Airway Patency
SB may be associated with airway patency,32 and SB episodes are increased in patients with airway
collapse (such as in OSA),146,206 suggesting a protective role in obstructive respiratory
events.156,207,208 Although the literature in this regard seems to be rather limited, it indicates that
bruxer movements may aid in restoring and maintaining the patency of the upper airway. However,
other researchers have failed to find any association.156 Mandibular advancement devices that
increase the cross-sectional diameter at the oropharynx have been found to reduce the frequency of
SB episodes.209-213 RMMA has also been proposed to be a physiological oromotor event necessary
to restore salivary flow and swallowing, which are normally decreased during sleep.28,214,215

Epidemiology
Incidence and Prevalence
The prevalence of bruxism is reported to be 5% through 40%31,216 in children and 10% through
30% in adults.217 There is a higher prevalence of SB in younger people and drops after the age of 50
years.21 In the pediatric population, SB is more prevalent in girls.218

Age
A peripubertal (mixed dentition) age predilection was observed. It is not clear, however, whether
this observation was related to the hormonal changes occurring in this age group.218 SB seems to
increase with age.219 Some authors have proposed an increase in bruxism during the mixed-
dentition stage, with a subsequent reduction as the person gets older.220 The apparent wide
range of reported differences in epidemiolgy may be due to the way bruxism has been defined and
diagnosed in various studies.

Assessment strategies
PSG
PSG with audio and video recordings has, for decades, been considered the reference standard for
SB analysis.2,221 Among the 11 channels, electroencephalography, electro-oculography, EMG,
electrocardiography, thoracoabdominal movements, oronasal airflow, and oxygen saturation are the

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Table 3. Proposed diagnostic and assessment criteria according to the International Classification of Sleep Disorders, 3rd edition in 20143 and grading
system from the International Consensus in 2018.5,*

DIAGNOSTIC
CONSIDERATIONS TYPE OF BRUXISM DESCRIPTION
International Classification of
Sleep Disorders, 3rd Edition

A SB† Positive regular or frequent tooth grinding sounds during sleep

B SB Presence of  1 of these clinical findings:

Excessive tooth wear (consistent with positive reports of nocturnal tooth grinding)
Momentary morning jaw muscle pain or fatigue, headache located on the temporal area, or jaw
locking on awakening (consistent with positive reports of nocturnal tooth grinding)

International Consensus

Possible SB, AB‡ Based on a positive self-report

Probable SB, AB Based on a positive clinical evaluation, with or without a positive self-report

Definite SB Based on positive polysomnography (possibly combined with audio or video recordings), with or
without a positive self-report or a positive clinical evaluation
AB Based on positive electromyography (possibly combined with ecological momentary assessment or
experience sampling methodology), with or without a positive self-report or a positive clinical
evaluation

* Priyanka Kodaganallur Pitchumani digitized the table. † SB: Sleep bruxism. ‡ AB: Awake bruxism.

most important elements recorded.18 Masticatory muscle activity is measured by means of grading
the information from EMG channels of masticatory muscles.222 PSG electrodes and portable devices
appear to have high sensitivity and specificity when analyzed simultaneously.221,223 Heart rate
measurements may aid in the assessment, in addition to portable home EMG monitoring of SB
events.221 The available data on PSG refer to the older criteria based on the number of EMG events
above a certain threshold of maximum voluntary contractions. The term muscle work has been
introduced in the literature to replace number of SB and EMG events, but definite criteria that
match the definition are still lacking.224

Portable Devices
Portable devices relying on EMG-dependent measurements record bruxism data over a single night
or multiple nights,225,226 based mostly on the number of bruxism episodes. The patients are divided
into nonbruxer (ie, no episodes recorded) and bruxer (ie, on at least 1 night had more than 2 SB
episodes for every hour of sleep).225 One of the shortcomings of this method is that wake after sleep
onset may not be recorded accurately.221,225 Wake after sleep onset may be an important factor in
contributing to false-positive readings for SB movements because the portable devices may not be
sensitive enough to differentiate between those wakefulness-associated movements and SB move-
ments. This may further skew such data. EMG-independent portable devices are proposed to
distinguish patients with SB from patients without SB using a specific software that identifies the
extent of wear from RMMA.223 Certain non-PSG techniques seem to be validated in assessing
SB.227,228 Instruments that can measure muscle work, as opposed to merely the number of muscle
contractions or movements, have gained momentum.224

Self-Reported and Clinical Approaches

A downside of both of these approaches is that the responses and findings may not be reliable.225,229
Therefore, PSG has long been considered a standard for bruxism assessment.225,230,231 However, the
use of these approaches may be limited, as they assess varied SB constructs.225,231,232

Diagnosis and assessment

The most widely accepted assessments are those proposed in the ICSD-33 and the International
Consensus in 20185 (Table 3). Clinical examination findings for bruxism include, but are not
limited to, excessive tooth wear, masticatory muscle hypertrophy, and muscle tenderness.21 How-
ever, abnormal tooth wear (such as dental attrition) is not only conceivably dependent on multiple
variables, such as acid reflux, acidic or coarse foods, and enamel or dentin abnormalities. A patient
predominantly exhibiting more of a static bruxism component (ie, clenching) may not have the

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same degree of abnormal tooth wear as a patient with dynamic bruxism. Headaches and myalgia are
often not symptoms in patients with SB. The term temporomandibular joint lock appears in the
ICSD-33 criteria for “sleep related bruxism,” however, we could not find a satisfactory explanation
of this lock in the ICSD-3 or in the associated literature.233,234 The Standardised Tool for the
Assessment of Bruxism encompasses strategies for patient-based, clinical-based, and instrument-
based assessment to collect information on bruxism status, etiology, comorbid conditions, and
consequences, and it is divided into 2 axes.6

Differential diagnosis
The differential diagnoses of secondary SB may include a variety of conditions that can result in
nocturnal orofacial movements, tooth wear, masticatory muscle pain, and fatigue. Figure 3 presents
the most common conditions to consider in the workup of a bruxism case.

Dental implications
Changes in dentition, destruction of restorations, attrition, condylar flattening, soft-tissue changes,
and periodontal changes have been suggested as sequelae of bruxism. A clinical entity known as
buttressing bone formation was proposed in the early 1960s235; however, there is no evidence of a
causal relation between the 2 entities. Bruxism has been reported as a factor affecting prognosis of
dental implants. However, a causal relationship between bruxism and implant failures has not been
established.236 Researchers performing systematic reviews in this regard found that most of the
failures reported were due to structural breakdown (fracture or chipping of prosthesis, prefabricated
components), rather than biological complications (eg, absence of osseointegration, peri-
implantitis, or marginal bone loss).236-238 To avoid mechanical complications, stress-reducing al-
ternatives, such as wider diameter implants, additional implants, eliminating cantilevers, metal
occlusal surfaces, and nightguards have been proposed.239,240 SB has not been conclusively found to
cause restoration failures.241

Clinical features
The major clinical features of SB are provided in the Box.

Management
In case of secondary bruxism, the offending factor and associated conditions should be identified
and addressed appropriately. When concurrent SB and OSA are diagnosed, it may be prudent to use
a mandibular advancement device for management of both conditions simultaneously. Bruxism
secondary to medication, such as selective serotonin reuptake inhibitors, may be managed by means
of a reduction in the dosage, addition of serotonin and norepinephrine reuptake inhibitors,
administration of buspirone, and elimination of the offending drug.181
Dental splints may lower the frequency of SB episodes temporarily245-248; however, there is a lack
of evidence for any difference in efficacy of various types of appliances. Bruxism episodes tend to
return to a preappliance level within approximately 4 through 6 weeks.246 Other modalities include
stress management and clenching awareness, with modalities such as cognitive behavioral ther-
apy,245 physical self-regulation,249 and biofeedback therapy,245 among others.

Clinical pearls
SB should be a consideration in treatment planning for dental restorative and reconstructive work.
The clinician should consider bruxism secondary to other factors. Management of bruxism sec-
ondary to medication should be considered in conjunction with, and after consultation with, the
appropriate prescribing medical specialist. The association of SB with conditions such as restless legs
syndrome, OSA, and possible associated cardiac events should be explored. Furthermore, when SB
coexists with dystonic movements, the possibility of neurodegenerative conditions, such as
parkinsonism syndromes, needs to be ruled out. Patients experiencing musculoskeletal pain seem-
ingly associated with SB may need to be assessed for systemic factors that may induce or condition
the pain entity. Splints may prevent additional tooth damage or restoration failure. Alternative
restorative materials and restoration types may be considered for a patient with SB. Until a universal
consensus can be reached about the classification and diagnosis of SB, the clinician should use

JADA n(n) n http://jada.ada.org n n 2024 9

 Systemic

• Facial myoclonus250-252
• Sleep talking253
• Movement disorders (oromandibular dystonia, Parkinson
disease, dyskinesia, drug-induced extrapyramidal reactions)21,254,255
• Parasomnias256,257
• Rapid eye movement sleep behavior disorder21,258
• Periodic limb movements and restless legs syndrome21
Based on
• Nocturnal seizures and sleep-related epilepsy256,259-263
positive report
• Drug induced21,176,181,255,264,265

Local

• Swallowing266
• Chewing-like movements266
• Rhythmic masticatory muscle activity267

Systemic

• Syndromes
• Gastroesophageal reflux disease139,268-270
• Bulimia nervosa271
• Age-related tooth wear

Local
Based on
positive tooth • Chemical erosion due to dietary factors (acidic content such as oranges,
wear apples, lemons, carbonated or soft drinks, fruit juices, acidic snacks,
sweets)269-274
• Frequent meals or snacks274
• Occupational factors (eg, exposition to acidic liquids or vapors)270
• Xerostomia269,275
• Oral hygiene271,273
• Vomiting270,271
• Medication and dietary supplements (eg, vitamin C)270,271,274
• Abrasion due to erosive substances (eg, acid or substances with
high-buffering capacity) 271,274

Systemic

• Carotidynia276
• Headache associated with temporomandibular disorder21
• Temporomandibular disorder21,277
• Stress, anxiety20,21,86,91,92,278

Based on Local
positive muscle
pain or fatigue • Obstructive parotitis 279
or hypertrophy • Muscle hypertrophy

Figure 3. Differential diagnoses based on a positive self-report, clinical finding of tooth wear, and history of muscle
pain or fatigue or hypertrophy.

prudence in screening for SB, with the view that it may affect or determine the prognosis and,
hence, treatment planning.

CONCLUSIONS
The American Academy of Sleep Medicine classifies SB as a sleep-related movement disorder. The
pathophysiology, classification, assessment, and diagnosis of SB are still evolving. It is our hope that,
in view of the literature reviewed in our article, the assessment protocol for SB is universally

10 JADA n(n) n http://jada.ada.org n n 2024

 Box. Clinical features of sleep bruxism.*

FINDINGS FEATURES
Extraoral Masseter and temporalis hypertrophy.
Intraoral Soft tissue: soft-tissue trauma, parotid obstruction,242 prominent linea alba bucca (maybe
static bruxism).
Hard tissue: enamel or dentin wear, implant failure, tooth fracture, restoration failure, tooth
loss, pulp exposure,242 vertical enamel craze lines.243 The association of tori with abnormal
tooth wear was proposed.244 A higher level of evidence for this association is with
mandibular tori as opposed to palatal tori.244 There is a lack of adequate literature to causally
associate tori with bruxism.244
* Priyanka Kodaganallur Pitchumani digitized the box.

accepted to accurately reflect the latest science. The astute clinician should consider the existence
of bruxism when contemplating dental treatment, particularly restorative therapy. The dental sci-
entific community looks forward to succinct research and management modalities of SB. n

DISCLOSURE
None of the authors reported any disclosures.

Dr. Thomas is an associate clinical professor, Center for
Temporomandibular Disorders and Orofacial Pain, Department of
Diagnostic Sciences, Rutgers School of Dental Medicine, Newark, NJ.
Address correspondence to Dr. Thomas, Department of Diagnostic
Sciences, Rutgers School of Dental Medicine, 110 Bergen St, Newark, NJ
07103, email davisct1@gmail.com.
Dr. Manfredini is a professor, Department of Biomedical Technology,
School of Dentistry, University of Sienna, Sienna, Italy.
Dr. Patel is a private dental practitioner, 32 PEARLS Multispecialty Dental
Clinics and Implant Centers, Ahmedabad, India.
Dr. George is an intern, SRM Kattankulathur Dental College and
Hospital, Chennai, India.
Dr. Chanamolu is a postgraduate student, University of North Texas,
Denton, TX.
Dr. Pitchumani is a postgraduate resident, Division of Periodontology,
College of Dentistry, The Ohio State University, Columbus, OH.
Dr. Sangalli is an assistant professor, College of Dental Medicine-Illinois,
Midwestern University, Downers Grove, IL.-
ORCID Numbers. Davis C. Thomas: https://orcid.org/0000-0002-6205-
2899; Daniele Manfredini: https://orcid.org/0000-0002-4352-3085;
Jaimin Patel: https://orcid.org/0000-0001-7792-279X; Aaron George:
https://orcid.org/0009-0000-1459-8646; Bindu Chanamolu: https://orci-
d.org/0009-0007-1958-5722; Priyanka Kodaganallur Pitchumani: https://
orcid.org/0000-0001-7897-5244; Linda Sangalli: https://orcid.org/0000-
0002-1386-5594. For information regarding ORCID numbers, go to http://
orcid.org.

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