Abstract
Bruxism is repetitive masticatory-muscle activity — clenching or grinding the teeth, or bracing and thrusting the mandible. It is not one behaviour but two distinct circadian phenomena: sleep bruxism, a largely involuntary motor event during sleep, and awake bruxism, a daytime clenching tied to psychological load. An international consensus now frames bruxism in otherwise healthy people as a behaviour rather than a disorder, grading its presence by the strength of the evidence. The modern account locates its regulation centrally, in the nervous system and sleep-arousal physiology, rather than peripherally in the bite. This article sets out what bruxism is, how its two types differ, how clinicians grade it from self-report to instrumented recording, and why its links to stress, arousal, and sleep place it between dentistry and the psychology of the self-regulating mind.
Keywords: bruxism, sleep bruxism, teeth grinding, masticatory muscle activity, arousal
Few everyday behaviours sit as squarely between the body and the mind as grinding one's teeth. A dentist sees worn enamel and a fractured molar; a sleep physician sees bursts of jaw-muscle activity riding on the micro-arousals of a restless night; a psychologist sees a somatic signature of stress. All three are looking at the same phenomenon, and the history of bruxism research is largely the story of those three viewpoints converging on a single, central account. Bruxism is common, often harmless, occasionally destructive, and — because it is driven more by how the brain regulates arousal than by how the teeth meet — genuinely a topic for cognitive and behavioural science as much as for dentistry.
- Bruxism is two behaviours, not one. Sleep bruxism and awake bruxism differ in their timing, their motor pattern, and their likely causes, and should be assessed separately (Lobbezoo et al., 2018). - It is defined as a behaviour, not a disorder, in otherwise healthy individuals — a shift codified by international consensus (Lobbezoo et al., 2013). - Its control is central, not peripheral. Decades of evidence moved the field away from the old occlusal (bite) model toward regulation by the nervous system and sleep-arousal physiology (Lobbezoo & Naeije, 2001; Klasser et al., 2015). - Grading follows the evidence. Assessment is graded possible (self-report), probable (plus clinical examination), or definite (plus instrumental recording such as polysomnography) (Lobbezoo et al., 2018). - Stress and arousal are reliable correlates, linking bruxism to the psychology of emotion regulation and self-control (Manfredini & Lobbezoo, 2009; Smardz et al., 2019).
What Bruxism Is
The current international consensus defines bruxism as a repetitive masticatory-muscle activity characterised by clenching or grinding of the teeth and/or by bracing or thrusting of the mandible (Lobbezoo et al., 2013). Two features of that definition are deliberate. First, it is built around muscle activity, not around tooth wear: worn teeth are a possible consequence of bruxism, not the behaviour itself, and many people with ground-down enamel are no longer actively bruxing while many active bruxers show little wear. Second, the consensus deliberately splits the behaviour by its circadian timing, because the daytime and night-time forms behave so differently that treating them as one construct obscures both.
Awake bruxism is a semi-voluntary activity of the jaw muscles during wakefulness, dominated by sustained, low-level clenching and bracing rather than the vigorous grinding of sleep. It waxes and wanes with attention and emotional state, and a person can often be made aware of it and asked to stop (Lavigne et al., 2008). Sleep bruxism, by contrast, is a largely involuntary motor behaviour that the sleeper cannot report and does not remember. It is distinguished by rhythmic masticatory muscle activity (RMMA) — brief, repetitive bursts of jaw-muscle contraction, sometimes with audible grinding — occurring in clusters through the night (Kato et al., 2001; Carra et al., 2012).
A second, equally important part of the consensus is a statement about status. In otherwise healthy people, bruxism is best regarded not as a disorder but as a behaviour that can be a risk factor for certain outcomes (such as tooth wear or masticatory-muscle pain), a protective factor for others (such as maintaining airway patency during sleep), or of no clinical consequence at all (Lobbezoo et al., 2018). This reframing matters: it moves the clinical question from does this person have a disease? to is this behaviour, in this person, doing any harm?
Types of Bruxism
In the Medical Subject Headings (MeSH) vocabulary, Bruxism (D002012) is classified under three parent headings at once — Tooth Diseases, Habits, and Psychological Distress — a triple placement that itself captures the behaviour's dental, behavioural, and psychological faces. The descriptor has one narrower heading beneath it.
| Type | MeSH identifier | What distinguishes it |
|---|---|---|
| Sleep Bruxism | D020186 | Grinding and clenching during sleep, expressed as rhythmic masticatory muscle activity tied to sleep micro-arousals; involuntary and unremembered. |
MeSH lists only Sleep Bruxism as a formal narrower descriptor; awake bruxism, though central to the clinical consensus (Lobbezoo et al., 2018), is not a separate MeSH heading and is indexed under the parent term. This is a useful reminder that a classification hierarchy such as MeSH is an indexing scheme built for retrieving literature, not a theory of the phenomenon: the two circadian types are clinically co-equal even though only one has its own descriptor. The sleep/awake distinction is also orthogonal to severity and to cause — a person may show mild sleep bruxism and marked awake clenching, or either in isolation, and the timing of the behaviour does not by itself fix how harmful or how treatable it is.
From the Bite to the Brain: The Shift to a Central Model
For much of the twentieth century, bruxism was blamed on the bite. The dominant occlusal (peripheral) theory held that premature tooth contacts and malocclusion triggered grinding, and that correcting the bite would cure it. That model drove a great deal of irreversible dental treatment, and it was wrong in its essentials. A pivotal re-analysis argued that the evidence pointed the other way: bruxism is mainly regulated centrally, by the nervous system, not peripherally by the occlusion (Lobbezoo & Naeije, 2001). Occlusal factors, on this account, play at most a minor role, and the grinding originates in the brain's motor and arousal systems.
The central model has only strengthened since. Reviews tracing the evolution of thinking describe sleep bruxism as an arousal-related motor phenomenon: the RMMA bursts do not occur at random through the night but cluster within the brief micro-arousals that punctuate normal sleep, typically preceded by a cascade of autonomic and cortical activation (Klasser et al., 2015; Carra et al., 2012). Heart rate rises, breathing changes, cortical activity shifts toward lighter sleep, and only then does the jaw-muscle burst fire. Sleep bruxism, in other words, is better understood as one possible motor expression of the sleeping brain's normal arousal machinery than as a dental problem that happens to occur at night. Dopaminergic and other central neurotransmitter systems have been implicated, consistent with the behaviour's responsiveness to centrally acting drugs and its associations with stress and certain medications (Lavigne et al., 2008).
Assessing and Grading Bruxism
Because bruxism cannot be read off the teeth and sleep bruxism cannot be self-reported, the consensus replaced the old yes/no diagnosis with a graded assessment that makes the strength of the evidence explicit (Lobbezoo et al., 2018). Three grades are defined:
- Possible bruxism rests on self-report alone — a questionnaire or a history of clenching or grinding. It is cheap and scalable but weak, since people are poor witnesses to their own sleep and inconsistent reporters of daytime clenching. - Probable bruxism adds a clinical examination — a clinician's inspection for tooth wear, masticatory-muscle tenderness, tongue or cheek indentations, and the like. More objective than self-report, but still indirect. - Definite bruxism adds an instrumental measure. For sleep bruxism the reference standard is polysomnography, ideally with audio-video, which records the jaw-muscle (masseter and temporalis) electromyographic bursts directly and scores RMMA against validated criteria (Carra et al., 2012). For awake bruxism, ecological momentary assessment and portable electromyography are increasingly used.
This graded scheme is deliberately epistemic rather than clinical: it does not grade how severe the bruxism is, but how confident one can be that it is present. A large epidemiological literature rests almost entirely on the possible grade, because polysomnography is expensive, which is one reason prevalence estimates vary so widely (Manfredini et al., 2013).
Consequences, and What To Do About Them
Bruxism's possible consequences include accelerated tooth wear and fracture, failure of dental restorations, masticatory-muscle pain and fatigue, and — contested — a contribution to temporomandibular disorders (TMD). The TMD link is the most debated: a systematic review of the 1998-2008 literature found the association real but weaker and less consistent than clinical lore assumes, complicated by the fact that both bruxism and TMD are hard to measure and may share upstream causes such as stress (Manfredini & Lobbezoo, 2010). An umbrella review of systematic reviews reached a similar verdict across outcomes — many associations are reported, but the evidence base is often low in quality and heterogeneous (Melo et al., 2019).
Management follows directly from the central model, and its guiding principle is conservatism. Because bruxism is a centrally driven behaviour rather than a bite defect, irreversible occlusal treatment is not justified as a cure. The consensus on management is often summarised as the three Ps: plates (occlusal splints or mouthguards that protect the teeth and redistribute load without claiming to stop the grinding), pharmacology (short-term or targeted use of centrally acting agents in selected cases), and psychology (stress management, relaxation, biofeedback, and behavioural strategies, especially for awake clenching) (Lobbezoo et al., 2008). A plain-language clinical overview for practitioners frames the same protect-first logic for everyday dental practice (Beddis et al., 2018). A neurology-oriented review of treatments reaches broadly the same place: splints protect, some drugs reduce motor events in the short term, and behavioural approaches target the arousal and stress that drive the behaviour — but no treatment reliably abolishes bruxism, and for many people protection rather than cure is the realistic goal (Guaita & Hogl, 2016). For the subset whose awake clenching is clearly stress-linked, relaxation therapy and other behaviour-therapy techniques are the most direct lever.
Arousal drives the jaw-muscle bursts
Rhythmic masticatory muscle activity (RMMA) clusters inside the brief micro-arousals of sleep. Raise the night’s arousal index and watch the expected number of sleep-bruxism episodes rise.
Over a 7-hour night: 15 expected bruxism episodes.
Illustrative model, not a diagnostic tool. The point is directional: the motor events track arousal, not the bite.
Grade the evidence
The 2018 consensus grades bruxism not by severity but by how confident one can be that it is present. Toggle the evidence you have.
How many bruxers in a population?
Self-report prevalence from the adult-epidemiology review (Manfredini et al., 2013): awake bruxism ~22–31%, sleep bruxism ~13%.
About 712 people (~36%) report clenching or grinding of some kind.
“Either” assumes statistical independence (overlap = 68); real co-occurrence runs somewhat higher. These are self-report figures — the polysomnography-confirmed sleep-bruxism rate is lower.
Figure
Worked Example
How many people in a given population are likely to brux? The most-cited systematic review of adult epidemiology gives working figures: awake bruxism affects roughly 22-31% of adults, while sleep bruxism affects roughly 13%, with both declining with age (Manfredini et al., 2013). These are almost entirely possible-grade estimates — based on self-report — so they are best read as orders of magnitude rather than precise rates.
Take a mid-sized workplace of 2,000 adults and apply the central estimates:
- Awake bruxism at 26% (the midpoint of the 22-31% range): 0.26 × 2,000 = 520 people. - Sleep bruxism at 13%: 0.13 × 2,000 = 260 people.
Suppose we want a rough count of people likely to show either form. If the two were statistically independent, the expected overlap would be 0.26 × 0.13 × 2,000 ≈ 68 people showing both, so the number showing at least one form would be 520 + 260 − 68 = 712 people, about 36% of the workforce. Independence is only an approximation — the two types do co-occur more than chance in some samples — but the arithmetic makes the headline point: on self-report figures, clenching or grinding of some kind is reported by roughly a third of adults, while the definite, polysomnography-confirmed rate of sleep bruxism is far lower. The PrevalenceExplorerDemo lets the reader vary the population size and the assumed rates and watch these counts update.
Discussion
The arc of bruxism research is a clean example of a field relocating a phenomenon from the periphery to the centre. The occlusal model treated grinding as a mechanical fault of the mouth; the modern model treats it as a behaviour of the brain, expressed through the mouth. That shift reorganised everything downstream — it dissolved the rationale for aggressive bite correction, it explained why stress and arousal are such reliable correlates, and it reframed sleep bruxism as a motor signature of normal sleep physiology rather than a disease of the teeth (Lobbezoo & Naeije, 2001; Klasser et al., 2015).
The cost of that reframing is humility about measurement. Because the two types have different causes and different methods of detection, because self-report is weak and polysomnography is scarce, and because the clinically important consequences (pain, TMD) are themselves contested and hard to measure, the evidence base is noisier than the volume of publication suggests (Melo et al., 2019; Manfredini & Lobbezoo, 2010). The graded assessment scheme is an honest response to that noise: it does not pretend to a certainty the data cannot support.
Cognitive and Psychological Implications
Bruxism is not, on its face, a cognitive process — but it is tightly bound to several that are. The most robust psychological finding is its association with stress and negative emotional states. A systematic review of psychosocial factors found consistent, if modest, links between bruxism and anxiety, stress sensitivity, and certain personality traits, placing the behaviour within the broader literature on how the body expresses psychological load (Manfredini & Lobbezoo, 2009). An instrumented polysomnographic study sharpened the picture: measuring sleep bruxism directly against validated stress and depression scales, it found the correlation held up under objective recording rather than being an artefact of self-report (Smardz et al., 2019).
This places bruxism squarely at the interface of cognition and the body. Its tie to arousal connects it to the psychophysiology of the activated nervous system; its clustering within sleep micro-arousals links it to the architecture of sleep itself; and its responsiveness to psychological stress makes it a somatic readout of emotion regulation and self-control. The behavioural treatments that help — relaxation, biofeedback, habit-reversal for awake clenching — are precisely interventions that target cognitive and emotional self-regulation rather than the mouth (Lobbezoo et al., 2008; Guaita & Hogl, 2016). For the cognitive scientist, bruxism is a reminder that the aroused, stressed, self-regulating mind leaves motor traces, and that one of the clearest of those traces is written into the muscles of the jaw.
Current Directions
Three threads dominate the recent literature. The first is standardisation: the 2018 international consensus formalised the graded (possible/probable/definite) assessment and pushed the field toward a shared, operational vocabulary, so that studies can finally be compared on a common footing (Lobbezoo et al., 2018). The second is instrumentation: portable electromyography and ecological momentary assessment are making the definite grade — once confined to the sleep laboratory — reachable in the field, and are beginning to characterise awake bruxism with the rigour previously reserved for sleep bruxism. The third is evidence synthesis: umbrella reviews are now aggregating the many systematic reviews, consistently finding that the associations the clinical world takes for granted rest on evidence of modest quality, and calling for better-controlled primary studies (Melo et al., 2019). Objective-measurement studies of the stress link, such as polysomnography paired with validated psychometrics, point to where the next advances lie — in pinning down which arousal and affective mechanisms drive the behaviour, rather than merely re-establishing that they do (Smardz et al., 2019).
Common Misconceptions
- Bruxism is caused by a bad bite.
- The occlusal model is largely abandoned. Bruxism is regulated centrally; malocclusion plays at most a minor role, and correcting the bite is not a cure (Lobbezoo & Naeije, 2001).
- Worn teeth mean active bruxism.
- Tooth wear is a cumulative, historical record, not a measure of current activity. Many worn dentitions belong to people who no longer brux, and many active bruxers have little wear (Lobbezoo et al., 2013).
- A night guard stops the grinding.
- Occlusal splints protect the teeth and redistribute load; they do not reliably abolish the underlying muscle activity, which is centrally driven (Guaita & Hogl, 2016).
- Bruxism is a disease everyone with it should treat.
- In otherwise healthy people the consensus treats bruxism as a behaviour, not a disorder — sometimes a risk factor, sometimes harmless, occasionally protective. Treatment is warranted only when it is doing harm (Lobbezoo et al., 2018).
Glossary
- Awake bruxism.
- Masticatory-muscle activity during wakefulness, dominated by sustained clenching and bracing rather than grinding; semi-voluntary and modulated by attention and emotion.
- Bracing.
- Holding the mandible rigidly in position by sustained muscle contraction, without necessarily moving or grinding the teeth.
- Clenching.
- Forceful static contact of the opposing teeth produced by jaw-muscle contraction, without the lateral movement that produces grinding.
- Definite bruxism.
- The highest assessment grade: self-report plus clinical examination plus an instrumental measure such as polysomnography.
- Electromyography (EMG).
- Recording of the electrical activity of muscle; in bruxism research, used to capture masseter and temporalis bursts.
- Grinding.
- Lateral or protrusive rubbing of the opposing teeth against one another, often audible, characteristic of sleep bruxism.
- Malocclusion.
- A misalignment of the teeth or bite; once thought to cause bruxism, now considered at most a minor factor.
- Masticatory muscles.
- The muscles that move the jaw — chiefly the masseter, temporalis, and pterygoids — whose activity constitutes bruxism.
- Micro-arousal.
- A brief, transient shift toward lighter sleep marked by autonomic and cortical activation, within which RMMA bursts cluster.
- Occlusal splint.
- A removable dental appliance (night guard) worn over the teeth to protect them and redistribute load; protective, not curative.
- Occlusion.
- The way the upper and lower teeth meet; the basis of the now-superseded peripheral model of bruxism.
- Polysomnography (PSG).
- Multi-channel sleep recording (EEG, EMG, ECG, respiration, and often audio-video) that provides the reference standard for diagnosing sleep bruxism.
- Possible bruxism.
- The lowest assessment grade, resting on self-report alone.
- Probable bruxism.
- The middle assessment grade: self-report plus a clinical examination.
- Rhythmic masticatory muscle activity (RMMA).
- The repetitive jaw-muscle bursts that constitute sleep bruxism, scored from EMG and clustered within sleep micro-arousals.
- Sleep bruxism.
- Involuntary grinding and clenching during sleep, expressed as RMMA tied to arousal; unremembered by the sleeper.
- Temporomandibular disorder (TMD).
- A group of conditions affecting the jaw joint and masticatory muscles; its relationship to bruxism is real but contested.
Key Researchers
Takafumi Kato
(contemporary). Professor of oral physiology at Osaka University; established the polysomnographic characterisation of sleep bruxism as rhythmic masticatory muscle activity tied to sleep micro-arousals. ORCID - Faculty
Gilles J. Lavigne
(contemporary). Professor at the Université de Montréal and McGill University; a founder of dental sleep medicine and of the rhythmic-masticatory-muscle-activity / sleep-arousal model of sleep bruxism. ORCID - Wikipedia - Google Scholar
Frank Lobbezoo
(contemporary). Professor of orofacial pain and dysfunction at ACTA (Academic Centre for Dentistry Amsterdam), VU University Amsterdam; lead author of the 2013 and 2018 international consensus definitions of bruxism. ORCID - Google Scholar - Faculty
Daniele Manfredini
(contemporary). Professor at the University of Siena; co-author of the bruxism consensus papers and lead author of the adult-epidemiology and bruxism–TMD systematic reviews. ORCID - Google Scholar
Peter Svensson
(contemporary). Professor of orofacial pain at Aarhus University; co-author of the bruxism consensus papers and a leader in the neurophysiology of jaw-muscle pain and motor control. Faculty
Frequently Asked Questions
What is bruxism in simple terms?
Bruxism is the repetitive clenching or grinding of the teeth, or the tensing and thrusting of the jaw, produced by activity of the chewing muscles. It comes in two forms: a daytime form (awake bruxism), which is mostly clenching under stress or concentration, and a night-time form (sleep bruxism), which involves involuntary grinding during sleep (Lobbezoo et al., 2013).
What causes teeth grinding?
The modern view is that bruxism is controlled centrally, by the brain, rather than by the bite. Sleep bruxism in particular is tied to the brief arousals that punctuate normal sleep, and both forms are linked to stress and to certain neurotransmitter and medication effects. The old idea that a bad bite causes grinding has been largely abandoned (Lobbezoo & Naeije, 2001; Klasser et al., 2015).
Is sleep bruxism different from daytime clenching?
Yes, and the distinction matters clinically. Sleep bruxism is an involuntary motor behaviour expressed as rhythmic bursts of jaw-muscle activity during sleep, which the sleeper cannot report. Awake bruxism is semi-voluntary clenching during the day, modulated by attention and emotion, which a person can often learn to notice and interrupt (Lobbezoo et al., 2018; Lavigne et al., 2008).
How is bruxism diagnosed?
Assessment is graded by the strength of the evidence: possible bruxism from self-report alone, probable bruxism from self-report plus a clinical examination, and definite bruxism when an instrumental measure (polysomnography for sleep bruxism) confirms it. Most large studies rely on the weakest, self-report grade (Lobbezoo et al., 2018; Carra et al., 2012).
How common is bruxism?
On self-report figures, awake bruxism affects roughly 22 to 31% of adults and sleep bruxism roughly 13%, with both declining with age. Because these rest almost entirely on self-report, they are best treated as rough magnitudes; the polysomnography-confirmed rate of sleep bruxism is considerably lower (Manfredini et al., 2013).
Does bruxism cause jaw problems (TMD)?
There is a real but contested association between bruxism and temporomandibular disorders. A systematic review found the link weaker and less consistent than clinical lore suggests, complicated because both conditions are hard to measure and may share upstream causes such as stress (Manfredini & Lobbezoo, 2010; Melo et al., 2019).
Can bruxism be cured?
No treatment reliably abolishes bruxism, because it is a centrally driven behaviour rather than a fixable mechanical fault. The realistic goals are protection and harm reduction: splints protect the teeth, some drugs reduce motor events in the short term, and behavioural approaches target the stress and arousal that drive it (Lobbezoo et al., 2008; Guaita & Högl, 2016).
How is bruxism connected to the mind and to stress?
Bruxism is one of the clearest somatic markers of psychological load. It correlates consistently with stress, anxiety, and negative affect, and sleep bruxism rides on the brain's arousal system during sleep. That is why it interests cognitive and behavioural science: it is a motor trace of how the aroused, self-regulating mind handles stress, and why relaxation and biofeedback (interventions aimed at the mind, not the mouth) can help (Manfredini & Lobbezoo, 2009; Smardz et al., 2019).
References
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Carra, M. C., Huynh, N., & Lavigne, G. (2012). Sleep bruxism: a comprehensive overview for the dental clinician interested in sleep medicine. Dental Clinics of North America, 56(2), 387-413. https://doi.org/10.1016/j.cden.2012.01.003
Guaita, M., & Hogl, B. (2016). Current treatments of bruxism. Current Treatment Options in Neurology, 18(2), 10. https://doi.org/10.1007/s11940-016-0396-3
Kato, T., Thie, N. M., Montplaisir, J. Y., & Lavigne, G. J. (2001). Bruxism and orofacial movements during sleep. Dental Clinics of North America, 45(4), 657-684. https://doi.org/10.1016/S0011-8532(22)00487-6
Klasser, G. D., Rei, N., & Lavigne, G. J. (2015). Sleep bruxism etiology: the evolution of a changing paradigm. Journal of the Canadian Dental Association, 81, f2. PMID: 25633110.
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Lobbezoo, F., & Naeije, M. (2001). Bruxism is mainly regulated centrally, not peripherally. Journal of Oral Rehabilitation, 28(12), 1085-1091. https://doi.org/10.1046/j.1365-2842.2001.00839.x
Lobbezoo, F., van der Zaag, J., van Selms, M. K. A., Hamburger, H. L., & Naeije, M. (2008). Principles for the management of bruxism. Journal of Oral Rehabilitation, 35(7), 509-523. https://doi.org/10.1111/j.1365-2842.2008.01853.x
Lobbezoo, F., Ahlberg, J., Glaros, A. G., Kato, T., Koyano, K., Lavigne, G. J., de Leeuw, R., Manfredini, D., Svensson, P., & Winocur, E. (2013). Bruxism defined and graded: an international consensus. Journal of Oral Rehabilitation, 40(1), 2-4. https://doi.org/10.1111/joor.12011
Lobbezoo, F., Ahlberg, J., Raphael, K. G., Wetselaar, P., Glaros, A. G., Kato, T., Santiago, V., Winocur, E., De Laat, A., De Leeuw, R., Koyano, K., Lavigne, G. J., Svensson, P., & Manfredini, D. (2018). International consensus on the assessment of bruxism: Report of a work in progress. Journal of Oral Rehabilitation, 45(11), 837-844. https://doi.org/10.1111/joor.12663
Manfredini, D., & Lobbezoo, F. (2009). Role of psychosocial factors in the etiology of bruxism. Journal of Orofacial Pain, 23(2), 153-166. PMID: 19492540.
Manfredini, D., & Lobbezoo, F. (2010). Relationship between bruxism and temporomandibular disorders: a systematic review of literature from 1998 to 2008. Oral Surgery, Oral Medicine, Oral Pathology, Oral Radiology, and Endodontology, 109(6), e26-e50. https://doi.org/10.1016/j.tripleo.2010.02.013
Manfredini, D., Winocur, E., Guarda-Nardini, L., Paesani, D., & Lobbezoo, F. (2013). Epidemiology of bruxism in adults: a systematic review of the literature. Journal of Orofacial Pain, 27(2), 99-110. https://doi.org/10.11607/jop.921
Melo, G., Duarte, J., Pauletto, P., Porporatti, A. L., Stuginski-Barbosa, J., Winocur, E., Flores-Mir, C., & De Luca Canto, G. (2019). Bruxism: An umbrella review of systematic reviews. Journal of Oral Rehabilitation, 46(7), 666-690. https://doi.org/10.1111/joor.12801
Smardz, J., Martynowicz, H., Wojakowska, A., Michalek-Zrabkowska, M., Mazur, G., & Wieckiewicz, M. (2019). Correlation between sleep bruxism, stress, and depression: a polysomnographic study. Journal of Clinical Medicine, 8(9), 1344. https://doi.org/10.3390/jcm8091344