Bruxism

Bruxism is excessive teeth grinding or jaw clenching.<ref name="p930">Template:Cite book</ref> It is an oral parafunctional activity;<ref name="Wassell 2008">Template:Cite book</ref> i.e., it is unrelated to normal function such as eating or talking. Bruxism is a common behavior; the global prevalence of bruxism (both sleep and awake) is 22.22%.<ref name="auto">Template:Cite journalTemplate:Creative Commons text attribution notice </ref> Several symptoms are commonly associated with bruxism, including aching jaw muscles, headaches, hypersensitive teeth, tooth wear, and damage to dental restorations (e.g. crowns and fillings).<ref name="Tyldesley 2003" /> Symptoms may be minimal, without patient awareness of the condition. If nothing is done, after a while many teeth start wearing down until the whole tooth is gone.

There are two main types of bruxism: one occurs during sleep (nocturnal bruxism) and one during wakefulness (awake bruxism). Dental damage may be similar in both types, but the symptoms of sleep bruxism tend to be worse on waking and improve during the course of the day, and the symptoms of awake bruxism may not be present at all on waking, and then worsen over the day.

The causes of bruxism are not completely understood, but probably involve multiple factors.<ref name="Cawson 2002" /><ref name="Shetty 2010" /> Awake bruxism is more common in women, whereas men and women are affected in equal proportions by sleep bruxism.<ref name="Shetty 2010" /> Awake bruxism is thought to have different causes from sleep bruxism. Several treatments are in use, although there is little evidence of robust efficacy for any particular treatment.<ref name="LOBBEZOO 2008" /> Template:TOC limit

Epidemiology

There is a wide variation in reported epidemiologic data for bruxism, and this is largely due to differences in the definition, diagnosis and research methodologies of these studies. E.g. several studies use self-reported bruxism as a measure of bruxism, and since many people with bruxism are not aware of their habit, self-reported tooth grinding and clenching habits may be a poor measure of the true prevalence.<ref name="Shetty 2010" />

The ICSD-R states that 85–90% of the general population grind their teeth to a degree at some point during their life, although only 5% will develop a clinical condition.<ref name=ICSD-R /> Some studies have reported that awake bruxism affects females more commonly than males,<ref name="Shetty 2010" /> while in sleep bruxism, males and females are affected equally.<ref name=ICSD-R /><ref name="Macedo 2007 (cochrane rv)" />

Children are reported to brux as commonly as adults. It is possible for sleep bruxism to occur as early as the first year of life, after the first teeth (deciduous incisors) erupt into the mouth, and the overall prevalence in children is about 14–20%.<ref name="Macedo 2007 (cochrane rv)" /> The ICSD-R states that sleep bruxism may occur in over 50% of normal infants.<ref name=ICSD-R /> Often sleep bruxism develops during adolescence, and the prevalence in 18- to 29-year-olds is about 13%.<ref name="Macedo 2007 (cochrane rv)" /> The overall prevalence in adults is reported to be 8%, and people over the age of 60 are less likely to be affected, with the prevalence dropping to about 3% in this group.<ref name="Macedo 2007 (cochrane rv)" />

According to a meta-analysis conducted in 2024, the global prevalence of bruxism (both sleep and awake) is 22.22%. The global prevalence of sleep bruxism is 21%, while the prevalence of awake bruxism is 23%. The occurrence of sleep bruxism, based on polysomnography, was estimated at 43%. The highest prevalence of sleep bruxism was observed in North America at 31%, followed by South America at 23%, Europe at 21%, and Asia at 19%. The prevalence of awake bruxism was highest in South America at 30%, followed by Asia at 25% and Europe at 18%.<ref name="auto"/> The review also concluded that overall, bruxism affects males and females equally, and affects elderly people less commonly.<ref name="Manfredini 2013">Template:Cite journal</ref><ref name="auto"/>

Signs and symptoms

Most people who brux are unaware of the problem, either because there are no symptoms, or because the symptoms are not understood to be associated with a clenching and grinding problem. The symptoms of sleep bruxism are usually most intense immediately after waking, and then slowly abate, and the symptoms of a grinding habit which occurs mainly while awake tend to worsen through the day, and may not be present on waking.<ref name="Scully 2008" /> Bruxism may cause a variety of signs and symptoms, including:

File:Topviewtooth.jpg

View from above of an anterior (front) tooth showing severe tooth wear which has exposed the dentin layer (normally covered by enamel). The pulp chamber is visible through the overlying dentin. Tertiary dentin will have been laid down by the pulp in response to the loss of tooth substance. Multiple fracture lines are also visible.

• A grinding or tapping noise during sleep, sometimes detected by a partner or a parent. This noise can be surprisingly loud and unpleasant, and can wake a sleeping partner. Noises are rarely associated with awake bruxism.<ref name="Macedo 2009" />
• Other parafunctional activity which may occur together with bruxism:<ref name="Macedo 2009" /> cheek biting (which may manifest as morsicatio buccarum or linea alba),<ref name="Scully 2008" /><ref name="Heasman 2008" /> or lip biting.
• A burning sensation on the tongue (see: glossodynia),<ref name="Macedo 2009" /> possibly related to a coexistent "tongue thrusting" parafunctional activity.
• Indentations of the teeth in the tongue ("crenated tongue" or "scalloped tongue").<ref name="Heasman 2008" />
• Hypertrophy of the muscles of mastication (increase in the size of the muscles that move the jaw),<ref name="Heasman 2008">Template:Cite book</ref> particularly the masseter muscle.<ref name="Macedo 2009" /><ref name="Scully 2008" /><ref name="Kalantzis 2005">Template:Cite book</ref>
• Tenderness, pain or fatigue of the muscles of mastication,<ref name="Macedo 2009" /> which may get worse during chewing or other jaw movement.<ref name="Scully 2008" />
• Trismus (restricted mouth opening).<ref name="Macedo 2009" />
• Pain or tenderness of the temporomandibular joints,<ref name="Macedo 2009" /> which may manifest as preauricular pain (in front of the ear), or pain referred to the ear (otalgia).<ref name="medline plus">{{#invoke:citation/CS1|citation

|CitationClass=web }}</ref>

• Clicking of the temporomandibular joints.<ref name="Shetty 2010" />
• Headaches, particularly pain in the temples,<ref name="Shetty 2010" /> caused by muscle pain associated with the temporalis muscle.
• Excessive tooth wear,<ref name="Heasman 2008" /> particularly attrition, which flattens the occlusal (biting) surface, but also possibly other types of tooth wear such as abfraction, where notches form around the neck of the teeth at the gumline.<ref name="Neville 2001">Template:Cite book</ref>
• Tooth fractures,<ref name="Macedo 2009" /> and repeated failure of dental restorations (fillings, crowns, etc.).<ref name="Tyldesley 2003">Template:Cite book</ref>
• Hypersensitive teeth,<ref name="Macedo 2009" /> (e.g. dental pain when drinking a cold liquid) caused by wearing away of the thickness of insulating layers of dentin and enamel around the dental pulp.
• Inflammation of the periodontal ligament of teeth, which may make them sore to bite on, and possibly also a degree of loosening of the teeth.<ref name="Macedo 2009" />

Bruxism is usually detected because of the effects of the process (most commonly tooth wear and pain), rather than the process itself. The large forces that can be generated during bruxism can have detrimental effects on the components of masticatory system, namely the teeth, the periodontium and the articulation of the mandible with the skull (the temporomandibular joints). The muscles of mastication that act to move the jaw can also be affected since they are being utilized over and above of normal function.<ref name="Wassell 2008" />

Pain

Most people with bruxism will experience no pain.<ref name="Cawson 2002" /> The presence or degree of pain does not necessarily correlate with the severity of grinding or clenching.<ref name="Cawson 2002" /> The pain in the muscles of mastication caused by bruxism can be likened to muscle pain after exercise.<ref name="Cawson 2002" /> The pain may be felt over the angle of the jaw (masseter) or in the temple (temporalis), and may be described as a headache or an aching jaw. Most (but not all) bruxism includes clenching force provided by masseter and temporalis muscle groups; but some bruxers clench and grind front teeth only, which involves minimal action of the masseter and temporalis muscles. The temporomandibular joints themselves may also become painful, which is usually felt just in front of the ear, or inside the ear itself. Clicking of the jaw joint may also develop. The forces exerted on the teeth are more than the periodontal ligament is biologically designed to handle, and so inflammation may result. A tooth may become sore to bite on, and further, tooth wear may reduce the insulating width of enamel and dentin that protects the pulp of the tooth and result in hypersensitivity, e.g. to cold stimuli.

The relationship of bruxism with temporomandibular joint dysfunction (TMD, or temporomandibular pain dysfunction syndrome) is debated. Many suggest that sleep bruxism can be a causative or contributory factor to pain symptoms in TMD.<ref name="Tyldesley 2003" /><ref name="Shetty 2010" /><ref name="Scully 2008">Template:Cite book</ref><ref name="Glick 2003" /> Indeed, the symptoms of TMD overlap with those of bruxism.<ref name="De Meyer 1997">Template:Cite journal</ref> Others suggest that there is no strong association between TMD and bruxism.<ref name="Cawson 2002" /> A systematic review investigating the possible relationship concluded that when self-reported bruxism is used to diagnose bruxism, there is a positive association with TMD pain, and when stricter diagnostic criteria for bruxism are used, the association with TMD symptoms is much lower.<ref name="Manfredini 2010">Template:Cite journal</ref> In severe, chronic cases, bruxism can lead to myofascial pain and arthritis of the temporomandibular joints.Template:Medical citation needed

Tooth wear

Many publications list tooth wear as a consequence of bruxism, but some report a lack of a positive relationship between tooth wear and bruxism.<ref name="Shetty 2010" /> Tooth wear caused by tooth-to-tooth contact is termed attrition. This is the most usual type of tooth wear that occurs in bruxism, and affects the occlusal surface (the biting surface) of the teeth. The exact location and pattern of attrition depends on how the bruxism occurs, e.g., when the canines and incisors of the opposing arches are moved against each other laterally, by the action of the medial pterygoid muscles, this can lead to the wearing down of the incisal edges of the teeth. To grind the front teeth, most people need to posture their mandible forwards, unless there is an existing edge to edge, class III incisal relationship. People with bruxism may also grind their posterior teeth (back teeth), which wears down the cusps of the occlusal surface. Once tooth wear progresses through the enamel layer, the exposed dentin layer is softer and more vulnerable to wear and tooth decay. If enough of the tooth is worn away or decayed, the tooth will effectively be weakened, and may fracture under the increased forces that occur in bruxism.

Abfraction is another type of tooth wear that is postulated to occur with bruxism, although some still argue whether this type of tooth wear is a reality.<ref name="Neville 2001" /> Abfraction cavities are said to occur usually on the facial aspect of teeth, in the cervical region as V-shaped defects caused by flexing of the tooth under occlusal forces. It is argued that similar lesions can be caused by long-term forceful toothbrushing. However, the fact that the cavities are V-shaped does not suggest that the damage is caused by toothbrush abrasion, and that some abfraction cavities occur below the level of the gumline, i.e., in an area shielded from toothbrush abrasion, supports the validity of this mechanism of tooth wear. In addition to attrition, erosion is said to synergistically contribute to tooth wear in some bruxists, according to some sources.<ref name="Pettengill 2011">Template:Cite journal</ref>

Tooth mobility

The view that occlusal trauma (as may occur during bruxism) is a causative factor in gingivitis and periodontitis is not widely accepted.<ref name="Davies 2001">Template:Cite journal</ref> It is thought that the periodontal ligament may respond to increased occlusal (biting) forces by resorbing some of the bone of the alveolar crest, which may result in increased tooth mobility, however these changes are reversible if the occlusal force is reduced.<ref name="Davies 2001" /> Tooth movement that occurs during occlusal loading is sometimes termed fremitus.<ref name="Wassell 2008" /> It is generally accepted that increased occlusal forces are able to increase the rate of progression of pre-existing periodontal disease (gum disease), however the main stay treatment is plaque control rather than elaborate occlusal adjustments.<ref name="Davies 2001" /> It is also generally accepted that periodontal disease is a far more common cause of tooth mobility and pathological tooth migration than any influence of bruxism, although bruxism may much less commonly be involved in both.<ref name="Wassell 2008" />

Causes

File:Gray382.png

The left temporalis muscle

File:Gray383.png

The left medial pterygoid muscle, and the left lateral pterygoid muscle above it, shown on the medial surface of the mandbilar ramus, which has been partially removed along with a section of the zygomatic arch

File:Gray378 (masseter highlight).png

The left masseter muscle (red highlight), shown partially covered by superficial muscles

The muscles of mastication (the temporalis muscle, masseter muscle, medial pterygoid muscle and lateral pterygoid muscle) are paired on either side and work together to move the mandible, which hinges and slides around its dual articulation with the skull at the temporomandibular joints. Some of the muscles work to elevate the mandible (close the mouth), and others also are involved in lateral (side to side), protrusive or retractive movements. Mastication (chewing) is a complex neuromuscular activity that can be controlled either by subconscious processes or by conscious processes. In individuals without bruxism or other parafunctional activities, during wakefulness the jaw is generally at rest and the teeth are not in contact, except while speaking, swallowing or chewing. It is estimated that the teeth are in contact for less than 20 minutes per day, mostly during chewing and swallowing. Normally during sleep, the voluntary muscles are inactive due to physiologic motor paralysis, and the jaw is usually open.<ref name="Kato 2003">Template:Cite journal</ref>

Ankyloglossia is suspected as a cause of bruxism.

Some bruxism activity is rhythmic with bite force pulses of tenths of a second (like chewing), and some have longer bite force pulses of 1 to 30 seconds (clenching). Some individuals clench without significant lateral movements. Bruxism can also be regarded as a disorder of repetitive, unconscious contraction of muscles. This typically involves the masseter muscle and the anterior portion of the temporalis (the large outer muscles that clench), and the lateral pterygoids, relatively small bilateral muscles that act together to perform sideways grinding.

Multiple causes

The cause of bruxism is largely unknown, but it is generally accepted to have multiple possible causes.<ref name="Cawson 2002">Template:Cite book</ref><ref name="Shetty 2010" /><ref name="Lobbezoo 2001">Template:Cite journal</ref> Bruxism is a parafunctional activity, but it is debated whether this represents a subconscious habit or is entirely involuntary. The relative importance of the various identified possible causative factors is also debated.

Awake bruxism is thought to be usually semivoluntary, and often associated with stress caused by family responsibilities or work pressures.<ref name="Shetty 2010" /> Some suggest that in children, bruxism may occasionally represent a response to earache or teething.<ref name="mayo clinic website" /> Awake bruxism usually involves clenching<ref name="Shetty 2010" /> (sometimes the term "awake clenching" is used instead of awake bruxism),<ref name="Manfredini 2009">Template:Cite journal</ref> but also possibly grinding,<ref name="Cawson 2002" /> and is often associated with other semivoluntary oral habits such as cheek biting, nail biting, chewing on a pen or pencil absent mindedly, or tongue thrusting (where the tongue is pushed against the front teeth forcefully).<ref name="Cawson 2002" />

There is evidence that sleep bruxism is caused by mechanisms related to the central nervous system, involving sleep arousal and neurotransmitter abnormalities.<ref name="Wassell 2008" /> Underlying these factors may be psychosocial factors including daytime stress which is disrupting peaceful sleep.<ref name="Wassell 2008" /> Sleep bruxism is mainly characterized by "rhythmic masticatory muscle activity" (RMMA) at a frequency of about once per second, and also with occasional tooth grinding.<ref name="Lavigne 2007">Template:Cite journal</ref> It has been shown that the majority (86%) of sleep bruxism episodes occur during periods of sleep arousal.<ref name="Lavigne 2007" /> One study reported that sleep arousals which were experimentally induced with sensory stimulation in sleeping bruxists triggered episodes of sleep bruxism.<ref name="LOBBEZOO 2006" /> Sleep arousals are a sudden change in the depth of the sleep stage, and may also be accompanied by increased heart rate, respiratory changes and muscular activity, such as leg movements.<ref name="Shetty 2010" /> Initial reports have suggested that episodes of sleep bruxism may be accompanied by gastroesophageal reflux, decreased esophageal pH (acidity), swallowing,<ref name="LOBBEZOO 2006" /> and decreased salivary flow.<ref name="Macedo 2009" /> Another report suggested a link between episodes of sleep bruxism and a supine sleeping position (lying face up).<ref name="LOBBEZOO 2006" />

Disturbance of the dopaminergic system in the central nervous system has also been suggested to be involved in the etiology of bruxism.<ref name="Macedo 2009" /> Evidence for this comes from observations of the modifying effect of medications which alter dopamine release on bruxing activity, such as levodopa, amphetamines or nicotine. Nicotine stimulates release of dopamine, which is postulated to explain why bruxism is twice as common in smokers compared to non-smokers.<ref name="Shetty 2010" />

Historical focus

Historically, many believed that problems with the bite were the sole cause for bruxism.<ref name="Macedo 2009" /><ref name="Lobbezoo 2001"/> It was often claimed that a person would grind at the interfering area in a subconscious, instinctive attempt to wear this down and "self equiliberate" their occlusion. However, occlusal interferences are extremely common and usually do not cause any problems. It is unclear whether people with bruxism tend to notice problems with the bite because of their clenching and grinding habit, or whether these act as a causative factor in the development of the condition. In sleep bruxism especially, there is no evidence that removal of occlusal interferences has any impact on the condition.<ref name=ICSD-R /> People with no teeth at all who wear dentures can still have bruxism,<ref name="Cawson 2002" /> although dentures also often change the original bite. Most modern sources state that there is no relationship, or at most a minimal relationship, between bruxism and occlusal factors.<ref name="Shetty 2010" /><ref name="LOBBEZOO 2006" /><ref name="Glick 2003" /> The findings of one study, which used self-reported tooth grinding rather than clinical examination to detect bruxism, suggested that there may be more of a relationship between occlusal factors and bruxism in children.<ref name="Shetty 2010" /> However, the role of occlusal factors in bruxism cannot be completely discounted due to insufficient evidence and problems with the design of studies.<ref name="Shetty 2010" /> A minority of researchers continue to claim that various adjustments to the mechanics of the bite are capable of curing bruxism (see Occlusal adjustment/reorganization).

Psychosocial factors

Many studies have reported significant psychosocial risk factors for bruxism, particularly a stressful lifestyle, and this evidence is growing, but still not conclusive.<ref name="Shetty 2010" /><ref name="LOBBEZOO 2006" /><ref name="Manfredini 2009" /> Some consider emotional stress and anxiety to be the main triggering factors.<ref name="Poveda Roda 2007">Template:Cite journal</ref><ref>Template:Cite journal</ref> It has been reported that persons with bruxism respond differently to depression, hostility and stress compared to people without bruxism. Stress has a stronger relationship to awake bruxism, but the role of stress in sleep bruxism is less clear, with some stating that there is no evidence for a relationship with sleep bruxism.<ref name="Manfredini 2009" /> However, children with sleep bruxism have been shown to have greater levels of anxiety than other children.<ref name="Shetty 2010" /> People aged 50 with bruxism are more likely to be single and have a high level of education.<ref name="LOBBEZOO 2006" /> Work-related stress and irregular work shifts may also be involved.<ref name="LOBBEZOO 2006" /> Personality traits are also commonly discussed in publications concerning the causes of bruxism,<ref name="LOBBEZOO 2006" /> e.g. aggressive, competitive or hyperactive personality types.<ref name="mayo clinic website" /> Some suggest that suppressed anger or frustration can contribute to bruxism.<ref name="mayo clinic website" /> Stressful periods such as examinations, family bereavement, marriage, divorce, or relocation have been suggested to intensify bruxism. Awake bruxism often occurs during periods of concentration such as while working at a computer, driving or reading. Animal studies have also suggested a link between bruxism and psychosocial factors. Rosales et al. electrically shocked lab rats, and then observed high levels of bruxism-like muscular activity in rats that were allowed to watch this treatment compared to rats that did not see it. They proposed that the rats who witnessed the electrical shocking of other rats were under emotional stress which may have caused the bruxism-like behavior.<ref name="LOBBEZOO 2006" />

Genetic factors

Some research suggests that there may be a degree of inherited susceptibility to develop sleep bruxism.<ref name="Wassell 2008" /> 21–50% of people with sleep bruxism have a direct family member who had sleep bruxism during childhood, suggesting that there are genetic factors involved,<ref name="Macedo 2007 (cochrane rv)">Template:Cite journal</ref> although no genetic markers have yet been identified.<ref name="Wassell 2008" /> Offspring of people who have sleep bruxism are more likely to also have sleep bruxism than children of people who do not have bruxism, or people with awake bruxism rather than sleep bruxism.<ref name=ICSD-R />

Medications

Certain stimulant drugs, including both prescribed and recreational drugs, are thought by some to cause the development of bruxism.<ref name="Wassell 2008" /> However, others argue that there is insufficient evidence to draw such a conclusion.<ref name="Winocur 2003">Template:Cite journal</ref> Examples may include dopamine agonists, dopamine antagonists, tricyclic antidepressants, selective serotonin reuptake inhibitors, alcohol, cocaine, and amphetamines (including those taken for medical reasons).<ref name="Scully 2008" /> In some reported cases where bruxism is thought to have been initiated by selective serotonin reuptake inhibitors, decreasing the dose resolved the side effect.<ref name="Glick 2003" /> Other sources state that reports of selective serotonin reuptake inhibitors causing bruxism are rare, or only occur with long-term use.<ref name="Buescher 2007" /><ref name="LOBBEZOO 2006" />

Specific examples include levodopa (when used in the long term, as in Parkinson's disease), fluoxetine, metoclopramide, lithium, cocaine, venlafaxine, citalopram, fluvoxamine, methylenedioxyamphetamine (MDA), methylphenidate (used in attention deficit hyperactive disorder),<ref name="Winocur 2003" /> and gamma-hydroxybutyric acid (GHB) and similar gamma-aminobutyric acid-inducing analogues such as phenibut.<ref name="Winocur 2003" /> Bruxism can also be exacerbated by excessive consumption of caffeine,<ref name="Winocur 2003" /> as in coffee, tea or chocolate. Bruxism has also been reported to occur commonly comorbid with drug addiction.<ref name="LOBBEZOO 2006" /> Methylenedioxymethamphetamine (MDMA, ecstasy) has been reported to be associated with bruxism,<ref name="Winocur 2003" /> which occurs immediately after taking the drug and for several days afterwards. Tooth wear in people who take ecstasy is also frequently much more severe than in people with bruxism not associated with ecstasy.

Occlusal factors

Occlusion is defined most simply as "contacts between teeth",<ref name="Davies 2001B">Template:Cite journal</ref> and is the meeting of teeth during biting and chewing. The term does not imply any disease. Malocclusion is a medical term referring to less than ideal positioning of the upper teeth relative to the lower teeth, which can occur both when the upper jaw is ideally proportioned to the lower jaw, or where there is a discrepancy between the size of the upper jaw relative to the lower jaw. Malocclusion of some sort is so common that the concept of an "ideal occlusion" is called into question, and it can be considered "normal to be abnormal".<ref name="Wassell 2008" /> An occlusal interference may refer to a problem which interferes with the normal path of the bite, and is usually used to describe a localized problem with the position or shape of a single tooth or group of teeth. A premature contact is one part of the bite meeting sooner than other parts, meaning that the rest of the teeth meet later or are held open, e.g., a new dental restoration on a tooth (e.g., a crown) which has a slightly different shape or position to the original tooth may contact too soon in the bite. A deflective contact/interference is an interference with the bite that changes the normal path of the bite. A common example of a deflective interference is an over-erupted upper wisdom tooth, often because the lower wisdom tooth has been removed or is impacted. In this example, when the jaws are brought together, the lower back teeth contact the prominent upper wisdom tooth before the other teeth, and the lower jaw has to move forward to allow the rest of the teeth to meet. The difference between a premature contact and a deflective interference is that the latter implies a dynamic abnormality in the bite.

Possible associations

Several associations between bruxism and other conditions, usually neurological or psychiatric disorders, have rarely been reported, with varying degrees of evidence (often in the form of case reports).<ref name="Wassell 2008" /><ref name="LOBBEZOO 2006" /> Examples include:

• Acrodynia<ref name="Neville 2001" />
• Atypical facial pain<ref name=ICSD-R />
• Autism<ref name="Jaganathan 2014 p. ">Template:Cite journal</ref><ref name="l850">Template:Cite book</ref>
• Cerebral palsy<ref name="Cawson 2002" /><ref name="Heasman 2008" />
• Disturbed sleep patterns and other sleep disorders, such as obstructive sleep apnea,<ref name="LOBBEZOO 2006" /> snoring,<ref name="LOBBEZOO 2006" /> moderate daytime sleepiness,Template:Medical citation needed and insomnia<ref name="medline plus" />
• Down syndrome<ref name="Cawson 2002" />
• Dyskinesias<ref name="Scully 2008" />
• Developmental delay or developmental disability<ref name="l850"/>
• Epilepsy<ref name="LOBBEZOO 2006" />
• Eustachian tube dysfunctionTemplate:Medical citation needed
• Infarction in the basal ganglia<ref name="LOBBEZOO 2006" />
• Intellectual disability, particularly in children<ref name=ICSD-R />
• Leigh disease<ref name="LOBBEZOO 2006" />
• Meningococcal septicaemia<ref name="LOBBEZOO 2006" />
• Multiple system atrophy<ref name="LOBBEZOO 2006" />
• Oromandibular dystonia<ref name="Persaud 2013" />
• Parkinson's diseases,<ref name="mayo clinic website">{{#invoke:citation/CS1|citation

|CitationClass=web }}</ref> (possibly due to long-term therapy with levodopa causing dopaminergic dysfunction)<ref name="Macedo 2009" />

• Rett syndrome<ref name="Scully 2008" />
• Torus mandibularis<ref name="Neville 2001" /> and buccal exostosis<ref name="Mehra2015">Template:Cite book</ref>
• Trauma,<ref name="LOBBEZOO 2006">Template:Cite journal</ref> e.g. brain injury or coma<ref name="Macedo 2009" />

Diagnosis

Early diagnosis of bruxism is advantageous, but difficult. Early diagnosis can prevent damage that may be incurred and the detrimental effect on quality of life.<ref name="Shetty 2010" /> A diagnosis of bruxism is usually made clinically,<ref name="Kalantzis 2005" /> and is mainly based on the person's history (e.g. reports of grinding noises) and the presence of typical signs and symptoms, including tooth mobility, tooth wear, masseteric hypertrophy, indentations on the tongue, hypersensitive teeth (which may be misdiagnosed as reversible pulpitis), pain in the muscles of mastication, and clicking or locking of the temporomandibular joints.<ref name="Shetty 2010" /> Questionnaires can be used to screen for bruxism in both the clinical and research settings.<ref name="Shetty 2010" />

For tooth grinders who live in a household with other people, diagnosis of grinding is straightforward: Housemates or family members would advise a bruxer of recurrent grinding. Grinders who live alone can likewise resort to a sound-activated tape recorder. To confirm the condition of clenching, on the other hand, bruxers may rely on such devices as the Bruxchecker,<ref>Template:Cite journal</ref> Bruxcore,<ref name="Shetty 2010" /> or a beeswax-bearing biteplate.<ref name=":2">Template:Cite journal</ref>

The Individual (personal) Tooth-Wear Index was developed to objectively quantify the degree of tooth wear in an individual, without being affected by the number of missing teeth.<ref name="Shetty 2010" /> Bruxism is not the only cause of tooth wear. Another possible cause of tooth wear is acid erosion, which may occur in people who drink a lot of acidic liquids such as concentrated fruit juice, or in people who frequently vomit or regurgitate stomach acid, which itself can occur for various reasons. People also demonstrate a normal level of tooth wear, associated with normal function. The presence of tooth wear only indicates that it had occurred at some point in the past, and does not necessarily indicate that the loss of tooth substance is ongoing. People who clench and perform minimal grinding will also not show much tooth wear. Occlusal splints are usually employed as a treatment for bruxism, but they can also be of diagnostic use, e.g. to observe the presence or absence of wear on the splint after a certain period of wearing it at night.<ref name="Shetty 2010" />

The most usual trigger in sleep bruxism that leads a person to seek medical or dental advice is being informed by a sleeping partner of unpleasant grinding noises during sleep.<ref name=ICSD-R /> The diagnosis of sleep bruxism is usually straightforward, and involves the exclusion of dental diseases, temporomandibular disorders, and the rhythmic jaw movements that occur with seizure disorders (e.g. epilepsy).<ref name=ICSD-R /> This usually involves a dental examination, and possibly electroencephalography if a seizure disorder is suspected.<ref name=ICSD-R /> Polysomnography shows increased masseter and temporalis muscular activity during sleep.<ref name=ICSD-R /> Polysomnography may involve electroencephalography, electromyography, electrocardiography, air flow monitoring and audio–video recording. It may be useful to help exclude other sleep disorders; however, due to the expense of the use of a sleep lab, polysomnography is mostly of relevance to research rather than routine clinical diagnosis of bruxism.<ref name="Shetty 2010" />

Tooth wear may be brought to the person's attention during routine dental examination. With awake bruxism, most people will often initially deny clenching and grinding because they are unaware of the habit. Often, the person may re-attend soon after the first visit and report that they have now become aware of such a habit.

Several devices have been developed that aim to objectively measure bruxism activity, either in terms of muscular activity or bite forces. They have been criticized for introducing a possible change in the bruxing habit, whether increasing or decreasing it, and are therefore poorly representative to the native bruxing activity.<ref name="Shetty 2010" /> These are mostly of relevance to research, and are rarely used in the routine clinical diagnosis of bruxism. Examples include the "Bruxcore Bruxism-Monitoring Device" (BBMD, "Bruxcore Plate"), the "intra-splint force detector" (ISFD), and electromyographic devices to measure masseter or temporalis muscle activity (e.g. the "BiteStrip", and the "Grindcare").<ref name="Shetty 2010" />

ICSD-R diagnostic criteria

The ICSD-R listed diagnostic criteria for sleep bruxism.<ref name=ICSD-R /> The minimal criteria include both of the following:

• A. symptom of tooth-grinding or tooth-clenching during sleep, and
• B. One or more of the following:
  • Abnormal tooth wear
  • Grinding sounds
  • Discomfort of the jaw muscles

With the following criteria supporting the diagnosis:

• C. polysomnography shows both:
  • Activity of jaw muscles during sleep
  • No associated epileptic activity
• D. No other medical or mental disorders (e.g., sleep-related epilepsy, which may cause abnormal movement during sleep).
• E. The presence of other sleep disorders (e.g., obstructive sleep apnea syndrome).

Definition examples

Bruxism is derived from the Greek word {{#invoke:Lang|lang}} (brykein) "to bite, or to gnash, grind the teeth".<ref>Template:Cite encyclopedia</ref><ref>Template:OEtymD</ref><ref>Template:LSJ.</ref> People with bruxism are called bruxists or bruxers and the verb itself is "to brux". There is no widely accepted definition of bruxism.<ref name="LOBBEZOO 2006" /> Examples of definitions include:

"Bruxism is a repetitive jaw-muscle activity characterized by clenching or grinding of the teeth and/or by bracing or thrusting of the mandible. Bruxism has two distinct circadian manifestations: it can occur during sleep (indicated as sleep bruxism) or during wakefulness (indicated as awake bruxism)."<ref>Template:Cite journal</ref>{{#if:|{{#if:|}}

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Classification by temporal pattern

Comparison of typical features of sleep bruxism and awake bruxism.<ref name="Manfredini 2013" /><ref name="Shetty 2010" /><ref name="Macedo 2009" />

	Sleep bruxism	Awake bruxism
Occurrence	While asleep, mostly during periods of sleep arousal	While awake
Time–intensity relationship	Pain worst on waking, then slowly gets better	Pain worsens throughout the day, may not be present on waking
Noises	Commonly associated	Rarely associated
Activity	Clenching and grinding	Usually clenching, occasionally clenching and grinding
Relationship with stress	Unclear, little evidence of a relationship	Stronger evidence for a relationship, but not conclusive
Prevalence (general population)	9.7–15.9%	22.1–31%
Gender distribution	Equal gender distribution	Mostly females
Heritability	Some evidence	Unclear

Bruxism can be subdivided into two types based upon when the parafunctional activity occurs – during sleep ("sleep bruxism"), or while awake ("awake bruxism").<ref name="Macedo 2009">Template:Cite journal</ref> This is the most widely used classification since sleep bruxism generally has different causes to awake bruxism, although the effects on the condition on the teeth may be the same.<ref name="ICSD-R" /> The treatment is also often dependent upon whether the bruxism happens during sleep or while awake, e.g., an occlusal splint worn during sleep in a person who only bruxes when awake will probably have no benefit.<ref name="Cawson 2002" /> Some have even suggested that sleep bruxism is an entirely different disorder and is not associated with awake bruxism.<ref name="Macedo 2009" /> Awake bruxism is sometimes abbreviated to AB,<ref name="Shetty 2010">Template:Cite journal</ref> and is also termed "diurnal bruxism",<ref name="Shetty 2010" /> DB, or "daytime bruxing". Sleep bruxism is sometimes abbreviated to SB,<ref name="Shetty 2010" /> and is also termed "sleep-related bruxism",<ref name="ICSD-R" /> "nocturnal bruxism",<ref name="ICSD-R" /> or "nocturnal tooth grinding".<ref name="ICSD-R" /> According to the International Classification of Sleep Disorders revised edition (ICSD-R), the term "sleep bruxism" is the most appropriate since this type occurs during sleep specifically rather than being associated with a particular time of day, i.e., if a person with sleep bruxism were to sleep during the day and stay awake at night then the condition would not occur during the night but during the day.<ref name="ICSD-R">{{#invoke:citation/CS1|citation |CitationClass=web }}</ref> The ICDS-R defined sleep bruxism as "a stereotyped movement disorder characterized by grinding or clenching of the teeth during sleep",<ref name="ICSD-R" /> classifying it as a parasomnia. The second edition (ICSD-2) however reclassified bruxism to a "sleep related movement disorder" rather than a parasomnia.<ref name="Macedo 2009" />

Classification by cause

Alternatively, bruxism can be divided into primary bruxism (also termed "idiopathic bruxism"), where the disorder is not related to any other medical condition, or secondary bruxism, where the disorder is associated with other medical conditions.<ref name="Macedo 2009" /> Secondary bruxism includes iatrogenic causes, such as the side effect of prescribed medications. Another source divides the causes of bruxism into three groups, namely central or pathophysiological factors, psychosocial factors and peripheral factors.<ref name="Shetty 2010" /> The World Health Organization's International Classification of Diseases 10th revision does not have an entry called bruxism, instead listing "tooth grinding" under somatoform disorders.<ref>{{#invoke:citation/CS1|citation |CitationClass=web }}</ref> To describe bruxism as a purely somatoform disorder does not reflect the mainstream, modern view of this condition (see causes).

Classification by severity

The ICSD-R described three different severities of sleep bruxism, defining mild as occurring less than nightly, with no damage to teeth or psychosocial impairment; moderate as occurring nightly, with mild impairment of psychosocial functioning; and severe as occurring nightly, and with damage to the teeth, temporomandibular disorders and other physical injuries, and severe psychosocial impairment.<ref name=ICSD-R />

Classification by duration

The ICSD-R also described three different types of sleep bruxism according to the duration the condition is present, namely acute, which lasts for less than one week; subacute, which lasts for more than a week and less than one month; and chronic which lasts for over a month.<ref name=ICSD-R />

Management

Treatment for bruxism revolves around repairing the damage to teeth that has already occurred, and also often, via one or more of several available methods, attempting to prevent further damage and manage symptoms, but there is no widely accepted, best treatment. Since bruxism is not life-threatening,<ref name="Shetty 2010" /> and there is little evidence of the efficacy of any treatment,<ref name="LOBBEZOO 2008">Template:Cite journal</ref> it has been recommended that only conservative treatment which is reversible and that carries low risk of morbidity should be used.<ref name="Cawson 2002" /> The main treatments that have been described in awake and sleep bruxism are described below.

Psychosocial interventions

Given the strong association between awake bruxism and psychosocial factors (the relationship between sleep bruxism and psychosocial factors being unclear), the role of psychosocial interventions could be argued to be central to the management. The most simple form of treatment is therefore reassurance that the condition does not represent a serious disease, which may act to alleviate contributing stress.<ref name="Cawson 2002" />

Sleep hygiene education should be provided by the clinician, as well as a clear and short explanation of bruxism (definition, causes and treatment options).<ref>Template:Citation</ref> Relaxation and tension-reduction have not been found to reduce bruxism symptoms, but have given patients a sense of well-being.<ref>Template:Cite journal</ref> One study has reported less grinding and reduction of EMG activity after hypnotherapy.<ref>Template:Cite journal</ref>

Other interventions include relaxation techniques, stress management, behavioural modification, habit reversal and hypnosis (self hypnosis or with a hypnotherapist).<ref name="Cawson 2002" /> Cognitive behavioral therapy has been recommended by some for treatment of bruxism.<ref name="van der Meulen 2000">Template:Cite journal</ref> In many cases awake bruxism can be reduced by using reminder techniques. Combined with a protocol sheet this can also help to evaluate in which situations bruxism is most prevalent.<ref>{{#invoke:citation/CS1|citation |CitationClass=web }}</ref>

Medication

Many different medications have been used to treat bruxism,<ref name="Macedo 2009" /> including benzodiazepines, anticonvulsants, beta blockers, dopamine agents, antidepressants, muscle relaxants, and others. However, there is little, if any, evidence for their respective and comparative efficacies with each other and when compared to a placebo.Template:Citation needed A multiyear systematic review to investigate the evidence for drug treatments in sleep bruxism published in 2014 (Pharmacotherapy for Sleep Bruxism. Macedo, et al.) found "insufficient evidence on the effectiveness of pharmacotherapy for the treatment of sleep bruxism."<ref>Macedo CR, Macedo EC, Torloni MR, Silva AB, Prado GF. Pharmacotherapy for sleep bruxism. Cochrane Database of Systematic Reviews 2014, Issue 10. Art. No.: CD005578. DOI: 10.1002/14651858.CD005578.pub2.</ref>

Specific drugs that have been studied in sleep bruxism are clonazepam,<ref name=Machado2011>Template:Cite journal</ref> levodopa,<ref name=Machado2011/> amitriptyline,<ref name=Machado2011/> bromocriptine,<ref name=Machado2011/> pergolide, clonidine, propranolol, and l-tryptophan, with some showing no effect and others appear to have promising initial results; however, it has been suggested that further safety testing is required before any evidence-based clinical recommendations can be made.<ref name="Macedo 2009" /> When bruxism is related to the use of selective serotonin reuptake inhibitors in depression, adding buspirone has been reported to resolve the side effect.<ref name="Glick 2003" /> Tricyclic antidepressants have also been suggested to be preferable to selective serotonin reuptake inhibitors in people with bruxism, and may help with the pain.<ref name="Buescher 2007">Template:Cite journal</ref>

Prevention of dental damage

Bruxism can cause significant tooth wear if it is severe, and sometimes dental restorations (crowns, fillings etc.) are damaged or lost, sometimes repeatedly.<ref name="Wassell 2008" /><ref name="Tyldesley 2003" /> Most dentists therefore prefer to keep dental treatment in people with bruxism very simple and only carry it out when essential, since any dental work is likely to fail in the long term.<ref name="Wassell 2008" /> Dental implants, dental ceramics such as Emax crowns<ref>Template:Cite journal</ref> and complex bridgework for example are relatively contraindicated in bruxists.<ref name="Wassell 2008" /> In the case of crowns, the strength of the restoration becomes more important, sometimes at the cost of aesthetic considerations. E.g. a full coverage gold crown, which has a degree of flexibility and also involves less removal (and therefore less weakening) of the underlying natural tooth may be more appropriate than other types of crown which are primarily designed for esthetics rather than durability. Porcelain veneers on the incisors are particularly vulnerable to damage, and sometimes a crown can be perforated by occlusal wear.<ref name="Wassell 2008" />

Occlusal splints (also termed dental guards) are commonly prescribed, mainly by dentists and dental specialists, as a treatment for bruxism. Proponents of their use claim many benefits, however when the evidence is critically examined in systematic reviews of the topic, it is reported that there is insufficient evidence to show that occlusal splints are effective for sleep bruxism<ref name="MacedoSilva2007">Template:Cite journal</ref> as well as bruxism overall.<ref name="Hardy Bonsor 2021 p=103621">Template:Cite journal</ref> Furthermore, occlusal splints are probably ineffective for awake bruxism,<ref name="Cawson 2002" /> since they tend to be worn only during sleep. However, occlusal splints may be of some benefit in reducing the tooth wear that may accompany bruxism,<ref name="MacedoSilva2007"/> but by mechanically protecting the teeth rather than reducing the bruxing activity itself. In a minority of cases, sleep bruxism may be made worse by an occlusal splint. Some patients will periodically return with splints with holes worn through them, either because the bruxism is aggravated, or unaffected by the presence of the splint. When tooth-to-tooth contact is possible through the holes in a splint, it is offering no protection against tooth wear and needs to be replaced.

Occlusal splints are divided into partial or full-coverage splints according to whether they fit over some or all of the teeth. They are typically made of plastic (e.g. acrylic) and can be hard or soft. A lower appliance can be worn alone, or in combination with an upper appliance. Usually lower splints are better tolerated in people with a sensitive gag reflex. Another problem with wearing a splint can be stimulation of salivary flow, and for this reason some advise to start wearing the splint about 30 mins before going to bed so this does not lead to difficulty falling asleep. As an added measure for hypersensitive teeth in bruxism, desensitizing toothpastes (e.g. containing strontium chloride) can be applied initially inside the splint so the material is in contact with the teeth all night. This can be continued until there is only a normal level of sensitivity from the teeth, although it should be remembered that sensitivity to thermal stimuli is also a symptom of pulpitis, and may indicate the presence of tooth decay rather than merely hypersensitive teeth.

Splints may also reduce muscle strain by allowing the upper and lower jaw to move easily with respect to each other. Treatment goals include: constraining the bruxing pattern to avoid damage to the temporomandibular joints; stabilizing the occlusion by minimizing gradual changes to the positions of the teeth, preventing tooth damage and revealing the extent and patterns of bruxism through examination of the markings on the splint's surface. A dental guard is typically worn during every night's sleep on a long-term basis. However, a meta-analysis of occlusal splints (dental guards) used for this purpose concluded "There is not enough evidence to state that the occlusal splint is effective for treating sleep bruxism."<ref>Template:Cite journal</ref>

A repositioning splint is designed to change the patient's occlusion, or bite.Template:Medical citation needed The efficacy of such devices is debated. Some writers propose that irreversible complications can result from the long-term use of mouthguards and repositioning splints. Random controlled trials with these type devices generally show no benefit over other therapies.<ref>Template:Cite book</ref><ref>Template:Cite journal</ref><ref name="Widmalm 1999">Template:Cite journal</ref> Another partial splint is the nociceptive trigeminal inhibition tension suppression system (NTI-TSS) dental guard. This splint snaps onto the front teeth only. It is theorized to prevent tissue damages primarily by reducing the bite force from attempts to close the jaw normally into a forward twisting of the lower front teeth. The intent is for the brain to interpret the nerve sensations as undesirable, automatically and subconsciously reducing clenching force. However, there may be potential for the NTI-TSS device to act as a Dahl appliance, holding the posterior teeth out of occlusion and leading to their over-eruption, deranging the occlusion (i.e. it may cause the teeth to move position). This is far more likely if the appliance is worn for excessive periods of time, which is why NTI type appliances are designed for night time use only, and ongoing follow-ups are recommended.Template:Citation needed

A mandibular advancement device (normally used for treatment of obstructive sleep apnea) may reduce sleep bruxism, although its use may be associated with discomfort.<ref name="Huynh 2007">Template:Cite journal</ref>

Botulinum toxin

Botulinum neurotoxin (BoNT) is used as a treatment for bruxism.<ref name="Buescher 2007" /> A 2020 overview of systematic reviews found that botulinum toxin type A (BTX-A) showed a significant pain and sleep bruxism frequency reduction when compared to placebo or conventional treatment (behavioral therapy, occlusal splints, and drugs), after 6 and 12 months.<ref name="Bussadori Motta Horliana Santos 2020 pp. 2413–2421">Template:Cite journal</ref>

Botulinum toxin causes muscle paralysis/atrophy by inhibition of acetylcholine release at neuromuscular junctions.<ref name="Glick 2003">Template:Cite book</ref> BoNT injections are used in bruxism on the theory that a dilute solution of the toxin will partially paralyze the muscles and lessen their ability to forcefully clench and grind the jaw, while aiming to retain enough muscular function to enable normal activities such as talking and eating. This treatment typically involves five or six injections into the masseter and temporalis muscles, and less often into the lateral pterygoids (given the possible risk of decreasing the ability to swallow) taking a few minutes per side. The effects may be noticeable by the next day, and they may last for about three months. Occasionally, adverse effects may occur, such as bruising, but this is quite rare. The dose of toxin used depends upon the person, and a higher dose may be needed in people with stronger muscles of mastication. With the temporary and partial muscle paralysis, atrophy of disuse may occur, meaning that the future required dose may be smaller or the length of time the effects last may be increased.Template:Citation needed

Biofeedback

Biofeedback is a process or device that allows an individual to become aware of, and alter physiological activity with the aim of improving health. Although the evidence of biofeedback has not been tested for awake bruxism, there is recent evidence for the efficacy of biofeedback in the management of nocturnal bruxism in small control groups.<ref name="Shetty 2010" /><ref name="Efficacy of biofeedback therapy">Template:Cite journal</ref> Electromyographic monitoring devices of the associated muscle groups tied with automatic alerting during periods of clenching and grinding have been prescribed for awake bruxism. Dental appliances with capsules that break and release a taste stimulus when enough force is applied have also been described in sleep bruxism, which would wake the person from sleep in an attempt to prevent bruxism episodes.<ref name=":0" /> "Large scale, double-blind, experiment confirming the effectiveness of this approach have yet to be carried out."<ref name=":2" />

Occlusal adjustment/reorganization

As an alternative to simply reactively repairing the damage to teeth and conforming to the existing occlusal scheme, occasionally some dentists will attempt to reorganize the occlusion in the belief that this may redistribute the forces and reduce the amount of damage inflicted on the dentition. Sometimes termed "occlusal rehabilitation" or "occlusal equilibration",<ref name="Shetty 2010" /> this can be a complex procedure, and there is much disagreement between proponents of these techniques on most of the aspects involved, including the indications and the goals. It may involve orthodontics, restorative dentistry or even orthognathic surgery. Some have criticized these occlusal reorganizations as having no evidence base, and irreversibly damaging the dentition on top of the damage already caused by bruxism.<ref name="Shetty 2010" />

History

Two thousand years ago, Shuowen Jiezi by Xu Shen documented the definition of Chinese character "齘" (bruxism) as "the clenching of teeth" (齒相切也).<ref>Template:Cite wikisource</ref> In 610, Zhubing yuanhou lun by Chao Yuanfang documented the definition of bruxism (齘齒) as "the clenching of teeth during sleep" and explained that it was caused by Qi deficiency and blood stasis.<ref>Template:Cite wikisource</ref> In 978, Taiping Shenghuifang by Wang Huaiyin gave a similar explanation and three prescriptions for treatment.<ref>{{#invoke:citation/CS1|citation |CitationClass=web }}</ref><ref>Template:Cite wikisource</ref>

"La bruxomanie" (a French term, translates to bruxomania) was suggested by Marie Pietkiewics in 1907.<ref name="Shetty 2010" /> In 1931, Frohman first coined the term bruxism.<ref name="Macedo 2009" /> Occasionally recent medical publications will use the word bruxomania with bruxism, to denote specifically bruxism that occurs while awake; however, this term can be considered historical and the modern equivalent would be awake bruxism or diurnal bruxism. It has been shown that the type of research into bruxism has changed over time. Overall between 1966 and 2007, most of the research published was focused on occlusal adjustments and oral splints. Behavioral approaches in research declined from over 60% of publications in the period 1966–86 to about 10% in the period 1997–2007.<ref name="LOBBEZOO 2008" /> In the 1960s, a periodontist named Sigurd Peder Ramfjord championed the theory that occlusal factors were responsible for bruxism.<ref name=Behr2011>Template:Cite journal</ref> Generations of dentists were educated by this ideology in the prominent textbook on occlusion of the time, however therapy centered around removal of occlusal interference remained unsatisfactory. The belief among dentists that occlusion and bruxism are strongly related is still widespread, however the majority of researchers now disfavor malocclusion as the main etiologic factor in favor of a more multifactorial, biopsychosocial model of bruxism.

Society and culture

Template:See also Clenching the teeth is generally displayed by humans and other animals as a display of anger, hostility or frustration. It is thought that in humans, clenching the teeth may be an evolutionary instinct to display teeth as weapons, thereby threatening a rival or a predator. The phrase "to grit one's teeth" is the grinding or clenching of the teeth in anger, or to accept a difficult or unpleasant situation and deal with it in a determined way.<ref>{{#invoke:citation/CS1|citation |CitationClass=web }}</ref>

In the Bible there are several references to "gnashing of teeth" in both the Old Testament,<ref>Template:Cite journal</ref> and the New Testament, where the phrase "weeping and gnashing of teeth" appears no less than 7 times in Matthew alone.

A Chinese proverb has linked bruxism with psychosocial factors. "If a boy clenches, he hates his family for not being prosperous; if a girl clenches, she hates her mother for not being dead."(男孩咬牙，恨家不起；女孩咬牙，恨妈不死。)<ref>Template:Cite journal</ref>

In David Lynch's 1977 film Eraserhead, Henry Spencer's partner ("Mary X") is shown tossing and turning in her sleep, and snapping her jaws together violently and noisily, depicting sleep bruxism. In Stephen King's 1988 novel The Tommyknockers, the sister of central character Bobbi Anderson also had bruxism. In the 2000 film Requiem for a Dream, the character of Sara Goldfarb (Ellen Burstyn) begins taking an amphetamine-based diet pill and develops bruxism. In the 2005 film Beowulf & Grendel, a modern reworking of the Anglo-Saxon poem Beowulf, Selma the witch tells Beowulf that the troll's name Grendel means "grinder of teeth", stating that "he has bad dreams", a possible allusion to Grendel traumatically witnessing the death of his father as a child, at the hands of King Hrothgar. The Geats (the warriors who hunt the troll) alternatively translate the name as "grinder of men's bones" to demonize their prey. In George R. R. Martin's A Song of Ice and Fire series, King Stannis Baratheon grinds his teeth regularly, so loudly it can be heard "half a castle away".

In rave culture, recreational use of ecstasy is often reported to cause bruxism. Among people who have taken ecstasy, while dancing it is common to use pacifiers, lollipops or chewing gum in an attempt to reduce the damage to the teeth and to prevent jaw pain.<ref name=CESAR>{{#invoke:citation/CS1|citation |CitationClass=web }}</ref> Bruxism is thought to be one of the contributing factors in "meth mouth", a condition potentially associated with long term methamphetamine use.<ref>Template:Cite journal</ref>