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|Classification and external resources|
Attrition (tooth wear caused by tooth to tooth contact) can be a manifestation of bruxism.
Bruxism refers to excessive grinding of teeth and/or excessive clenching of the jaw. Bruxism is an oral parafunctional activity, that is to say, it is not activity related to normal function such as eating or talking. Bruxism is a common problem, with some sources stating 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. Bruxism may cause minimal symptoms, and therefore people may not be aware of the condition. Several symptoms are commonly associated, including hypersensitive teeth, aching jaw muscles and headaches. Bruxism may also cause tooth wear, or even cause teeth to break and dental restorations (e.g. crowns and fillings) to be repeatedly lost or damaged.
There are two main types of bruxism, namely bruxism which occurs during sleep (sleep bruxism) and bruxism which occurs during wakefulness (awake bruxism). The damage to the teeth is similar in both types, but the symptoms of sleep bruxism are usually worst upon waking and then slowly get better over the day, and the symptoms of awake bruxism may not be present at all upon waking, and then slowly get worse over the day. The causes of bruxism are not totally understood, but probably involves multiple factors. Awake bruxism is thought to have different causes to sleep bruxism, and is more common in females whereas males and females are affected in equal proportions by sleep bruxism. There are several treatments in use, although there is very little evidence for any particular treatment in the management of bruxism.
Bruxism is derived from the Greek word βρυγμός (brygmós), meaning "gnashing of teeth". People who suffer with bruxism may also be called "bruxists", and the act itself "to brux". There is no widely accepted definition of bruxism, but some suggested definitions include:
"Non-functional contact of the mandibular and maxillary teeth resulting in clenching or tooth grinding due to repetitive, unconscious contraction of the masseter and temporalis muscles."
"Parafunctional grinding of teeth or an oral habit consisting of involuntary rhythmic or spasmodic non functional gnashing, grinding or clenching of teeth in other than chewing movements of the mandible which may lead to occlusal trauma."
"Periodic repetitive clenching or rhythmic forceful grinding of the teeth."
Classification by temporal pattern 
|Sleep bruxism||Awake bruxism|
|Pattern||Whilst asleep, mostly during periods of sleep arousals||Whilst awake|
|Pain pattern||Worst upon waking, then slowly gets better||Gets worse throughout the day, may not be present upon waking|
|Noises||Commonly associated||Rarely associated|
|Bruxing pattern||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|
|Gender distribution||Equal gender distribution||Mostly females|
Bruxism can be subdivided into two types based upon when the parafunctional activity occurs - during sleep ("sleep bruxism"), or whilst awake ("awake bruxism"). This distinction is most widely referred to since sleep bruxism generally has different causes to awake bruxism, although the affects of condition on the teeth may be the same. The treatment is also often dependent upon whether the bruxism happens during sleep or whilst awake. E.g., an occlusal splint worn during sleep in a person who only bruxes when they are awake will probably have no benefit. Some have even suggested that sleep bruxism is an entirely different disorder and is not associated with awake bruxism. Awake bruxism is sometimes abbreviated to AB, and is also termed "diurnal bruxism", DB, or "daytime bruxing". Sleep bruxism is sometimes abbreviated to SB, and is also termed "sleep-related bruxism", "nocturnal bruxism", or "nocturnal tooth grinding". 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. The ICDS-R defined sleep bruxism as "a stereotyped movement disorder characterized by grinding or clenching of the teeth during sleep", classifying it as a parasomnia. The second edition (ICSD-2) however reclassified bruxism to a "sleep related movement disorder" rather than a parasomnia.
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. Secondary bruxism includes iatrogenic causes, such as the side effect of prescribed medications. Another source divides the causes of bruxism into 3 groups, namely central or pathophysiological factors, psychosocial factors and peripheral factors. 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. 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 occuring nightly, and with damage to the teeth, tempormandibular disorders and other physical injuries, and severe psychosocial impairment.
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 1 week; subacute, which lasts for more than a week and less than a month; and chronic which lasts for over a month.
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 get better, and the symptoms of a bruxing habit which occurs mainly while awake tend to slowly get worse throughout the day, and may not be present upon waking. Bruxism may cause a variety of signs and symptoms, including:
- Excessive tooth wear, 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.
- Tooth fractures, and repeated failure of dental restorations (fillings, crowns, etc.).
- Hypersensitive teeth, (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.
- A grinding 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.
- Cheek biting (which may manifest as morsicatio buccarum and/or linea alba), and/or lip biting, (other parafunctional activity which may occur together with bruxism).
- A burning sensation on the tongue (see: glossodynia), possibly related to a coexistent "tongue thrusting" parafunctional activity.
- Indentations of the teeth in the tongue ("crenated tongue" or "scalloped tongue").
- Hypertrophy of the muscles of mastication (increase in the size of the muscles that move the jaw), particularly the masseter muscle.
- Tenderness, pain or fatigue of the muscles of mastication, which may get worse during chewing or other jaw movement.
- Trismus (restricted mouth opening).
- Pain or tenderness of the temporomandibular joints, which may manifest as preauricular pain (infront of the ear), or pain referred to the ear (otalgia).
- Clicking of the temporomandibular joints.
- Headaches, particularly pain in the temples, (caused by muscle pain associated with the temporalis muscle).
The muscles of mastication (the temporalis, masseter, medial and lateral pterygoid muscles) 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. Whilst awake, and at times other than speaking, swalling or chewing, the jaw is generally at rest and the teeth are not in contact. Normally during sleep, the voluntary muscles are inactive due to physiologic motor paralysis, and the jaw is usually open.
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.
The cause of bruxism is largely unknown, but it is generally accepted to have multiple possible causes. Bruxism is a parafunctional activity, but it is debated whether this represents a subconscious habit or is entirely involuntary.
Awake bruxism is thought to be usually semivoluntary, and often associated with stress caused by family responsibilities or work pressures. Some suggest that in children, bruxism may occasionally represent a response to earache or teething. Awake bruxism usually involves clenching, (sometimes the term "awake clenching" is used instead of awake bruxism), but also possibly grinding, 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 trusting (where the tongue is pushed against the front teeth forcefully).
There is evidence that sleep bruxism is caused by mechanisms related to the central nervous system, involving sleep arousal and neurotransmitter abnormalities. Underlying these factors may be psychosocial factors including daytime stress which is disrupting peaceful sleep. 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. It has been shown that the majority (86%) of sleep bruxism episodes occur during periods of sleep arousal. One study reported that sleep arousals which were experimentally induced with sensory stimulation in sleeping bruxists triggered episodes of sleep bruxism. Sleep arousals are a sudden change in the depth of the sleep stage, and may be also be accompanied by increased heart rate, respiratory changes and muscular activity, such as leg movements. Initial reports have suggested that episodes of sleep bruxism may be accompanied by gastroesophageal reflux, decreased esophageal pH (acidity), swallowing, and decreased salivary flow. Another report suggested a link between episodes of sleep bruxism and a supine sleeping position (lying face up).
Disturbance of the dopaminergic system in the central nervous system has also been suggested to be involved in the etiology of bruxism. Evidence for this comes from observations such as the effect of medications which alter dopamine release, 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.
Many studies have reported significant psychosocial risk factors for bruxism, particularly a stressful lifestyle, and this evidence is growing, but still not conclusive. Some consider emotional stress to be the main triggering factor. 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. However, children with sleep bruxism have been shown to have greater levels of anxiety than other children. People aged 50 with bruxism are more likely to be single and have a high level of education. Work related stress and irregular work shifts may also be involved. Personality traits are also commonly discussed in publications concerning the causes of bruxism, e.g. aggressive, competitive or hyperactive personality types. Some suggest that suppressed anger or frustration can be contribute to bruxism. Animal studies have also suggested a link between bruxism and psychosocial factors. Rosales et al. electrocuted 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 electrocution of other rats were under emotional stress which may have caused the bruxism-like behavior.
Some research suggests that there may be a degree of inherited susceptibility to develop sleep bruxism. 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, although no genetic markers have yet been identified. 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.
Certain drugs, including both prescribed and recreational drugs are thought to cause bruxism to develop, however others argue that there is insufficient evidence to draw conclusion between the effect of any medication and bruxism. Examples include dopamine agonists, dopamine antagonists, tricyclic antidepressants, selective serotonin reuptake inhibitors, alcohol, cocaine, amphetamines (including those taken for medical reasons). In some reported cases when bruxism is thought to have been initiated by selective serotonin reuptake inhibitors, decreasing the dose resolved the side effect, Other sources state that reports of selective serotonin reuptake inhibitors causing bruxism are rare, and only happens with long term use.
Specific examples include levodopa (when used in the long term, as in Parkinson's disease), methylphenidate (used in attention deficit hyperactive disorder), venlafaxine, citalopram, fluvoxamine, methylenedioxymethamphetamine (MDMA, ecstasy), methylenedioxyamphetamine (MDA), methylphenidate, and gamma-hydroxybutyric acid (GHB) and similar gamma-aminobutyric acid-inducing analogues such as phenibut. Bruxism can also be exacerbated by excessive consumption of caffeine, such as coffee, tea or chocolate. Bruxism was also reported to occur more commonly in drug addiction.
Occlusal interference 
Occlusion is defined most simply as "contacts between teeth", and refers to 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 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". An 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 a term that refers to 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 interference refers to a interference with the bite that changes the normal path of the bite. A common example of a deflective is an over-erupted upper wisdom tooth, often because the lower wisdom tooth has been removed. In this example, when the jaws are brought together, the lower back teeth contact the prominent wisdom tooth before the other teeth, and the lower jaw has to move forward to get 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.
Historically, many believed that problems with the bite were the sole cause for bruxism. It was often claimed that a person would grind at the interefering 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 intereferences has any impact on the condition. People with no teeth at all, who wear dentures can still suffer from bruxism, (although dentures too 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. 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. However, the role of occlusal factors in bruxism cannot be completely discounted due to insufficient evidence and problems with the design of studies. A minority of researchers continue to claim that various adjustments to the mechanics of the bite are capable of curing bruxism (see Occlusal adjustments/reorganization).
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). Examples include:
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.
Tooth wear 
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. side to side grinding on the back teeth will flatten the biting surfaces of the back teeth, or posturing the mandible forwards and grinding on the incisor teeth will preferentially wear these (posturing may not be involved if there is an existing edge to edge, class III incisal relationship).
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. Abfraction cavities are said to occur usually on the facial aspect of teeth, in 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 toothbush 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.
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.
In a typical case involving lateral motion (side to side grinding), the canines and incisors of the opposing arches are moved against each other laterally, i.e., with a side-to-side action by the medial pterygoid muscles that lie medial to the temporomandibular joints bilaterally. This movement abrades tooth structure and can lead to the wearing down of the incisal edges of the teeth. People with bruxism may also grind their posterior teeth, which wears down the cusps of the occlusal surface. 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 neither masseter nor temporalis muscle groups.
Tooth mobility 
The view that occlusal trauma (as may occur during bruxism) is a causative factor in gingivitis and periodontitis is not widely accepted. 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. Tooth movement that occurs during occlusal loading is sometimes termed fremitus. 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. 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.
Most people with bruxism will not experience any pain. Furthermore, the presence or degree of pain does not necessarily correlate with the severity of grinding or clenching that is occurring. The pain in the muscles of mastication caused by bruxism can be likened to muscle pain that occurs after exercise. The pain may be felt over the angle of the jaw (masseter) or in the temple (temporalis), and is may be described as a headache or an aching jaw. 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. The 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 disorder (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. Indeed, the symptoms of TMD overlap with those of bruxism. Others suggest that there is no strong association between TMD and bruxism. 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 more strict diagnostic criteria for bruxism are used, the association with TMD symptoms is much lower. In severe, chronic cases, bruxism can lead to myofascial pain and arthritis of the temporomandibular joints.[medical citation needed]
The most usual trigger in sleep bruxism that leads a person to seek medical or dental advice is being informed by sleeping partner of unpleasant grinding noises during sleep. A diagnosis of bruxism is usually made clinically. Bruxism is not the only cause of tooth wear, making it difficult to diagnose by visual evidence alone. Abraded teeth are usually brought to the patient's attention during a routine dental examination.
The most reliable diagnostic technique is measuring EMG (electromyography). These measurements pick up electrical signals from the chewing muscles (masseter and temporalis). This method is commonly used in sleep labs. Three forms of EMG measurement are available outside of sleep labs.
"Bedside" EMG units are similar to those used by sleep labs. These units pick up their signals from facial muscles through wires connecting the bedside unit to electrodes that are adhesively attached to the user's face. TENS electrodes or ECG electrodes may be used.
A biofeedback headband may be used in silent mode to record the total number of clenching incidents and the total clenching time each night. These two numbers easily distinguish clenching from rhythmic grinding and allow dentists to quantify severity levels. Biofeedback headbands do not require adhesive electrodes or wires attached to the face. They do not record the exact time, duration, and strength of each clenching incident as bedside EMG monitors do.
Bedside EMG units and biofeedback headbands can both be used either as a diagnosis measurement or in biofeedback mode as a treatment to help patients reduce their bruxism.
"Disposable" EMG monitors adhesively mount to the side of the face over the masseter muscle. They monitor one night and provide a single-digit measure of bruxism severity.
ICSD-R Diagnostic criteria 
The ICSD-R listed diagnostic criteria for sleep bruxism. The minimal criteria include both of the following criteria:
- 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).
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, and there is little evidence of the efficacy of any treatment, it has been recommended that only conservative treatment which is reversible and that carries low risk of morbidity should be used.
Repairing the damage to teeth 
Bruxism can cause significant tooth wear if it is severe, and sometimes dental restorations (crowns, fillings etc) are damaged or lost, sometimes repeatedly. 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. Dental implants and complex bridgework for example are relatively contraindicated in bruxists. In the case of crowns, the strength of the restoration becomes more important, sometimes at the cost of esthetic 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.
Dental guards and occlusal splints 
A dental guard or splint can reduce tooth abrasion. Dental guards are devided into partial or full-coverage splints and are typically made of plastic and fit over some or all of upper and/or lower teeth. The guard protects the teeth from abrasion and can 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."
A repositioning splint is designed to change the patient's occlusion, or bite. 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. Randomly controlled trials with these type devices generally show no benefit over other therapies. Another partial splint option is an NTI (nociceptive trigeminal inhibitor) dental guard. Nociceptor nerves sense and respond to pressure. The trigeminal nerve supplies the face and mouth. The NTI appliance snaps onto the front teeth. The NTI prevents 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. Patients who subconsciously clench their teeth are clenching less, even during sleeping hours, when using an NTI device. The NTI device must be fitted by a skilled and experienced practician. The NTI patients who require ongoing follow-ups can be monitored by a general dentist.
In a 2010 review in Journal of Orofacial Pain of 47 publications that involved 44 randomized controlled trials with a total of more than 2200 participants, Fricton et al. concluded: "Hard stabilization appliances, when adjusted properly, have good evidence of modest efficacy in the treatment of TMJD pain compared to non-occluding appliances and no treatment. Other types of appliances, including soft stabilization appliances, anterior positioning appliances, and anterior bite appliances, have some RCT evidence of efficacy in reducing TMJD pain. However, the potential for adverse events with these appliances is higher and suggests the need for close monitoring in their use."
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. Other interventions include relaxation techniques, stress management and hypnosis (self hypnosis or with a hypnotherapist). Cognitive behavioral therapy has been recommended by some for treatment of bruxism.
Many different medications have been used to treat bruxism, 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. A systematic review is underway to investigate the evidence for drug treatments in sleep bruxism.
Specific drugs which have been studied in sleep bruxism include 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 evidenced based clinical recommendations can be made. When bruxism is related to the use of selective serotonin reuptake inhibitors in depression, adding buspirone has been reported to resolve the side effect. Tricyclic antidepressants have also been been suggested to be preferable to selective serotinin reuptake inhibitors in people with bruxism, and may help with the pain.
Botulinum toxin (Botox) has been suggested as a treatment for bruxism, however there is only one randomized control trial which has reported that Botox reduces the myofascial pain symptoms. This scientific study was based on thirty people with bruxism who received Botox injections into the muscles of mastication and a control group of people with bruxism who received placebo injections. Normally multiple trials with larger cohorts are required to make any firm statement about the efficacy of a treatment. In 2013, a further randomized control trial investigating Botox in bruxism started. There is also little information available about the safety and long term follow up of this treatment for bruxism.
Botulinum toxin causes muscle paralysis by inhibition of acetylcholine release at neuromuscular junctions. Botox 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, whilst 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 termporalis muscles, and less often into the lateral pterygoids, (given the possible risk of decreasing the ability to swallow). It takes a few minutes per side, and the patient may start feeling the effects by the next day, and may last for about three months. Occasionally, adverse effects may occur, such as bruising can occur, 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.
|This section does not cite any references or sources. (May 2013)|
The principle behind biofeedback in treating bruxism is to automatically detect bruxing behavior, and provide a conscious or subconscious awareness signal to the user so that the user can decrease that behavior, preferably even while asleep. Some clinical trials have shown nighttime biofeedback to be effective at reducing nighttime bruxism behavior (though daytime biofeedback alone has not been shown to be effective at altering nighttime behavior).
The first wearable nighttime EMG biofeedback device (the biofeedback headband) became available in 2001. The awareness signal it provides is a sound which comes on quietly and gradually gets louder until the clenching incident stops, or until a maximum volume level (set by the user) is reached. Daytime practice is advised to facilitate responding in sleep without waking.
The biofeedback headband also tallies nightly data on the number of events that last for at least two seconds and the total accumulated duration of those events. A "fast-response" headband catches events that last for as little as 0.2 seconds. Since the same muscles used in clenching are also used in yawning and swallowing, a fast-response headband may sound during yawns and swallowing, so a standard-response headband is better for use during sleep, and will not include swallowing incidents in its time and clench count tallies. Studies indicate that the reduction in bruxism available during ongoing use of nighttime biofeedback relapses if biofeedback is discontinued, so this treatment should be considered long-term just as mouth guards are if long-term benefit is desired.
Another type of wearable EMG biofeedback device became available in 2005. It uses a mild electric shock as the biofeedback, producing an undesirable sensation intended to interrupt bruxing. The shock current is referred to by the manufacturer as "contingent electrical stimulation". The manufacturer's marketing literature speaks of triggering an "inhibitory reflex", but the only inhibitory reflex from the nerves stimulated is a pain reflex, and normally the device is not set to a high enough level to trigger such a reflex. If the shock current is set lower so the user can remain asleep through the shock, the response is less of a reflex response and requires conscious or subconscious participation on the part of the user, similar to the acoustic biofeedback headband. Some patients report desensitizing of nerves after a night of use. Some users report referred pain that appears to come from non-facial locations when the facial shock happens. Bruxism reduction clinical trial results are similar to those for the biofeedback headband. Typical consumer cost of an electric stimulation biofeedback device is about $1000. Electric stimulation units are not available in headband form in the US due to patents on the biofeedback headband, but rather are arm-band mounted, with a wire that runs to a disposable three-contact electrode which attaches adhesively to the face (typically over the masseter muscle at the jaw joint).
The NTI dental guard is technically also a biofeedback device (translating physical bite force into an uncomfortable feeling in the front teeth), so it is mentioned here as well as above in the section on dental guards and splints.
Another type of biofeedback therapy relies on stimulating the taste buds. The therapy involves suspending sealed packets containing a harmless but bad-tasting substance (e.g. hot sauce, vinegar, denatonium benzoate, etc.) between the rear molars using an orthodontic-style appliance. Attempts to bring the teeth together ruptures the packets, alerting the user. One major difference between this biofeedback method and all the others is that the undesirable sensation (taste) does not go away immediately when clenching stops. Thus this method is more likely to wake the user.
Occlusal adjustment/reorganization 
An alternative to simply re-actively 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", 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.
More data are available for the prevalence of sleep bruxism compared to bruxism generally, or specifically to awake bruxism. In a Scandinavian study of over 1000 people in the general population, 27.2% reported some form of bruxism, however 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. 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. One study reported the prevalence of awake and sleep bruxism to be 20% and 8-16% respectively. Awake bruxism affects females more commonly than males, whilst in sleep bruxism, males are as equally affected as females.
Children are reported to brux as commonly, if not more commonly, compared to 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%. The ICSD-R states that sleep bruxism may occur in over 50% of normal infants. Often sleep bruxism develops during adolescence, and the prevalence in 18 to 29 year olds is about 13%. The overall prevalence in adults is reported to be 8%, and people aver the age of 60 are less likely to be affected, with the prevalence dropping to about 3% in this group.
"La bruxomanie" (a french term roughly equivalent to bruxomania), is suggested by Marie Pietkiewics in 1907. In 1931, Frohman first coined the term bruxism. Occasionally recent medical publications will use the word bruxomania with bruxism, to denote specifically bruxism that occurs whilst awake, however this term can be considered historical and the modern equivalent would be awake bruxism or diurnal bruxism.
Society and culture 
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 threaten a rival or a predator.
In the Bible there are several references to "gnashing of teeth" (derived from the same Greek word "brygmos" from which bruxism originates) in both the Old Testament, and the New Testament particularly, where the phrase "wailing and gnashing of teeth" is used to described the fate of sinners in hell (Matthew 22:13).
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 rave culture, recreational use of ecstasy causes many health problems, and bruxism is often reported by users. Whilst 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.
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