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. 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. 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 thrusting (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 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 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. historical focus 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 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. people with no teeth at all who wear dentures can still have bruxism, 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. 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 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. some consider emotional stress and anxiety to be the main triggering factors. 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 contribute to bruxism. 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. genetic factors 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. medications certain stimulant drugs, including both prescribed and recreational drugs, are thought by some to cause the development of bruxism. however, others argue that there is insufficient evidence to draw such a conclusion. examples may include dopamine agonists, dopamine antagonists, tricyclic antidepressants, selective serotonin reuptake inhibitors, alcohol, cocaine, and amphetamines (including those taken for medical reasons). in some reported cases where 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, or only occur with long-term use. 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), 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, as in coffee, tea or chocolate. bruxism has also been reported to occur commonly comorbid with drug addiction. methylenedioxymethamphetamine (mdma, ecstasy) has been reported to be associated with bruxism, 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", 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". 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). examples include: acrodynia atypical facial pain autism cerebral palsy disturbed sleep patterns and other sleep disorders, such as obstructive sleep apnea, snoring, moderate daytime sleepiness, and insomnia down syndrome dyskinesias epilepsy eustachian tube dysfunction infarction in the basal ganglia intellectual disability, particularly in children leigh disease meningococcal septicaemia multiple system atrophy oromandibular dystonia parkinson's diseases, (possibly due to long-term therapy with levodopa causing dopaminergic dysfunction) rett syndrome torus mandibularis and buccal exostosis trauma, e.g. brain injury or coma 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. a diagnosis of bruxism is usually made clinically, 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. questionnaires can be used to screen for bruxism in both the clinical and research settings. 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, bruxcore, or a beeswax-bearing biteplate. 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. 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. 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. 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