The left temporalis muscle 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 The left masseter muscle (red highlight), shown partially covered by superficial muscles 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. In individuals without<unk>  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. Some<unk>  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.<unk>  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<unk>  is largely unknown, but it is generally accepted to have multiple possible causes.<unk>  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<unk>  is thought to be usually semivoluntary, and often associated with stress caused by family responsibilities or work pressures. Some suggest that in children,<unk>  may occasionally represent a response to earache or teething. Awake<unk>  usually involves clenching (sometimes the term "awake clenching" is used instead of awake<unk> , 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<unk>  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<unk>  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<unk>  episodes occur during periods of sleep arousal. One study reported that sleep arousals which were experimentally induced with sensory stimulation in sleeping<unk> s triggered episodes of sleep<unk> . 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<unk>  may be accompanied by gastroesophageal reflux, decreased esophageal pH (acidity), swallowing, and decreased salivary flow. Another report suggested a link between episodes of sleep<unk>  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<unk> . 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<unk>  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<unk> . 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<unk>  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<unk>  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 suffer from<unk> , although dentures also often change the original bite. Most modern sources state that there is no relationship, or at most a minimal relationship, between<unk>  and occlusal factors. The findings of one study, which used self-reported tooth grinding rather than clinical examination to detect<unk> , suggested that there may be more of a relationship between occlusal factors and<unk>  in children. However, the role of occlusal factors in<unk>  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<unk>  (see Occlusal adjustment/reorganization). Psychosocial factors Many studies have reported significant psychosocial risk factors for<unk> , 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<unk>  respond differently to depression, hostility and stress compared to people without<unk> . Stress has a stronger relationship to awake<unk> , but the role of stress in sleep<unk>  is less clear, with some stating that there is no evidence for a relationship with sleep<unk> . However, children with sleep<unk>  have been shown to have greater levels of anxiety than other children. People aged 50 with<unk>  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<unk> , e.g. aggressive, competitive or hyperactive personality types. Some suggest that suppressed anger or frustration can contribute to<unk> . Stressful periods such as examinations, family bereavement, marriage, divorce, or relocation have been suggested to intensify<unk> . Awake<unk>  often occurs during periods of concentration such as while working at a computer, driving or reading. Animal studies have also suggested a link between<unk>  and psychosocial factors. Rosales et al. electrically shocked lab rats, and then observed high levels of<unk> -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<unk> -like behavior. Genetic factors Some research suggests that there may be a degree of inherited susceptibility to develop sleep<unk> . 21–50% of people with sleep<unk>  have a direct family member who had sleep<unk>  during childhood, suggesting that there are genetic factors involved, although no genetic markers have yet been identified. Offspring of people who have sleep<unk>  are more likely to also have sleep<unk>  than children of people who do not have<unk> , or people with awake<unk>  rather than sleep<unk> . Medications Certain stimulant drugs, including both prescribed and recreational drugs, are thought by some to cause the development of<unk> . 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<unk>  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<unk>  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.<unk>  can also be exacerbated by excessive consumption of caffeine, as in coffee, tea or chocolate.<unk>  has also been reported to occur commonly comorbid with drug addiction. Methylenedioxymethamphetamine (MDMA, ecstasy) has been reported to be associated with<unk> , 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<unk>  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.
Bruxism
Vitalism
Rape trauma syndrome
Manganism
Cherubism
Stiff skin syndrome
Oral galvanism
Mirror syndrome