<unk>  is a symptom complex (i.e. a group of symptoms occurring together and characterizing a particular disease), which is thought to be caused by multiple, poorly understood factors, but the exact etiology is unknown. There are factors which appear to predispose to<unk>  (genetic, hormonal, anatomical), factors which may precipitate it (trauma, occlusal changes, parafunction), and also factors which may prolong it (stress and again parafunction). Overall, two hypotheses have dominated research into the causes of<unk> , namely a psychosocial model and a theory of occlusal dysharmony. Interest in occlusal factors as a causative factor in<unk>  was especially widespread in the past, and the theory has since fallen out of favor and become controversial due to lack of evidence. Disc displacement In people with<unk> , it has been shown that the lower head of lateral pterygoid contracts during mouth closing (when it should relax), and is often tender to palpation. To theorize upon this observation, some have suggested that due to a tear in the back of the<unk>  capsule, the articular disc may be displaced forwards (anterior disc displacement), stopping the upper head of lateral pterygoid from acting to stabilize the disc as it would do normally. As a biologic compensatory mechanism, the lower head tries to fill this role, hence the abnormal muscle activity during mouth closure. There is some evidence that anterior disc displacement is present in a proportion of<unk>  cases. Anterior disc displacement with reduction refers to abnormal forward movement of the disc during opening which reduces upon closing. Anterior disc displacement without reduction refers to an abnormal forward, bunched-up position of the articular disc which does not reduce. In this latter scenario, the disc is not intermediary between the condyle and the articular fossa as it should be, and hence the articular surfaces of the bones themselves are exposed to a greater degree of wear (which may predispose to osteoarthritis in later life). Degenerative<unk>  disease The general term "degenerative<unk>  disease" refers to arthritis (both osteoarthritis and rheumatoid arthritis) and arthrosis. The term arthrosis may cause confusion since in the specialized<unk>  literature it means something slightly different from in the wider medical literature. In medicine generally, arthrosis can be a nonspecific term for a<unk> , any disease of a<unk>  (or specifically degenerative<unk>  disease), and is also used as a synonym for osteoarthritis. In the specialized literature that has evolved around<unk>  research, arthrosis is differentiated from arthritis by the presence of low and no inflammation respectively. Both are however equally degenerative. The TMJs are sometimes described as one of the most used<unk> s in the body. Over time, either with normal use or with parafunctional use of the<unk> , wear and degeneration can occur, termed osteoarthritis. Rheumatoid arthritis, an autoimmune<unk>  disease, can also affect the TMJs. Degenerative<unk>  diseases may lead to defects in the shape of the tissues of the<unk> , limitation of function (e.g. restricted mandibular movements), and<unk>  pain. Psychosocial factors Emotional stress (anxiety, depression, anger) may increase pain by causing autonomic, visceral and skeletal activity and by reduced inhibition via the descending pathways of the limbic system. The interactions of these biological systems have been described as a vicious "anxiety-pain-tension" cycle which is thought to be frequently involved in<unk> . Put simply, stress and anxiety cause grinding of teeth and sustained muscular contraction in the face. This produces pain which causes further anxiety which in turn causes prolonged muscular spasm at trigger<unk> s, vasoconstriction, ischemia and release of pain mediators. The pain discourages use of the masticatory system (a similar phenomenon in other chronic pain conditions is termed "fear avoidance" behavior), which leads to reduced muscle flexibility, tone, strength and endurance. This manifests as limited mouth opening and a sensation that the teeth are not fitting properly. Persons with<unk>  have a higher prevalence of psychological disorders than people without<unk> . People with<unk>  have been shown to have higher levels of anxiety, depression, somatization and sleep deprivation, and these could be considered important risk factors for the development of<unk> . In the 6 months before the onset, 50–70% of people with<unk>  report experiencing stressful life events (e.g. involving work, money, health or relationship loss). It has been postulated that such events induce anxiety and cause increased jaw muscle activity. Muscular hyperactivity has also been shown in people with<unk>  whilst taking examinations or watching horror films. Others argue that a link between muscular hyperactivity and<unk>  has not been convincingly demonstrated, and that emotional distress may be more of a consequence of pain rather than a cause. Bruxism Bruxism is an oral parafunctional activity where there is excessive clenching and grinding of the teeth. It can occur during sleep or whilst awake. The cause of bruxism itself is not completely understood, but psychosocial factors appear to be implicated in awake bruxism and dopaminergic<unk>  and other central nervous system mechanisms may be involved in sleep bruxism. If<unk>  pain and limitation of mandibular movement are greatest upon waking, and then slowly resolve throughout the day, this may indicate sleep bruxism. Conversely, awake bruxism tends to cause symptoms that slowly get worse throughout the day, and there may be no pain at all upon waking. The relationship of bruxism with<unk>  is debated. Many suggest that sleep bruxism can be a causative or contributory factor to pain symptoms in<unk> . Indeed, the symptoms of<unk>  overlap with those of bruxism. Others suggest that there is no strong association between<unk>  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<unk>  pain, and when more strict diagnostic criteria for bruxism are used, the association with<unk>  symptoms is much lower. Self-reported bruxism is probably a poor method of identifying bruxism. There are also very many people who grind their teeth and who do not develop<unk> . Bruxism and other parafunctional activities may play a role in perpetuating symptoms in some cases. Other parafunctional habits such as pen chewing, lip and cheek biting (which may manifest as morsicatio buccarum or linea alba), are also suggested to contribute to the development of<unk> . Other parafunctional activities might include jaw thrusting, excessive gum chewing, nail biting and eating very hard foods. Trauma Trauma, both micro and macrotrauma, is sometimes identified as a possible cause of<unk> ; however, the evidence for this is not strong. Prolonged mouth opening (hyper-extension) is also suggested as a possible cause. It is thought that this leads to microtrauma and subsequent muscular hyperactivity. This may occur during dental treatment, with oral intubation whilst under a general anesthetic, during singing or wind instrument practice (really these can be thought of as parafunctional activities). Damage may be incurred during violent yawning, laughing, road traffic accidents, sports injuries, interpersonal violence, or during dental treatment, (such as tooth extraction). It has been proposed that a link exists between whiplash injuries (sudden neck hyper-extension usually occurring in road traffic accidents), and the development of<unk> . This has been termed "post-traumatic<unk> ", to separate it from "idiopathic<unk> ". Despite multiple studies having been performed over the years, the cumulative evidence has been described as conflicting, with moderate evidence that<unk>  can occasionally follow whiplash injury. The research that suggests a link appears to demonstrate a low to moderate incidence of<unk>  following whiplash injury, and that pTMD has a poorer response to treatment than<unk>  which has not developed in relation to trauma. Occlusal factors Occlusal factors as an etiologic factor in<unk>  is a controversial topic. Abnormalities of occlusion (problems with the bite) are often blamed for<unk>  but there is no evidence that these factors are involved. Occlusal abnormalities are incredibly common, and most people with occlusal abnormalities do not have<unk> . Although occlusal features may affect observed electrical activity in masticatory muscles, there are no statistically significant differences in the number of occlusal abnormalities in people with<unk>  and in people without<unk> . There is also no evidence for a causal link between orthodontic treatment and<unk> . The modern, mainstream view is that the vast majority of people with<unk> , occlusal factors are not related. Theories of occlusal factors in<unk>  are largely of historical interest. A causal relationship between occlusal factors and<unk>  was championed by Ramfjord in the 1960s. A small minority of dentists continue to prescribe occlusal adjustments in the belief that this will prevent or treat<unk>  despite the existence of systematic reviews of the subject which state that there is no evidence for such practices, and the vast majority of opinion being that no irreversible treatment should be carried out in<unk>  (see Occlusal adjustment). Genetic factors<unk>  does not obviously run in families like a genetic disease. It has been suggested that a genetic predisposition for developing<unk>  (and chronic pain syndromes generally) could exist. This has been postulated to be explained by variations of the gene which codes for the enzyme catechol-O-methyl transferase
Temporomandibular joint dysfunction
Impacted wisdom teeth
Facial nerve paralysis
Eustachian tube dysfunction
Orofacial myofunctional disorders
Barodontalgia
Ear pain
Orofacial pain