TMD does not obviously run in families like a genetic disease. It has been suggested that a genetic predisposition for developing TMD (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 (COMT) which may produce 3 different phenotypes with regards pain sensitivity. COMT (together with monoamine oxidase) is involved in breaking down catecholamines (e.g. dopamine, epinephrine, and norepinephrine). The variation of the COMT gene which produces less of this enzyme is associated with a high sensitivity to pain. Females with this variation, are at 2–3 times greater risk of developing TMD than females without this variant. However this theory is controversial since there is conflicting evidence.

Occlusal factors as an etiologic factor in TMD is a controversial topic. Abnormalities of occlusion (problems with the bite) are often blamed for TMD but there is no evidence that these factors are involved. Occlusal abnormalities are incredibly common, and most people with occlusal abnormalities do not have TMD. 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 TMD and in people without TMD. There is also no evidence for a causal link between orthodontic treatment and TMD. The modern, mainstream view is that the vast majority of people with TMD, occlusal factors are not related. Theories of occlusal factors in TMD are largely of historical interest. A causal relationship between occlusal factors and TMD 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 TMD 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 TMD (see Occlusal adjustment).

Fractures, particularly those of the mandible and fractures of zygomatic arch and zygomatic arch complex, accidental incorporation of foreign bodies due to external traumatic injury.

Treatment: fracture reduction, removal of foreign bodies with antibiotic coverage

Traditionally causes of trismus are divided into intra-articular (factors within the temporomandibular joint [TMJ]) and extra-articular (factors outside the joint, see table).

The temporomandibular joints (TMJ) are the two joints connecting the jawbone to the skull. It is a bilateral synovial articulation between the temporal bone of the skull above and the mandible below; it is from these bones that its name is derived.

Condylar resorption is an idiopathic condition, though there are some theories relating to its possible cause. Because condylar resorption is more likely to be in young females, hormonal mediation may be involved. Strain on the temporomandibular joint from orthodontics or orthognathic surgery may be related to the condition. Reactive arthritis, rheumatoid arthritis, and psoriatic arthritis are other possible causes.

Condylar resorption, also called idiopathic condylar resorption, ICR, and condylysis, is a temporomandibular joint disorder in which one or both of the mandibular condyles are broken down in a bone resorption process. This disorder is nine times more likely to be present in females than males, and is more common among teenagers.

Jaw dislocation is common for people who are in car, motorcycle or related accidents and also sports related activities. This injury does not pin point specific ages or genders because it could happen to anybody. People who dislocate their jaw do not usually seek emergency medical care. In most cases, jaw dislocations are acute and can be altered by minor manipulations. It was reported from one study that over a seven-year period at an emergency medical site, with 100,000 yearly visits, there were only 37 patients that were seen for a dislocated jaw.

Temporomandibular joint pain is generally due to one of four reasons.

- Myofascial pain dysfunction syndrome, primarily involving the muscles of mastication. This is the most common cause.

- Internal derangements, an abnormal relationship of the disc to any of the other components of the joint. Disc displacement is an example of internal derangement.

- Osteoarthritis of the temporomandibular joint, a degenerative joint disease of the articular surfaces.

- Temporal arteritis, for which it is considered a reliable diagnostic criteria.

Pain or dysfunction of the temporomandibular joint is sometimes referred to as "TMJ", and temporomandibular joint disorder (or "dysfunction") may be abbreviated TMD. This term is used to refer to a group of problems involving the temporomandibular joints and the muscles, tendons, ligaments, blood vessels, and other tissues associated with them.

Although rare, other pathologic conditions may also affect the function of temporomandibular joints, causing pain and swelling. These conditions include chondrosarcoma, osteosarcoma, giant cell tumor and aneurysmal bone cyst.

The exact cause is unknown. Mechanical factors, dietary and long term use of some antidepressants may be of significance. There is a correlation between these factors but not a cause or effect. The distinctive radiological feature of DISH is the continuous linear calcification along the antero-medial aspect of the thoracic spine. The disease is usually found in people in their 60s and above, and is extremely rare in people in their 40s and 30s. The disease can spread to any joint of the body, affecting the neck, shoulders, ribs, hips, pelvis, knees, ankles, and hands. The disease is not fatal, however some associated complications can lead to death. Complications include paralysis, dysphagia (the inability to swallow), and pulmonary infections. Although DISH manifests in a similar manner to ankylosing spondylitis, these two are totally separate diseases. Ankylosing spondylitis is a genetic disease with identifiable marks, and affects organs. DISH has no indication of a genetic link, and does not affect organs other than the lungs, which is only indirect due to the fusion of the rib cage.

Long term treatment of acne with vitamin derived retinoids, such as etretinate and acitretin, have been associated with "extraspinal" hyperostosis.

Stenosing tenosynovitis is most commonly caused by overuse from chronic repetitive activities using the hand or the involved finger. Examples include work activities (e.g., computer use, materials handling) or recreational activities (e.g., knitting, golf, racket sports). Carpenters who use hammers suffer from this as well as those who continuously grip wood or other materials when cutting them due to having to use your hands as a clamp to hold things in place.

Primary stenosing tenosynovitis can be idiopathic, occurring in middle age women more frequently than in men, but can present also in infancy.

Secondary stenosing tenosynovitis can be caused by disease or entities that cause connective tissue disorders including the following:

- Rheumatoid arthritis and psoriatic arthritis—therefore the clinician must assess the hands for rheumatologic deformities.

- Gout

- Diabetes mellitus

- Amyloidosis

- Systemic lupus erythematosus

Others causes may include the following:

- Direct trauma to the site

- During the postpartum period

- Congenital

Fibrous ankylosis is a fibrous connective tissue process which results in decreased range of motion. Symptoms present as bony ankylosis, in which osseous tissue fuses two bones together reducing mobility, which is why fibrous ankylosis is also known as false ankylosis.

Pathology may be the result of trauma, disease, chronic inflammation, or surgery.

Some research suggests fibrous ankylosis may precede the development of bony ankylosis

There is strong evidence to show that chronic orofacial pain (including AFP) is associated with psychological factors. Sometimes stressful life events appear to precede the onset of AFP, such as bereavement or illness in a family member. Hypochondriasis, especially cancerophobia, is also often cited as being involved. Most people with AFP are "normal" people who have been under extreme stress, however other persons with AFP have neuroses or personality disorders, and a small minority have psychoses. Some have been separated from their parents as children.

Depression, anxiety and altered behavior are strongly correlated with AFP. It is argued whether this is a sole or contributing cause of AFP, or the emotional consequences of suffering with chronic, unrelieved pain. It has been suggested that over 50% of people with AFP have concomitant depression or hypochondria. Furthermore, about 80% of persons with psychogenic facial pain report other chronic pain conditions such as listed in the table.

Mandible fracture causes vary by the time period and the region studied. In North America, blunt force trauma (a punch) is the leading cause of mandible fracture whereas in India, motor vehicle collisions are now a leading cause. On battle grounds, it is more likely to be high velocity injuries (bullets and shrapnel). Prior to the routine use of seat belts, airbags and modern safety measures, motor vehicle collisions were a leading cause of facial trauma. The relationship to blunt force trauma explains why 80% of all mandible fractures occur in males. Mandibular fracture is a rare complication of third molar removal, and may occur during the procedure or afterwards. With respect to trauma patients, roughly 10% have some sort of facial fracture, the majority of which come from motor vehicle collisions. When the person is unrestrained in a car, the risk of fracture rises 50% and when an unhelmeted motorcyclist the risk rises 4-fold.

Otitis media is a particularly common cause of otalgia in early childhood, often occurring secondary to other infectious illnesses, such as colds, coughs, or conjunctivitis.

Jaw claudication is pain in the jaw associated with chewing. It is a classic symptom of Giant-cell arteritis, but can be confused with symptoms of Temporomandibular joint disease, Rheumatoid arthritis of the temporomandibular joint, Myasthenia gravis, tumors of the Parotid gland, or occlusion or stenosis of the External carotid artery. The term is derived by analogy from claudication of the leg, where pain is caused by arterial insufficiency.

The healing time for a routine mandible fractures is 4–6 weeks whether MMF or rigid internal fixation (RIF) is used. For comparable fractures, patients who received MMF will lose more weight and take longer to regain mouth opening, whereas, those who receive RIF have higher infection rates.

The most common long-term complications are loss of sensation in the mandibular nerve, malocclusion and loss of teeth in the line of fracture. The more complicated the fracture (infection, comminution, displacement) the higher the risk of fracture.

Condylar fractures have higher rates of malocclusion which in turn are dependent on the degree of displacement and/or dislocation. When the fracture is intracapsular there is a higher rate of late-term osteoarthritis and the potential for ankylosis although the later is a rare complication as long as mobilization is early. Pediatric condylar fractures have higher rates of ankylosis and the potential for growth disturbance.

Rarely, mandibular fracture can lead to Frey's syndrome.

AFP is sometimes described as being fairly common, and one estimated prevalence is about 1–2% of the general population. However, the IASP described PIFP as being rare, less common than trigeminal neuralgia (which has a prevalence of about 0.01–0.3% in the general population), and possessing no available epidemiologic data for estimated prevelence in the general population. The predominant age group is 30–50, and females are more often affected than males, with most reports stating that about 80% of people with AFP are female.

Diffuse idiopathic skeletal hyperostosis (DISH) is a non-inflammatory spondyloarthropathy which predominantly affects the spine. It is characterized by ankylosis and enthesopathy (ossification of the ligaments and entheses). It most commonly affects the thoracic and thoraco-lumbar spine, but involvement is variable and can include the entire spine.

Some studies suggest a hormonal link. Specifically, the hormone relaxin has been indicated.

A genetic factor is indicated since the trait runs in families and there is an increased occurrence in some ethnic populations (e.g., Native Americans, Lapps / Sami people). A locus has been described on chromosome 13. Beukes familial dysplasia, on the other hand, was found to map to an 11-cM region on chromosome 4q35, with nonpenetrant carriers not affected.

Hip dysplasia is considered to be a multifactorial condition. That means that several factors are involved in causing the condition to manifest.

The cause of this condition is unknown; however, some factors of congenital hip dislocation are through heredity and racial background. It is also thought that the higher rates in some ethnic groups (such as some Native American groups) is due to the practice swaddling of infants, which is known to be a potential risk factor for developing dysplasia. It also has a low risk in African Americans and southern Chinese.

Increased risk of developing knee and hip osteoarthritis was found in those who:

- work with manual handling (e.g. lifting)

- have physically demanding work

- walk at work

- have climbing tasks at work (e.g. climb stairs or ladders)

Increased risk of developing hip osteoarthritis over time was found among those who work in bent or twisted positions.

Increased risk of knee osteoarthritis was found in those who:

- work in a kneeling or squatting position

- experience heavy lifting in combination with a kneeling or squatting posture

- work standing up

A number of studies have shown that there is a greater prevalence of the disease among siblings and especially identical twins, indicating a hereditary basis. Although a single factor is not generally sufficient to cause the disease, about half of the variation in susceptibility has been assigned to genetic factors.

As early human ancestors evolved into bipeds, changes occurred in the pelvis, hip joint and spine which increased the risk of osteoarthritis. Additionally genetic variations that increase the risk were likely not selected against because usually problems only occur after reproductive success.

The development of osteoarthritis is correlated with a history of previous joint injury and with obesity, especially with respect to knees. Since the correlation with obesity has been observed not only for knees but also for non-weight bearing joints and the loss of body fat is more closely related to symptom relief than the loss of body weight, it has been suggested that there may be a metabolic link to body fat as opposed to just mechanical loading.

Changes in sex hormone levels may play a role in the development of osteoarthritis as it is more prevalent among post-menopausal women than among men of the same age. A study of mice found natural female hormones to be protective while injections of the male hormone dihydrotestosterone reduced protection.

There is no single factor that is consistently found in the prenatal history of individuals affected with amyoplasia and, in some cases, there is no known cause of the disorder.

Amyoplasia is a sporadic condition that occurs due to lack of fetal movement in the womb. There is no specific gene that is known to cause the disorder. It is thought to be multifactorial, meaning that numerous genes and environmental factors play a role in its development. The recurrence risk is minimal for siblings or children of affected individuals. There have been no reports of recurrent cases of amyoplasia in a family.

The fetal akinesia in amyoplasia is thought to be caused by various maternal and fetal abnormalities. In some cases, the mother's uterus does not allow for adequate fetal movement because of a lack of amniotic fluid, known as oligohydramnios, or an abnormal shape to the uterus, called a bicornuate uterus.

There may also be a myogenic cause to the fetal akinesia, meaning that fetal muscles do not develop properly due to a muscle disease (for example, a congenital muscular dystrophy). Similarly, connective tissue tendon and skeletal defects may contribute to the fetal akinesia and be the primary cause of amyoplasia. Additionally, malformations may occur in the central nervous system and/or spinal cord that can lead to a lack of fetal movement in utero. This neurogenic cause is often accompanied by a wide range of other conditions. Other causes of fetal akinesia may include a maternal fever during pregnancy or a virus.

It is normally possible to establish the cause of ear pain based on the history. It is important to exclude cancer where appropriate, particularly with unilateral otalgia in an adult who uses tobacco or alcohol.Often migraines are caused by middle ear infections which can easily be treated with antibiotics. Often using a hot washcloth can temporarily relieve ear pain.