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).

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).

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.

Both sex are equally affected

Any age group can develop a parapheryngeal abscess but it is most commonly seen in children and adolescents. Adults who are immunocompromised are also at high risk.

Infection can occur from:

- Pharynx: acute and chronic infection of tonsil and adenoids

- Teeth: dental infection occurs from lower last molar tooth

- Ear: bezold abscess and petrositis

- Other space: infection of parotid retropharyngeal space

- External trauma: penetrating injuries of neck, injection of local anaesthetic

The incidence of the disease is higher in people from certain parts of the world including South-East Asia, South Africa and the Middle East.

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.

Pathologic fracture of the mandible is a possible complication of OM where the bone has been weakened significantly.

Pericoronitis usually occurs in young adults, around the time when wisdom teeth are erupting into the mouth. If the individual has reached their twenties without any attack of pericoronitis, it becomes substantially less likely one will occur thereafter.

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 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.

OM is usually a polymicrobial, opportunistic infection, caused primarily by a mixture of alpha hemolytic streptococci and anaerobic bacteria from the oral cavity such as "Peptostreptococcus", "Fusobacterium" and "Prevotella", (in contrast to OM of the long bones, usually caused by isolated "Staphylococcus aureus" infection). These are the same as the common causative organisms in odotonogenic infections. However, when OM in the jaws follows trauma, is the likely cause is still staphylococcal (usually "Staphylococcus epidermis".

Other risk factors can be any familial hypercoagulation tendency, including for example, Factor V (Five) Leiden heterozygosity.

Once the plaque stagnation area is removed either through further complete tooth eruption or tooth removal then pericoronitis will likely never return. A non-impacted tooth may continue to erupt, reaching a position which eliminates the operculum. A transient and mild pericoronal inflammation often continues while this tooth eruption completes. With adequate space for sustained improved oral hygiene methods, pericoronitis may never return. However, when relying on just oral hygiene for impacted and partially erupted teeth, chronic pericoronitis with occasional acute exacerbation can be expected.

Dental infections such as a pericoronal abscess can develop into septicemia and be life-threatening in persons who have neutropenia. Even in people with normal immune function, pericoronitis may cause a spreading infection into the potential spaces of the head and neck. Rarely, the spread of infection from pericoronitis may compress the airway and require hospital treatment (e.g. Ludwig's angina), although the majority of cases of pericoronitis are localized to the tooth. Other potential complications of a spreading pericoronal abscess include peritonsillar abscess formation or cellulitis.

Chronic pericoronitis may be the etiology for the development of paradental cyst, an inflammatory odontogenic cyst.

In some cases Meige's syndrome can be reversed when it is caused by medication. It has been theorized that it is related to cranio-mandibular orthopedic misalignment, a condition that has been shown to cause a number of other movement disorders (Parkinon's, tourettes, and torticollis). This theory is supported by the fact that the trigeminal nerve is sensory for blink reflex, and becomes hypertonic with craniomandibular dysfunction. Palliative treatments are available, such as botulinum toxin injections.

It is a commonly encountered otorhinolaryngological (ENT) emergency.

The number of new cases per year of peritonsillar abscess in the United States has been estimated approximately at 30 cases per 100,000 people. In a study in Northern Ireland, the number of new cases was 10 cases per 100,000 people per year.

In Denmark, the new number of new cases is higher and reaches 41 cases per 100,000 people per year. Younger children who develop a peritonsillar abscess are often immunocompromised and in them, the infection can cause airway obstruction.

Dried products such as paan masala and gutkha have higher concentrations of areca nut and appear to cause the disease. Other causes include:

- Immunological diseases

- Extreme climatic conditions

- Prolonged deficiency to iron and vitamins in the diet

The main symptoms involve involuntary blinking and chin thrusting. Some patients may experience excessive tongue protrusion, squinting, light sensitivity, muddled speech, or uncontrollable contraction of the platysma muscle. Some Meige's patients also have "laryngeal dystonia" (spasms of the larynx). Blepharospasm may lead to embarrassment in social situations, and oromandibular dystonia can affect speech, making it difficult to carry on the simplest conversations. This can cause difficulty in both personal and professional contexts, and in some cases may cause patients to withdraw from social situations.

The condition tends to affect women more frequently than men.

PTA usually arises as a complication of an untreated or partially treated episode of acute tonsillitis. The infection, in these cases, spreads to the peritonsillar area (peritonsillitis). This region comprises loose connective tissue and is hence susceptible to formation of an abscess. PTA can also occur "". Both aerobic and anaerobic bacteria can be causative. Commonly involved aerobic pathogens include "Streptococcus, Staphylococcus" and "Haemophilus". The most common anaerobic species include "Fusobacterium necrophorum", " Peptostreptococcus", "Prevotella species", and "Bacteroides".

In general, chronic periodontal conditions do not cause any pain. Rather, it is acute inflammation which is responsible for the pain.

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.

Common marginal gingivitis in response to subgingival plaque is usually a painless condition. However, an acute form of gingivitis/periodontitis, termed acute necrotizing ulcerative gingivitis (ANUG), can develop, often suddenly. It is associated with severe periodontal pain, bleeding gums, "punched out" ulceration, loss of the interdental papillae, and possibly also halitosis (bad breath) and a bad taste. Predisposing factors include poor oral hygiene, smoking, malnutrition, psychological stress, and immunosuppression. This condition is not contagious, but multiple cases may simultaneously occur in populations who share the same risk factors (such as students in a dormitory during a period of examination). ANUG is treated over several visits, first with debridement of the necrotic gingiva, homecare with hydrogen peroxide mouthwash, analgesics and, when the pain has subsided sufficiently, cleaning below the gumline, both professionally and at home. Antibiotics are not indicated in ANUG management unless there is underlying systemic disease.

Masticatory muscle myositis (MMM) is an inflammatory disease in dogs affecting the muscles of mastication (chewing). It is also known as atrophic myositis or eosinophilic myositis. MMM is the most common inflammatory myopathy in dogs. The disease mainly affects large breed dogs. German Shepherd Dogs and Cavalier King Charles Spaniels may be predisposed. There is a similar disease of the eye muscles found in Golden Retrievers. Symptoms of acute MMM include swelling of the jaw muscles, drooling, and pain on opening the mouth. Ophthalmic signs may include third eyelid protrusion, red eyes, and exophthalmos (protruding eyeballs). In chronic MMM there is atrophy of the jaw muscles, and scarring of the masticatory muscles due to fibrosis may result in inability to open the mouth (trismus). The affected muscles include the temporalis, masseter, and pterygoid muscles. The disease is usually bilateral.

MMM is caused by the presence of 2M fibers in the muscles of the jaw. 2M fibers are not found elsewhere in the body. The immune system recognizes these proteins as foreign to the body and attacks them, resulting in inflammation. Diagnosis of MMM is through either biopsy of the temporalis or masseter muscles or the 2M antibody assay, in which blood serum of the possible MMM-dog is reacted with temporalis tissue of a normal dog, or both. False negatives by the 2M antibody assay may be obtained if MMM is end-stage with destruction of type 2M fibers and marked fibrosis. Treatment is usually with corticosteroids such as prednisone, often with decreasing doses for up to 4–6 months, and in the case of trismus, manual opening of the mouth under anesthesia. Feeding very soft or liquid food during this time is usually necessary. The ultimate degree of recovery of jaw function and muscle mass will depend upon the extent of damage to the muscle tissue. Recurrence of MMM may occur. Misdiagnosis of MMM as a retroorbital abscess based on physical examination and finding of trismus leads to inappropriate treatment with antibiotics, which will not impede the progress of MMM.

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.

Since the advent of penicillin in the 1940s, a major preoccupation in the treatment of streptococcal tonsillitis has been the prevention of rheumatic fever, and its major effects on the nervous system (Sydenham's chorea) and heart. Recent evidence would suggest that the rheumatogenic strains of group A beta hemolytic strep have become markedly less prevalent and are now only present in small pockets such as in Salt Lake City, USA. This brings into question the rationale for treating tonsillitis as a means of preventing rheumatic fever.

Complications may rarely include dehydration and kidney failure due to difficulty swallowing, blocked airways due to inflammation, and pharyngitis due to the spread of infection.

An abscess may develop lateral to the tonsil during an infection, typically several days after the onset of tonsillitis. This is termed a peritonsillar abscess (or quinsy).

Rarely, the infection may spread beyond the tonsil resulting in inflammation and infection of the internal jugular vein giving rise to a spreading septicaemia infection (Lemierre's syndrome).

In chronic/recurrent cases (generally defined as seven episodes of tonsillitis in the preceding year, five episodes in each of the preceding two years or three episodes in each of the preceding three years), or in acute cases where the palatine tonsils become so swollen that swallowing is impaired, a tonsillectomy can be performed to remove the tonsils. Patients whose tonsils have been removed are still protected from infection by the rest of their immune system.

In strep throat, very rarely diseases like rheumatic fever or glomerulonephritis can occur. These complications are extremely rare in developed nations but remain a significant problem in poorer nations. Tonsillitis associated with strep throat, if untreated, is hypothesized to lead to pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections (PANDAS).

The hypothesized causes of meth mouth are a combination of MA side effects and lifestyle factors which may be present in users:

- Dry mouth (xerostomia)

- Clenching and grinding of the teeth (bruxism)

- Infrequent oral hygiene

- Frequent consumption of sugary, fizzy drinks

- Caustic nature of methamphetamine

The dental effects of long-term methamphetamine use are often attributed to its effects on saliva. The reduction in saliva increases the likelihood of dental caries, enamel erosion, and periodontal disease. Although it is clear that use of the drug decreases saliva, the mechanism by which it does so is unclear. One theory is that the drug causes vasoconstriction (narrowing of the blood vessels) in salivary glands, decreasing salivary flow. This constriction is thought to be due to the activation of alpha-adrenergic receptors by both methamphetamine itself and norepinephrine, the levels of which are dramatically increased by methamphetamine use. These factors can be compounded by dehydration, which occurs in many methamphetamine users after drug-induced increases in metabolism. The characteristics of the saliva produced during use of the drug, which includes high protein content, may also contribute to the sensation of dry mouth.

Long-term methamphetamine use can cause parafunctional habits, routine actions of a body part that are different than their common use, which can result in tooth wear and exacerbate periodontal diseases. One such habit that may affect the development of meth mouth is bruxism, particularly as the drug's effects wane and stereotypy occurs, a phase that is often referred to as "tweaking". This bruxism may be due to a drug-induced increase in monoamines. Other behaviors of long-term methamphetamine users that may cause or accelerate the symptoms of meth mouth are the failure to pay attention to oral hygiene and excessive food intake during binges, especially sugary foods; the drug's users often report strong cravings for sugar and consume large amounts of high-sugar beverages. The altered mental state that accompanies methamphetamine use lasts longer than that of some other common drugs, increasing the amount of time the user engages in drug-induced behavior.

Hydrochloric acid is used in methamphetamine's manufacturing process, but academic reviews have not supported the idea that the acid contributes to dental decay. Speculation that oral consumption of the drug causes tooth decay by raising the acidity of users' mouths is also unsupported. Meth mouth is generally most severe in users who inject the drug, rather than those who smoke, ingest or inhale it.