Orofacial myofunctional disorders (OMD) (sometimes called “oral myofunctional disorder", and “tongue thrust”) are muscle disorders of the face, mouth, lips, or jaw.

Recent studies on incidence and prevalence of tongue thrust behaviors are not available. However, according to the previous research, 38% of various populations have OMD. The incidence is as high as 81% in children exhibiting speech/articulation problems (Kellum, 1992).

The adaptation from nasal to mouth breathing takes pace when changes such as chronic middle ear infections, sinusitis, allergic rhinitis, upper airway infections, and sleep disturbances (e.g., snoring) take place. In addition, mouth breathing is often associated with a decrease in oxygen intake into the lungs. Mouth breathing can particularly affect the growing face, as the abnormal pull of these muscle groups on facial bones slowly deforms these bones, causing misalignment. The earlier in life these changes take place, the greater the alterations in facial growth, and ultimately an open mouth posture is created where the upper lip is raised and the lower jaw is maintained in an open posture. The tongue, which is normally tucked under the roof of the mouth, drops to the floor of the mouth and protrudes to allow a greater volume of air intake. Consequently, an open mouth posture can lead to malocclusions and problems in swallowing. Other causes of open-mouth posture are weakness of lip muscles, overall lack of tone in the body or hypotonia, and prolonged/chronic allergies of the respiratory tract. A.union

Factors that can contribute to tongue thrusting include macroglossia (enlarged tongue), thumb sucking, large tonsils, hereditary factors, ankyloglossia (tongue tie), and certain types of artificial nipples used in feeding infants, also allergies or nasal congestion can cause the tongue to lie low in the mouth because of breathing obstruction and finally contributing to tongue thrusting. In addition, it is also seen after prolonged therapy by levodopa in Parkinsonism, also it occurs as extra pyramidal side effect (Acute muscular dystonia) after use of Neuroleptics (Anti-Psychotics).

Tongue thrust is normal in infants until approximately the age of six months. The loss of this normal infant behavior is one of the signs that the baby is ready to begin eating baby food.

Tongue thrusting can adversely affect the teeth and mouth. A person swallows from 1,200 to 2,000 times every 24 hours with about four pounds (1.8 kg) of pressure each time. If a person suffers from tongue thrusting, this continuous pressure tends to force the teeth out of alignment. Many people who tongue thrust have open bites; the force of the tongue against the teeth is an important factor in contributing to "bad bite" (malocclusion). Many orthodontists have completed dental treatment with what appeared to be good results, only to discover that the case relapsed because of the patient's tongue thrust. If the tongue is allowed to continue its pushing action against the teeth, it will continue to push the teeth forward and reverse the orthodontic work.

Speech is not frequently affected by the tongue thrust swallowing pattern. The "S" sound (lisping) is the one most affected. The lateral lisp (air forced on the side of the tongue rather than forward) shows dramatic improvement when the tongue thrust is corrected. However, lisping and tongue thrust are not always associated.

Opinion varies regarding how frequently ankyloglossia truly causes problems. Some professionals believe it is rarely symptomatic, whereas others believe it is associated with a variety of problems. The disagreement among professionals was documented in a study by Messner and Lalakea (2000). The authors sent a survey to a total of 1598 otolaryngologists, pediatricians, speech-language pathologists and lactation consultants with questions to ascertain their beliefs on ankyloglossia. 797 of the surveys were fully completed and used in the study. It was found that 69% of lactation consultants, but only a minority of pediatricians answered that ankyloglossia is frequently associated with feeding difficulties; 60% of otolaryngologists and 50% of speech pathologists answered that ankyloglossia is sometimes associated with speech difficulties compared to only 23% of pediatricians; 67% of otolaryngologists compared with 21% of pediatricians answered that ankyloglossia is sometimes associated with social and mechanical difficulties. Limitations of this study include a reduced sample size due to unreturned or incomplete surveys.

Ankyloglossia can affect eating, speech, and oral hygiene as well as have mechanical/social effects. Ankyloglossia can also prevent the tongue from contacting the anterior palate. This can then promote an infantile swallow and hamper the progression to an adult-like swallow which can result in an open bite deformity. It can also result in mandibular prognathism; this happens when the tongue contacts the anterior portion of the mandible with exaggerated anterior thrusts.

The cause of talon cusp is unknown. The anomaly can occur due to genetic and environmental factors but the onset can be spontaneous. Prevention is difficult because the occurrence happens during the development of teeth.

Talon cusp affects men and women equally, however the majority of reported cases are of the male gender. Individuals of Asian, Arabic, Native American and Inuit descent are affected more commonly. Talon cusp is also highly observed in patients with orofacial digital II syndrome and Rubinstein Taybi syndrome. Other anomalies that occur with talon cusp can include peg laterals, supernumerary teeth, dens envaginatus, agenesis and impaction. A person belonging to one of these particular demographics or one who has any of these deformities or syndromes may have a higher risk of having a talon cusp.

Future studies will look further into the relationship of talon cusp and Rubinstein-Taybi syndrome and other oral-facial-digital syndromes. A former study showed a direct correlation in which 45 affected patients with Rubinstein-Taybi syndrome, 92% of these patients had talon cusp. Other researchers are attempting to trace talon cusp to ancestors and comparing dentition to modern humans. Another study done in 2007 examined the dentition of 301 Native American Indian skeletons for the presence or absence of talon cusp. The results showed five skeletons (2 percent) in the population had the trait.

In 2011, only 21 cases of talon cusp have been reported and are in literature. It appears that as of 2014 and 2015, additional research continues in hopes of finding the cause and mechanism of talon cusp. With the majority of cases of talon cusp being unreported, it remains difficult to conduct tests, come up with conclusions, conduct surgery and perform research with small numbers.

Dentin hypersensitivity is a relatively common condition. Due to differences in populations studied and methods of detection, the reported incidence ranges from 4-74%. Dentists may under-report dentin hypersensitivity due to difficulty in diagnosing and managing the condition. When questionnaires are used, the reported incidence is usually higher than when clinical examination is used. Overall, it is estimated to affect about 15% of the general population to some degree.

It can affect people of any age, although those aged 20–50 years are more likely to be affected. Females are slightly more likely to develop dentin hypersensitivity compared to males. The condition is most commonly associated with the maxillary and mandibular canine and bicuspid teeth on the facial (buccal) aspect, especially in areas of periodontal attachment loss.

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).

Trauma, both micro and macrotrauma, is sometimes identified as a possible cause of TMD; 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 TMD. This has been termed "post-traumatic TMD", to separate it from "idiopathic TMD". Despite multiple studies having been performed over the years, the cumulative evidence has been described as conflicting, with moderate evidence that TMD can occasionally follow whiplash injury. The research that suggests a link appears to demonstrate a low to moderate incidence of TMD following whiplash injury, and that pTMD has a poorer response to treatment than TMD which has not developed in relation to trauma.

A great many diseases involve the mouth, jaws and orofacial skin. Some example pathologies which can involve the oral and maxillofacial region are listed. Some are more common than others, and this list is by no means complete. The examples are considered according to a surgical sieve.

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.

Genetic counseling for VWS involves discussion of disease transmission in the autosomal dominant manner and possibilities for penetrance and expression in offspring. Autosomal dominance means affected parents have a 50% chance of passing on their mutated "IRF6" allele to a their child. Furthermore, if a cleft patient has lip pits, he or she has a ten times greater risk of having a child with cleft lip with or without cleft palate than a cleft patient who does not have lip pits. Types of clefting between parents and affected children are significantly associated; however, different types of clefts may occur horizontally and vertically within the same pedigree. In cases where clefting is the only symptom, a complete family history must be taken to ensure the patient does not have non-syndromic clefting.

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.

Dentin hypersensitivity may affect individuals' quality of life. Over time, the dentin-pulp complex may adapt to the decreased insulation by laying down tertiary dentin, thereby increasing the thickness between the pulp and the exposed dentin surface and lessening the symptoms of hypersensitivity. Similar process such as formation of a smear layer (e.g. from toothbrushing) and dentin sclerosis. These physiologic repair mechanisms are likely to occur with or without any form of treatment, but they take time.

Oral and maxillofacial pathology (also termed oral pathology, stomatognathic disease, dental disease, or mouth disease) refers to the diseases of the mouth ("oral cavity" or "stoma"), jaws ("maxillae" or "gnath") and related structures such as salivary glands, temporomandibular joints, facial muscles and perioral skin (the skin around the mouth). The mouth is an important organ with many different functions. It is also prone to a variety of medical and dental disorders.

The specialty oral and maxillofacial pathology is concerned with diagnosis and study of the causes and effects of diseases affecting the oral and maxillofacial region. It is sometimes considered to be a specialty of dentistry and pathology. Sometimes the term head and neck pathology is used instead, but this might imply that the pathologist deals with otorhinolaryngologic disorders (i.e. ear, nose and throat) in addition to maxillofacial disorders. In this role there is some overlap between the expertise of head and neck pathologists and that of endocrine pathologists.

Environmental influences may also cause, or interact with genetics to produce, orofacial clefting. An example of how environmental factors might be linked to genetics comes from research on mutations in the gene "PHF8" that cause cleft lip/palate (see above). It was found that PHF8 encodes for a histone lysine demethylase, and is involved in epigenetic regulation. The catalytic activity of PHF8 depends on molecular oxygen, a fact considered important with respect to reports on increased incidence of cleft lip/palate in mice that have been exposed to hypoxia early during pregnancy. In humans, fetal cleft lip and other congenital abnormalities have also been linked to maternal hypoxia, as caused by e.g. maternal smoking, maternal alcohol abuse or some forms of maternal hypertension treatment. Other environmental factors that have been studied include: seasonal causes (such as pesticide exposure); maternal diet and vitamin intake; retinoids — which are members of the vitamin A family; anticonvulsant drugs; nitrate compounds; organic solvents; parental exposure to lead; alcohol; cigarette use; and a number of other psychoactive drugs (e.g. cocaine, crack cocaine, heroin).

Current research continues to investigate the extent to which folic acid can reduce the incidence of clefting.

Lip pits may be surgically removed either for aesthetic reasons or discomfort due to inflammation caused by bacterial infections or chronic saliva excretion, though spontaneous shrinkage of the lip pits has occurred in some rare cases. Chronic inflammation has also been reported to cause squamous-cell carcinoma. It is essential to completely remove the entire lip pit canal, as mucoid cysts can develop if mucous glands are not removed. A possible side effect of removing the lip pits is a loose lip muscle. Other conditions associated with VWS, including CL, CP, congenital heart defects, etc. are surgically corrected or otherwise treated as they would be if they were non-syndromic.

Most dental pain can be treated with routine dentistry. In rare cases, toothache can be a symptom representing a life-threatening condition, such as a deep neck infection (compression of the airway by a spreading odontogenic infection) or something more remote like a heart attack.

Dental caries, if left untreated, follows a predictable natural history as it nears the pulp of the tooth. First it causes reversible pulpitis, which transitions to irreversible pulpitis, then to necrosis, then to necrosis with periapical periodontitis and, finally, to necrosis with periapical abscess. Reversible pulpitis can be stopped by removal of the cavity and the placement of a sedative dressing of any part of the cavity that is near the pulp chamber. Irreversible pulpitis and pulp necrosis are treated with either root canal therapy or extraction. Infection of the periapical tissue will generally resolve with the treatment of the pulp, unless it has expanded to cellulitis or a radicular cyst. The success rate of restorative treatment and sedative dressings in reversible pulpitis, depends on the extent of the disease, as well as several technical factors, such as the sedative agent used and whether a rubber dam was used. The success rate of root canal treatment also depends on the degree of disease (root canal therapy for irreversible pulpitis has a generally higher success rate than necrosis with periapical abscess) and many other technical factors.

Toothache may occur at any age, in any gender and in any geographic region. Diagnosing and relieving toothache is considered one of the main responsibilities of dentists. Irreversible pulpitis is thought to be the most common reason that people seek emergency dental treatment. Since dental caries associated with pulpitis is the most common cause, toothache is more common in populations that are at higher risk of dental caries. The prevalence of caries in a population is dependent upon factors such as diet (refined sugars), socioeconomic status, and exposure to fluoride (such as areas without water fluoridation). In the United States, an estimated 12% of the general population reported that they suffered from toothache at some point in the six months before questioning. Individuals aged 18–34 reported much higher experience of toothache than those aged 75 or over. In a survey of Australian schoolchildren, 12% had experienced toothache before the age of five, and 32% by the age of 12. Dental trauma is extremely common and tends to occur more often in children than adults.

This type of gingival enlargement is sometimes termed "drug induced gingival enlargement" or "drug influenced gingival enlargement", abbreviated to "DIGO". Gingival enlargement may also be associated with the administration of three different classes of drugs, all producing a similar response: Gingival overgrowth is a common side effect of phenytoin, termed "Phenytoin-induced gingival overgrowth" (PIGO).

- anticonvulsants (such as phenytoin, phenobarbital, lamotrigine, vigabatrin, ethosuximide, topiramate and primidone NOT common for valproate)

- calcium channel blockers (antihypertensives such as nifedipine, amlodipine, and verapamil). The dihydropyridine derivative isradipidine can replace nifedipine and does not induce gingival overgrowth.

- cyclosporine, an immunosuppresant.

Of all cases of DIGO, about 50% are attributed to phenytoin, 30% to cyclosporins and the remaining 10-20% to calcium channel blockers.

Drug-induced enlargement has been associated with a patient's genetic predisposition, and its association with inflammation is debated. Some investigators assert that underlying inflammation is necessary for the development of drug-induced enlargement, while others purport that the existing enlargement induced by the drug effect compounds plaque retention, thus furthering the tissue response. Careful attention to oral hygiene may reduce the severity of gingival hyperplasia. In most cases, discontinuing the culprit drug resolves the hyperplasia.

OFG is uncommon, but the incidence is increasing. The disease usually presents in adolescence or young adulthood. It may occur in either sex, but males are slightly more commonly affected.

Many genes associated with syndromic cases of cleft lip/palate (see above) have been identified to contribute to the incidence of isolated cases of cleft lip/palate. This includes in particular sequence variants in the genes "IRF6", "PVRL1" and "MSX1". The understanding of the genetic complexities involved in the morphogenesis of the midface, including molecular and cellular processes, has been greatly aided by research on animal models, including of the genes "BMP4", "SHH", "SHOX2", "FGF10" and "MSX1".

It is commonly seen in Boxer dogs and other brachycephalic breeds, and in the English Springer Spaniel. It usually starts around middle age and progresses. Some areas of the gingiva can become quite large but have only a small attachment to the rest of the gingiva, and it may completely cover the teeth. Infection and inflammation of the gingiva is common with this condition. Under anesthesia, the enlarged areas of gingiva can be cut back with a scalpel blade or CO laser, but it often recurs. Gingival enlargement is also a potential sequela of gingivitis. As in humans, it may be seen as a side effect to the use of ciclosporin.