Extra teeth, lost teeth, impacted teeth, or abnormally shaped teeth have been cited as causes of malocclusion. A small underdeveloped jaw, caused by lack of masticatory stress during childhood, can cause tooth overcrowding. Ill-fitting dental fillings, crowns, appliances, retainers, or braces as well as misalignment of jaw fractures after a severe injury are other causes. Tumors of the mouth and jaw, thumb sucking, tongue thrusting, pacifier use beyond age 3, and prolonged use of a bottle have also been identified as causes.

In an experiment on two groups of rock hyraxes fed hardened or softened versions of the same foods, the animals fed softer food had significantly narrower and shorter faces and thinner and shorter mandibles than animals fed hard food. Experiments have shown similar results in other animals, including primates, supporting the theory that masticatory stress during childhood affects jaw development. Several studies have shown this effect in humans. Children chewed a hard resinous gum for two hours a day and showed increased facial growth.

During the transition to agriculture, the shape of the human mandible went through a series of changes. The mandible underwent a complex series of shape changes not matched by the teeth, leading to incongruity between dental and mandibular form. These changes in human skulls may have been "driven by the decreasing bite forces required to chew the processed foods eaten once humans switched to growing different types of cereals, milking and herding animals about 10,000 years ago."

Crowding of the teeth is treated with orthodontics, often with tooth extraction, clear aligners, or dental braces, followed by growth modification in children or jaw surgery (orthognathic surgery) in adults. Surgery may be required on rare occasions. This may include surgical reshaping to lengthen or shorten the jaw (orthognathic surgery). Wires, plates, or screws may be used to secure the jaw bone, in a manner similar to the surgical stabilization of jaw fractures. Very few people have "perfect" alignment of their teeth. However, most problems are very minor and do not require treatment.

Behavior therapy is important especially when the kids are in their primary dentition in the pre-adolescent age. Improving habits at this time may lead to self-correction of open bite in many cases. Sometimes presence of infantile swallowing into early childhood may lead to an anterior open bite in patients. Habit control through appliances such as Tongue crib or Tongue spurs may be used in adolescent ages if the behavior modification fails to stop the habit.

Man-Suk Baek and others evaluated long-term stability of anterior open bite by intrusion of maxillary posterior teeth. Their results showed that the molars were intruded by 2.39mm during treatment and relapsed back by 0.45mm or 22.8%. The incisal overbite increased by 5.56mm during treatment and relapsed back by 1.20mm or 17%. They concluded that majority of the relapse occurred during first year of treatment.

Reduced salivary flow rate is associated with increased caries since the buffering capability of saliva is not present to counterbalance the acidic environment created by certain foods. As a result, medical conditions that reduce the amount of saliva produced by salivary glands, in particular the submandibular gland and parotid gland, are likely to lead to dry mouth and thus to widespread tooth decay. Examples include Sjögren's syndrome, diabetes mellitus, diabetes insipidus, and sarcoidosis. Medications, such as antihistamines and antidepressants, can also impair salivary flow. Stimulants, most notoriously methylamphetamine, also occlude the flow of saliva to an extreme degree. This is known as meth mouth. Tetrahydrocannabinol (THC), the active chemical substance in cannabis, also causes a nearly complete occlusion of salivation, known in colloquial terms as "cotton mouth". Moreover, 63% of the most commonly prescribed medications in the United States list dry mouth as a known side-effect. Radiation therapy of the head and neck may also damage the cells in salivary glands, somewhat increasing the likelihood of caries formation.

Susceptibility to caries can be related to altered metabolism in the tooth, in particular to fluid flow in the dentin. Experiments on rats have shown that a high-sucrose, cariogenic diet "significantly suppresses the rate of fluid motion" in dentin.

The use of tobacco may also increase the risk for caries formation. Some brands of smokeless tobacco contain high sugar content, increasing susceptibility to caries. Tobacco use is a significant risk factor for periodontal disease, which can cause the gingiva to recede. As the gingiva loses attachment to the teeth due to gingival recession, the root surface becomes more visible in the mouth. If this occurs, root caries is a concern since the cementum covering the roots of teeth is more easily demineralized by acids than enamel. Currently, there is not enough evidence to support a causal relationship between smoking and coronal caries, but evidence does suggest a relationship between smoking and root-surface caries.

Exposure of children to secondhand tobacco smoke is associated with tooth decay.

Intrauterine and neonatal lead exposure promote tooth decay. Besides lead, all atoms with electrical charge and ionic radius similar to bivalent calcium,

such as cadmium, mimic the calcium ion and therefore exposure to them may promote tooth decay.

Poverty is also a significant social determinant for oral health. Dental caries have been linked with lower socio-economic status and can be considered a disease of poverty.

Forms are available for risk assessment for caries when treating dental cases; this system using the evidence-based Caries Management by Risk Assessment (CAMBRA). It is still unknown if the identification of high-risk individuals can lead to more effective long-term patient management that prevents caries initiation and arrests or reverses the progression of lesions.

Saliva also contains iodine and EGF. EGF results effective in cellular proliferation, differentiation and survival. Salivary EGF, which seems also regulated by dietary inorganic iodine, plays an important physiological role in the maintenance of oral (and gastro-oesophageal) tissue integrity, and, on the other hand, iodine is effective in prevention of dental caries and oral health.

Literature states that very few crossbites tend to self-correct which often justify the treatment approach of correcting these bites as early as possible. Only 0–9% of crossbites self-correct. Lindner et al. reported that in a 50% of crossbites were corrected in 76 four year old children.

Crossbite is a form of malocclusion where a tooth (or teeth) has a more buccal or lingual position (that is, the tooth is either closer to the cheek or to the tongue) than its corresponding antagonist tooth in the upper or lower dental arch. In other words, crossbite is a lateral misalignment of the dental arches.

Overbite medically refers to the extent of vertical (superior-inferior) overlap of the maxillary central incisors over the mandibular central incisors, measured relative to the incisal ridges.

The term overbite does not refer to a specific condition, nor is it a form of malocclusion. Rather an absent or excess overbite would be a malocclusion. Normal overbite is not measured in exact terms, but as a proportion (approximately 30–50% of the height of the mandibular incisors) and is commonly expressed as a percentage.

There are certain diseases and disorders affecting teeth that may leave an individual at a greater risk for cavities.

Molar incisor hypomineralization, which seems to be increasingly common. While the cause is unknown it is thought to be a combination of genetic and environmental factors. Possible contributing factors that have been investigated include systemic factors such as high levels of dioxins or polychlorinated biphenyl (PCB) in the mother’s milk, premature birth and oxygen deprivation at birth, and certain disorders during the child’s first 3 years such as such as mumps, diphtheria, scarlet fever, measles, hypoparathyroidism, malnutrition, malabsorption, hypovitaminosis D, chronic respiratory diseases, or undiagnosed and untreated coeliac disease, which usually presents with mild or absent gastrointestinal symptoms.

Amelogenesis imperfecta, which occurs in between 1 in 718 and 1 in 14,000 individuals, is a disease in which the enamel does not fully form or forms in insufficient amounts and can fall off a tooth. In both cases, teeth may be left more vulnerable to decay because the enamel is not able to protect the tooth.

In most people, disorders or diseases affecting teeth are not the primary cause of dental caries. Approximately 96% of tooth enamel is composed of minerals. These minerals, especially hydroxyapatite, will become soluble when exposed to acidic environments. Enamel begins to demineralize at a pH of 5.5. Dentin and cementum are more susceptible to caries than enamel because they have lower mineral content. Thus, when root surfaces of teeth are exposed from gingival recession or periodontal disease, caries can develop more readily. Even in a healthy oral environment, however, the tooth is susceptible to dental caries.

The evidence for linking malocclusion and/or crowding to dental caries is weak; however, the anatomy of teeth may affect the likelihood of caries formation. Where the deep developmental grooves of teeth are more numerous and exaggerated, pit and fissure caries is more likely to develop (see next section). Also, caries is more likely to develop when food is trapped between teeth.

In disease states, maxillary prognathism is associated with Cornelia de Lange syndrome; however, so-called false maxillary prognathism, or more accurately, retrognathism, where there is a lack of growth of the mandible, is by far a more common condition.

Prognathism, if not extremely severe, can be treated in growing patients with orthodontic functional or orthopaedic appliances. In adult patients this condition can be corrected by means of a combined surgical/orthodontic treatment, where most of the time a mandibular advancement is performed. The same can be said for mandibular prognathism.

Not all alveolar prognathism is anomalous, and significant differences can be observed among different ethnic groups.

Harmful habits such as thumb sucking or tongue thrusting can result in or exaggerate an alveolar prognathism, causing teeth to misalign. Functional appliances can be used in growing children to help modify bad habits and neuro-muscular function, with the aim of correcting this condition.

Alveolar prognathism can also easily be corrected with fixed orthodontic therapy. However, relapse is quite common, unless the cause is removed or a long-term retention is used.

Repair with cementum or dentin occurs after partial root resorption, fusing the tooth with the bone. It may occur following dental trauma, especially occlusal trauma, or after periapical periodontitis caused by pulp necrosis. Ankylosis itself is not a reason to remove a permanent tooth, however teeth which must be removed for other reasons are made significantly more difficult to remove if they are ankylosed.

Overbite is often confused with overjet, which is the distance between the maxillary anterior teeth and the mandibular anterior teeth in the anterior-posterior axis.

"Overbite" may also be used commonly to refer to Class II malocclusion or retrognathia, though this usage can be considered incorrect. This is where the mesiobuccal cusp of the maxillary first molar is situated anterior to the buccal groove of the mandibular first molar; in other words, the mandible (lower jaw) appears too far behind the maxilla. A person presenting with Class II malocclusion may exhibit excessive overbite as well, or may have the opposite problem, which is referred to as openbite (or apertognathia). In the case of apertognathia, the teeth do not overlap enough or at all. The upper teeth protrude past the lower teeth.

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

Ankylosis of deciduous teeth ("submerged teeth") may rarely occur. The most commonly affected tooth is the mandibular (lower) second deciduous molar. Partial root resorption first occurs and then the tooth fuses to the bone. This prevents normal exfoliation of the deciduous tooth and typically causes impaction of the permanent successor tooth. As growth of the alveolar bone continues and the adjacent permanent teeth erupt, the ankylosed deciduous tooth appears to submerge into the bone, although in reality it has not changed position. Treatment is by extraction of the involved tooth, to prevent malocclusion, periodontal disturbance or dental caries.

While it is rare before the age of 3, about 30 percent of children between 7 and 10 years of age and 45 percent of teenagers engage in nail biting. Finally, prevalence decreases in adults. Figures may vary between studies, and could be related to geographic and cultural differences. The proportion of subjects that have ever had the habit (lifetime prevalence) may be much higher than the proportion of current nail-biters (time-point prevalence). Although it does not seem to be more common in either sex, results of epidemiological studies on this issue are not fully consistent. It may be underrecognized since individuals tend to deny or be ignorant of its negative consequences, complicating its diagnosis. Having a parent with a mental disorder is also a risk factor.

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).

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).

Prosthetic replacement of missing teeth is possible using dental implant technology or dentures. This treatment can be successful in giving patients with anodontia a more aesthetically pleasing appearance. The use of an implant prosthesis in the lower jaw could be recommended for younger patients as it is shown to significantly improve the craniofacial growth, social development and self-image. The study associated with this evidence worked with individuals who had ectodermal dysplasia of varying age groups of up to 11, 11 to 18 and more than 18 years. It was noted that the risk of implant failure was significantly higher in patients younger than 18 years, but there is significant reason to use this methodology of treatment in those older. Overall the use of an implant-prosthesis has a considerable functional, aesthetic and psychological advantage when compared to a conventional denture, in the patients.

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.

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.

Some researchers suggest that HGF is transmitted as a Mendelian trait since both autosomal dominant and autosomal recessive transmission has been reported since the early 1970s. (SOURCE 1) In more recent scientific literature, there is evidence in which pedigree analyses confirm autosomal dominant, autosomal recessive or even as X-linked inherited cases of the HGF trait.

In 2002, researchers described the SOS1 gene and proved for the first time that a single-nucleotide–insertion mutation of the SOS1 gene on codon 1083 is the preliminary cause of HGF1 in humans. (Source 1) Later on in 2010, there was a case study done on a 16-year-old male with severe gingival overgrowth, almost covering all teeth. Researchers approached this issue with periodontics - a partial gingivectomy and flap surgery. This case study concluded that surgery followed by regular follow-ups is a good way to treat HGF despite the fact that the risks of re-occurrence of the condition remain high.

Even more recently, a study was done in 2013 on a family that showed history of autosomal recessive inheritance of HGF. The study did not dismiss the return of HGF after treatment but did claim that general surgical intervention after scaling and root planning of teeth supplemented with good oral hygiene is good enough to prevent the re-occurrence of HGF. This case study also acknowledged how HGF can be part of a multi-system syndrome associated with disorders such as Zimmermann Laband syndrome (ear, nose, bone, and nail defects with hepatosplenomegaly), Rutherford syndrome (microphthalmia, mental retardation, athetosis, and hypopigmentation), Murray-Puretic Drescher syndrome and Ramon syndrome.

The following can occur if left untreated:

- Too much gingiva exposure

- Oral morbidity

- Chronic infection of areas between the gums and teeth, or at the gum line

- various degrees of Periodontitis - most likely due to the inability and difficulty of keeping the gingival margin and surrounding tissue clean due to the overgrowth

- Improper tooth eruption and/or complete prevention of tooth eruption as a result of too much gingiva exposure

- Systemic every-day troubles including functional and aesthetic problems of the mouth

- Malocclusion

In dentistry, anodontia, also called anodontia vera, is a rare genetic disorder characterized by the congenital absence of all primary or permanent teeth. It is associated with the group of skin and nerve syndromes called the ectodermal dysplasias. Anodontia is usually part of a syndrome and seldom occurs as an isolated entity.

Congenital absence of permanent teeth can present as hypodontia, usually missing 1 or 2 permanent teeth, or oligodontia that is the congenital absence of 6 or more teeth. Congenital absence of all wisdom teeth, or third molars, is relatively common. Anodontia is the congenital absence of teeth and can occur in some or all teeth (partial anodontia or hypodontia), involve two dentitions or only teeth of the permanent dentition (Dorland's 1998). Approximately 1% of the population suffers from oligodontia. Many denominations are attributed to this anomaly: partial anodontia, hypodontia, oligodontia, the congenital absence, anodontia, bilateral aplasia. Anodontia being the term used in controlled vocabulary Medical Subject Headings (MeSH) from MEDLINE which was developed by the United States National Library of Medicine. The congenital absence of at least one permanent tooth is the most common dental anomaly and may contribute to masticator dysfunction, speech impairment, aesthetic problems, and malocclusion (Shapiro and Farrington 1983). Absence of lateral incisors represents a major stereotype. Individuals with this condition are perceived as socially most aggressive compared with people without anodontia (Shaw 1981).

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.