The cause of isolated missing teeth remains unclear, but the condition is believed to be associated with genetic or environmental factors during dental development. Missing teeth have been reported in association with increased maternal age, low birth weight, multiple births and rubella virus infection during embryonic life.

There is a possible correlation between tooth agenesis and innervation. A relationship was also postulated between abnormalities of the brainstem and the presence of agenesis.

Hypodontia is often familial, and can also be associated with genetic disorders such as ectodermal dysplasia or Down syndrome. Hypodontia can also be seen in people with cleft lip and palate.

Among the possible causes are mentioned genetic, hormonal, environmental and infectious.

Cause due to hormonal defects: idiopathic hypoparathyroidism and pseudohypoparathyroidism. Exists the possibility that this defect depends on a moniliasis (candidiasis, "candida endocrinopathy syndrome").

Environmental causes involving exposure to PCBs (ex.dioxin), radiation, anticancer chemotherapeutic agents, allergy and toxic epidermal necrolysis after drug.

Infectious causes of hypodontia: rubella, candida.

The Journal of the American Dental Association published preliminary data suggesting a statistical association between hypodontia of the permanent teeth and epithelial ovarian cancer (EOC). The study shows that women with EOC are 8.1 times more likely to have hypodontia than are women without EOC. The suggestion therefore is that hypodontia can serve as a "marker" for potential risk of EOC in women.

Also the increased frequency of hypodontia in twins and low birth weight in twins with hypodontia suggests that environmental factors during perinatal are responsible hypodontia.

Females are affected more than males, and the condition occurs in permanent (adult) teeth more than deciduous (baby teeth or milk teeth).

In the 1960s and 1970s, several studies were conducted sponsored by the U.S. Atomic Energy Commission, with the aim of finding a link between genetics and hypodontia.

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.

Although the etiology is unclear and it is speculated to be multifactorial. Contributing factors may include the following:

1. children born preterm and those with poor general health or systemic conditions in their first 3 years may develop MIH.

2. environmental changes

3. exposure to dioxine by prolonged breast-feeding could lead to an increase in the risk of MIH

4. respiratory diseases and oxygen shortage of the ameloblasts

5. oxygen shortage combined with low birth weight

It can be caused by any of the following:

- Nutritional factors.

- Some diseases (such as undiagnosed and untreated celiac disease, chicken pox, congenital syphilis).

- Hypocalcemia.

- Fluoride ingestion (dental fluorosis).

- Birth injury.

- Preterm birth.

- Infection.

- Trauma from a deciduous tooth.

There are many potential factors involved.

- Congenital hypopituitarism

- Ectodermal dysplasia

- Down syndrome

- Ionizing radiation to the jaws during tooth development (odontogenesis)

- Chemotherapy during tooth development

- Marshall syndrome

- Rieger syndrome

- Focal dermal hypoplasia

- Silver-Russell syndrome

- Williams syndrome

- Gorlin-Chaudhry-Moss syndrome

- Coffin–Siris syndrome

- Salamon syndrome

- Cleft lip and palate

Others include trichorhinopharyngeal, odontotrichomelic, neuroectodermal and dermo-odontodysplasia syndromes.

Turner's hypoplasia is an abnormality found in teeth. Its appearance is variable, though usually is manifested as a portion of missing or diminished enamel on permanent teeth. Unlike other abnormalities which affect a vast number of teeth, Turner's hypoplasia usually affects only one tooth in the mouth and, it is referred to as a Turner's tooth.

Another abnormal condition is hypodontia, in which there are fewer than the usual number of teeth.

Hyperdontia is seen in a number of disorders, including Gardner's syndrome and cleidocranial dysostosis, where multiple supernumerary teeth are seen that are usually impacted.

There is evidence of hereditary factors along with some evidence of environmental factors leading to this condition. While a single excess tooth is relatively common, multiple hyperdontia is rare in people with no other associated diseases or syndromes. Many supernumerary teeth never erupt, but they may delay eruption of nearby teeth or cause other dental or orthodontic problems. Molar-type extra teeth are the rarest form. Dental X-rays are often used to diagnose hyperdontia.

It is suggested that supernumerary teeth develop from a third tooth bud arising from the dental lamina near the regular tooth bud or possibly from splitting the regular tooth bud itself. Supernumerary teeth in deciduous (baby) teeth are less common than in permanent teeth.

There have been many syndromes which have been identified to be related to failure of eruption of teeth. These syndromes are Cleidocranial dyspalsia, Osteoporosis, Rutherford syndrome, GAPO syndrome and Osteoglophonic dysplasia.

It is estimated that tooth loss results in worldwide productivity losses in the size of about US$63 billion yearly.

The distribution of disease in those affected with MIH can vary greatly. It can be common for the enamel of one molar to be affected while the enamel of the contralateral molar is clinically unaffected, or with minor defects only.

Smoking and tobacco use of any kind are associated with increased risk of dry socket. This may be partially due to the vasoconstrictive action of nicotine on small blood vessels. Abstaining from smoking in the days immediately following a dental extraction reduces the risk of a dry socket occurring.

The etiology, or cause of edentulism, can be multifaceted. While the extraction of non-restorable or non-strategic teeth by a dentist does contribute to edentulism, the predominant cause of tooth loss in developed countries is periodontal disease. While the teeth may remain completely decay-free, the bone surrounding and providing support to the teeth may reabsorb and disappear, giving rise to tooth mobility and eventual tooth loss. In the radiograph at the beginning of the article, tooth #21 (the lower left first premolar, to the right of #22, the lower left canine) exhibits 50% bone loss, presenting with a distal horizontal defect and a mesial vertical defect. Tooth #22 exhibits roughly 30% bone loss.

This type of failure of eruption takes place when the affected tooth is ankylosed to the bone around it. This is different than primary failure of eruption where the affected tooth/teeth were not ankylosed. In mechanical failure of eruption, affected tooth has partial or complete loss of PDL in a panoramic radiograph and teeth distal to affected tooth do not have this condition. On a percussion test, a tooth with mechanical failure of eruption will have a dull metallic sound.

Taurodontism is a condition found in the molar teeth of humans whereby the body of the tooth and pulp chamber is enlarged vertically at the expense of the roots. As a result, the floor of the pulp and the furcation of the tooth is moved apically down the root. The underlying mechanism

of taurodontism is the failure or late invagination of Hertwig's epithelial root sheath, which is responsible for root formation and shaping causing an apical shift of the root furcation.

The constriction at the amelocemental junction is usually reduced or absent. Taurodontism is most commonly found in permanent dentition although the term is traditionally applied to molar teeth.

In some cases taurodontism seems to follow an autosomal dominant type of inheritance.

Taurodontism is found in association with amelogenesis imperfecta, ectodermal dysplasia and tricho-dento-osseous syndrome.

The term means "bull like" teeth derived from similarity of these teeth to those of ungulate or cud-chewing animals.

According to Shaw these can be classified as hypotaurodont, hypertaurodont and mesotaurodont.

According to Mangion taurodontism may be:

- A (mentally retarded) character

- A primitive pattern

- Mendelian recessive character

- Atavistic feature

- A mutation

It has also been reported in Klinefelter's syndrome, XXYY and Down's syndrome .

The teeth involved are invariably molars, sometimes single and at the other times multiple teeth may be involved. The teeth themselves may look normal and do not have any particular anatomical character on clinical examination.

On a dental radiograph, the involved tooth looks rectangular in shape without apical taper. The pulp chamber is extremely large and the furcations may be only a few millimeters long at times.

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."

Mulberry molars are a dental condition usually associated with congenital syphilis, characterized by multiple rounded rudimentary enamel cusps on the permanent first molars. Mulberry molars are physically defective permanent molars. The deformity is caused by congenital syphilis. This type of abnormality is characterized by dwarfed molars with cusps covered with globular enamel growths. These teeth are functional but can be cosmetically fixed with crowns, bridges, or implants.

Just above the gum line, the mulberry molar looks normal. A deformity becomes apparent towards the cusp or top grinding surface of the tooth. Here, the size of the mulberry molar is diminished in all aspects, creating a stumpy version of a conventional molar. The cause of the molar atrophy is thought to be enamel hypoplasia, or a deficiency in tooth enamel. The underlying dentin and pulp of the tooth is normal, but the enamel covering or molar sheath is thin and deformed, creating a smaller version of a typical tooth.

The grinding surface of a mulberry molar is also corrupted. Normally, the grinding surface of a molar has a pit and is surrounded by a circular ridge at the top of the tooth, which is used for grinding. The cusp deformity of the mulberry molar is characterized by an extremely shallow or completely absent pit. Instead, the pit area is filled with globular structures bunched together all along the top surface of the cusp. This type of deformity is also thought to be caused by enamel hypoplasia. Mulberry molars are typically functional and do not need treatment. If the deformity is severe or the person is bothered by the teeth, there are several options. The teeth can be covered with a permanent cast crown, stainless steel crown, or the molars can be removed and an implant or bridge can be put in place of the mulberry molar.

A mulberry molar is caused by congenital syphilis, which is passed from the mother to the child in the uterus through the placenta. Since this particular symptom of congenital syphilis manifests later in childhood with the eruption of the permanent molars, it is a late stage marker for the disease. Hutchinson’s teeth, marked by dwarfed teeth and deformed cusps that are spaced abnormally far apart, are another dental deformity caused by congenital syphilis. Mulberry molars and Hutchinson’s teeth will often occur together. Pregnant women with syphilis should tell their doctors about the condition and be treated for it during pregnancy, otherwise the baby should be screened for the disease after birth and treated with penicillin if necessary.

Dry socket is more likely to occur following a difficult tooth extraction. It is thought that excessive force applied to the tooth, or excessive movement of the tooth burnishes the bony walls of the socket and crushes blood vessels, impairing the repair process. It has also been shown that dry socket is more likely to occur when an inexperienced surgeon performed the extraction, possibly because excessive force or excessive tooth movements are used.

The prognosis for impacted wisdom teeth depends on the depth of the impaction. When they lack a communication to the mouth, the main risk is the chance of cyst or neoplasm formation which is relatively uncommon.

Once communicating with the mouth, the onset of disease or symptoms cannot be predicted but the chance of it does increase with age. Less than 2% of wisdom teeth are free of either periodontal disease or caries by age 65. Further, several studies have found that between 30% – 60% of people with previously asymptomatic impacted wisdom teeth will have them extracted due to symptoms or disease, 4–12 years after initial examination.

Extraction of the wisdom teeth removes the disease on the wisdom tooth itself and also appears to improve the periodontal status of the second molar, although this benefit diminishes beyond the age of 25.

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.

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.

Few studies have looked at the percentage of the time wisdom teeth are present or the rate of wisdom teeth eruption. The lack of up to five teeth (excluding third molars, i.e. wisdom teeth) is termed hypodontia. Missing third molars occur in 9-30% of studied populations.

One large scale study on a group of young adults in New Zealand showed 95.6% had at least 1 wisdom tooth with an eruption rate of 15% in the maxilla and 20% in the mandible. Another study on 5000 army recruits found 10,767 impacted wisdom teeth. The frequency of impacted lower third molars has been found to be 72% and the frequency of retained impacted wisdom teeth that are free of disease and symptoms is estimated at 11.6% to 29% which drops with age.

The incidence of wisdom tooth removal was estimated to be 4 per 1000 person years in England and Wales prior to the 2000 NICE guidelines.