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.

The cause of germination is still unknown. However, there are a few possible factors contributing to germination:

- Vitamin deficiency

- Hormonal irregularities

- Infection or inflammation of areas near to the developing tooth bud

- Drug induced

- Genetic predisposition

- Radiotherapy that caused damage to the developing tooth germ

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).

Genetic causes also involve the genes MSX1 and PAX9.

Genetic associations for selective tooth agenesis ("STHAG") include:

Before root canal treatment or extraction are carried out, the clinician should have thorough knowledge about the root canal morphology to avoid complications.

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.

No intervention is usually recommended unless they are causing difficulty to the infant or mother.

However some recommend that they be removed as the tooth can cut or amputate the tip of the tongue.

They should be left in the mouth as long as possible to decrease the likelihood of removing permanent tooth buds with the natal tooth. They should also not be removed if the infant has hypoprothrombinemia. In case of complications when the natal teeth need to be removed, dental radiographs should be obtained whenever possible, and evaluated and followed up with pediatric dentists.

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.

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.

Most of the time, natal teeth are not related to a medical condition. However, sometimes they may be associated with:

- Ellis–van Creveld syndrome

- Hallermann–Streiff syndrome

- Pierre Robin syndrome

- Sotos syndrome

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

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.

An anterior open bite occurs in humans when the front teeth fail to touch and there is no overlap between upper incisors and lower incisors. Anterior open can be caused by functional habits such as digit sucking, tongue thrust or long-term pacifier use. When digit sucking habit is present in the late primary to early mixed dentition stages, it can lead to different side-effects such as upper teeth flaring out, lower teeth flaring in, increase in the open bite and the overjet. A posterior crossbite in these children along with decrease in intercanine and intermolar width is also found. The more intense (longer) the habit, the worse the malocclusion may be.

Pacifier use has also shown to cause anterior open bites in children. Pacifier use which lasts longer than 18 months, may cause this malocclusion. It is shown that as long as the sucking habit stops before the eruption of permanent teeth, the open bite self-corrects. In some cases, behavior modification may be necessary to eliminate the dental habits. If all else fails, then a tongue crib can be used.

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).

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.

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.

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.

Unilateral crossbite involves one side of the arch. The most common cause of unilateral crossbite is a narrow maxillary dental arch. This can happen due to habits such as digit sucking, prolonged use of pacifier or upper airway obstruction. Due to the discrepancy between the maxillary and mandibular arch, neuromuscular guidance of the mandible causes mandible to shift towards the side of the crossbite. This is also known as Functional mandibular shift. This shift can become structural if left untreated for a long time during growth, leading to skeletal asymmetries. Unilateral crossbites can present with following features in a child

- Lower midline deviation to the crossbite side

- Class 2 Subdivision relationships

- Temporomandibular disorders

Overjet is the extent of horizontal (anterior-posterior) overlap of the maxillary central incisors over the mandibular central incisors. In class II (division I) malocclusion the overjet is increased as the maxillary central incisors are protruded.

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.

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.

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."

1-increased localised pressure.

2- focal growth retardation and stimulation.