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.

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.

Prevention of early childhood caries begins before the baby is born; women are advised to maintain a well-balanced diet of high nutritional value, especially during the third trimester and within the infants first year of life. This is since enamel undergoes maturation; if the diet is not sufficient, a common condition that may occur is enamel hypoplasia.

Enamel hypoplasia is a developmental defect of enamel that occurs during tooth development, mainly pre-natally or during early childhood. Teeth affected by enamel hypoplasia are commonly at a higher risk of caries since there is an increased loss of minerals and therefore the tooth surface is able to breakdown more easily than in comparison to a non-hypoplastic tooth. It is therefore suggested to the mother to maintain a healthy diet since evidence suggests malnourishment during the perinatal period increases the risk of hypoplastic teeth in an infant.

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.

Fluorosis is extremely common, with 41% of adolescents having definite fluorosis, and another 20% "questionably" having fluorosis according to the Centers for Disease Control.

The U.S. Centers for Disease Control found a 9 percentage point increase in the prevalence of confirmed dental fluorosis in a 1999-2002 study of American children and adolescents than was found in a similar survey from 1986-1987 (from 22.8% in 1986-1987 to 32% in 1999-2002). In addition, the survey provides further evidence that African Americans suffer from higher rates of fluorosis than Caucasian Americans.

The condition is more prevalent in rural areas where drinking water is derived from shallow wells or hand pumps. It is also more likely to occur in areas where the drinking water has a fluoride content greater than 1 ppm (part per million).

If the water supply is fluoridated at the level of 1 ppm, one must consume one litre of water in order to take in 1 mg of fluoride. It is thus improbable a person will receive more than the tolerable upper limit from consuming optimally fluoridated water alone.

Fluoride consumption can exceed the tolerable upper limit when someone drinks a lot of fluoride-containing water in combination with other fluoride sources, such as swallowing fluoridated toothpaste, consuming food with a high fluoride content, or consuming fluoride supplements. The use of fluoride supplements as a prevention for tooth decay is rare in areas with water fluoridation, but was recommended by many dentists in the UK until the early 1990s.

Dental fluorosis can be prevented by lowering the amount of fluoride intake to below the tolerable upper limit.

In November 2006 the American Dental Association published information stating that water fluoridation is safe, effective and healthy; that enamel fluorosis, usually mild and difficult for anyone except a dental health care professional to see, can result from ingesting more than optimal amounts of fluoride in early childhood; that it is safe to use fluoridated water to mix infant formula; and that the probability of babies developing fluorosis can be reduced by using ready-to-feed infant formula or using water that is either free of fluoride or low in fluoride to prepare powdered or liquid concentrate formula. They go on to say that the way to get the benefits of fluoride but minimize the risk of fluorosis for a child is to get the right amount of fluoride, not too much and not too little. "Your dentist, pediatrician or family physician can help you determine how to optimize your child’s fluoride intake."

Fluoride is a natural mineral that naturally occurs throughout the world – it is also the active ingredient of many toothpastes specifically for its remineralizing effects on enamel, often repairing the tooth surface and reducing the risk of caries.

The use of fluoridated toothpaste is highly recommended by dental professionals; whereby studies suggest that the correct daily use of fluoride on the dentition of children has a high caries-preventive effect and therefore prevents has potential to prevent ECC. However, it is important to use fluoridated toothpastes correctly; children below the age of two do not usually require toothpaste unless they are already at a high risk of ECC as diagnosed by a dental professional, and therefore it is it is recommended to use a small sized ‘smear’ of toothpaste to incorporate fluoride, with caution removing the toothpaste from within the mouth and not allowing the child to swallow the substances.

Amelogenesis imperfecta hypomaturation type with taurodontism are often confused. Amelogenesis imperfecta of the hypomaturation type with taurodontism (AIHHT) has no hair or bone changes which helps to differentiate between TDO cases and AIHHT. Polymerase chain reaction also known as PCR is used to amply pieces of DNA and observed for the 141 base pair allele as a result of a deletion of four nucleotides in exon 3 of the DLX-3 gene. Additionally, the current research shows that there is heavy reliance on the physical characteristics in the differentiation of TDO verses AIHHT and the severity and prevalence of their expression. For instance, taurodontism is severely expressed in TDO, but mildly expressed in AIHHT. Currently, researchers are trying to identify the reason for the alteration in the DLX-3 and DLX-7 genes that are responsible for AIHHT versus TDO.

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.

The most superficial concern in dental fluorosis is aesthetic changes in the permanent dentition (the adult teeth). The period when these teeth are at highest risk of developing fluorosis is between when the child is born up to 6 years old, though there has been some research which proposes that the most crucial course is during the first 2 years of the child's life. From roughly 7 years old thereafter, most children's permanent teeth would have undergone complete development (except their wisdom teeth), and therefore their susceptibility to fluorosis is greatly reduced, or even insignificant, despite the amount of intake of fluoride. The severity of dental fluorosis depends on the amount of fluoride exposure, the age of the child, individual response, weight, degree of physical activity, nutrition, and bone growth. Individual susceptibility to fluorosis is also influenced by genetic factors.

Many well-known sources of fluoride may contribute to overexposure including dentifrice/fluoridated mouthrinse (which young children may swallow), excessive ingestion of fluoride toothpaste, bottled waters which are not tested for their fluoride content, inappropriate use of fluoride supplements, ingestion of foods especially imported from other countries, and public water fluoridation. The last of these sources is directly or indirectly responsible for 40% of all fluorosis, but the resulting effect due to water fluoridation is largely and typically aesthetic. Severe cases can be caused by exposure to water that is naturally fluoridated to levels well above the recommended levels, or by exposure to other fluoride sources such as brick tea or pollution from high fluoride coal.

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.

Research has shown that there are five million teeth knocked-out each year in the United States.

Up to 25% of school-aged children and military trainees and fighters experience some kind of dental trauma each year. The incidence of dental avulsion in school aged children ranges from 0.5 to 16% of all dental trauma. Many of these teeth are knocked-out during school activities or sporting events such as contact sports, football, basketball, and hockey.It is important for anyone whom is related, working, or witnessing sports that they be educated on this subject matter. Being educated could aid in minimizing injuries that could do further harm to the victim. Being informed and spreading awareness of dental avulsion in the state of knowledge, treatment, and prevention could make an impact.

Bisphosphonates have recently been introduced to treat several bone disorders, which include osteogenesis imperfecta.

A recognized risk of this drug relevant to dental treatments is bisphosphonate-associated osteonecrosis of the jaw (BRONJ). Occurrences of this risk is associated with dental surgical procedures such as extractions.

Dental professionals should therefore proceed with caution when carrying out any dental procedures in patients who have Type 2 DI who may be on bisphosphonate drug therapy.

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.

A single copy of the abnormal gene from one parent is able to cause the disease; this is called autosomal dominance. A mutation in the DLX3 gene has been confirmed as the cause of TDO. The onset of TDO begins with a 4 base pair deletion on chromosome 17q21, causing a mutation, specifically frameshift, and the termination codon to be the cause of the lack of complete maturation of the tooth enamel; this mutation is also responsible for the osseous defects in the bone. DLX-3 is expressed in the placenta and is significantly important during embryonic development in regards to hard bone tissue which is present in the teeth, skull, and long bones such as in the arms and legs. During normal tooth development, DLX 3 shifts from predominant expression in the inner enamel epithelium; the outer layer does not express DLX 3. In TDO cases, the DLX-3 is present on the outer enamel epithelium and leads to the dental abnormalities seen in this disease. Improper expression of DLX-3 causes the tooth enamel to be thinner, which leads to attrition and is most often the cause of dental abscess seen in TDO persons.

During osseous, connective tissue, and dermal cell differentiation, DLX 3 in TDO is also responsible for upper cranial thickness, calvaria, osteosclerosis of the long bones, long narrow head (dolichocephaly), abnormally thin brittle nails, and premature closing of fibrous joints. Consequently, 95% of people with TDO that are 16 years old or younger show skeletal abnormalities before full maturation takes place. Lack of mastoid pneumatization by mastoid cells occurs in 82% of the cases and is rarely prevalent outside of TDO diagnosis. Mastoid pneumatization occurs at about 6 months of ages and acts to minimize pressure fluctuations in the Eustachian tubes of the ear. The mastoid lies posterior to the lower jawbone (mandible) and distal to the ear. The Eustachian tube connects the middle ear to the back of the nose, and acts to create a specific pressure in the ear canal that causes vibrations to the eardrum; if adequate pressure is not attained, muffled, dull hearing results. In addition to the mastoid pneumatization assisting the Eustachian tubes for normal hearing, lack of mastoid pneumatization causes inflammation of the ear, general irritation, and does not allow enough air in to assist with mucus flowing out. It is not completely understood why gene mutations occur, but it is known that genetic mutations that cause disease are acquired from either or both parents at fertilization.

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.

Discoloration of the front teeth is one of the most common reasons people seek dental care. However, many people with teeth of normal shade ask for them to be whitened. Management of tooth discoloration depends on the cause. Most discoloration is harmless and may or may not be of cosmetic concern to the individual. In other cases it may indicate underlying pathology such as pulp necrosis or rarely a systemic disorder.

Most extrinsic discoloration is readily removed by cleaning the teeth, whether with "whitening" (i.e., abrasive) toothpaste at home, or as treatment carried out by a professional (e.g., scaling and/or polishing). To prevent future buildup of extrinsic stains, identification of the cause (e.g., smoking) is required.

Intrinsic discoloration generally requires one of the many types of tooth bleaching. Alternatively the appearance of the tooth can be hidden with dental restorations (e.g., composite fillings, veneers, crowns).

The mutation in collagen type 1 (COL1 A1, COL1 A2) causes DI-1. It is similar to the systemic condition dental features known as osteogenesis imperfect. DI-2, DI-3 and DD-2 share the same genetic mutation of dentin sialophosphoprotein, that is located on chromosome 4. They are autosomal-dominant diseases with complete penetrance and variable expressivity. Due to the same genetic mutation, these diseases would often result in overlapping clinical and radiographic features. Therefore, prevailing theories suggests that DI-2, DI-3 and DD-2 are categorized as a single disease entity with variable severity of expression. However, the causes of DD-1 have yet to be theorized.

The best method of maintaining the health of teeth is to practice exemplary oral hygiene. More tooth loss is likely to occur if intervention takes place. However, factors such as present complaint, patient age, severity of the problem, can affect the treatment plan or options.

Several genetic disorders affect tooth development (odontogenesis), and lead to abnormal tooth appearance and structure. Enamel hypoplasia and enamel hypocalcification are examples of defective enamel that potentially gives a discolored appearance to the tooth. Teeth affected in this way are also usually more susceptible to further staining acquired throughout life.

Amelogenesis imperfecta is a rare condition that affects the formation of enamel (amelogenesis). The enamel is fragile, the teeth appear yellow or brown, and surface stains build up more readily.

Dentinogenesis imperfecta is a defect of dentin formation, and the teeth may be discolored yellow-brown, deep amber or blue-grey with increased translucency. Dentinal dysplasia is another disorder of dentin.

Congenital erythropoietic porphyria (Gunther disease) is a rare congenital form of porphyria, and may be associated with red or brown discolored teeth.

Hyperbilirubinemia during the years of tooth formation may make bilirubin incorporate into the dental hard tissues, causing yellow-green or blue-green discoloration. One such condition is hemolytic disease of the newborn (erythroblastosis fetalis).

Thalassemia and sickle cell anemia may be associated with blue, green or brown tooth discoloration.

A high proportion of children with cystic fibrosis have discolored teeth. This is possibly the result of exposure to tetracycline during odontogenesis, however cystic fibrosis transmembrane regulator has also been demonstrated to be involved in enamel formation, suggesting that the disease has some influence on tooth discoloration regardless of exposure to tetracyclines.

Preventive and restorative care are important as well as esthetics as a consideration. This ensures preservation of the patient's vertical face height between their upper and lower teeth when they bite together. The basis of treatment is standard throughout the different types of DI where prevention, preservation of occlusal face height, maintenance of function, and aesthetic needs are priority. Preventive efforts can limit pathology occurring within the pulp, which may render future endodontic procedures less challenging, with better outcomes.

- Challenges are associated with root canal treatment of teeth affected by DI due to pulp chamber and root canal obliteration, or narrowing of such spaces.

- If root canal treatment is indicated, it should be done in a similar way like with any other tooth. Further consideration is given for restoring the root-treated tooth as it has weaker dentine which may not withstand the restoration.

Preservation of occlusal face height may be tackled by use of stainless steel crowns which are advocated for primary teeth where occlusal face height may be hugely compromised due to loss of tooth tissue as a result of attrition, erosion of enamel.

In most cases, full-coverage crowns or veneers (composite/porcelain) are needed for aesthetic appearance, as well as to prevent further attrition. Another treatment option is bonding, putting lighter enamel on the weakened enamel of the teeth and with lots of treatments of this bonding, the teeth appear whiter to the eye, but the teeth on the inside and under that cover are still the same. Due to the weakened condition of the teeth, many common cosmetic procedures such as braces and bridges are inappropriate for patients with Dentinogenesis imperfecta and are likely to cause even more damage than the situation they were intended to correct.

Dental whitening (bleaching) is contraindicated although it has been reported to lighten the color of DI teeth with some success; however, because the discoloration is caused primarily by the underlying yellow-brown dentin, this alone is unlikely to produce normal appearance in cases of significant discoloration.

If there is considerable attrition, overdentures may be prescribed to prevent further attrition of remaining teeth and for preserving the occlusal face height.

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.

Acidic drinks and foods lower the pH level of the mouth so consuming them causes the teeth to demineralise. Drinks low in pH levels that cause dental erosion include fruit juices, sports drinks, wine, beer and carbonated drinks. Orange and apple juices are common culprits among fruit juices. Carbonated drinks such as colas, lemonades are also very acidic, as are fruit-flavoured drinks and dilutables. Frequency rather than total intake of acidic juices is seen as the greater factor in dental erosion; infants using feeding bottles containing fruit juices (especially when used as a comforter) are therefore at greater risk of acid erosion.

Saliva acts as a buffer, regulating the pH when acidic drinks are ingested. Drinks vary in their resistance to the buffering effect of saliva. Studies show that fruit juices are the most resistant to saliva's buffering effect, followed by, in order: fruit-based carbonated drinks and flavoured mineral waters, non-fruit-based carbonated drinks, sparkling mineral waters; Mineral water being the least resistant. Because of this, fruit juices in particular, may prolong the drop in pH levels.

A number of medications such as vitamin C, aspirin and some iron preparations are acidic and may contribute towards acid erosion.

Dental erosion can occur by non-extrinsic factors too. Intrinsic dental erosion is known as perimolysis, whereby gastric acid from the stomach comes into contact with the teeth. People with illnesses such as anorexia nervosa, bulimia, and gastroesophageal reflux disease (GERD) often suffer from this. GERD is quite common and an average of 7% of adults experience reflux daily. The main cause of GERD is increased acid production by the stomach. This is not exclusive to adults, as GERD and other gastrointestinal disorders may cause dental erosions in children. Rumination also may cause acid erosion.

Preventive and restorative dental care is very important as well as considerations for esthetic issues since the crown are yellow from exposure of dentin due to enamel loss. The main objectives of treatment is pain relief, preserving patient's remaining dentition, and to treat and preserve the patient's occlusal vertical height.

Many factors are to be considered to decide on treatment options such as the classification and severity of AI, the patient's social history, clinical findings etc. There are many classifications of AI but the general management of this condition is similar.

Full-coverage crowns are sometimes being used to compensate for the abraded enamel in adults, tackling the sensitivity the patient experiences. Usually stainless steel crowns are used in children which may be replaced by porcelain once they reach adulthood. These aid with maintaining occlusal vertical dimension.

Aesthetics may be addressed via placement of composite or porcelain veneers, depending on patient factors eg age. If the patient has primary or mixed dentition, lab-made composite veneers may be provided temporarily, to be replaced by permanent porcelain veneers once the patient has stabilized permanent dentition. The patient's oral hygiene and diet should be controlled as well as they play a factor in the success of retaining future restorations.

In the worst-case scenario, the teeth may have to be extracted and implants or dentures are required. Loss of nerves in the affected teeth may occur.