If Turner's hypoplasia is found on a canine or a premolar, the most likely cause is an infection that was present when the primary (baby) tooth was still in the mouth. Most likely, the primary tooth was heavily decayed and an area of inflamed tissues around the root of the tooth (called a periapical inflammation), affecting the development of the permanent tooth. The tooth most likely affected by this cause is the canine tooth. The appearance of the abnormality will depend on the severity and longevity of the infection.

If Turner's hypoplasia is found in the front (anterior) area of the mouth, the most likely cause is a traumatic injury to a primary tooth. The traumatized tooth, which is usually a maxillary central incisor, is pushed into the developing tooth underneath it and consequently affects the formation of enamel. Because of the location of the permanent tooth's developing tooth bud in relation to the primary tooth, the most likely affected area on the permanent tooth is the facial surface (the side closer to the lips or cheek). White or yellow discoloration may accompany Turner's hypoplasia. Enamel hypoplasia may also be present.

Turner's hypoplasia usually affects the tooth enamel if the trauma occurs prior to the third year of life. Injuries occurring after this time are less likely to cause enamel defects since the enamel is already calcified.

The same type of injury is also associated with the dilaceration of a tooth.

Enamel hypoplasia is a defect of the teeth in which the enamel is hard but thin and deficient in amount, caused by defective enamel matrix formation. Usually the condition involves part of the tooth having a pit in it. In some cases, the natural enamel crown has a hole in it, and in extreme cases, the tooth has no enamel, exposing the dentin.

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.

Hair abnormalities are very prominent in majority of the cases of TDO. Kinky/curly hair that is unusually dry and easily sheds is present at birth. In 80% of cases, the hair has a more relaxed appearance by adolescence. The presence of this hair texture type is a defining characteristic between a diagnosis of TDO verses amelogenesis imperfecta with hypomaturation. Additionally, in TDO the nails are usually abnormally thin, brittle, and split frequently. Cranial deficiencies are marked by the presence of having a long skull relative to its width, or protrusive foreheads due to increased thickness of the cranial bones and premature closing of the associated sutures in the skull. The long bones in the body (arms, legs) are also abnormally long and tend to fracture very easily. Osteosclerosis, commonly seen in TDO cases is characterized by an increase in bone density, affecting the skull and the mastoid process located behind the jawbone on the skull, as well as a shortened ramus seen in people with TDO. There are no known pathological problems associated with hair and bone changes in people with this disease. Changes in the long bones tend to appear later in development, but changes in the teeth appear once the teeth being to form, called primary dentition. The hair and bone abnormalities are evaluated radiographically during initial diagnosis, and visually during the course of the disease. Radiographic exams may be repeated if there is suspect of fracture.

Type II would mostly cause discolouration to the primary teeth. Affected teeth usually appear as brownish-blue, brown or yellow. Translucent “opalescence” is often one of the characteristics to describe teeth with DD-2. In some cases teeth might show slightly amber coloured but in most of the cases permanent teeth are unaffected and appear normal regardless of colour, shape and size. Dental X-rays is the key to diagnose dentine dysplasia, especially on permanent teeth. Abnormalities of the pulp chamber is the main characteristic to make a definitive diagnosis.

In the primary teeth, coronal dentin dysplasia may appear similar to Dentinogenesis Imperfecta type II (DG-II) but if abnormalities features appear to be more pronounced in the permanent teeth, then consider changing the diagnosis to DGI-II instead of DD-2.

In other words, affect primary teeth usually have abnormal shaped or shorter than normal roots . “Crescent/ half-moon shaped” pulp chamber remnant in permanent teeth can be seen on x-rays. The roots may appear to be darker or radiolucent/ pointy and short with apical constriction. Dentine is laid down abnormally and causes excessive growth within the pulp chamber. This will reduce the pulp space and eventually cause incomplete and total pulp chamber obliteration in permanent teeth. Sometimes periapical pathology or cysts can be seen around the root apex. Most cases of DD associated with peri-apical radiolucency/ pathology have been diagnosed as radicular cysts, but some of them have been as diagnosed peri-apical grauloma instead.

In the oral cavity 100% of people diagnosed with TDO have taurodontism which is characterized by vertically enlarged pulp chambers at the expense of the roots of the teeth; the floor of the pulp chamber and furcation is moved apically down. This is due to the failure of the Hertwig epithelial root sheath which maps the shape of the forming tooth roots during active differentiation. Amelogenesis imperfecta, an abnormal formation of the enamel or external layer of the crown of the tooth, may also be present where the tooth enamel may be thin or absent. There are several clinical subsets of amelogenesis imperfecta, but common to TDO is the hypoplastic-hypomaturation subtype; the hypomaturation-hypoplastic is less common in individuals with TDO. The difference between the 2 dominant subtypes is the changes seen in the enamel matrix, and the phenotypic type that predominates. The hypoplastic-hypomaturation type of amelogenesis imperfecta with TDO occurs where the tooth enamel depicts a generalized pitted pattern, with open contacts between the teeth as well as an open bite. A smaller amount of cases are of the hypomaturation-hypoplastic case type, in which the enamel structure is softer due to the under maturation of ameloblasts during development. Mandibular prognathism also called a severe underbite, is also a prominent feature in TDO. Prognathism defects are diagnosed based the level of severity that this condition interferes with being able to chew or speak properly.

Due to improper tooth development, TDO patients suffer from high rates of dental caries causing dental abscess. The under maturation of the enamel causes the tooth structure to be softer, and more susceptible to the effects of bruxism due to abnormalities in skeletal development. The oral abnormalities are evaluated by radiographs and visual examination. Oral radiographs are frequently repeated due to the high incidence of infection due to abnormal biting patterns seen in TDO cases.

Clinical appearance is variable with presentation ranging from gray to yellowish brown, but the characteristic features is the translucent or opalescent hue to the teeth.

In Type I, primary teeth are more severely affected compared to the permanent dentition which has more varied features, commonly involving lower incisors & canines. Primary teeth have a more obvious appearance as it has a thinner layer of enamel overlying dentine, hence the color of dentine is more noticeable.

In Type II, both the dentitions are equally affected.

Enamel is usually lost early because it is further inclined to attrition due to loss of scalloping at the dentoenamel junction (DEJ). It was suggested that the scalloping is beneficial for the mechanical properties of teeth as it reinforces the anchor between enamel and dentine. However, the teeth are not more susceptible to dental caries than normal ones.

However, certain patients with dentinogenesis imperfecta will suffer from multiple periapical abscesses apparently resulting from pulpal strangulation secondary to pulpal obliteration or from pulp exposure due to extensive coronal wear. They may need apical surgery to save the involved teeth.

These features are also present in dentine dysplasia and hence, the condition may initially be misdiagnosed.

Talon Cusp will show physical signs of the irregular dental formation of the teeth and cause other symptoms of the disease that could possibly lead to dental problems in the future depending on severity of the deformity. Most commonly, the extra cusp is located on the lingual surface, giving a three-pronged appearance which has been described as an eagle talon. Rarely however the extra cusp may be situated on the facial surface, or there may be extra cusps on both lingual and facial surfaces. There may be a deep groove between the talon cusp and the rest of the tooth. The extra cusp typically contains pulp tissue. When viewing talon cusp from the occlusal, the projection will appear "x-shaped" as well as appears conical and mimicking the shape of an "eagle's talon".

Symptoms of talon cusp include:

- Interference with occlusion or bite

- Irritation of soft tissues and tongue

- Accidental cusp fracture

- Susceptible to dental caries

The lesions that appear in teeth affected with MIH can present as opacities that vary from white to yellow-brown. They are usually asymmetrical in appearance, with a sharp demarcation that distinguishes between normal and affected enamel. The lesions usually do not involve the cervical third of affected teeth.

1-increased localised pressure.

2- focal growth retardation and stimulation.

Type I and II have similar radiographic features

- Total obliteration of the pulp chamber and root canals due to deposition of dentine

- Bulbous crowns with apparent cervical constriction

- Reduced root length with rounded apices

Type III shows thin dentin and extremely enormous pulp chamber. These teeth are usually known as "shell teeth".

Periapical radiolucency may be seen on radiographs but may occur without any apparent clinical pathology.

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.

Clinical signs of TRs are often minimal since the discomfort can be minor. However, some authors have described discomfort while chewing, anorexia, dehydration, weight loss, and tooth fracture. The lower third premolar is the most commonly affected tooth.

Talon Cusp is a rare dental anomaly. Generally a person with this develops "cusp-like" projections located on the inside surface of the affected tooth. Talon cusp is an extra cusp on an anterior tooth. Other names for talon cusp is eagle's talon, dens evaginatus, interstitial cusp, tuberculated premolar, evaginated odontoma and supernumerary cusp. Although talon cusp may not appear serious (and in some people may be completely benign), it can cause clinical, diagnostic, functional problems and alters the aesthetic appeal.

The term refers to the same condition as dens evaginatus, but the talon cusp is the manifestation of dens evaginatus on anterior teeth. Talon cusp can simply be defined as hyperplasia of the cingulum of an anterior tooth.Talon cusp was first described by W.H. Mitchell in 1982 and named by J. Kimball Mellor B.S., D.D.S. and Louis W. Ripa, D.D.S., M.S. due to its similar appearance to an eagle's talon. Some sources define a talon cusp as an extra cusp which extends at least half the distance between the cementoenamel junction and the incisal edge of the tooth. Other sources classify all enlarged cingula as talon cusps and classify them according to the degree of enlargement.

The incidence has been found to range from 1% to 6% of the population. Talon cusp tends to occur on permanent teeth only. They are vary rare in (deciduous) baby teeth. In most cases the involved teeth are the permanent maxillary lateral incisors (55%), followed by maxillary central incisors (33%), mandibular incisors (6%), and maxillary canines (4%).

Dens invaginatus, also known as dens in dente ("tooth within a tooth") is a condition found in teeth where the outer surface folds inward. There are coronal and radicular forms, with the coronal form being more common.

Dens invaginatus is a malformation of teeth most likely resulting from an infolding of the dental papilla during tooth development or invagination of all layers of the enamel organ in dental papillae. Affected teeth show a deep infolding of enamel and dentine starting from the foramen coecum or even the tip of the cusps and which may extend deep into the root. Teeth most affected are maxillary lateral incisors and bilateral occurrence is not uncommon. The malformation shows a broad spectrum of morphologic variations and frequently results in early pulp necrosis. Root canal therapy may present severe problems because of the complex anatomy of the teeth. Cause, prevalence, classification, and therapeutic considerations including root canal therapy, apical surgery and prevention of pulpal involvement are reviewed.

Ectopic enamel is an abnormality in the shape of teeth. It is tooth enamel that is found in an unusual location, such as at the root of a tooth.

Dental fluorosis (also termed mottled enamel) is an extremely common disorder, characterized by hypomineralization of tooth enamel caused by ingestion of excessive fluoride during enamel formation.

It appears as a range of visual changes in enamel causing degrees of intrinsic tooth discoloration, and, in some cases, physical damage to the teeth. The severity of the condition is dependent on the dose, duration, and age of the individual during the exposure. The "very mild" (and most common) form of fluorosis, is characterized by small, opaque, "paper" white areas scattered irregularly over the tooth, covering less than 25% of the tooth surface. In the "mild" form of the disease, these mottled patches can involve up to half of the surface area of the teeth. When fluorosis is moderate, all of the surfaces of the teeth are mottled and teeth may be ground down and brown stains frequently "disfigure" the teeth. Severe fluorosis is characterized by brown discoloration and discrete or confluent pitting; brown stains are widespread and teeth often present a corroded-looking appearance.

People with fluorosis are relatively resistant to dental caries (tooth decay caused by bacteria), although they may be of cosmetic concern. In moderate to severe fluorosis, teeth are physically damaged.

Feline Tooth Resorption (TR) is a syndrome in cats characterized by resorption of the tooth by odontoclasts, cells similar to osteoclasts. TR has also been called "feline odontoclastic resorption lesion" (FORL), neck lesion, cervical neck lesion, cervical line erosion, feline subgingival resorptive lesion, feline caries, or feline cavity. It is one of the most common diseases of domestic cats, affecting up to two-thirds. TRs have been seen more recently in the history of feline medicine due to the advancing ages of cats, but 800-year-old cat skeletons have shown evidence of this disease. Purebred cats, especially Siamese and Persians, may be more susceptible.

TRs clinically appear as erosions of the surface of the tooth at the gingival border. They are often covered with calculus or gingival tissue. It is a progressive disease, usually starting with loss of cementum and dentin and leading to penetration of the pulp cavity. Resorption continues up the dentinal tubules into the tooth crown. The enamel is also resorbed or undermined to the point of tooth fracture. Resorbed cementum and dentin is replaced with bone-like tissue.

The two main classification systems are described below. Others include the tooth surface fluorosis index (Horowitz et al. 1984), which combines Deans index and the TF index; and the fluorosis risk index (Pendrys 1990), which is intended to define the time at which fluoride exposure occurs, and relates fluorosis risk with tooth development stage.

Amelogenesis imperfecta (AI) is a congenital disorder that presents with a rare abnormal formation of the enamel or external layer of the crown of teeth, unrelated to any systemic or generalized conditions. Enamel is composed mostly of mineral, that is formed and regulated by the proteins in it. Amelogenesis imperfecta is due to the malfunction of the proteins in the enamel (ameloblastin, enamelin, tuftelin and amelogenin) as a result of abnormal enamel formation via amelogenesis.

People afflicted with amelogenesis imperfecta have teeth with abnormal color: yellow, brown or grey; this disorder can afflict any number of teeth of both dentitions. The teeth have a lower risk for dental cavities and are hypersensitive to temperature changes as well as rapid attrition, excessive calculus deposition, and gingival hyperplasia.

An enamel pearl is a condition of teeth where enamel is found in locations where enamel is not supposed to be, such as on a root surface. They are usually found in the area between roots, which is called a furcation, of molars. Enamel pearls are not common in teeth with a single root. The most common location of enamel pearls is the furcation areas of the maxillary and mandibular third molar roots.

Enamel pearls are formed from the Hertwig's Epithelial root sheath. After the initiation of the formation of dentin in the root area of the tooth, the root sheath disintegrates and moves away from the root surface so that the cells of the dental sac can come in contact with predentin to differentiate into cementoblasts and start deposition of cementum. However, if the cells of epithelial root sheath remain adherent to predentin, they may differentiate into fully functional ameloblasts and deposit enamel. Such droplets of enamel are called enamel pearls.

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.

AI can be classified according to their clinical appearances:

- Type 1 - Hypoplastic

Enamel of abnormal thickness due to malfunction in enamel matrix formation. Enamel is very thin but hard & translucent, and may have random pits & grooves. Condition is of autosomal dominant, autosomal recessive, or x-linked pattern. Enamel differs in appearance from dentine radiographically as normal functional enamel.

- Type 2 - Hypomaturation

Enamel has sound thickness, with a pitted appearance. It is less hard compared to normal enamel, and are prone to rapid wear, although not as intense as Type 3 AI. Condition is of autosomal dominant, autosomal recessive, or x-linked pattern. Enamel appears to be comparable to dentine in its radiodensity on radiograpshs.

- Type 3 - Hypocalcified

Enamel defect due to malfunction of enamel calcification, therefore enamel is of normal thickness but is extremely brittle, with an opaque/chalky presentation. Teeth are prone to staining and rapid wear, exposing dentine. Condition is of autosomal dominant and autosomal recessive pattern. Enamel appears less radioopaque compared to dentine on radiographs.

- Type 4: Hypomature hypoplastic enamel with taurodontism

Enamel has a variation in appearance, with mixed features from Type 1 and Type 2 AI. All Type 4 AI has taurodontism in common. Condition is of autosomal dominant pattern.

Other common features may include an anterior open bite, taurodontism, sensitivity of teeth.

Differential diagnosis would include dental fluorosis, molar-incisor hypomineralization, chronological disorders of tooth development.

There are two main types: compound and complex.

- A "compound" odontoma still has the three separate dental tissues (enamel, dentin and cementum), but may present a lobulated appearance where there is no definitive demarcation of separate tissues between the individual "toothlets" (or denticles). It usually appears in the anterior maxilla.

- The "complex" type is unrecognizable as dental tissues, usually presenting as a radioopaque area with varying densities. It usually appears in the posterior maxilla or in the mandible.

In addition to the above forms, the dilated odontoma is an infrequent developmental alteration that appears in any area of the dental arches and can affect deciduous, permanent and supernumerary teeth. Dens invaginatus is a developmental anomaly resulting from invagination of a portion of crown forming within the enamel organ during odontogenesis. The most extreme form of dens invaginatus is known as dilated odontoma.