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.

Males tend to have larger teeth than females, and tooth size also varies according race. Abnormal tooth size is defined by some as when the dimensions are more than 2 standard deviations from the average. Microdontia is when the teeth are abnormally small, and macrodontia is when the teeth are abnormally large.

All the teeth are smaller than the normal size. True generalized microdontia is very rare, and occurs in pituitary dwarfism. Due to decreased levels of growth hormone the teeth fail to develop to a normal size.

Regional odontodysplasia or odontogenesis imperfecta is an uncommon developmental abnormality of teeth, usually localized to a certain area of the mouth. The condition is nonhereditary. There is no predilection for race, but females are more likely to get regional odontodysplasia. The enamel, dentin, and pulp of teeth are affected, to the extent that the affected teeth do not develop properly. These teeth are very brittle. On radiographs the teeth appear more radiolucent than normal, so they are often described as "ghost teeth". Most cases are considered , but some cases are associated with syndromes, growth abnormalities, neural disorders, and vascular malformations.

Permanent teeth usually show effects of regional odontodysplasia if the deciduous tooth was affected. Many of these teeth do not erupt, and those that do have an increased risk of caries and periapical inflammation.

Supernumerary teeth can be classified by shape and by position. The shapes include the following:

- Supplemental (where the tooth has a normal shape for the teeth in that series);

- Tuberculate (also called "barrel shaped");

- Conical (also called "peg shaped");

- Compound odontoma (multiple small tooth-like forms);

- Complex odontoma (a disorganized mass of dental tissue)

When classified by position, a supernumerary tooth may be referred to as a "mesiodens", a "paramolar", or a "distomolar".

The most common supernumerary tooth is a mesiodens, which is a malformed, peg-like tooth that occurs between the maxillary central incisors.

Fourth and fifth molars that form behind the third molars are another kind of supernumerary teeth.

Classifications enable the oral surgeon to determine the difficulty in removal of the impacted tooth. The primary factor determining the difficulty is accessibility, which is determined by adjacent teeth or other structures that impair access or delivery pathway. The majority of classification schemes are based on analysis on a radiograph. The most frequently considered factors are discussed below.

1-increased localised pressure.

2- focal growth retardation and stimulation.

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.

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.

This type of classification is based on the amount of impacted tooth that is covered with the mandibular ramus. It is known as the Pell and Gregory classification, classes 1, 2, and 3.

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.

A single tooth is larger than the rest. This is unusual and could be the result of fusion and germination that cause enlarged crowns.

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.

The presence of a supernumerary tooth, particularly when seen in young children, is associated with a disturbance of the maxillary incisor region. This commonly results in the impaction of the incisors during the mixed dentition stage. The study debating this also considered many other factors such as: the patient’s age, number, morphology, growth orientation and position of the supernumerary tooth. Therefore, the presence of a supernumerary tooth when found must be appropriately approached with the correct treatment plan incorporating the likelihood of incisal crowding.

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.

Invaginatus is an anomaly resulting from invagination forming within the enamel organ. Invagination ranges pitting occupying most of the crown and root. Although examination may reveal a fissure on the surface of anterior tooth, radiographic examination is the way.

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.

All teeth appear slightly larger than normal, usually occurring in cases with small jaws. It is called pseudomacrodontia because the small jaws give the illusion that they are abnormally large. Genetics plays a major role in this type of macrodontia, as the offspring inherits small jaw size from one of the parents and large teeth from the other parent.

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.

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.

Impacted wisdom teeth without a communication to the mouth, that have no pathology associated with the tooth and have not caused tooth resorption on the blocking tooth rarely have symptoms. In fact, only 12% of impacted wisdom teeth are associated with pathology.

When wisdom teeth communicate with the mouth, the most common symptom is localized pain, swelling and bleeding of the tissue overlying the tooth. This tissue is called the operculum and the disorder called pericoronitis which means inflammation around the crown of the tooth. Low grade chronic periodontitis commonly occurs on either the wisdom tooth or the second molar, causing less obvious symptoms such as bad breath and bleeding from the gums. The teeth can also remain asymptomatic (pain free), even with disease. As the teeth near the mouth during normal development, people sometimes report mild pressure of other symptoms similar to teething.

The term asymptomatic means that the person has no symptoms. The term asymptomatic should not be equated with absence of disease. Most diseases have no symptoms early in the disease process. A pain free or asymptomatic tooth can still be infected for many years before pain symptoms develop.

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

Other kinds of malocclusions can be due to tooth size or horizontal, vertical, or transverse skeletal discrepancies, including skeletal asymmetries. Long faces may lead to "open bite malocclusion", while short faces can be coupled to a "Deep bite malocclusion". However, there are many other more common causes for open bites (such as tongue thrusting and thumb sucking), and likewise for deep bites. Upper or lower jaw can be overgrown or undergrown, leading to Class II or Class III malocclusions that may need corrective jaw surgery or orthognathic surgery as a part of overall treatment, which can be seen in about 5% of the general population.

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.