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

Dental open bite occurs in patients where the anterior teeth fail to touch. However, this is not accompanied by the skeletal tendency of having an open bite. Thus this type of open bite may happen in patients who have horizontal or hypodivergent growth pattern. These patients have normal jaw growth and do not have the long face syndrome. The anterior open bite in these patients may be caused by Macroglossia, Tongue thrusting habit or digit sucking habits. Some of the characteristics of a dental open bite include:

- Normal lower anterior facial height

- Horizontal/Hypodivergent growth pattern

- Occlusal plane diverges after the premolar contact

- Under-eruption of the anterior incisors

- Over-eruption of the posterior incisors

- Proclined upper and lower incisors

- No vertical maxillary excess or gummy smile

- Presence of habits such as thumb sucking, tongue thrusting

- Spacing between anterior incisors due to their proclination

Patient with skeletal open bites that accompany dental open bites may have Adenoid faces or Long face syndrome. They are said to have what is known as "Hyperdivergent Growth Pattern" which includes characteristics such as:

- Increased Lower Anterior Facial Height

- Occlusal plane diverges after the 1st molar contact

- May accompany dental open bite

- Narrow nostrils with upturned nose

- Dolicofacial or Leptoprosopic face pattern

- Constricted maxillary arch

- Bilateral Posterior Crossbite

- High and narrow palatal vault

- Presence of crowding in teeth

- Mentalis muscle strain upon forcibly closing of lips

- Possible gummy smile with increased interlabial gap

Cephalometric analysis features of skeletal open bite may include:

- Increased Frankfurt-Mandibular Plane angle

- Steep Occlusal Plane Angle

- Increased SN-MP Angle

- Short Mandibular ramus

- Increased mandibular body length

- Downward and backward position of mandible

- Increased gonial angle

- Proclined upper incisors, retroclined or upright lower incisors

- Posterior part of maxilla is tipped downwards

- Posterior facial height equals 1/2 of anterior facial height

- Increased hard tissue Lower Anterior Facial Height

- Increased total anterior facial height

- Short mandibular ramus

Viken Sassouni developed Sassouni analysis which indicates that patient's with long face syndrome have 4 of their bony planes (mandibular plane, occlusal plane, palatal plane, SN plane) steep to each other.

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

This anomaly is large enough to be seen with the naked eye. One can see the projection on the incisal edge of a tooth looking into the mouth of the affected person. The structure is described to be "T'shaped" or "X-shaped" however will differ depending on its shape, size, structure, location and site of origin. X-rays and radiographs can also show evidence of the abnormality. The digital images would show a tooth with talon cusp as if it were "double teeth".

When looking at a radiograph some features to look for would be location, edge, shape and number. The location would be on an anterior tooth, the edge would be clear and well defined and can be seen even by the naked eye, and the shape would appear "talon-like" over the top portion or crown of the affected tooth. There could potentially be one, two or multiple protrusions depending on the type of cusp.

Talon cusp can fall under three categories: Type I, Type II and Type III. They are created based on the cusp formation shape and length of extension.

- Type I - Talon: The additional cusp or talon projects from the palatal surface of a primary or permanent anterior (front) tooth that extends at least half of the distance from the cemento enamel junction to the incisal edge.

- Type II - Semi Talon: The semi talon cusp measures about 1mm or more in length but extends less than half of the distance seen in Type I Talon.

- Type III - Trace Talon: The projection originates from the cingulum (also known as the "cervical third") of the root and is enlarged or prominent in any form (conical, or tubercle-like)

Since many cases of Talon cusp go unreported, it is hard to draw linkage maps but it is safe to assume that dental formation is influenced by genetic factors. Talon cusp is also seen in association with conditions such as Rubinstein-Taybi syndrome, Mohr syndrome, Ellis–van Creveld syndrome, Incontinentia pigmenti achromians, Berardinelli-Seip syndrome, and Sturge–Weber syndrome.

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.

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.

An anterior crossbite in a child with baby teeth or mixed dentition may happen due to either dental misalignment or skeletal misalignment. Dental causes may be due to displacement of one or two teeth, where skeletal causes involve either mandibular hyperplasia, maxillary hypoplasia or combination of both.

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.

Most commonly the individual complains of food getting lodged beneath the gums and a soreness that is usually confused with throat infections. In slightly milder forms a swelling is visible and mouth opening becomes difficult in severe cases. Pain is invariably present.

Oral habits and pressure on teeth or the maxilla and mandible are causes of malocclusion.

In the active skeletal growth, mouthbreathing, finger sucking, thumb sucking, pacifier sucking, onychophagia (nail biting), dermatophagia, pen biting, pencil biting, abnormal posture, deglutition disorders and other habits greatly influence the development of the face and dental arches.

Pacifier sucking habits are also correlated with otitis media.

Dental caries, periapical inflammation and tooth loss in the deciduous teeth alter the correct permanent teeth eruptions.

The phenomenon of gemination arises when two teeth develop from one tooth bud and, as a result, the patient has an extra tooth, in contrast to fusion, where the patient would appear to be missing one tooth.

Fused teeth arise through union of two normally separated tooth germs, and depending upon the stage of development of the teeth at the time of union, it may be either complete or incomplete. On some occasions, two independent pulp chambers and root canals can be seen. However, fusion can also be the union of a normal tooth bud to a supernumerary tooth germ. In these cases, the number of teeth is also normal and differentiation from gemination may be very difficult, if not impossible. In geminated teeth, division is usually incomplete and results in a large tooth crown that has a single root and a single canal. It is an asymptomatic condition.

The prevalence of germination or fusion is 2.5% in primary dentition, and 0.1 - 0.2% in permanent dentition. It is more frequently observed in primary than permanent dentition; anterior than posterior teeth; unilaterally than bilaterally. It commonly occurs in the primary upper incisors.

All the teeth are normal size but appear smaller relative to enlarged jaws. Relative generalized microdontia may be the result of inheritance of a large jaw from one parent, and normal sized teeth from the other.

There may or may not be any evidence of history of HGF in the family nor any usage of taking long-term medicines for any particular disease when it comes to diagnosing HGF. There also may or may not be any signs of medical and/or family history of mental retardation, hypertrichosis, nor clinical symptoms that can be associated with gingival enlargement. Although, enlargement of gingiva, interdental papilla, hindered speech, and secondary inflammatory changes taking place in the mouth commonly at the marginal gingiva are all very indicative of this condition. Commonly the patient will have mandiblular and maxilliary inflammation and overgrowth as opposed to the traditional pink, firm, and fleshy consistency of healthy gingiva. The patient's jaw may also appear distorted because of the gingiva englargements. Overgrowth of the gingiva can range from slightly covering the surface of teeth or it can even completely cover the surrounding teeth. The patient can also experience damage or loss of teeth.

Most commonly used classification system with respect to treatment planning. Depending on the angulation the tooth might be classified as:

- Mesioangular

- Horizontal

- Vertical

- Distoangular

- Palatal

- Buccal

- Lingual

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.

Tooth gemination is a dental phenomenon that appears to be two teeth developed from one. There is one main crown with a cleft in it that, within the incisal third of the crown, looks like two teeth, though it is not two teeth. The number of the teeth in the arch will be normal.

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.

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.

Prognathism in humans can be due to normal variation among phenotypes. In human populations where prognathism is not the norm, it may be a malformation, the result of injury, a disease state or a hereditary condition. Prognathism is considered a disorder only if it affects mastication, speech or social function as a byproduct of severely affected aesthetics of the face.

Clinical determinants include soft tissue analysis where the clinician assesses nasolabial angle, the relationship of the soft tissue portion of the chin to the nose, and the relationship between the upper and lower lips; also used is dental arch relationship assessment such as Angle's classification.

Cephalometric analysis is the most accurate way of determining all types of prognathism, as it includes assessments of skeletal base, occlusal plane angulation, facial height, soft tissue assessment and anterior dental angulation. Various calculations and assessments of the information in a cephalometric radiograph allow the clinician to objectively determine dental and skeletal relationships and determine a treatment plan.

Prognathism is less prevalent in East Asians and Caucasians. It is not to be confused with micrognathism, although combinations of both may be found. It affects the middle third of the face, causing it to jut out, thereby increasing the facial area, similar in phenotype of archaic hominids and apes. Mandibular prognathism is a protrusion of the mandible, affecting the lower third of the face. Alveolar prognathism is a protrusion of that portion of the maxilla where the teeth are located, in the dental lining of the upper jaw. Prognathism can also be used to describe ways that the maxillary and mandibular dental arches relate to one another, including malocclusion (where the upper and lower teeth do not align). When there is maxillary and/or alveolar prognathism which causes an alignment of the maxillary incisors significantly anterior to the lower teeth, the condition is called an overjet. When the reverse is the case, and the lower jaw extends forward beyond the upper, the condition is referred to as retrognathia (reverse overjet).

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.

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.

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.

All teeth are classified as either developing, erupted (into the mouth), embedded (failure to erupt despite lack of blockage from another tooth) or impacted. An impacted tooth is one that fails to erupt due to blockage from another tooth.

Wisdom teeth develop between the ages of 14 and 25, with 50% of root formation completed by age 16 and 95% of all teeth erupted by the age of 25. However, tooth movement can continue beyond the age of 25.

Impacted wisdom teeth are classified by the direction and depth of impaction, the amount of available space for tooth eruption. and the amount of soft tissue or bone (or both) that covers them. The classification structure helps clinicians estimate the risks for impaction, infections and complications associated with wisdom teeth removal. Wisdom teeth are also classified by the presence (or absence) of symptoms and disease.

One review found that 11% of teeth will have evidence of disease and are symptomatic, 0.6% will be symptomatic but have no disease, 51% will be asymptomatic but have disease present and 37% will be asymptomatic and have no disease.

Impacted wisdom teeth are often described by the direction of their impaction (forward tilting, or mesioangular being the most common), the depth of impaction and the age of the patient as well as other factors such as pre-existing infection or the presence of pathology. Of these predictors, age correlates best with extraction difficulty and complications during wisdom teeth removal rather than the orientation of the impaction.

Another classification system often taught in U.S. dental schools is known as "Pell and Gregory Classification". This system includes a horizontal and vertical component to classify the location of third molars (predominately applicable to mandibular third molars): the third molar's relationship to the occlusal plane being the vertical or "x-component" and to the anterior border of the ramus being the horizontal or "y-component". Vertically, Class A impaction is one in which the occlusal surface of the impacted tooth is level or nearly level with the occlusal plane and the cervical line of the adjacent second molar.

In dentistry, hypodontia is the condition at which the patient has missing teeth as a result of the failure of those teeth to develop (also called tooth agenesis). Hypodontia describes a situation where the patient is missing up to five permanent teeth, excluding the 3rd molars. Missing third molars occur in 9–30% of studied populations. In primary dentition the maxilla is more affected, with the condition usually involving the maxillary lateral incisor.

The condition of missing over five (six or more) permanent teeth, excluding 3rd molars or wisdom teeth, has been called oligodontia. The condition for missing all teeth, either primary and/or permanent), is called anodontia. A similar condition is hyperdontia, in which there are more than the usual number of teeth, more commonly called supernumerary teeth.

Many other terms to describe a reduction in number of teeth appear in the literature: aplasia of teeth, congenitally missing teeth, absence of teeth, agenesis of teeth and lack of teeth.