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.

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.

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.

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.

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.

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.

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.

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

Macrodontia of a single tooth is attributed to a disturbance of morphodifferentiation. Generalized macrodontia is usually attributed to some hormonal imbalance (e.g., pituirary gigantism). It can also be associated with facial hemihyperplasia. Macrodontia stems from systematic disturbances. These include KBG syndrome, otodental syndrome, and insulin-resistant diabetes. Ethnicity and gender also factors that influence macrodontia. Asians and males are more likely to be effected.

All teeth, although the same size, grow in larger than normal. This is seen in cases of growth hormone excess called pituitary gigantism. It is the rarest of the types.

PLS is characterized by periodontitis and palmoplantar keratoderma. The severe destruction of periodontium results in loss of most primary teeth by the age of 4 and most permanent teeth by age 14. Hyperkeratosis of palms and soles of feet appear in first few years of life. Destructions of periodontium follows almost immediately after the eruption of last molar tooth. The teeth are involved in roughly the same order in which they erupt.

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.

Hereditary gingival fibromatosis (HGF), also known as idiopathic gingival hyperplasia, is a rare condition of gingival overgrowth. HGF is characterized as a benign, slowly progressive, nonhemorrhagic, fibrous enlargement of keratinized gingiva. It can cover teeth in various degrees, and can lead to aesthetic disfigurement. Fibrous enlargement is most common in areas of maxillary and mandibular tissues of both arches in the mouth. Phenotype and genotype frequency of HGF is 1:175,000 where males and females are equally affected but the cause is not entirely known. It mainly exists as an isolated abnormality but can also be associated with a multi-system syndrome.

Most often natal teeth are mandibular central incisors. They have little root structure and are attached to the end of the gum by soft tissue and are often mobile.

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

- Ellis–van Creveld syndrome

- Hallermann–Streiff syndrome

- Pierre Robin syndrome

- Sotos syndrome

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.

Another abnormal condition is hypodontia, in which there are fewer than the usual number of teeth.

Hyperdontia is seen in a number of disorders, including Gardner's syndrome and cleidocranial dysostosis, where multiple supernumerary teeth are seen that are usually impacted.

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.

Papillon–Lefèvre syndrome (PLS), also known as palmoplantar keratoderma with periodontitis, is an autosomal recessive genetic disorder caused by a deficiency in cathepsin C.

Posterior open bite is caused when posterior teeth such as molars or premolars fail to touch their counterpart tooth. This is more likely to occur in segments where there may be unilateral open bite or open bite related to one or more teeth. Failure of eruption of teeth either due to primary failure or mechanical obstruction during eruption phase can cause the open bite. Sometimes lateral tongue thrust may also prevent the eruption of the posterior teeth, thus eliminating this habit maybe key to eruption in those instances.

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.

In the early stages, periodontitis has very few symptoms, and in many individuals the disease has progressed significantly before they seek treatment.

Symptoms may include:

- Redness or bleeding of gums while brushing teeth, using dental floss or biting into hard food (e.g., apples) (though this may occur even in gingivitis, where there is no attachment loss)

- Gum swelling that recurs

- Spitting out blood after brushing teeth

- Halitosis, or bad breath, and a persistent metallic taste in the mouth

- Gingival recession, resulting in apparent lengthening of teeth. (This may also be caused by heavy-handed brushing or with a stiff toothbrush.)

- Deep pockets between the teeth and the gums (pockets are sites where the attachment has been gradually destroyed by collagen-destroying enzymes, known as collagenases)

- Loose teeth, in the later stages (though this may occur for other reasons, as well)

Patients should realize gingival inflammation and bone destruction are largely painless. Hence, people may wrongly assume painless bleeding after teeth cleaning is insignificant, although this may be a symptom of progressing periodontitis in that patient.

In persons of European ancestry, the most common missing teeth are the wisdom teeth (25–35%), the permanent upper lateral incisors (2%), the lower second premolars (3%), or the upper second premolar, with a higher prevalence in females than in males. The prevalence of missing primary teeth is found at 0.1–0.9%, with a 1:1 male to female ratio. Excluding the third molars, missing permanent dentition accounts for 3.5–6.5%. Similar trends of missing teeth can be seen in approximately 3–10% of orthodontic patients.

30-50% of people with missing primary teeth will have missing permanent teeth, as well.

The "severity" of disease refers to the amount of periodontal ligament fibers that have been lost, termed "clinical attachment loss". According to the American Academy of Periodontology, the classification of severity is as follows:

- Mild: of attachment loss

- Moderate: of attachment loss

- Severe: ≥ of attachment loss