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.

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.

Teeth affected by macrodontia are either contoured, aligned or extracted. Contouring involves shaving the tooth down to change shape and size. However, the result is minimal change as this could be dangerous for the dentin and dental pulp. Aligning involves the use of braces to straighten, align, and make space for larger teeth to grow. When extracted, they are replaced with an implant or bridge. This is done in cases in which the patient suffers from pain that cannot be treated by other methods.

Preventive maintenance therapy for the oral effects of TDO involve frequent dental cleanings, professional application of desensitizing medication, diet counseling, and oral hygiene instructions in proper home care and maintenance; medicated dental rinses and toothpastes are also prescribed as people suffering from TDO are more prone to oral hard tissue disease and early tooth loss. If restorative dentistry is performed without orthodontics to correct the protrusion of the lower jaw, a dental night guard worn at bedtimes on the upper or lower teeth to protect them from the effects of grinding may be recommended.

In extreme cases, tooth loss is inevitable, and the patient will consult with a prosthodontist to determine tooth replacement options such as dental implants, or partial dentures. There is no cure for TDO, but managing its oral and systemic affects is key to having the most favorable outcome from the disease. As the person affected by TDO ages, increased bone fractures may occur. The person suffering from TDO should watch for any pimple like masses on the gum tissue, pain or soreness in the teeth and gums, broken or chipped teeth, feeling of water in the ear or severe pain in the extremities which could indicate fracture.

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.

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.

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.

The condition is of anthropological importance as it was seen in Neanderthals.

The trait ""is common among extant New World monkeys, apes, and fossil hominins"".

Otodental syndrome, also known as otodental dysplasia, is an exceptionally rare disease that is distinguished by a specific phenotype known as globodontia, that in rare cases can be associated with eye coloboma and high frequency hearing loss. Globodontia is an abnormal condition that can occur in both the primary and secondary dentition, except for the incisors which are normal in shape and size. This is demonstrated by significant enlargement of the canine and molar teeth. The premolars are either reduced in size or are absent. In some cases, the defects affecting the teeth, eye and ear can be either individual or combined. When these conditions are combined with eye coloboma, the condition is also known as oculo-otodental syndrome. The first known case of otodental syndrome was found in Hungary in a mother and her son by Denes and Csiba in 1969. Prevalence is less than 1 out of every 1 million individuals.

The cause of otodental syndrome is considered to be genetic. It is an autosomal dominant inheritance and is variable in its expressivity. Haploinsufficiency in the fibroblast growth factor 3 (FGF3) gene (11q13) has been reported in patients with otodental syndrome and is thought to cause the phenotype. Both males and females are equally affected. Individuals diagnosed with otodental syndrome can be of any age; age is not a relevant factor.

Currently there are no specific genetic treatments for otodental syndrome. Dental and orthodontic management are the recommended course of action.

Otodental syndrome is a rare condition that is genetically inherited in an autosomal dominant manner. Although there is no specific biological mechanism for otodental syndrome, what is recognized is that there is a genetic mutation, known as haploinsufficiency, that occurs in the fibroblast growth factor 3 (FGF3) gene (11q13). This is the alleged cause of the physical abnormalities and symptoms associated with otodental syndrome. Although in individuals with signs of ocular coloboma, a microdeletion in the Fas-associated death domain (FADD) gene (11q13.3) was also found to be responsible. There is variable penetrance and variable gene expression within these genetic mutations. Individuals with sensorineural hearing loss are believed to have a local lesion in the auditory segment of the inner ear, known as the cochlea. The biological mechanism for this is currently unknown as well.

Ackerman syndrome is a familial syndrome of fused molar roots with a single canal (taurodontism), hypotrichosis, full upper lip without a cupid’s bow, thickened and wide philtrum, and occasional juvenile glaucoma.

It was described by James L. Ackerman, A. Leon Ackerman, and A. Bernard Ackerman.

It can also refer to interstitial granulomatous dermatitis.

As the syndrome is due to a chromosomal non-disjunction event, the recurrence risk is not high compared to the general population. There has been no evidence found that indicates non-disjunction occurs more often in a particular family.

In mild cases, individuals with XXXY syndrome may lead a relatively good life. These individuals may face difficulties in communicating with others due to their language-based deficits. These deficits may make forming bonds with others difficult, but fulfilling relationships with others are still achievable. Those with higher scores in adaptive functioning are likely to have higher quality of life because they can be independent.