Anomaly in pulp cavity Contents 1. Introduction 2. Gemination 3. Fusion 4. Taurodontism 5. Dens in Dente (dens invaginatus) 6. Dens Evaginatus 7.

Dentinogenesis imperfecta 8. Dentinal dysplasia 9. Odontodyplasia 10. Hyperparathyroidism 11. Hypopitutarism

Introduction Pulp cavity Is defined as a space located in the center of tooth surrounded by dentin. In vital condition it contains a soft connective tissue termed dental pulp or pulp organ, which continues apical with periapical tissues.

The primary function of the dental pulp is to form dentin (by the odontoblasts) Other functions include

Nutritive: the pulp keeps the organic components of the surrounding mineralized tissue supplied with moisture and nutrients; Sensory: extremes in temperature, pressure, or trauma to the dentin or pulp are perceived as pain; Protective: the formation of reparative or secondary dentin (by the odontoblasts).

Anomalies in pulp cavitycan be understood under following heads : Anomalies of Shape 1. 2. 3. Gemination Fusion Taurodontism

4. Dens in Dente (dens invaginatus) 5. Dens Evaginatus Anomalies of Structure 1. Dentinogenesis imperfecta 2. Dentinal dysplasia 3. Odontodyplasia Anomalies associated with Glandular diseases 1. 2. Hyperparathyroidism Hypopitutarism

Gemination The partial development of two teeth from a single tooth bud following incomplete division.

An incomplete division of a single tooth bud resulting in a bifid crown with a single pulp chamber. It is also known as schizodontia, twinning. It occurs in mandibular anterior teeth mostly. It occur in both deciduous and permanent dentition.

Fusion The dentinal union of two embryologically developing teeth. Fused teeth can contain two separate pulp chamber, may appear as large bifid crowns with one chamber.

Taurodontism Taurodont teeth are characterized by having a significantly elongated pulpchamber with short stunted roots, resulting from the failure of the proper level of horizontal invagination of Hertwigs epithelial root sheath..The

condition has sometimesbeen seen in association with amelogenesis imperfecta, tricho-dento-osseous syndrome,and Klinefelter's syndrome. This anomaly is not recognizable clinically but on a radiograph,the rectangular pulp chamber is seen in an elongated tooth body with shortened roots androot canals.

Dens invaginatus Dens invaginatus in a human tooth was first described by a dentist named Socrates in 1856 (Schulze 1970). In 1873 Mhlreiter reported on anomalous cavities in human teeth, Baume in 1874 and Busch in 1897 published on this malformation. In 1887 Tomes described the dens invaginatus in his textbook A System of Dental Surgery, as follows:

Synonyms for this malformation are: Dens in dente, invaginated odontome, dilated gestant odontome, dilated composite odontome, tooth inclusion, dentoid in dente. consider dens invaginatus as a deep folding of the foramen coecum during tooth development which in some cases even may result in a second apical foramen (Schulze 1970) The first classification of invaginated teeth was published by Hallet (1953). The most commonly used classification proposed by Oehlers (1957a) is shown in

Fig. 3. He described the anomaly occurring in three forms: Type I: an enamel-lined minor form occurring within the confines of the crown not extending beyond the amelocemental junction. Type II: an enamel-lined form which invades the root but remains confined as a blind sac. It may or may not communicate with the dental pulp. Type III: a form which penetrates through the root perforating at the apical area showing a second foramen in the apical or in the periodontal area. There is no immediate communication with the pulp. The invagination may be completely

lined by enamel, but frequently cementum will be found lining the invagination. Oehlers (1957a,b) also described different crown forms (normal with a deep lingual or palatal pit; conical, barrel-shaped or peg-shaped with an incisal pit) relating to the three groups mentioned above. In addition, Ulmansky & Hermel (1964) and VincentTownend (1974) described an incipient dens in dente, a deep palatal or lingual pit completely lined by enamel with no communication to the pulp. Oehlers (1958) also presented radicular invaginations. Schulze & Brand (1972) proposed a more detailed

classification (Fig. 4), also including invaginations starting at the incisal edge or the top of the crown and also including dysmorphic root configurations.

Dens evaginatus Dens evaginatus (DE) is a developmental aberration of a tooth resulting in formation of an accessory cusp whose morphology has been variously described as an abnormal tubercle, elevation, protuberance, excrescence, extrusion, or bulge This uncommon anomaly projects above the adjacent tooth surface, exhibiting enamel covering

a dentinal core that usually contains pulp tissue that on occasion may have a slender pulp horn which extends various distances up to the full length of the tubercles dentin core (1). The presence of pulp within the cusp-like tubercle has great clinical significance and distinguishes the anomaly from supplemental cusps, such as the cusp of Carabelli (2), which contain no pulp DE is thought to develop from an abnormal proliferation and folding of a portion of the inner enamel epithelium and subjacent ectomesenchymal cells of the dental papilla into the stellate reticulum of the enamel organ during the bell stage of tooth

formation (24 26). The resultant formation is defined as a tubercle, or supplemental solid elevation on some portion of the crown surface.

Schulge (1987) distinguishes the following five types of DE for posterior teeth by the location of the tubercle (5).

1. A cone-like enlargement of the lingual cusp. 2. A tubercle on the inclined plane of the lingual cusp. 3. A cone-like enlargement of the buccal cusp. 4. A tubercle on the inclined plane of the buccal cusp. 5. A tubercle arising from the occlusal surface obliterating the central groove. Accordingly, Lau further classified each type of tubercle on the basis of four anatomical shapes of smooth, grooved, terraced and ridged. Finally, Oehlers identified the evagination according to the pulp contents within the tubercle by examining the histological appearance of the pulp using decalcified serial sections of extracted teeth with DE. These categories are listed as follows along with their percentage of occurrence: 1. Wide pulp horns (34%)

2. 3. 4. 5.

Narrow pulp horns (22%) Constricted pulp horns (14%) Isolated pulp horn remnants (20%) No pulp horn (10%).

Dentinal Dysplasia Dentin dysplasia is a genetic disorder of teeth, commonly exhibiting an autosomal dominant inheritance. It is characterized by presence of normal enamel but atypical dentin with abnormal pulpal morphology. There are two types. Type I is the radicular

type, and type II is the coronal type. In the radicular type, the roots of teeth are shorter than normal and the pulp chamber may be nearly gone. The pulp chamber is sometimes described as having a "crescent shaped" appearance. In the coronal type, the pulps are enlarged and are described as having a "thistle tube" appearance, in permanent dentition. In the deciduous dentition, coronal dentin dysplasia bears a resemblance to Dentinogenesis Imperfecta type II. Radiographic Features Type 1: Roots are short, blunt and conical. In deciduous teeth, pulp chambers and root canals are completely obliterated in permanent they may be crescent shaped.

Type 2: The pulp chamber of the deciduous teeth become obliterated in deciduous teeth. While in permanent teeth, large pulp chamber is seen in coronal portion of the tooth - referred to as thistle tube appearance.Pulp stones may be found.

Dentinogenesis imperfecta Dentinogenesis imperfecta (hereditary Opalescent Dentin) is a genetic disorder of tooth development. This condition causes teeth to be discolored (most often a blue-gray or yellow-brown color) and translucent. Teeth are also weaker than normal, making them prone to rapid wear, breakage, and loss. These problems can affect both primary (baby) teeth and permanent teeth. This condition is inherited in an autosomal dominant pattern, which means one copy of the altered gene in each cell is sufficient to cause the disorder.

Dentinogenesis imperfecta affects an estimated 1 in 6,000 to 8,000 people. Types Types of dentinogenesis imperfecta with similar dental formalities usually an autosomal dominant trait with variable expressivity but can be recessive if the associated osteogenesis imperfecta is of recessive type. This type is no l Type II : Occurs in people without other inherited disorders (i.e. Osteogenesis imperfecta).It is an autosomal dominant trait. A few families with type II have progressive hearing loss in addition to dental abnormalities. Mutations in the DSPP gene have been identified in people with type II and type III dentinogenesis imperfecta. Type I

occurs as part of osteogenesis imperfecta. Radiographic features Type I and II show total obliteration of the pulp chamber. Type III shows thin dentin and extremely enormous pulp chamber.These teeth are usually known as Shell Teeth. Histology Dentinal tubules are irregular and are bigger in diameter. Areas of uncalcified matrix are seen. Sometimes odontoblasts are seen in dentin

ODONTODYSPLASIA (Odontogenesis imperfecta, ghost teeth) Odontodysplasia or "ghost teeth" is a relatively rare developmental abnormality of unknown cause. It results in marked hypoplasia and hypocalcification of enamel and dentin. The cementum is much thinner than normal. The affected teeth are small and have short roots. They are brittle and fracture readily, resulting in pulpal infection. Both dentitions, deciduous and permanent, may be involved. A single tooth or several teeth in a localized area may exhibit the abnormality. The maxillary anterior teeth are affected more than the

other teeth. Radiographic appearance shows thin and poorly mineralized enamel and dentin surrounding large pulp chambers and wide root canals. This thinness of enamel, dentin, and cementum gives the teeth the characteristic "egg shell" appearance and gives rise to the term "ghost teeth". Many of these teeth remain unerupted and may, therefore, be mistaken as teeth undergoing resorption.

Hyperparathyroidism Hyperparathyroidism is overactivity of the parathyroid glands resulting in excess production of parathyroid hormone (PTH). The parathyroid hormone regulates calcium and phosphate levels and helps to maintain these levels. Excessive PTH secretion

may be due to problems in the glands themselves, in which case it is referred to as primary hyperparathryroidism and which leads to hypercalcemia (raised calcium levels).

there are excessive amounts of calcium in the bloodstream, and calcium salts are deposited into soft tissues throughout the body. Without medical intervention, these can be deposited into the heart, lungs, liver, etc., which can result in calcinosis. Without medical intervention, calcinosis can be lethal. More subtle calcium deposits can also be detected in other soft tissues, such as the pulp of a tooth. This is where radiographic interpretation and medical referral can assist in the early intervention of CKD and secondary

hyperparathyroidism. It is likely that calcification of the dental pulp in patients with secondary hyperparathyroidism would not appear as classic pulp stones, but rather a more subtle narrowing of the pulp chamber. Left untreated, the complete pulp chamber could become calcified. See Table 1 for additional symptoms of secondary hyperparathyroidism.

Hypopituitarism Hypopituitarism is the decreased (hypo) secretion of one or more of the eight hormones normally produced by the pituitary gland at the base of the brain.[1] [2] If there is decreased secretion of most

pituitary hormones, the term panhypopituitarism (pan meaning "all") is used.[3] Hypofunction of the pituitary gland may lead to retarded euption of teeth and to open root apices.

Reference Grossmans endodontic Practice Shafers textbook of oral pathology Wikipedia.com,