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Anomaly in pulp cavity

Contents1. Introduction2. Gemination3. Fusion4. Taurodontism5. Dens in Dente (dens

invaginatus)6. Dens Evaginatus7. Dentinogenesis

imperfecta8. Dentinal dysplasia

9. Odontodyplasia10. Hyperparathyroidism11. Hypopitutarism

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IntroductionPulp cavity Is defined as a spacelocated in the center of tooth

surrounded by dentin.

In vital condition it contains a softconnective tissue termed dentalpulp or pulp organ, which

continues apical with periapicaltissues.

The primary function of the dental

pulp is to form dentin (by theodontoblasts)

Other functions include

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Nutritive: the pulp keeps theorganic components of the

surrounding mineralized tissuesupplied with moisture andnutrients;

Sensory: extremes intemperature, pressure, ortrauma to the dentin or pulp are

perceived as pain; Protective: the formation of

reparative or secondary dentin(by the odontoblasts).

Anomalies in pulp cavitycan beunderstood under following heads :

Anomalies of Shape

1. Gemination

2. Fusion3. Taurodontism

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4. Dens in Dente (densinvaginatus)

5. Dens EvaginatusAnomalies of Structure

1. Dentinogenesis imperfecta2. Dentinal dysplasia3. Odontodyplasia

Anomalies associated withGlandular diseases

1. Hyperparathyroidism

2. Hypopitutarism

GeminationThe partial development of two teeth

from a single tooth bud followingincomplete division.

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An incomplete division of a singletooth bud resulting in a bifid crown

with a single pulp chamber.

It is also known as schizodontia,twinning.It occurs in mandibular anterior teethmostly.

It occur in both deciduous andpermanent dentition.

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Fusion

The dentinal union of twoembryologically developing teeth.

Fused teeth can contain two separatepulp chamber, may appear as largebifid crowns with one chamber.

TaurodontismTaurodont teeth are characterized byhaving a significantly elongated

pulpchamber with short stunted roots,resulting from the failure of the properlevel of horizontal invagination ofHertwigs epithelial root sheath..The

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condition has sometimesbeen seen inassociation with amelogenesis

imperfecta, tricho-dento-osseoussyndrome,and Klinefelter's syndrome.

This anomaly is not recognizableclinically but on a radiograph,therectangular pulp chamber is seen in

an elongated tooth body withshortened roots androot canals.

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Dens invaginatus

Dens invaginatus in a human tooth wasfirst describedby a dentist named Socrates in 1856(Schulze 1970).

In 1873 Mhlreiter reported onanomalous cavities inhuman teeth, Baume in 1874 and Buschin 1897published on this malformation. In 1887

Tomesdescribed the dens invaginatus in histextbookA Systemof Dental Surgery, as follows:

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Synonyms for this malformation are:Dens in dente,invaginated odontome, dilated gestantodontome,dilated composite odontome, tooth

inclusion, dentoid indente.consider dens invaginatus asa deep folding of the foramen coecumduring tooth

development which in some cases evenmay result in asecond apical foramen (Schulze 1970)The first classification of invaginatedteeth was publishedby Hallet (1953). The most commonly

usedclassification proposed by Oehlers(1957a) is shown in

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Fig. 3. He described the anomalyoccurring in three

forms:Type I: an enamel-lined minor formoccurring withinthe confines of the crown not extendingbeyond the amelocemental junction.Type II: an enamel-lined form which

invades the rootbut remains confined as a blind sac. Itmay ormay not communicate with the dentalpulp.

Type III: a form which penetrates throughthe root perforatingat the apical area showing a secondforamen in the apical or in theperiodontalarea. There is no immediate

communicationwith the pulp. The invagination may becompletely

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lined by enamel, but frequentlycementum

will be found lining the invagination.Oehlers (1957a,b) also describeddifferent crown forms(normal with a deep lingual or palatal pit;conical,barrel-shaped or peg-shaped with an

incisal pit) relatingto the three groups mentioned above. Inaddition,Ulmansky & Hermel (1964) and Vincent-Townend

(1974) described an incipient dens indente, a deeppalatal or lingual pit completely lined byenamel with nocommunication to the pulp. Oehlers(1958) also

presented radicular invaginations.Schulze & Brand (1972) proposed a moredetailed

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classification (Fig. 4), also includinginvaginations

starting at the incisal edge or the top ofthe crown andalso including dysmorphic rootconfigurations.

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D ens evaginatus

Dens evaginatus (DE) is a developmentalaberration of a tooth resulting informationof an accessory cusp whose morphology

has been variously described as anabnormaltubercle, elevation, protuberance,excrescence, extrusion, or bulge

This uncommon

anomaly projects above the adjacenttooth surface, exhibiting enamel covering

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a dentinal core that usually contains pulptissue that on occasion may have a

slenderpulp horn which extends variousdistances up to the full length of thetubercles dentincore (1). The presence of pulp within thecusp-like tubercle has great clinical

significanceand distinguishes the anomaly fromsupplemental cusps, such as the cusp ofCarabelli (2), which contain no pulp

DE is thought to develop from anabnormal proliferation and folding of aportionof the inner enamel epithelium andsubjacent ectomesenchymal cells of thedental

papilla into the stellate reticulum of theenamel organ during the bell stage oftooth

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formation (24 26). The resultantformation is defined as a tubercle, or

supplemental solid elevation on someportion of the crown surface.

Schulge (1987) distinguishes the

following five typesof DE for posterior teeth by the locationof the tubercle (5).

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1. A cone-like enlargement of the lingualcusp.

2. A tubercle on the inclined plane of thelingual cusp.3. A cone-like enlargement of the buccalcusp.4. A tubercle on the inclined plane of thebuccal cusp.

5. A tubercle arising from the occlusalsurface obliterating the central groove.Accordingly, Lau further classified eachtype of tubercle on the basis of fouranatomical shapes of smooth, grooved,

terraced and ridged.Finally, Oehlers identified the evaginationaccording to the pulp contents within thetubercle by examining the histologicalappearance of the pulp using decalcifiedserial sections of extracted teeth with

DE. These categories are listed as followsalong with their percentageof occurrence:1. Wide pulp horns (34%)

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2. Narrow pulp horns (22%)3. Constricted pulp horns (14%)

4. Isolated pulp horn remnants (20%)5. No pulp horn (10%).

Dentinal Dysplasia

Dentin dysplasia is a genetic disorderofteeth, commonly exhibiting anautosomal dominant inheritance. It is

characterized by presence of normalenamel but atypical dentin withabnormal pulpal morphology. Thereare two types. Type I is the radicular

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type, and type II is the coronal type. Inthe radicular type, the roots of teeth

are shorter than normal and the pulpchamber may be nearly gone. Thepulp chamber is sometimes describedas having a "crescent shaped"appearance. In the coronal type, thepulps are enlarged and are described

as having a "thistle

tube" appearance, in permanentdentition. In the deciduous dentition,

coronal dentin dysplasia bears aresemblance to DentinogenesisImperfecta type II.

Radiographic Features

Type 1: Roots are short, blunt and

conical. In deciduous teeth, pulpchambers and root canals are completelyobliterated in permanent they may becrescent shaped.

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Type 2: The pulp chamber of the

deciduous teeth become obliterated indeciduous teeth. While in permanentteeth, large pulp chamber is seen incoronal portion of the tooth - referred toas thistle tube appearance.Pulp stones

may be found.

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Dentinogenesis imperfecta

Dentinogenesis imperfecta (hereditaryOpalescent Dentin) is a genetic disorderoftooth development. This conditioncauses teeth to be discolored (most oftena blue-gray or yellow-brown color) andtranslucent. Teeth are also weaker than

normal, making them prone to rapidwear, breakage, and loss. Theseproblems can affect both primary (baby)teeth and permanent teeth. Thiscondition is inherited in an autosomal

dominant pattern, which means one copyof the altered gene in each cell issufficient to cause the disorder.

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Dentinogenesis imperfecta affects anestimated 1 in 6,000 to 8,000 people.

Types

Types of dentinogenesis imperfecta withsimilar dental formalities usually an

autosomal dominant trait with variableexpressivity but can be recessive if theassociated osteogenesis imperfecta is ofrecessive type. This type is no l

Type II : Occurs in people without other

inherited disorders (i.e. Osteogenesisimperfecta).It is an autosomal dominanttrait. A few families with type II haveprogressive hearing loss in addition todental abnormalities.

Mutations in the DSPPgene have beenidentified in people with type II and typeIII dentinogenesis imperfecta. Type I

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occurs as part of osteogenesisimperfecta.

Radiographic features

Type I and II show total obliteration of thepulp chamber.

Type III shows thin dentin and extremely

enormous pulp chamber.These teeth areusually known as Shell Teeth.

Histology

Dentinal tubules are irregular and arebigger in diameter. Areas of uncalcified

matrix are seen. Sometimes odontoblastsare seen in dentin

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ODONTODYSPLASIA (Odontogenesisimperfecta, ghost teeth)Odontodysplasia or "ghost teeth" is arelatively rare developmentalabnormality of unknown

cause. It results in marked hypoplasiaand hypocalcification of enamel anddentin. Thecementum is much thinner than normal.The affected teeth are small and have

short roots.They are brittle and fracture readily,resulting in pulpal infection. Bothdentitions,deciduous and permanent, may beinvolved. A single tooth or several teeth

in a localized area may exhibit the

abnormality. The maxillary anteriorteeth are affected more than the

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other teeth. Radiographic appearanceshows thin and poorly mineralized

enamel anddentin surrounding large pulp chambersand wide root canals. This thinness ofenamel,dentin, and cementum gives the teeththe characteristic "egg shell" appearance

and givesrise to the term "ghost teeth". Many ofthese teeth remain unerupted and may,therefore,be mistaken as teeth undergoing

resorption.

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Hyperparathyroidism

Hyperparathyroidism is overactivity ofthe parathyroid glands resulting inexcess production ofparathyroidhormone (PTH). The parathyroidhormone regulates calcium andphosphate levels and helps to maintainthese levels. Excessive PTH secretion

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may be due to problems in the glandsthemselves, in which case it is referred to

asprimaryhyperparathryroidism andwhich leads to hypercalcemia (raisedcalcium levels).

there are excessive amounts of calciumin the bloodstream, and calcium salts aredeposited into soft tissues throughoutthe body. Without medical intervention,these can be deposited into the heart,

lungs, liver, etc., which can result incalcinosis. Without medical intervention,calcinosis can be lethal.

More subtle calcium deposits can also bedetected in other soft tissues, such as

the pulp of a tooth. This is whereradiographic interpretation and medicalreferral can assist in the earlyintervention of CKD and secondary

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hyperparathyroidism. It is likely thatcalcification of the dental pulp in patients

with secondary hyperparathyroidismwould not appear as classic pulp stones,but rather a more subtle narrowing of thepulp chamber. Left untreated, thecomplete pulp chamber could becomecalcified. See Table 1 for additional

symptoms of secondaryhyperparathyroidism.

Hypopituitarism

Hypopituitarism is the decreased (hypo)

secretion of one or more of the eighthormones normally produced by thepituitary gland at the base of the brain.[1][2] If there is decreased secretion of most

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pituitary hormones, the termpanhypopituitarism (pan meaning "all") is

used.

[3]

Hypofunction of the pituitary gland maylead to retarded euption of teeth and toopen root apices.

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Reference

Grossmans endodontic Practice

Shafers textbook of oral pathology

Wikipedia.com,