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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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    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 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.


    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


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    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 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



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

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    Grossmans endodontic Practice

    Shafers textbook of oral pathology