ODONTOGENESIS-

DEVELOPMENTAL
AN0MALIES OF TOOTH
CONTENTS
• Introduction.
• Stages in Tooth development
• Classification of developmental anomalies of tooth
• Clinical features
• Radiological features
• Clinical considerations
• Syndromes associated with developmental anomalies
• Conclusion
• References
• Development – it refers to all the
naturally occurring unidirectional
changes in the life of an individual
from its existence as a single cell to its
elaboration as a multifunctional unit
terminating in death

• Disturbance- The act of disturbing

something or someone; setting
something in motion
Stages of Tooth
development & parts

TOOTH & RELATED TISSUES: Developmental goal

WABeresford

ENAMEL
GINGIVA
DENTINE

PULP
CEMENTUM

PERIODONTAL
ALVEOLAR BONE LIGAMENT/ PDL
• Why study growth &development of teeth?

Diagnose developmental anomalies of teeth

treat them successfully

restore function, esthetics and comfort of the patient

Tooth development

Morphological stage Physiological stages

Bud stage Initiation
Cap stage Proliferation
Early bell stage Histo-differentiation
Advanced bell stage Morpho-differentiation
Apposition

Introduction
Tooth formation / development is a continuous process where
each and every tooth pass though similar stages which has
been divided as morphologic and physiologic stages.
Steps in tooth development

• formation of primary epithelial band

• formation of dental and vestibular lamina
• Condensation of ectomesenchymal cells
• enamel organ formation
• formation of dental papilla & dental sac
Formation of vestibular and dental
lamina
Primary epithelial band

Vestibular Dental lamina

lamina Milk teeth
(lingually)
(labially)
Its Lingual Distally gives rise to
extension permanent molars

(successional)

All permanents except molars

Dental lamina
• it is lingually located to primary epithelial band, progressing
bilaterally forming 2 horse shoe shaped bands defining
prospective upper and lower dental arches which are shallow
initially but gets deeply established with in a week. Which is a
germinal band of epithelium circumscribing future maxillary
and mandibular arches.
Formation of enamel organ
10 small swellings develop in the region of future
primary teeth
They form enamel organ and give rise to the enamel of
the teeth
Vestibular lamina
• Lip furrow band or labial or buccal
lamina or buccogingival lamina
Contributes to development of
vestibule delineating the lips and
cheeks from tooth bearing regions.
Initially the cells of vestibular lamina
proliferates which subsequently
shows degeneration in central
epithelial cells resulting is formation
of sulcus i.e. vestibule.
Future
• Tooth germ = enamel organ
Enamel
+
dental papilla
+ Dentin
dental sac/follicle Cementum
Periodontal ligament
bone
Clinical considerations
• Lack of intiation results in the absence of teeth.
• Abnormal intiation may result in development of
supernumerary teeth.
• In vitamin A deficiency ameloblasts fail to differentiate
properly. This results osteodentin formation.
• Endocrine disturbances affect the size or form of teeth of the
crown if such occurs in morpho-differentiation in utero and 1 st
year of life , alterations in root may occur by disturbences in
later period.
• Disturbances in morpho-differentiation may effect the size and
form of teeth with out impairing of odntoblasts function.
• Number of teeth: it can be Hyperdontia or Hypodontia

• Size of teeth: Is correlated with the abnormality during

cap and bell stages.

• Shape of teeth: Abnormality any where between bud to

advanced bell stage.

• Structure teeth: abnormality during late Bell stage and

during root formation.
Developmental anomalies of teeth
• Variation : is a minor deviation from normal.eg-large oral
orifice or enlarged medullary space.
• Anomaly :Are more severe deviations, but they do not
interfere with function.eg-enamel hypoplasia, Peg laterals.
• malformation: Are even more severe deviations and do
interfere with function.eg-cleft lip, cleft palate.
• Monstrosities : Are extreme deviations that severely interfere
with Function. Eg-Aganthia.
• Malformation complex (Anomalad) : A malformation
together with its subsequently derived structure E.g.:- Pierre-
Robin Anomalad.
• Congenital : anomaly or defect present at birth.
• Hereditary : characteristic, condition or disease transmitted
from parent to offspring.
• Acquired : originating after birth, not caused by hereditary or
developmental factors, but by reaction to environmental
influence outside the organism.
• Agenesis : A condition which is its clinical and radiological
absence at an age when it is ordinarily expected to be present.
factors effecting the development of dentition

Systemic factors : • Local factors

• Accelerating effect
• Hyperthyroidism
• Hyperpitutarism
• Turner’s syndrome
• Retarding effect
• Hypopitutarism
• Hypothyroidism
• Cleidocranial dysostosis
• Downs syndrome
• Hypovitaminosis
• Amelogenesis imperfecta
• Aberrant tooth position
• Lack of space in the arch
• very early loss of
predecessor
• Ectopic eruption
• Congenital absence of
teeth
• Supernumerary tooth
• Tumor
• Cyst
 classifications
Number Shape
• Hypodontia • Gemination
• Hyperdontia • Fusion
• Twinning
• Concrescence
Size • Accessory cusps
• Microdontia • Dens invaginatus
• Macrodontia • Ectopic enamel
• Taurodontism
• Hypercementosis
• Accessory roots
• Dilaceration
• Enamel pearl or droplet or nodule
• Carabelli cusp
• Shovel shaped incisor.
Disturbance in eruption.
• Premature eruption
• Delayed eruption
• Transposition
• Transmigration
• Impacted tooth
• Ankylosed deciduous tooth
Structure
• Amelogenesis imperfecta
• Dentinogenesis imperfecta
• Dentin dysplasia type I &II
• Regional odontodysplasia
• Dentin hypo calcification
 • Abnormalities in morpho-
histodiffrentiation will cause
abnormality in size of tooth

• Tooth size is variable among different

races and between sexes.
Disturbance in
size of teeth
• Although heredity is the major
Microdontia factor ,both genetic and environment
Macrodontia influences affect the size .

• The deciduous dentition appears to be

affected more by maternal
influences ;the permanent teeth seem to
be more affected by environment
Microdontia
• “Teeth which are smaller than normal size’’-MICRODONTIA .
• According to Boyle, “in general Microdontia , the teeth are
small, the crowns short, and normal contact areas between the
teeth are frequently missing”.
• Transmitted as an autosomal dominant type.
• Females demonstrate a higher frequency of Microdontia and
Hypodontia.
• Microdontia is associated with strongly with Hypodontia.
• Microdontia is much more common than macrodontia.
 Microdontia

True generalized Relative generalized Localized

• All teeth are involved
• Occurs in pituitary dwarfism
Down’s syndrome
Congenital heart disease
Fanconi’s anemia
• Diffuse true Microdontia
may Occur as in isolated
finding in Downs syndrome
•Single tooth is
•Normal or slightly normal involved
teeth present in jaws •Types :Entire tooth
somewhat larger Only crown
than normal Root alone
• Hereditary role . •Commonly involves
Max.lateral&3rd
•Spaced dentition. molar>
Mand& max 2nd molar
•Can be seen in hemi
Facial hypoplasia

•Ex: peg lateral

Dwarfed roots
• Disturbance in root development.

• Usually found in premolars and 3rd molars.

• See in dentin dysplasia and dentinogenesis

imperfecta.
• Detected during routine radiological
examinations.
• Undo pressure put by orthodontic forces during
root development eg: Maxillary anterior
• Rammers et al reported Microdontia as a late effect of
chemotherapy on dental development in a pt with
neuroblastoma.
• syndromes : Goblin -Chaudhry-Moss syndrome,
Williams’s syndrome,
Chromosome 13, Hallermann-Streiff,
Orofaciodigital syndrome (type 3),
Oculo-mandibulo-facialsyndrome,
Tricho-Rhino-Phalangeal
 Microdontia as later effect of
chemotherapy and radiotherapy

Initial radiograph of the affected tooth

(Three-year
follow-up)

Initial radiograph of the affected tooth

• Peg lateral :it is one most common form of localized
Microdontia in which the mesio-disatal sides converges or
taper incisally ,forming peg shaped or cone shaped crown
• Prevalence varies from 0.8% to 8.4 %
• Appears as autosomal dominant type.

Radiographic features :
• radiograph will permit evaluation of size of tooth
Diagnosis :
• Clinically diagnosis can be made by looking at the size of tooth
Management:
• Esthetic restorations
• Prosthetic crowns & bridge work
• Extractions
 Macrodontia
• Refers to teeth that are larger than normal
• The word should not be used to describe teeth that have altered
by fusion or gemination.
• Three types .
• Macrodontia often seen with Hyperdontia & males have a
greater prevalence of Macrodontia with Hyperdontia.

True Relative Localized

generalized generalized Macrodontia

•Extremely rare
• importance
•Seen hemi
•Commonly of
hyperplasia
associated hereditary • relatively
with pituitary must be
gigantism uncommon
considered
Clinical features:
• Teeth most commonly affected are maxillary central incisors,
canines followed by maxillary lateral and third molars where
as in primary tooth Max. Canine, mand.2nd molar are affected.
• Crowding of teeth resulted in malocclusion
• It causes less available of space ,so there is impaction of teeth
Radiological features
• It will permit evaluation of size

Treatment:
• If necessary orthodontic treatment is done
• Extraction of impacted teeth.
• Double veneering.
Rhizomegaly (Radiculomegaly)
• Condition where in root of the teeth is larger than normal
• Most commonly affected teeth are maxillary & mandibular
cuspids

• Clinical significance
- Extraction difficulties
- Oro-antral fistula

Rhizomegaly
 Disturbance
in number
of teeth
Increase in number
(hyperdontia)
2. Decrease in
number (hypodontia
• Anodontia refers to a total lack of tooth development.
• Hypodontia denotes the lack of development of one or more
teeth.
• Oligodontia (a subdivision of hypodontia) indicates the lack of
development of six or more teeth.
• Hyperdontia is the development of an increased number of
teeth and the additional teeth are termed Supernumerary.
• Congenital refers to a condition that exists at birth.
Anodontia
• True anodontia may be two types –Total/partial.
• True total anodontia-all teeth are absent, involve both the
dentitions but it is very rare condition, is frequently associated
with a more generalized disturbence. eg-ectodermal dysplasia
• False anodontia occurs as a result of extraction of teeth, while
pseudoanodontia is applied when multiple unerupted teeth in
the jaw.
• True partial Anodontia: Hypodonta and oligodontia- invloves
one or more teeth and it is a rather common condition.
Hypodontia
• Hypodontia is best defined as agenesis of one or more number
of teeth.
• May be total / partial.
• Involve both the dentitions, but far common in premanent
teeth.
• Hypodontia was almost twice as common in femles , agenesis
of the maxillary laterals incisor was more frequent in males.
• Hypodontia may be symmetric hypodontia, involving
particular teeth or group of teeth whereas hapahazard
involvement is other one.
• Order of frequency-3rd molars, premolars, maxillary laterals.
• In primary teeth it effects maxillary lateral and mandibular
central and laterals.
• Agenesis of premolars is constant in PHC syndrome.
• Pathogenesis – correlates with the absence of dental lamina
• Genetic - Autosomal Dominant / Recessive / Sex linked
• Environment
• Evolution
• Clinical significance - reduced alveolar development, increased
freeway space and retained primary teeth, Abnormal spacing of
teeth late permanent tooth eruption.
Hypodontia
Panoramic radiograph is more
helpful in evaluating the
number of missing teeth and the
collapse of the arches
Syndromes associated with hypodontia
• Ankyloglossia superior
• Crouzon
• Down
• Ectodermal dysplasia
• Ehlers danlos
• Hurlers
• Sturge‐weber
• Turner
• Incontinentia pigmenti
• Ellis von creveld
Treatment –
1. Single missing tooth – replaced by fixed or removal partial
dentures or implants

2. Multiple missing teeth - prosthetic replacement with fixed

prosthodontics, resin-bonded bridges or osseointegrated
implants with associated crowns.

3. For children and young adults, a resin-bonded bridge often

is appropriate while waiting for full dental maturation.
Hyperdontia
Development of an increased number of teeth and the additional
teeth are termed as Supernumerary teeth. They may resemble
the teeth of the group to which it belongs.
Pathogenesis:-
• Caused by the development of excess dental lamina, which
presumably leads to the formation of additional tooth germs.

• Many theories have been postulated for the formation of

supernumerary teeth

It develops from the third tooth bud arising from the dental
lamina near the permanent tooth bud.

It may also possibly develop from splitting of the permanent

tooth bud itself
  Atavism, the reappearance of an ancestral condition.

Hyperactivity theory.

Another theory proposes the hereditary tendency for the

development of supernumerary teeth.

• Accessory teeth usually do not resemble the normal form one

whereas supernumerary teeth look like a normal shape.
• Supplemental teeth are extra but have the shape that resemble a
normal set of teeth.
Classification of supernumerary teeth
1.According to Morphology
• Conical
• Tuberculate
• Supplemental
• Odontoma.
2.According to Shape
• Supplemental
• Rudimentary
3.According to Location
• Mesiodens
• Paramolar
• Distomolar
Clinical features

• A supernumerary tooth may closely resemble the teeth of the

group to which it belongs, i.e. molars, premolars, or anterior
teeth.
• Dentition affected – permanent, less common in primary teeth.
• Jaws – maxilla >mandible.

• Site – maxilary anteriors.

• Gender – 2to5 times :1

• Prevalence – 1 to 3% of the populations. 76 to 86% - single
hyperdontia; 12 – 23% two supernumerary teeth; three or more
supernumerary teeth less than 1%.

• Primosch (1981) reported that 90 to 98% of supernumerary

occur in the maxilla especially premaxilla area
Syndromes associated with hyperdontia
Associated syndromes –
1. Cleft lip and cleft palate
2. Cleido-cranial dysplasia
3. Ehlers-Danlos syndrome
4. Garden syndrome .
5. Crozon syndrome.
6. Loepard syndrome.
 • Abnormalities in morpho-
Disturbence histodiffrentiation.
in shape of
teeth
Gemination
• synonyms – Schizodontia.
• Defined as an attempt of a single tooth bud to divide, with the
resultant formation of a tooth with a bifid crown and , a
common root and root canal
• It occurs in during the proliferation stage of the growth cycle .
• It has got familial and hereditary tendency.
• Aquilo et al (1999) classified gemination into four types based
on morphology :Type I
Type II
Type III
Type IV
• Type I: Bifid crown with a single root
crown is larger than normal with a notch on the incisal edge
and a bifid pulp Chamber. The root and pulp chamber are of
normal size
• Type II :large crown with a large root
crown is larger than normal and has no groove or notch. The
pulp chamber is single and large. The root is wider than normal
and has one large root canal.
• Type III : Two fused crowns with a single root
There are two crowns with a vertical groove. The cervical
portion of both crowns may be joined . The pulp camber may
be separate . The root is conical shaped with larger than
normal.
• Type IV :Two fused crowns with two fused roots.
There are two crowns with a vertical groove. The cervical
portion of both crowns is joined along with the pulp chambers.
Clinical features:
• Both sex are equally effected
• It is seen in deciduous as well as permanent dentition
• Site :deciduous mandibular incisors and permanent incisors.
• Appearance –Bifid crown on single root
• It does not increase or decrease number of teeth.
• It is not always possible to differentiate between gemination
and a fusion between a normal and supernumerary teeth.
Crown features :
• There are common pulp canals and either single or partially
divided pulp chambers.
• Crown is wider than normal with shallow groove extending
from incisal edge to cervical region . Enamel or dentin of crown
of geminated teeth may be hypo plastic or hypo calcified.
Complication :
• Hypo plastic areas & invagination lines represents caries
susceptible area ,which may lead to pulpal infections .
• It may also cause malocclusion and periodontal pathos is
Radiographic features :
• Cleft crown –cleft in the crown and invagination are usually
outlined by the radiopaque enamel which accentuates
• Pulp chamber –pulp chamber is single ,enlarged and may be
partially divided
Diagnosis :
• Clinical diagnosis –crown appear as bifid on a single root
• Radiological diagnosis-pulp chamber is single and enlarged
Fusion
• “Synodontia”, “connate teeth”.
• “Fusion "defined as a single enlarged tooth or joined
(double )tooth in which the tooth count reveals a missing tooth
when the anomalous tooth is counted as one.
• It represents the embryonic union of normally separated two
tooth germs.
• It represents junction at the level of dentin between juxtaposed
normal tooth germs .
• Two separate developing tooth germs being initially close
together ; they grow and expand ; they contact with each other
and the germs fuse to varying degrees
Etiology :
• Genetic -it is transmitted as autosomal dominant
• Physical –pressure generated during development causes
contact of tooth germs.
Clinical features
• Anterior teeth is more commonly involved
• Deciduous teeth >permanent teeth
• It tends occur more frequently in mandible whereas gemination
is more common in maxilla
• Size of tooth is almost twice than normal.
• Tooth may have separate or fusion canals
• It may cause clinical problems related to appearance ,spacing
and periodontal conditions.
• Significance:caries is common in fused teeth. it may result in
reduced number of teeth ,when deciduous teeth fuse, the
corresponding teeth may be absent.
Radiographic features :
• True nature and extent of the union will be more evident.
Diagnosis
• Clinical diagnosis –large tooth with missing adjacent tooth will
aid in diagnosis
• Radiographic diagnosis –can be seen easily
Differential diagnosis:
• Gemination.
Early diagnosis is important to avoid various complications such
as compromised aesthetics, space loss, midline shift, and
carious exposure .
Case report one
Clinical photograph depicting fusion
between permanent maxillary
central and lateral incisiors
Intraoral periapical radiograph
revealing
fusion between crowns of
permanent central and lateral
incisiors associated with carious
exposure and periapical
radiolucencies
Concrescence
• It is the union of two adjacent teeth by cementum alone
without confluence of the underlying dentin.
• It is form of fusion
• Due to:
• Traumatic injury, lack of space ,distortion of tooth germs.
• Crowding of teeth with resorption of adjacent interdental
bone – contact of two roots – fused by cementum deposition
• May occur before or after tooth eruption.
• Types : True concrescence-roots are bound during
development.
Acquired concrescence-occurs after development.
• Usually involves two teeth. But a case involving three teeth has
been reported.
• Diagnosed by radiographic examination. It is difficult to
differentiate between fusion and concrescence.
• Should be noted during extraction procedures.
• Mitchell(1892)first described talon cusp as a prominent
accessory cusp on the lingual surface of max.incisor.
• Talon cusp was later defined by gorlin and godman as a very
high accessory cusp ,which meet the incisal edge of tooth to
give rise to a T or a Y –shaped.
• Dental anomaly resembled the claw of an eagle.
Dens invaginatus
• Synonyms: palatal invaginations ,dens in dente ,bilateral
composite odontome ,gestant odontome, dilated composite
odontome.
• Tomes (1859) was first to describe a case of coronal dens in
dente .
• Swanson and Mc carthy have been described both radicular
and coronal type.
• The word “dens invaginatus” introduced by hallet.
• Dens invaginatus is a developmental anomaly thought to arise
as a result of an invagination in the surface of crown before
tooth calcification
Etiology :
• Increased localized external pressure.
• Focal growth retardation-relative retardation in growth of a
portion of the enamel.
• Focal growth stimulation-due proliferation of enamel organ at
the inner enamel epithelium apically into dental papilla during
the stage of differentiation
• Local causes –trauma ,periapical infection of deciduos tooth
Classification –based on the site
• Coronal dens invaginatus –formed by the folding of the enamel
organ into dental pulp
• Radicular dens invaginatus –invagination of hertwig’s epithelial
root sheath
• Cementum –lined invaginations of the root are considered
variations in the root morphology ,not a type.
• The redicular variety explained by bhatt and dholkia who
discussed that usually results from an infolding of hertwig’s
sheath after crown is formed.
• Extremely rare ,represented as enamel lined invagination with in
root.
• Based on depth of invagination oehlers(1957) classified into
three types
Type I-invagination ends in blind sac ,limited to the dental crown
Type II-invagination extends to the CEJ.
Type III-invagination extends to the interior of the root,providing
an opening to the periodontium, sometimes presenting another
foramen n the apical region.
Clinical features:
• In a review of pindborg ,the prevalence is 0.25 to 5.1 % affecting
maxillary lateral.
• Order of frequency -max.latreal
>central>premolars>canine>molars.
• Very rare in mandible,supernumerary,especially mesiodens often
have invaginatus.
• Clinically the suspicion of an invagination may arise if foramen
caecum is extremely marked.
• Histology-enamel ,dentin of outer enamel are not effected, the
enamel covering the invagination is more defective at the bottom
Radiological features:
• common appearance is pear shaped or loop-like defect lined by
a radiopaque line with density equal to enamel-TOOTH WITH
IN TOOTH.
• Radio graphically, it is impossible accurately to determine the
precise relationship of the invagination portion with the pulp
chamber.
• Palatogingival groove is the maxillary incisor was described
among chinese and indian population by lee and colleagues.
• The defect commences at the junction of the cingulum and one
of the lateral marginal ridge and extends on to the root.
• The groove probably represents an infolding of enamel organa
and hertwig sheath.
• The effected tooth has wider apical foramen.
• The tooth resembles INVERTED OPEN UMBRELLA, the
handle of which is short ,being represented by the conical shaped
crown.
Diagnosis :clinically seen infolding of tooth, characteristic
radiographic appearance of tooth will be diagnosed.
Management:
• The point of invagination is caries prone and as a preventive
measure ,restoration is recommended.
• If the tooth is carious and the invagination is close to the pulp
indirect pulp is to be done. However pulpally invaginated tooth
then best managed by root canal treatment.
Dens evaginatus
• Definition – is a cusp like elevation of enamel located in the
central grove or lingual ridge of the buccal cusp of permanent
premolar or molar teeth.
• Synonyms: occlusal enamel pearl ,leong’s premolar,
tuberclated cusp, accessory tubercele, evagianted odontomas.
• Pathogenesis – it is due to proliferation and evagination of an
area of the inner enamel epithelium and subsequent
odontogenic mesenchyme into the dental organ during early
tooth development.
• It is a rare developmental anamolay charecterized by the
presence of an acceossory cusp/enamel on occlusal surfaces of
premolar occuring between two cusps
Classification of dens evaginatus –
• According to location of the tubercle (schulge 1987)
• A cone-like enlargement of the lingual cusp
• A tubercle on the inclined plane of the lingual cusp
• A cone-like enlargement of the buccal cusp
• A tubercle on the inclined plane of the buccal cusp
• A tubercle arising from the occlusal surface obliteratng the
central groove
• Lau further classified each tubercle into four anatomical shapes
of smooth, grooved, terraced, and ridged.
• According to pulp contents within tubercle (Oehlers)
• Wide pulp horns
• Narrow pulp horns
• Constricted pulp horns
• Isolated pulp horn remnants
• No pulp horn
Dens evaginatus
Clinical features:
• Prevalence ranges between 1-4 %.
• Site –premolar(more common) and molar &
usually it is unilateral/bilateral.
• Common-mandible>maxilla.(five times)
• Composed of enamel,dentin,pulp.
R/F: tuberculated appearance.
• Significance-presence of occlusal tubercle can lead to occlusal
disharmony, attirition, and tendency to fracture therby resulting
in pulpal Exposure.The involved tooth can turn non-vital.
• May also cause Incomplete eruption, Displacement of teeth
• Some authors have reported fascial space infection and
osteomyelitis.
• The lack of 2º dentin is significant because it usually indicates
sudden death of pulp
• Shovel – shaped incisors: dens evaginatus which is seen in
association with maxillary incisors. Affected incisors
demonstrate prominent lateral margins creating a hollowed
lingual surface that resembles the scoop of a shovel.
• Typically the thickened margins converge at the cingulum, not
uncommonly there is deep pit, fissure,at this junction.
Maxillary lateral and central incisors most frequently affected,
with mandibular incisors and canines less commonly reported.
Taurodontism((Tauro- Bull, dont –
tooth)
Definition - it is an enlargement of the body and pulp chamber of
a multirooted tooth with apical displacement of the pulpal
floor and bifurcation of the roots.

• The term taurodontism was given by Sir Arthur Keith in 1913.

• According to witkop ‘taurodont teeth have pulp chambers in

which the bifurcaion or trifurcation is displaced apically, so
that the chamber has a grater apico-occlusal height than in
cynodont and lacks a constriction at CEJ level.
Etiology –
• A mendelian recessive trait
• Mutation resulting in odontoblastic deficiency during
dentinogenesis of roots.
Hammer and his associates - taurodontism is caused by failure
of Hertwig's epithelial sheath to invaginate at the proper
horizontal level.
• Appears to be genetically controlled and familial in nature.
Clinical features:
• Affect either deciduous or permanent teeth (more common in
permanent teeth).
• Usually molars – single/multiple-1st molar>2nd molar>3rd molar
followed by premolars.
• Prevalence – (0.5 to 46%)
• Unilateral or bilateral involvement.
• No unusual morphology.
• Affected teeth tend to be rectangular in shape.
• Pulp chamber is extremely large with greater apico-occlusal
height.
Shaw classified it as,
• – Hypotaurodont – mildest form
• – Mesotaurodont – moderate
• – Hypertaurodont – severe form with furcation near the apices
of the roots.
Measurement of taurodontism

If AB > '/2 AC the tooth was considered to be taurodontic – Witkop et al in

1988
Tulensalo et al. (1989) – connecting line between the CEJ to the floor of
the pulp chamber on panoramic radiographs. If the distance was >3.5 mm
the tooth was circumscribed as being taurodontic
 Syndromes associated with
taurodontism
• AI – Type IE, IV.
• Ectodermal dysplasia.
• Hyper/Hypo phosphatasia.
• Klinefelter syndrome.
• Oculo‐dental‐digital dysplasia.
• Tricho‐dento‐osseous syndrome.
• Down’s syndrome.
• Sex chromosomal aberrations.
Clinical significance
• Endodontic therapy – difficult
• Furcation involvement
• Stability & strength as abutment

Treatment
No specific therapy
 Click icon to add picture

Dilaceration
Scorpion tooth or
hand of a traffic
police men
DEFINITIONS
• The term Dilaceration was first coined in 1848 by Tomes , who
defined the phenomenon as the forcible separation of the cap of
the developed dentine from the pulp in which the development
of the dentine is still progressing.
• According to the glossary of dental terms, Dilaceration is
defined as the deformity of a tooth due to a disturbance
between the un mineralized and mineralized portions of the
developing tooth germ.
• Andreasen et al defined Dilaceration as the abrupt deviation of
the long axis of the crown or root portion of the tooth, which is
due to a traumatic non axial displacement of already formed
hard tissue in relation to the developing soft tissue .
• Due to trauma during tooth formation, the position of calcified
portion of the tooth is changed and the remaining tooth
develops at an angle.
• Dilaceration in a permanent tooth often follows traumatic
injury (avulsion or intrusion) to the deciduous predecessor in
which the tooth is driven apically into the jaw.
• Can also develop secondary to adjacent cyst, tumor or
odontogenic hamartoma.
• The curve or bend can occur anywhere along the length of the
tooth depending on the amount of tooth formed at the time of
injury
• Commonly effects the anterior teeth and the teeth may be non-
vital.
• Dilaceration of decidous teeth can cause delayed eruption of
permanent teeth.
• Malcic et al(2006)assesed prevalence is more in caucasians. The
results showed it found more common in maxillary and posterior
teeth were highest effected.
• According to hamasha et al(2002) mandibular 3rd molar were the
most commonly effected followed by mandibular 1st molar.
• The maxillary and mandibular teeth were least effected, almost
2/3-rd were in mandible and approximately 5%were in anterior
teeth.
• According to chohayeb(1983) conducted a study on 480
extracted teeth. In the study the root dilaceration was defined
as a deviation of 20º or more of the apical end of the root from
the normal long axis of the tooth and also disto-labial direction
root is major factor in the failure of endodontic therapy of
maxillary lateral.
Radiographic features :
• It will show angular distortion of unusual relationship between
coronal and radicular portion of the tooth.
• If the root bends mesially or distally condition will clearly
appear on radiograph.
• When the tilt is buccaly or lingually, dilacerated portion will
appear at apical end as a round opaque area with dark shadow
in central region by apical foramen. Periodontal space about
this is evident as a radiolucent halo.
• “Bull’s-eye” phenomena in a central incisor with a
dilacerated root
• The dilacerated portion then appears at the apical end of the
unaltered root as a rounded opaque area with a dark “spot” in
its center that is caused by the apical foramen of the root canal
(this appearance has been likened to a bull’seye or a target)
• Diagnosis: radiograph will show the curve of root, clinically
not possible to identify.
• Significance -complicated extractions and fialure of endodontic
therapy.
Talon’s cusp
• it is a supernumerary cusp, project from lingually from
cingulum are of maxillary and mandibular teeth.
Pathogenesis
• Focal proliferation
• Exuberant development.
Mellor and ripa(1970) described the talon cusp as a markedly
enlarged cingulum on a maxillary incisor teeth ,a rare finding
in the normal population.
• It resembles an eagle’s talon and blend smoothly with the tooth
except for a deep developmental groove.
Clinical features
• Sex –found in both sexes
• Location-seen in both dentitions in those max.lateral or central.
Predominantly affects permanent dentition .
• Composition –enamel , dentin, some times pulp
• Significance –esthetic ,high incidence of caries , occlusal
interferences.
• Syndrome –rubinstien-taybi syndrome .
• classification(Hattab et al)- type I( talon)-well delineated
additional cusp(CEJ to incisal edge )’type II(semi talon)-half of
distance from CEJ to incisal edge ;type III(trace talon)-
enlarged cingulum /prominent cingulum.
• This classification did not take consideration of talon on facial
aspect. later this was modified by stephen-ying
Type I-Major talon.
Type II-Minor talon.
Type iii-Trace talon.
Radiological appearance :
• It is seen as radiopaque structure ,in which enamel ,dentin,and
occasionally pulp.
• Typically it resembles V shaped superimposed over the normal
image of crown .
• Diagnosis :T shaped elevation on the tooth .
• Management :Restoration, endodontic therapy, periodic
grinding.
cusp of carabelli
• it was first described by Georg
carabelli in 1841, also known as
carabelli’s tubercle.
• It is accessory lingual cusp located on
the mesio palaptal cusp of maxillary
primary 2nd molar and 1st ,2nd, 3rd
permanent molar. May be
unilateral/bilateral.
• In some cases , accessory cusp is seen
occasionally on lower
permanent/deciduous molar –
Protostylid.
Protostylid
• First described by dahlberg(1945).
• It is a feature on the mesiobuccal surface of the crown of the mandibular
molar.
• It is seen in almost 40% population.
• In rare instances it can be seen on disto buccal cusp of the upper molars.
• There were five subdivisions of the classification which was proposed
by Snyder
• (0) no cusp – completely un interruptedsurface.
• 1) pit – a pit with a vertical wrinkle or irregular irregularities.
• (2) eminence – eminence of cusp without groove outline.
• (3) elevation – a small but positive elevation
• (4) cusp – well defined cusp.
• R/f: faint v shaped radio opacity.
Clinical significance:
• fissure is present between cusp tip and tooth surface prone for
caries.
• Interferes with bracket placement.
• Treatment: Enameloplasty
Ectopic enamel
Definition - Ectopic enamel refers to the presence of enamel in
unusual locations mainly in the tooth root

Types –
1. Enamel pearls
2. Cervical enamel projection
Enamel pearls
Enameloma, ectopic enamel
• They are droplets of white, dome-shaped calcific
concentrations of enamel , usually located at the furcation areas
of molar teeth.
• Most often attached to the CEJ, in some instances attached to
dentin, or cementum.
• Cavanha(1965) found that contain enamel only, others contain
core of dentin, rarely a small stand of pulp.
• Worth (1963) stated that there is no pulp cavity in enamel
pearl, and if it contains a pulp , it is geminated tooth.
• prevalence is high in eskimos.
• Pathogenesis –– they are thought to arise from localized
bulging of the odontoblastic layer. This bulge may provide
prolonged contact between Hertwig’s root sheath and the
developing dentin, triggering the induction of enamel
formation.
• Most common trifurcation of upper molars(usually found on
mesial/distal), followed by bifurcation of lower molars(on
buccal/lingual aspect).
• Clinical significance depends on site, if it happens to occupy
such a position at the CEJ that leads to pocket ,then it is
important to predisposing periodontal problems.
Radiographic features:
• Appears as Circumscribed ,dense,
smooth projection at the CEJ.
• This mass of enamel absorbs more x-rays
than dentin, so it appears as white image
that’s hemi-sperical in size of 1to 3mm.
• Diagnosis made radio graphically –
rounded opacity in furcation areas.
D/D- 1.calculus
2. pulp stones .
Cervical enamel extension
• These extensions represent a dipping of the enamel from the
cemento-enamel junction toward the bifurcation of the molar
teeth.
• Clinical features– buccal surface, man> max, Greater
prevalence in asians.
• There no real attachment of PDL fibers to the tooth.
• Clinical significance – early furcation involvement and
development of inflammatory cysts, pocket formation,
predisposing in periodontal diseases.
Masters and Hoskins suggested a classification system in 1964
that was based on the extent of cervical enamel projecting into
the furcation area.
• Grade I - The enamel projection extends from the
cementoenamel junction of the tooth toward the furcation
entrance.
• Grade II - The enamel projection approaches the entrance to
the furcation. It does not enter the furcation, and therefore, no
horizontal component is present.
• Grade III - The enamel projection extends horizontally into the
furcation.
Treatment : The enamel projection may be eliminated down to
the crestal bone level by ‘saucerization. Osteoplasty,
odontoplasty, or regenerative procedures may be required to treat
the osseous defect due to cervico-enamel projections.
Supernumerary roots
• Teeth that are normally single rooted exhibit two roots.
• These supernumerary roots may occur due to the disturbances
of the hertwig’s epithelial root sheath during root formation.
• Both maxillary and mandibular molars particularly 3rd molar
exhibits this tendency.
• The lower canine is often bifid, upper 1st molar may have three
roots that are arranged in manner similar to those of upper 1 st
molar.
• Freenezy reported that a bifurcation of root canal is seen in
13% of mandibular 1st premolars but only in 1% of the 2nd
premolar.
• Supernumerary roots can be either fully developed in size and
shape or small and rudimentary. Sometimes , they are fused to
the other roots.
• The presence of these roots is established by radiographic
examination. Two radiographs may have to be made from
slightly different angles to reveal hidden roots.
• When they are not superimposed on other roots, they are easier
to detect. An extra root canal or double periodontal membrane
space may be clue.
• Supernumerary root may be suspected when there is a sudden
diminution in the size of the root canal space or when it
appears divide into several smaller canal spaces.
• Mesial or distally roots can be easily identified but when they
are in buccal or lingual they may be superimposed on each
other appearing a bulbous root which may mimic
hypercementosis.
• Significance: Extracted teeth should be examined closely to
ensure that all roots have been removed. During endodontic
treatment the extra canal should be searched and treated
accordingly otherwise may lead to endodontic failure.
• Requires no specific treatment
 • Premature eruption
• Delayed eruption
Disturbances • Transposition
of eruption of • Transmigration
tooth • Impacted tooth
• Ankylosed deciduous tooth
premature eruption
• Congenital teeth ,fetal deciduous teeth, dentition praecox.
• There is premature eruption of teeth or teeth like structures that
are present at birth.
• Masseler and savara suggested the terms natal and neonatal
teeth.
• Natal teeth: teeth are present at the time of birth.
• Neonatal teeth: these teeth are erupting within 30 days after
birth.
• may be divided into mature and immature.
• Incidence -0.3 to 0.5%
• Position of eruption as same as deciduous.
• Etiology: unknown etiology. May be hereditary, hormonal
influence(hyperthyrodism).
• Common site –mandibular anterior region.
• In review of reports site of eruption-mandibular incisor(85%),
max.incisor(11%), mandibular canine(3%),
max.canine&molar(1%).
Clinical features:
• These teeth are well formed and normal in all aspects, except
that they may be somewhat mobile-cause possible aspiration
• Difficulty in sucking.
• Riga –fede-disease.
• Treatment -Eliminate the source of trauma so healing can take
place.
Conservative methods:
1.smoothening off the incisor edges,
2. covering the rough incisor edges with composite resin,
3.changing feeding habits by using a bottle with a larger hole in the
nipple, or placing a nasogastric tube
4.application of a local corticosteroid.
If conservative methods fail to resolve the lesion, or when the child
is severely dehydrated or malnourished extraction of the incisors
might be considered. Alternatively, excision of the lesion itself
might be performed
Delayed eruption
• May effect both the dentitions

• Can be localized or generalized.

• Lack of eruptive force.

Causes
• Systemic factors
- Rickets
- Cleidocranial dysplasia
- Cretinism

• Local factors
- Fibromatosis gingivae
- Cleft lip & palate
- Retained deciduous tooth
• Idiopathic.
• Treatment :removal of local causes.
Transposition
• Peck et al described dental transposition as the positional
interchanges of two adjacent teeth, or the development or
eruption of a tooth in a position normally occupied by a non-
adjacent tooth.
• Can be either complete(crown the roots of involved teeth
exchange or incomplete (crowns are transposed , but the roots
are remain in their original position).
• Prevalence -1% total population.
• Maxilla Region: Canine-premolar; Mandible: Canine-lateral.
• Duncan et al reported the fusion and transposition of maxillary
central and lateral primary incisors.
Etiology
• Interchange of developing tooth buds
• Inherited condition
• Altered eruption paths
• Trauma and presence of retained primary tooth.
• Root Dilaceration of adjacent tooth may be a potential
etiological factor of canine-premolar transpositions.
• Since they are asymptomatic no active management is
necessary.
• Tooth transposition can hinder esthetic and functional aspects
of dentition.
• Traumatic injuries to primary teeth and bone pathologies such
as cyst formation may cause displacement of permanent tooth
germs and lead to an abnormal eruption path
• peck and peck classified transpositions based on teeth involved
as :
 Maxillary canine-1st premolar.
 Maxillary canine –lateral.
 Maxillary canine to 1st molar.
 Maxillary lateral-central.
 Maxillary lateral-canine.
 Maxillary canine-central.
Transmigration
• It is described as pre-eruptive migration of a tooth across
midline of the jaw.
• It is unique in mandible permanent canines.
• Aras et al reported transmigration of maxillary canines.
• various authors proposed diagnostic criteria for
transmigrations.
• canine that has crossed the midline more than half of its length should
be considered.
• Others suggest that the tendency of a canine to cross the mandibular
midline is a more important consideration than the distance of migration
after crossing midline.
• Mupparapu proposed (2002) proposed a classification.
• Type 1: The canine is impacted mesioangularly across the
midline, labial, or lingual to the anterior teeth with the crown
portion of the teeth crossing the midline.
• Type 2: the canine is horizontally impacted near the inferior
border of the mandible below apices of incisors.
• Type 3: the canine has erupted either mesial or distal the
opposite canine.
• Type 4 : the canine is horizontally impacted near the inferior
border of the mandible below the apices of either premolars or
molars on the opposite side.
• Type 5: the canine is positioned vertically in the midline with
long axis of the tooth crossing the midline.
Impacted tooth
• is a tooth that fails to erupt into its normal functioning position
in the dental arch within the expected time
• The term Unerupted includes both impacted teeth and teeth
that are in the process of erupting.
• Impaction of tooth occurs when its eruption is impeded by a
physical barrier.
causes
A. A hereditary syndrom of cliedocranial dysistosis termed
primary Retention.
B. endocrinal deficiency (hypothyrodism, hypopituitarism).
C. febrile disease, down syndrom, irradiation (all cause
multiple teeth impaction).
D. prolonged deciduous tooth retention
E. malposed tooth germ
F. arch length deficiency
G. odontoginic tumors abnormal eruption path
H. cleft lip and palate
Frequency of impaction
1. mandibular 3rd molar
2. maxillary 3rd molar
3. maxillary cuspid
4. mandibular cuspid
5. Mandibular premolar
6. maxillary premolars
7. maxillary central and lateral incisors.
Classifications: - Relation of the tooth to the ascending
ramus of the mandible and to the distal surface of the 2nd
molar: (Pell &Gregory
 B - Relative depth of the third molar in
bone:
- this show the superior inferior
relationship of the tooth in relation
to the occlusal plan. (Pell &
Gregory)
Position A:
the highest portion of the tooth is
on level with or above the occlusal
plane.
Position B:
the highest portion is below the
occlusal
plane but above the cervical
margin of the 2nd molar
Position C:
the highest point of the tooth is
below the
cervical margins of the 2nd molar
(deep impaction)
C - the position of the long axis of the impacted tooth in
relation to the long axis of the 2nd molar (winter's
classification):

1-vertical: the long axis of the third

molar is parallel to that of the 2nd
molar.
2-horizontal:the long axis of the third
molar is at right angle to that of the
2nd molar .
3-mesioangular impaction.
4-destoangular impaction:
all the previous four classes can
come in:
a - lingual deflection.
b - buccal deflection.
5-inverted impaction
2 -Classification of impacted
maxillary third molar:
1. The relationship of the tooth to occlusal plane of the 2nd
molar (as before)
2. The relationship of tooth to maxillary sinus :
a-sinus approximation :
(s.a) where no bone or very thin bone exist
between the impacted teeth and floor of sinus.
b-no sinus approximation :
(n.s.a) where 2 mm or more of bone exist
between the floor of sinus and impacted teeth.
3-Classification of impacted
maxillary cuspids:
• Class1:
palatally impacted cuspids ,these could be in vertical,
horizontal, semivertical position.
• Class2:
labialy impacted cuspide which could be in vertical,
horizontal, semivertical.
• Class3:
impacted cuspid located both in the palatal and labial surfaces.
• Class4:
impacted cuspid that are present in an edentulous maxilla and
may assume any of the previous three classes.
• Treatment: Surgical removal of impacted teeth:
Ankylosis
• Cessation of eruption after emergence occuring from an
anatomic fusion of tooth cementum or dentin to alveolar bone
• Etiology unknown-trauma, local change of metabolism,
thermal irritation, and genetic predisposition have been
suggested.
• Can occur at any age but is clinically most evident when it
develops during first two decades of life
• Peak prevalence- 8-9 years of age
• Reported prevalence of clinically
• detectable ankylosis- 1.5% to 9%
• Primary molars are most commonly involved teeth with most
cases in mandible
• Radiographic findings
• Sound on percussion
• Treatment considerations
 • Enamel
Enamel hypoplasia
Amelogenesis
Developmental imperfecta
disturbances
in structure of • Dentin
teeth
Dentinogenesis
imperfecta
Dentin dysplasia
• Enamel + Dentin
Regional
odontodysplasia
Enamel hypoplasia:
• Enamel hypoplasia may be defined as an incomplete or
defective formation of the organic enamel matrix of the teeth.

Two types –
1. Hereditary type – Amelogenesis imperfecta
2. Environmental enamel hypoplasia.
Amelogenesis imperfecta
• Also called hereditary enamel dysplasia, hereditary brown
enamel, hereditary brown opalescent teeth.

• It represents a group of hereditary defects of enamel

unassociated with any other generalized defects.

• It is entirely an ectodermal disturbance and the mesodermal

components of the teeth are basically normal.
Definitions
A group of disfiguring hereditary conditions
which affect the clinical appearance of enamel of all or nearly
all teeth which occur in kindred, show essentially the same
defect & which are unassociated with known morphologic or
biochemical changes elsewhere in the body
- Witkop & Rao 1971
• In normal development of enamel, three stages can be
appreciated,
• Formative stage – deposition of organic matrix – defective –
Hypoplastic AI.
• Calcification stage – matrix mineralization – defective –
Hypocalcification (Hypomineralization) AI.
• Maturation stage – Crystallites mature and enlarge –
defective – Hypomaturation AI (immature crystallites).
• By Witkop and Sauk,
• Hypoplastic – enamel is not formed to full, normal thickness
on newly erupted, developing teeth.
• Hypocalcified – enamel is so soft that it can be removed by
prophylaxis instrument.
• Hypomaturation – enamel can be pierced by an explorer
point under firm pressure and can be lost by chipping off
from the underlying normal dentin.
Classification –

• Prevalence :
• 1: 718 – 1: 14,000
Hypoplastic amelogenesis imperfecta
The basic alteration centers on inadequate deposition of enamel
matrix.

Types –
1. Generalized pitting
2. Localized pitting
3. Autosomal dominant smooth pattern
4. X-linked dominant smooth pattern
5. Rough pattern
6. Enamel agenesis
Hypomaturation amelogenesis imperfecta

• In this type the enamel matrix is laid down and mineralization

begins. However there is defect in the maturation of the
enamel’s crystal structure.

• Affected teeth are normal in shape but exhibit a mottled,

opaque white-brown discoloration. The enamel is softer than
normal and tends to chip from the underlying dentin.

• Radiographically the enamel demonstrates radiodensity similar

to the underlying dentin.
 pigmented form

The snow-capped pattern

 Hypocalcified amelogenesis imperfecta
• In this type, the enamel matrix is laid down appropriately but
no significant mineralization occurs.
• The teeth are appropriately shaped on eruption, but the enamel
is very soft and easily lost.
• On eruption the enamel is yellow-brown or orange, but it often
becomes stained brown to black and exhibits rapid calculus
apposition.
• With the years of function much of the enamel is removed,
except for the cervical portion that is occasionally calcified
better.
 Hypomaturation/hypoplastic amelogenesis imperfecta
• Has enamel hypoplasia in combination with hypomaturation.
• Both the dentition are affected.
• Two patterns based on thickness of enamel and overall tooth
size.
Two types –
1. Hypomaturation –hypoplastic type
2. Hypoplastic-Hypomaturation type
• Hypomaturation – Hypoplastic
• Enamel hypomaturation is the dominant feature.
• Enamel is yellowish-white to yellowish-brown.
• Pits are seen on buccal surface.
• Enamel is similar to dentin in density.
• Large pulp chambers with varying degrees of taurodontism.
Hypoplastic-Hypomaturation type
• Enamel hypoplasia is the dominant feature.
• Enamel is thin.
• Other features are similar
Clinical features
• Extremely variable, clinical presentation.
• All teeth of both dentitions affected to some degree.
• Crowns may show discoloration varying from yellow to dark
brown.
• Enamel may be totally lost or have chalky texture or cheesy
consistency or relatively hard.
• Enamel may be smooth or show vertical wrinkles or grooves.
• May be chipped or show depressions with exposed dentin at its
base.
• Contact points are open
• Occlusal and incisal edges are severely abraded.
• Overall shape of the tooth may not be normal depending on
the,
• Amount of enamel present
• Amount of occlusal and incisal wear
• Enamel may be totally absent or seen only on the cusp tips and
inter-proximal surfaces.
• It may have similar radiodensity to dentin.
Clinical significance –
• Aesthetics
• Loss of vertical dimension
• Dental sensitivity
• Increased prevalence of caries
• Delayed eruption
• Associated gingival inflammation
Treatment –
• Appropriate diagnosis - Preservation of VD and Aesthetics
• Full coverage
• Full dentures or overdentures
• Facial veneers
Environmental enamel hypoplasia
• Nutritional deficiency- vitamin A,C,D.
• Exanthematous diseases- measles, chicken pox, scarlet fever
Congenital syphilis
• Hypocalcaemia
• Birth injury
• Local infection or trauma
• Ingestion of chemicals
• Idiopathic
Enamel hypoplasia due to congenital syphilis
Enamel hypoplasia due to hypocalcemia –
• Tetany
• Serum calcium level fall as low as 6 – 8 mg per 100ml
• Hypoplasia usually of pitting type

Hypoplasia due to birth injuries –

• Multiple pregnancy; prematurely born
• Neonatal line – Schour in 1936 Produced in enamel and
dentin
• In Rh hemolytic disease – staining and enamel hypoplasia
Hypoplasia due to local infection/ trauma
Turner’s hypoplasia and turner’s tooth
Etiology –
1. Inflammatory origin
2. Traumatic origin
Clinical features-

Treatment -
Enamel hypoplasia due to fluoride (mottled enamel)

• Dr.Frederick S. Mckay in 1901

• Etiology – ingestion of fluoride containing drinking water. > 0.9 –

1ppm

• Pathogenesis – disturbance of the ameloblasts during formative

stage of tooth dev.
Clinical features –
Depending of the severity – wide range of severity
1. Questionable changes characterized by occasional flecking or
spotting of enamel
2. Mild changes manifested by white opaque areas
3. Moderate and severe changes showing pitting and brownish staining
of the surface
4. Corroded appearance of the teeth.
Treatment of mottled enamel –
1. Microabrasion
2. Vital bleaching
3. Acid etched composite resin
4. Labial veneers or full crowns
Hereditary Defects Acquired Defects

Affect enamel or dentine Affect enamel and dentine

Affect both dentitions Affects one dentition usually

the permanent

Usually affect all teeth Usually affect single or

group of teeth

Produce vertically or Produce horizontally

randomly oriented pits or oriented pits or defects
defects
Dentinogenesis imperfecta :(Hereditary
opalecent dentin)
• Dentinogenesis imperfecta is a hereditary developmental
disturbance of the dentin in the absence of any systemic
disorder.
• Autosomal dominant condition. The gene maps to chromosome
#4. It encodes a protein called dentin sialophosphoprotein
(DSPP).
• Classification –
• shields:1) Dentinogenesis imperfecta -I
2) Dentinogenesis imperfecta -II
3) Dentinogenesis imperfecta -III
WITKOP:1) Dentinogenesis imperfecta
2) Hereditary opalacent teeth
3)Brandywine isolate
C/F:
• Race – more common in whites
• Prevalence – 1:8000.
• Dentition –. Deciduous teeth are affected severely, followed by the
permanent incisors and first molars,
• The dentitions have a blue-to-brown discoloration, The enamel frequently
separates easily from the underlying defective dentin. Once exposed, the
dentin often demonstrate significantly accelerated attrition
• Significant clinically obvious enamel
hypoplasia is noted in some patients.
Radiographic Features

1. DI – I, II

2. DI – III (Shell teeth)

Treatment
• Difficult to perform rct
• The teeth are not good candidates for full crowns because of
cervical fracture
• Overlay dentures placed on teeth that are covered with fluoride
releasing gic have been used with success in some cases.
• Metal crowns
DENTIN DYSPLASIA
It is a rare disturbance of dentin formation characterized by normal
enamel but atypical dentin formation with abnormal pulpal
morphology.

The first description of this disease was made by Ballschmiede in

1920.

Classification –
1. By shields and associates

• Type I – dentin dysplasia

• Type II – anomalous dysplasia of dentin
2. By witkop
• Radicular dentin dysplasia (type I)
• Coronal dentin dysplasia (type II)
Etiology –autosomal dominant characteristics.
Clinical features -
1. Dentin dysplasia type I-rootless teeth because the loss of
organization of the root dentin often leads to a shortened root length.
prevalence is 1:100,000., the initial clinical signs are extreme tooth
mobility, and premature exfoliation, spontaneously or secondary to
trauma. The radicular strength of the dentin is reduced, with the
teeth being predisposed to fracture during extraction
2. Dentin dysplasia type II-In contrast to type I, the root length is normal
in both dentitions. Clinically, the teeth demonstrate a blue–to–amber
-to-brown translucence. The permanent dentition demonstrates
normal clinical coloration.
Pulpal calcifications are more here .
Radiographic features –

Dentin dysplasia type I

Dentin dysplasia type II

Treatment and prognosis –
In type I dentin dysplasia –
• Restoration
• Extractions
In type II dentin dysplasia –
The deciduous teeth are managed in similar manner to
dentinogenesis imperfecta. Because the pulp canals are not
usually obliterated completely in permanent dentition,
endodontic treatment can be accomplished readily.
Regional odontodysplasia
• Synonyms - (Odontodysplasia, odontogenic dysplasia,
odontogenesis imperfecta, Ghost teeth)
• Definition - It is a localized, nonhereditary developmental
abnormality of teeth with extensive adverse effects on the
formation of enamel, dentin, and pulp.
• Crawford discribed the first report of ROD to Hitchin in
1934, while others suggested that McCall and Wald were the
first to describe in 1947. It was not until 1963, Zegarelli et al
coined the term Odontodysplasia and Pindborg added the
prefix Regional in 1970.
• Etiology –
1.Abnormal migration of neural crest cells
2.Latent virus
3.Local circulatory deficiency
4.Local trauma
5.Hyperpyrexia
6.Malnutrition
7.Medication used during pregnancy
8.Radiation therapy
9.Somatic mutation
Clinical features-
• Dentition affected –
• Gender – f>m
• Jaws – maxillary > mandibular
• Unilateral rarely crosses the midline
• Teeth are small, brown, grooved, and hypoplastic
• Common presenting signs and symptoms include delayed or failure
of eruption, early exfoliation, abscess formation, malformed teeth,
and non inflammatory gingival enlargement.
• Caries and associated periapical inflammatory lesions are fairly
common. Because of dentinal clefts and very long pulp horns, pulpal
necrosis is common.
Treatment
The therapy is directed towards retention of the altered teeth,
whenever possible, to allow for appropriate development and
preservation of the surrounding alveolar ridge.
1. Erupted teeth
 Intermediate restoration - etched retained restoration / SS crown
 Nonvital – endodontic therapy/ extraction
 Severely affected and infected teeth need to be removed
• 2. Unerupted teeth
 Undisturbed
• 3. Premature exfoliation
 Removable prosthesis
References
1.Oral Pathology by Shafer Hine Levi.6 th edition
2.Oral Development & Histology by James K. Avery
3.Oral Histology & Embryology by Orbans.
4.Oral & maxillofacial pathology – Neville, Damm, Allen,
Bouquot.
5.Diagnostic imaging of jaws –robert langlais, langland.
6.Anil ghom textbook of oralmedicine-4 th edition .
7.Ravikiran ongole text book of oral medicine & radiology.
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