DEVELOPMENTAL
DISTURBANCES OF TEETH
Dr. Saleem Shaikh
DEVELOPMENTAL DISTURBANCES
IN STRUCTURE OF TEETH
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Enamel hypoplasia
Dentinogenesis imperfecta
Dentin dysplasia
Regional odontogenic dysplasia
ENAMEL HYPOPLASIA
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Defect of enamel due to disturbance during its
formative process
Ameloblasts are among the most sensitive cells in the
body
During the formative stages of enamel the ameloblast
cells are susceptible to various factors which can
disturb the process and the effect of which are
reflected on the surface enamel after the eruption of
tooth
Types

Based on causative factors:
Enamel hypoplasia
Hereditary
(Amelogenesis Imperfecta)
Environmental
Generalized
Focal
(Turners hypoplasia)
Differences between hereditary & environmental
enamel hypoplasia

Hereditary
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1.
Both
affected
dentition
1.
Only
enamel
affected
1.
Affected
tooth
shows diffuse or
vertical orientation
of defects
is
Environmental
1.
Either
one
dentition affected
2.
Affects enamel and
other
calcified
structures
1.
Affected
tooth
shows defect which
is
horizontally
arranged
Hereditary enamel hypoplasia
Amelogenesis imperfecta

Hereditary enamel dysplasia; Hereditary brown enamel; Hereditary
brown opalescent tooth
It is a heterogenous group of hereditary disorders of enamel formation
Entirely an ectodermal disturbance.
The condition involves only the enamel while dentin, cementum & pulp
remain normal

3 types
1.
Hypoplastic type - Defective matrix deposition
2. Hypocalcification type – Defective calcification
3. Hypomaturation type- Defective maturation
Classification
1. Hypoplastic type
Generalized Pitted, autosomal dominant
Localized Pitted, autosomal dominant
Localized Pitted, autosomal recessive
Diffuse Smooth, autosomal dominant
Diffuse Smooth, X-linked dominant
Diffuse Rough, autosomal dominant
Enamel agenesis autosomal recessive
2. Hypomaturation type
Diffuse pigmented, autosomal recessive
Diffuse, X-linked recessive
Snow capped, X-linked
Snow capped, autosomal dominant
3. Hypocalcification type
Diffuse,Autosomal dominant
Diffuse,Autosomal recessive
Hypoplastic type
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The disease affects the stage of matrix formation
Teeth exhibit complete absence of enamel or there may be presence of
enamel on some focal areas
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Enamel thickness is usually below normal
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Quantity is affected, but quality of formed enamel is normal
Tooth appears as though prepared for receiving a prosthetic crown
Radiographic features Enamel may appear totally absent or as a thin line
Radiodensity of affected enamel is similar to that of normal enamel
(greater than dentin)
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Hypocalcification type
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The disease affects the stage of early mineralization
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Enamel is of normal thickness(quantity not affected)
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Tooth is normal in shape on eruption, but the enamel is lost very easily
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Enamel is soft & can be easily removed with a blunt instrument
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Enamel is yellowish brown on eruption
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Radiodensity of affected enamel is lesser than that of normal enamel
and is equivalent to normal dentin
Hypomaturation type
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The disease affects the stage of maturation
Enamel is of normal thickness (quantity not affected)
Teeth are normal in shape but enamel is opaque white or brownish
in colour
Enamel does not have normal hardness & translucency and tend to
chip off easily
It Can be pierced with an explorer tip with firm pressure
Snow capped teeth - It is the mildest form of hypomaturation type
of amelogenesis imperfecta.
The enamel is of near normal hardness & has a zone of white
opaque enamel on the incisal or occlusal one quarter to one third of
crown.
Demonstrates an anterior to posterior distribution and have been
compared to a denture dipped in white paint
Radiodensity of affected enamel is much lesser than that of normal
enamel
Environmental enamel hypoplasia
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FOCAL ENAMEL HYPOPLASIA; Also known as Turner’s hypoplasia;
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Most common form of enamel hypoplasia
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Occurs due to trauma or infection to deciduous teeth
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Usually affects single tooth & is called as Turners tooth
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Hypoplasia ranges from a mild, brownish discolouration to a severe
pitting of enamel surface on the labial aspect
Frequently involved teeth are permanent maxillary/mandibular
bicuspids & maxillary incisors
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Severity of hypoplasia depends on severity of infection, degree of tissue
involvement and stage of tooth formation
Pathogenesis
Trauma
Periapical Infection
Deciduous teeth
Affect the ameloblastic layer
of permanent tooth
Disturb the enamel formation
Enamel defects
Generalized Enamel Hypoplasia
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The ameloblasts in the developing tooth germ are sensitive to external
stimuli
Any systemic or environmental disturbance can result in abnormalities
in enamel formation which manifests as defects on the surface of tooth
It affects numerous teeth which are being formed at the time of
disturbance
Clinically the defects can manifests as
1. Hypoplasia
2. Diffuse opacities
3. Demarcated opacities
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Most often it manifests as a horizontal line of enamel hypoplasia with
pits & grooves
CHRONOLOGIC HYPOPLASIA -
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The line on the tooth surface indicates the zone of enamel
hypoplasia
The location of the line corresponds with the developmental
stage of affected tooth & width indicates the duration of the
disturbances
Causes
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Prenatal
Infections (Rubella, Syphilis)
Malnutrition, Metabolic & Neurological disorders during
pregnancy
Chromosomal abnormalities
Excess chemical intake (Tetracycline, Fluoride)
Neonatal
Birth injury
Premature delivery
Prolonged labor
Low birth weight
Postnatal
Severe childhood infections (Viral exanthematous fever)
Congenital heart diseases
Nutritional deficiencies (Vit-B, Vit-D)
Endocrinal disorders
Enamel hypoplasia due to nutritional deficiency and
exanthematous fevers
Serious nutritional deficiency is potentially capable of producing
enamel hypoplasia
The teeth that form within the first year after birth are affected.
Teeth most frequently affected are central & lateral incisors,
cuspids and first molars.
Premolars, 2nd & 3rd molars are rarely affected, since their
formation does not begin until the age of 3 or later
Presents as pitting of the tooth surface
Enamel hypoplasia due to congenital
syphilis
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Hypoplasia is not of pitted variety
Involves the permanent maxillary & mandibular incisors and 1st molars
Anterior teeth are referred to as Hutchinson’s incisors and posterior teeth
are referred to as mulberry molars.
Characteristically, the upper central is screw driver shaped, the mesial
and distal surfaces tapering and converging towards the incisal edge.
Incisal edge is usually notched.
Middle lobe of tooth is affected
The crowns of first molars are irregular & constricted, and the enamel of
the occlusal surface and occlusal third of tooth appears to be arranged in
an agglomerate mass of globules rather that well formed cusps.
Resembles a mulberry, hence the name mulberry molars
Enamel hypoplasia due to fluoride
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Excess amounts of fluoride can result in enamel defect known as dental
fluorosis./ mottled enamel
The severity increases with an increase in amount of fluoride in the
water.
The optimum range of fluoride in drinking water is 0.7 -1.2 ppm
Increased levels of fluoride interferes with calcification process of the
enamel matrix leading to the formation of hypomineralized enamel
These alterations results in an increased surface and subsurface
porosity of the enamel which alters the light reflection and creates the
appearance of white chalky areas which later gets stained
Clinical features
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Affected teeth are caries resistant
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Wide range of manifestations depending on fluoride levels
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Grading
 Questionable changes
 White flecking or spotting of enamel
 Mild changes
 White opaque areas involving more of tooth surface areas
 Moderate and severe changes
 Pitting and brownish staining of surface
 Corroded appearance
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Mild cases- Bleaching of teeth
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Severe cases- Prosthetic crowns
Dentinogenesis Imperfecta
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A hereditary defect of dentin in the absence of any systemic disorder,
consisting of opalescent teeth composed of irregularly formed and
undermineralized dentin that obliterates the coronal and root pulpal
chambers.
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Also known as “Hereditary opalescent dentin”, “Capdepont’s teeth”
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Severely affects the deciduous teeth than permanent teeth (Incisors & 1st
molars; Least involved teeth- 2nd & 3rd molars)
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Teeth exhibits a gray to brownish violet or yellowish brown appearance
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Involved teeth exhibits a characteristic unusual translucent or opalescent
hue.
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Enamel is normal but fractures and chips away easily leads to exposed
dentin and functional attrition presumably because of defective DEJ
Teeth are not particularly sensitive & are not caries prone
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Type I
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Type II
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Associated with osteogenesis imperfecta, blue sclera
Not associated with osteogenesis imperfecta unless by
chance
This type is most frequently referred to as Hereditary
opalescent dentin
Most common type
Type III
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Brandywine type, racial isolate in Maryland state
Same clinical presentation of Type I or II with multiple
pulpal exposures in deciduous dentition
Classification (Shafer)
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DENTINOGENESIS IMPERFECTA 1: Dentinogenesis
imperfecta without osteogenesis imperfecta (opalescent
dentin), this corresponds to dentinogenesis imperfecta
type II of Shields classification.
DENTINOGENESIS IMPERFECTA 2: Brandywine
type dentinogenesis imperfecta: this corresponds to
dentinogenesis imperfecta type III of Shields classification.
There is no substitute in the present classification for the
category designated as DI Type I of the previous
classification (Shield’s ).
Radiological features
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Exhibit bulb-shaped or bell shaped crowns with constricted CEJ (tulip
shaped)
Thin & blunted roots
Early obliteration of root canals and pulp chamber
Cementum, PDL & bone appears normal
Type II exhibits great variability in deciduous teeth, ranging from
normal to those changes of type I
Shell teeth
Apparently normal enamel
Extremely thin dentin (may involve entire tooth or isolated to the
root)
Enormous pulp chambers (not as a result of resorption, but due to
insufficient dentin)
Appear as shells of enamel & dentin surrounding enormous pulp
chambers and root canals.
Histopathological features
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Enamel & mantle dentin are normal
Remaining dentin is severely dysplastic & exhibits vast areas of interglobular dentin
Dentinal tubules are short, disoriented, irregular & widely spaced
Scanty odontoblasts line the pulp and they can be seen in the
defective dentin
Smooth DEJ
Treatment is aimed at preventing excessive tooth attrition &
improving esthetics
Metal / Ceramic crowns & over dentures can be given
Dentin dysplasia
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A hereditary defect characterized by defective dentin formation &
abnormal pulpal morphology
Autosomal dominant disorder
Type I – Radicular dentin dysplasia
 Also known as “Rootless teeth”
Type II – Coronal dentin dysplasia
Severe
Mild
Clinical features
Type I
Disturbance in
radicular dentin
development
Type II
of Disturbance in development of coronal
dentin
Normal crowns both structurally & Semi-transparent
opalescent
primary
morphologically
teeth
Normal appearance in the permanent teeth
Color of teeth normal with slight bluish Amber – grey color
translucency in cervical region
Early loss of dentin organization
results in extremely short roots
Later disorganization results in
minimal root changes
Affected teeth exhibits short roots,
delayed eruption , severe mobility &
premature exfoliation
Radiological features
Type I
Type II
Permanent teeth: Features vary on the
proportion of organized versus
disorganized dentin
Early disorganization - extremely short
roots with little or no pulp
Somewhat Later disorganization crescent or chevron shaped pulp
chambers overlying shortened roots
that exhibit no pulp canals
Late disorganization – normal pulp
chamber with large pup stone
Permanent teeth: Exhibits abnormally
large pulp chambers and apical
extension described as flame shaped
or thistle-tube in shape. Pulp stones
present
Deciduous teeth affected severely with
little or no detectable pulp
Deciduous teeth shows bulbous
crowns, cervical constriction and early
obliteration of pulp (Resembles DI)
Periapical radiolucencies around the
defective roots
Absence of periapical radiolucencies
Histopathological features
Type I
Normal enamel
Type II
Normal enamel and radicular dentin with
partial obliteration of root canals
Portion of coronal dentin is usually Near normal coronal dentin with
normal and may show tubular dentin numerous areas of interglobular dentin
apical to it
near the pulp
Pulp is obliterated by calcified tubular
dentin, osteodentin & fused denticles
Normal dentinal tubule formation Abnormally large pulp chambers with
appears to be blocked so that new pulp stones
dentin forms around obstacles and takes
on characteristic appearance described
as lava / stream flowing around boulders
Regional Odontodysplasia
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It is a uncommon non-hereditary developmental disturbances of tooth
characterized by defective formation of enamel & dentin with abnormal
calcifications of pulp & follicle
Also known as “Ghost teeth”
Cause
- Local ischemic change during odontogenesis
Clinical features:
 More common in permanent dentition
 More common in maxilla
 Affects several teeth in a single quadrant
 Maxillary anterior teeth affected more
 Failure of eruption or delayed eruption of affected teeth
 Teeth are deformed, yellowish – brown in color with a soft leathery surface
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Radiological features
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Marked decrease in radio density of teeth
Enamel & dentin are very thin & radiological distinction not
possible
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Extremely large & open pulp chamber with pulp stones
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Ghostly appearance of affected teeth
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Abnormal enamel & dentin
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Large pulp chamber with pulp stones
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Calcification in follicular connective