DEVELOPMENTAL DISTURBANCES

OF ORAL AND PARAORAL

STRUCTURES

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 Malformations or defects resulting from
disturbance of growth and development are
known as developmental anomalies.

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Developmental disturbances of teeth

• Size of teeth

• Shape of teeth

• Number of teeth

• Structure of teeth

• Growth (Eruption) of teeth

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DD in size of teeth

• Microdontia

• Macrodontia

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1. Microdontia

• teeth are smaller than normal

• Three types:

– True generalized

– Relative generalized

– Involving a single tooth

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True generalized type:

• All the teeth are smaller than normal.

• Teeth are well formed but small in size.

• Seen in Pituitary dwarfism, Down’s syndrome.

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Relative generalized type:

• Teeth are Normal or slightly smaller than normal, but the jaws

are somewhat larger than normal

• Inheritance of jaw size from one parent and tooth size from

other parent can lead to this variations.

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Involving a single tooth:

• Also called localized microdontia.

• Affects mostly the maxillary lateral incisor (PEGLATERALS) and

third molars.

• Supernumerary teeth are frequently small in size.

• Can be seen in Facial Hemiatrophy.

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2. Macrodontia (Megalodontia or megadontia)

• teeth are larger than normal.

Three types:

– True generalized

– Relative generalized

– Macrodontia of single teeth

Rhizomegaly / Radiculomegaly

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True generalized type:

• Extremely rare.

• All the teeth are larger than normal.

• Associated with pituitary gigantism.

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Relative generalized type:

• Some what more common.

• Normal or slightly larger sized teeth in smaller jaws.

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Involving a single tooth:

• Relatively uncommon.

• Tooth may appear normal in every aspect except for its size.

• Should not confused with fusion of teeth.

• Can be seen in facial hemi-hypertrophy

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DD in shape of teeth
• Gemination
• Fusion
• Enamel pearl
• Concrescence
• Dilaceration
• Talon cusp
• Dens in dente
• Dens evaginatus
• Taurodontism
• Supernumerary roots
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1. Gemination
• arise from incomplete division of single tooth germ by

invagination, result incomplete formation of two teeth.

• Appearence - Two completely or incompletely separated crowns

& with single Root.

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• Seen in both deciduous and permanent teeth,

• higher frequency in the anterior and maxillary region.

• Twinning – division of one tooth bud resulting in one normal

and one supernumerary tooth.

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Gemination

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2. Fusion
• union of two separate tooth germs

• may have separated or single root canal based on time of fusion

• both dentitions are effected
• mostly seen in decidous dentition
• may also occur between normal and supernumerary tooth

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Fusion
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3. Dilaceration
Abnormal angulation/ bend in the root or less frequently the crown
of a tooth

Etiology
– Trauma to tooth
– Cyst, tumor, odontogenic hamartoma
– Idiopathic

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C/F

– Perm teeth > deciduous teeth

– >Max Incisor
– Results - Altered path of eruption
– Posterior teeth – mostly at apical ½
Treatment
Deciduous teeth – extraction
Permanent teeth
Minor – no treatment
Extensive - extraction , orthodontic movement CI

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4. Taurodontism Tauro - Bull, dont – tooth
• Means bull-like tooth

• It is an enlargement of the body and pulp chamber of a

multi-rooted tooth with apical displacement of the pulpal floor
and bifurcation of the roots.

Pathogenesis

Failure of HERS to invaginate at

the proper horizontal level

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Causes :
1. Mendelian recessive trait
2. Atavistic feature
3. Component of various syndromes
Classified as,
• Hypotaurodont –mildest form
• Mesotaurodont –moderate
• Hypertaurodont –severe form with furcation near the apices of
the roots.

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C/F

• Both the dentitions are affected

• Molars - usually 2nd & 3rd molars are affected

• It may be Unilateral or bilateral & any quadrant may be affected

Radiographically,
• ↑Apico- cervical height
• with Short roots

Clinical significance
Endodontic therapy – difficult
↓Stability & strength of tooth
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5. Supernumerary roots
• It is↑ number of roots

• Both dentitions are involved

• Permanent molars are affected commonly (3rd molar)

R/G

• These roots may be Small & superimposed

Treatment – there is no particular Rx

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6. ECTOPIC ENAMEL
• Refers to the presence of enamel in unusual locations.

• known as enamel pearls/ Enameloma

• They project from the surface of root.
• These are hemispheric structures that consist of,
– Entirely of enamel or
– Enamel, dentin and pulp tissue.

Pathogenesis - Bulging of odontoblastic layer - Prolonged contact

b/w HERS & dentin

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C/F

Prevalence -1.1 – 5.7%

Eskimos – 9.7%

• mostly seen in the bifurcation of the mand molars

R/G – radio-opacity growth on root
Clinical significance
Furcation involvement
Treatment

oral hygiene maintainence

Flattening & removal with furcation plasty
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7. Dens evaginatus

• Also called leong’s premolar, evaginated odontome, occlusal

tubercle
Definition: tubercle or protuberance on posterior teeth
Pathogenesis :
Proliferation & evagination of IEE (Tartman)
Etiology
Hereditary – Autosomal dominant
Prevalence: 1- 4.3%
> mongoloid

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Clinical Features
Bilateral
Assoc with - Shovel shaped incisor

Clinical significance
Fracture / Wear → Pulpal pathosis
Eruption interference
Malocclusion
Dilaceration
Caries
Radiographically:

• Tuberculated occlusal surface with pulpal extension

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Treatment

Vital teeth -Selective grinding

Nonvital teeth - Apexification followed endodontic treatment

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8. Dens invaginatus (Dens in dente)
• It is Deep surface invagination of crown or root

• Two forms– coronal & radicular

Pathogenesis:
• It occurs as a result of an invagination in the surface of the tooth
crown before calcification occur
Etiology: it is due to
• ↑ localized external pressure, focal growth retardation and focal
growth stimulation

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C/F

• Its prevalence – 0.04 to 10%

• Permanent max LI, CI, PM, Canines & molars are affected

• Depth varies from slight enlargement of cingulum pit to deep

infolding upto apex

• Coronal dens invaginatus is of - 3 types

Type I – confined to crown

Type II – extends below CEJ
Type III – extends till root apex
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Radicular dense invaginatus

• relatively rare
• It arises 2ry to proliferation of Hertwig’s root sheath

R/G- Dilated invagination lined by enamel with opening at the lateral

aspect of the invagination is seen
Diagnosis
Thorough examination of teeth
Clinical significance – accumulation of debris
Predisposition to caries
Pulpal pathology
T/t

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9. Concrescence
• is union of two adjacent teeth by cementum alone

• it may occur before or after eruption of tooth.

• Seen most commonly in posterior maxilla regions

• Makes tooth extraction difficult

Etiology - trauma or overcrowding

Treatment: no specific treatment

• Surgical removal is indicated when extraction is advised

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10. Talon cusp
• So called as it resembles Eagle’s talon

• additional cusp that projects from the lingual surface of primary

or permanent anterior teeth

Pathogenesis : Proliferation & evagination of IEE

• More common in lingual surface of perm dentition (Max LI & CI)

Makes

• Eruption interference →Malocclusion

• Tongue irritation, Caries

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Prevalence: 0.17- 7.7%
> Chinese, Caucasians
M : F – 3.2 : 1.8
Clinical Features
LI (55%)>CI(33%)> Mand incisors(6%)> Max canine(4%)
Deciduous – rare (Max CI)
Appearance - Conical, Bifid and talon-like.
Syndromes associated with talons cusp are
• Rubinstein – Taybi syndrome
• Sturge –Weber syndrome

• Ellis van crevald syndrome

T/t
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D-D of growth (eruption) of teeth
• Premature Eruption
• Delayed Eruption

• Ankylosed Deciduous Teeth

• Impacted Teeth

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Premature eruption
• Natal teeth – these are deciduous teeth that erupt into the oral
cavity at birth in infants

• Neonatal teeth - teeth erupting prematurely in the first 30 days

of life (mandibular central incisors mostly).

• Premature shedding of deciduous teeth lead to premature

eruption of permanent teeth.

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DELAYED ERUPTION

• Systemic conditions - rickets, cretinism, cleidocranial dysplasia.

• Local factors - fibromatosis gingivae

• Delayed eruption in permanent dentition: Retained deciduous
teeth, impaction, ankylosis, cysts & tumors & endocrinal
disturbances.
Treatment

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Ankolysed deciduous teeth (Submerged teeth)

Synonyms : Ankylosed teeth, Infraocclusion, Secondary retention,

Reimpaction, Reinclusion
Etiology
Ankylosis
Pathogenesis
Prevalence
1. Disturbances in local metabolism 1.3 – 8.9 %
2. Trauma 7-18 yrs (8-9 yrs)
3. Local infection Mand > Max
4. Chemical / Thermal irritation 1st molar > 2nd molar

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• It has a solid sound on percussion when compared to the dull,
Clinical significance
– Occlusal & periodontal problem
– Supraeruption of opposite tooth
– Impaction of underlying permanent teeth
R/G
• Absence of PDL between the root and alveolar bone.
Complications - Development of malocclusion
T/T – Surgical removal

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Impacted teeth

• These teeth are not erupted due to barrier in the path of

eruption of tooth
Causes
• Due to lack of space in the dental arch
• Trauma during tooth formation
• Cysts & tumors, endocrinal disturbances
Most commonly impacted tooth are
• Perm teeth - Mand 3rd molar, maxll 3rd molar & maxll canine.
• 1ry teeth – mand 2nd molars.
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• Classification

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Clinical Significance

Partially Impacted tooth – Infection & Dental caries

Root resorption

Dentigerous cyst/ Ameloblastoma

Treatment
Molar – Extraction

Cuspid - Extraction of Deciduous canine

Surgical exposure & orthodontic traction

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DD affecting Number of teeth

• Anodontia

• Hypodontia

• Hyperdontia

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Anodontia

• Lack of development of tooth results in absence of teeth.

• Common tooth showing anodontia are – laterals, 3rd molars

Classification
True Anodontia - lack of development of tooth
• Total – seen in ECTODERMAL DYSPLASIA
• Partial – maxillary laterals, 3rd molars
Pseudo-Anodontia – due to multiple unerupted tooth

False Anodontia – due to extraction of tooth

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C/F – results in
• Masticatory dysfunction
• Speech impairment
• Aesthetic problems
• Malocclusion
T/T
• Dentures
• Crowns
• Implants

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Hypodontia

• Partial anodontia or oligodontia

• Patient has missing up to 6 teeth – hypodontia

• missing over 6 teeth – oligodontia

• Commonly involved are
wisdom teeth (25-35%), upper laterals (2%), lower 2nd premolars
(3%) & upper 2nd premolar.

• Female predilection
• Primary teeth – maxillary laterals
• Etiology – genetic, harmonal, environmental & infections
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Hyperdontia (supernumerary tooth)

• Presence of extra teeth in addition to normal series of teeth.

Etiology

Hereditary – Autosomal dominant/ sex linked

Atavism
Hyperactivity of dental lamina
Environmental factors
Pathogenesis

It is suggested, they may develop from extra tooth bud formation

near regular tooth bud or from splitting of single tooth bud.
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In permanent teeth

• Mesiodens

• Paramolars

• Distomolars

In Primary tooth – max laterals & canines

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Classification of supernumerary teeth

• Conical teeth – ex: mesiodens

• Tuberculate – ex: talons cusp in incisors

• Supplemental – duplication of teeth in normal series (max lateral)

• Odontome – is a odontogenic tumor

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Disorders assoc with supernumerary tooth

• Gardner’s syndrome
• Cleidocranial dysostosis

• Cleft lip & palate

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Gardener’s syndrome
• Multiple polyposis of large intestine
• Osteomas of bone
• Multiple sebaceous cysts
• Desmoid tumor
• Impacted supernumerary or permanent teeth

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D-D in STRUCTURE of teeth
•Amelogenesis imperfecta
•Environmental enamel hypoplasia
•Dentinogenesis imperfecta
•Dentin dysplasia
•Regional odontodysplasia

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AMELOGENESIS IMPERFECTA

• Also called hereditary brown opalescent teeth, hereditary

enamel dysplasia.
• represents a heterogenous group of genetic disorders, exhibiting
faulty enamel formation
• Can affects both dentitions
• only confined to the enamel and other components of the teeth
are normal

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Etiology

Inherited disorders:

• Mutations & Chromosomal alterations

• Alteration of gene coding for enamel protein (Amelogenin) which

is located at DXS 85 gene locus of chromosome Xp22

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3 basic types of AI can be appreciated,

• Hypoplastic – defective organic matrixformation

• Hypocalcified – defective mineralization of matrix

• Hypomaturation – enamel is fail to mature.

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C/F
Type I (Hypoplastic)
In pitted pattern (generalized / localized) ,
show Pinpoint pits that undergo staining.
buccal surface of teeth are more affected
In smooth pattern,
enamel – thin, glossy with opaque white/translucent brown
color
In rough pattern,
enamel – dense, rough with yellow to white in color.
In agenesis type - total lack of enamel surface
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Type II (Hypocalcified)
• enamel is more softer with normal shape

• enamel can be removed by prophylaxis instrument.

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Type III (Hypomaturation)
• Enamel can be pierced by an explorer with firm pressure

• Enamel can be lost by chipping off from the underlying normal

dentin.

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Other fatures
• Crowns may show discoloration (varying from yellow to dark
brown)

• Enamel may be totally lost or have chalky texture or cheesy

consistency.

• Enamel may be smooth or show vertical wrinkles or grooves.

• Enamel may be chipped or show depressions with exposed
dentin at its base.
• Contact points are open
• Occlusal and incisal edges are severely abraded.

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 Hypoplastic

yellow teeth

Hypocalcified

Diffuse yellow brown discoloration,

Hypomaturation

Mottled opaque white enamel

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R/G

• enamel may be completely absent

• If present, it appears as thin layer over the cusp tips &
interproximal areas.
• If calcification is defective, Radiodensity of enamel becomes same
as that of dentin

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Histologic features

• Hypoplasia – seen as defective matrix formation

• Hypocalcification - shows defects in matrix structure and mineral

deposition.

• Hypomaturation - shows alterations in enamel rods and rod

sheath structures.

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Treatment

• Crowns and veneers – ↑ cosmetic appearence

• Complete denture – in enamel agenesis

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ENAMEL HYPOPLASIA
• Enamel hypoplasia is incomplete/ defective formation of organic
enamel matrix of teeth.
• Two types - 1. hereditary
hereditary
Both dentitions affected
Only enamel is affected
2. environmental.
environmental
Either of the dentition is
affected including single tooth
hypoplasia
Enamel & certain extent
dentin is affected
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 This hypoplasia occurs, only if the injury occurs to the ameloblast

during the formative stage of enamel or before the calcification of

enamel.

• In mild cases, it manifests as few small grooves, pits or fissures

• In severe cases, rows of deep pits arranged horizontally across the

surface are seen.

• There may be a single row or series of rows of such pits indicating

a series of injuries

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Factors causing injury to the ameloblasts

• Nutritional deficiencies – vit A,C, D

• Exanthematous diseases – measles, chicken pox, scarlet fever

• Congenital syphilis
• Hypocalcemia
• Birth injuries, prematurity, Rh hemolytic disease
• Local infection and trauma
• Ingestion of chemicals – Flourides

• Idiopathic causes

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Nutritional deficiencies:

• such as rickets, vit A & D def can cause enamel hypoplasia

• Because, ameloblasts are most sensitive to metabolic function.

• It results in pitting type of enamel defect

• CI, LI, cuspids and 1st molar (especially those formed within the

first year after birth) are involved.

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Hypocalcemic conditions such as

• Tetany – due to vit D def and PTH def may cause EH

• Wherein Cal level falls to – < 6 to 8 mg/100ml

• Enamel hypoplasia in this case is of Pitting variety

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Congenital syphilis:
• Max & mand perm CI & 1st molars are affected
• It is of pitting variety
• Upper Incisor is screw driver shaped with notched incisal edge –
called Hutchinson’s teeth
• In1st molars – enamel of the occlusal surface & occlusal 3rd
appears like a mass of globules – called Mulberry molars.

Hutchinson’s teeth- Mulberry molars (moon molars or fournier’s molars)

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Due to local infection or trauma
• Only Single tooth is involved– like per max CI,PM or mand PM

• EH ranges from mild brownish discoloration to severe pitting.

• Such teeth are called Turner’s teeth/ Turners hypoplasia

• deciduous teeth (trauma/ Caries) →disturb the ameloblastic layer

of permanent tooth germ → EH

• It is manifested as a Yellowish or brownish stain or pigmentation

of the enamel on the labial surface.

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Due to fluoride - Mottled enamel

• Ingestion of high F containing drinking water (>1ppm) during

tooth formation can lead to EH
• Mild cases– white opaque areas involving more of the tooth
surface is seen
• Moderate cases – pitting & brownish staining of enamel is seen
• Severe cases- corroded appearance of the teeth is seen

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 DENTINOGENESIS IMPERFECTA

• HEREDITARY OPALESCENT DENTIN

• Is hereditary disturbance of dentin

• it is Autosomal dominant- affecting both deciduous & permanent

teeth
• DI is associated with mutation of DSPP (Dentin
sialophosphoprotein) gene that is present on chromosome 4.

• Dentin defects associated with this bone disease is termed as

osteogenesis imperfecta with opalescent teeth

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 Shield’s classification of DI

TYPES OF DI CLINICAL PRESENTATION

Type - I DI without osteogenesis imperfecta

TYPE– II DI with osteogenesis imperfecta

TYPE - III Seen as racial isolate in Maryland

(Called BRANDYWINE TYPE)

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Revised classification proposed is

1) Dentinogenesis imperfecta 1 --- DI without osteogenesis

imperfecta (Corresponds to DI type II of Shields type)

2) Dentinogenesis imperfecta II--- brandywine type DI---

corresponds to DI type III of shield’s classification

• There is no substitute in the present classification for category

designated as DI type I of the previous shield’s classification

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DENTINOGENESIS IMPERFECTA 1

• Affected teeth are blue, gray or amber brown & opalescent

• Enamel frequently separates from the underlying defective dentin

• Dentin demonstrates significantly accelerated attrition

R/G
• teeth having bulbous crown
• Pulp chambers are smaller than the normal or completely
obliterated

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DENTINOGENESIS IMPERFECTA 2

• Crowns wear rapidly leading to multiple pulp exposures

• Dentin is amber colored and smooth

• Teeth are called as SHELL TEETH - demonstrate normal enamel

thickness, thin dentin and enlarged pulps
R/G
• Deciduous teeth - large Pulp chambers & Root canals

• Permanent teeth - pulp space is smaller or obliterated

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H/p
• Enamel - normal
• Dentin –
shows irregular tubules with large areas of uncalcified matrix
Tubules are large in diameter & less numerous
Complete absence of tubules may also be seen
• Pulp chamber - Obliterated

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T/t

• crowns are indicated to prevent loss of enamel and subsequent

loss of dentin

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 DENTIN DYSPLASIA

• is an autosomal dominant hereditary disturbance in dentin

formation chzd by normal enamel but atypical dentin formation
with abnormal pulp morphology
Classification
• Type I – Radicular type
• Type II – Coronal type

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Etiology

• Both type I & type II --- are hereditary in nature

• autosomal dominant type of inheritence

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Radicular DD (rootless teeth)
• Dentin & pulp - disorganized
• Teeth roots – shorter & because of this teeth are mobile
• Enamel & coronal dentine – normal
R/g
• Shorter & blunt roots, obliterated pulp chambers with pulp stones
H/p – crown dentine - normal
Root dentine
• Dentinal tubules – appears to be blocked,
• Lawa flowing around boulders –new dentine is formed around
obstacles in repetitive attempts.

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Coronal DD
• Teeth crown: 1ry – yellowish brown & permanent – normal
R/g
• Pulp chamber:
1ry – obliterated
permanent –more coronal (thistle tube appearance)
H/p
• Dentine,
1ry – amorphous & atubular in root
permanent – normal
• Pulp stones

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T/ t
• No specific treatment

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 REGIONAL ODONTODYSPLASIA
• Ghost teeth
• is a rare developmental anomaly involving both mesodermal and
ectodermal dental components of teeth
Etiology
1. Abnormal migration of neural crest cells
2. Latent virus
3. Local circulatory deficiency
4. Local trauma or infection
5. Malnutrition
6. Medication used during pregnancy
7. Radiation therapy
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C/f
• F>M
• maxilla >mandible (2:1)
• Affects both dentitions
• Limited to only one arch and sometimes crosses the midline.
• Incisors > posterior teeth
• Enamel, dentin and pulp all are involved
• Affected teeth fail to erupt
• Affected teeth – show abnormal morphology with pitting and
grooves on the surface.
• The teeth appear to be discolored, hypoplastic and hypocalcified.
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R/g
• There is lack of contrast between the dentin and the enamel
• Altered teeth demonstrate extremely thin enamel and dentin
surrounding an enlarged radiolucent pulp resulting in a pale wispy
images of a tooth.
• Hence the term “Ghost teeth”.

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H/p
• Dentine - ↑ predentine, interglobular dentine, irregular tubular

arrangement

• Pulp shows free and attached denticles

• Reduced enamel epithelium around the nonerupted teeth shows

many irregular calcified bodies

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