PRESENTED BY

Dr . APARNA. M
P.G STUDENT
DEPARTMENT OF PUBLIC HEALTH
DENTISTRY

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 Introduction

 Oral Ectoderm

 Buccopharyngeal Membrane

2
 Initiation of Tooth Development

 Primary Epithelial Band

2 sub divisions:

 Dental lamina

 Vestibular lamina

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 Dental lamina

 Primordium for ectodermal portion of the

tooth

 Permanent molars

 Distal proliferation of the dental lamina

 Successional lamina

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 Fate of dental lamina
 5 yrs

 Loose connection with the dental lamina

 Mesenchymal invasion

 Cell rests of Serre

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 Vestibular lamina

 Forms labial and buccal to dental lamina

later

 Lip furrow band

 Oral vestibule

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 Tooth development

 Knobs growing into mesenchyme

 Beginning of enamel organ

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 Components of tooth germ

A. Enamel organ

B. Dental papilla

C. Dental follicle or sac

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Tooth development is a continuous process
divided into 3 stages:

 Bud Stage
 Cap Stage
 Bell Stage
 Early
 Advanced (late)

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 Bud stage

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 Cap stage

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  Bell stage
 Early

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 Advanced

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Root formation

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 Histophysiology

Initiation

Proliferation

Histodifferenciation

Morphodifferenciation

Apposition

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Developmental disturbances of teeth

 Size of teeth

 Shape of teeth

 Number of teeth

 Structure of teeth

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Developmental disturbances in size of
teeth
 Microdontia

 Macrodontia

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 Microdontia

 True generalized
 Relative generalized
 Involving a single tooth

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True generalized type:

 Pituitary dwarfism

 Down’s syndrome

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Relative generalized type:

 Inheritance of jaw size from one parent and

tooth size from other parent

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Involving a single tooth:

 Maxillary lateral incisor- Peg lateral

 Third molars

 Supernumerary

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 Macrodontia

 Megalodontia or megadontia.

 True generalized macrodontia

 Relative generalized macrodontia

 Macrodontia of single teeth

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True generalized type:

 Rare

 Associated with pituitary gigantism

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Relative generalized type:

 Common

 Hereditary factors

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Involving a single tooth:

 Uncommon

 Unknown etiology

 Facial hemi‐hypertrophy

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 Developmental disturbances in shape of
teeth
 Gemination
 Fusion
 Concrescence
 Dilaceration
 Talon cusp
 Dens in dente
 Dens evaginatus
 Taurodontism
 Supernumerary roots
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 Gemination

 Twinning

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Fusion

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 Separate or fused root canals

 Clinical problems - esthetics, spacing and

periodontal conditions

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Concrescence

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 After root formation

 Traumatic injury/Crowding with resorption of

adjacent interdental bone

cementum deposition contact of two

roots

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Dilaceration

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 Trauma during tooth formation

position of calcified portion of the tooth is

changed

remaining tooth develops at an angle

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 The curve or bend can occur anywhere along
the length of the tooth
 Cervical

 Midway

 Apex

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 Talon cusp

Blends smoothly with the lingual tooth surface

except for a deep developmental groove
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 Resembling an eagle’s talon

 Composed of normal enamel, dentin and a

horn of pulp tissue

 Rubinstein –Taybi syndrome

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 Dens in dente

Dens invaginatus
Dilated composite odontome.

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Due to,

 Increased localized external pressure

 Focal growth retardation

 Permanent maxillary lateral incisors

 Maxillary central incisor

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 Radiographs- pear shaped invagination of

enamel and dentine

 Food debris accumulates - caries and pulpal

infection

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 Dens evaginatus

•Leong’s premolar
•Evaginated odontome
•Occlusal enamel pearl
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 By proliferation & evagination of an area of

the inner enamel epithelium into the dental

organ during early tooth development

 Extra cusp

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 Taurodontism

Body of the tooth is enlarged at the expense

of the roots.

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 Bull‐like tooth

 Could be due to failure of Hertwig’s

epithelial sheath to invaginate at the
proper horizontal level

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 Occur concomitantly with amelogenesis

imperfecta

 Reported in Klinefelter’s syndrome.

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Supernumerary roots

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 Mandibular cuspids and bicuspids

 Maxillary and mandibular molars may exhibit

additional roots

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 Ectopic enamel

 Known as enamel pearls

 Project from the surface of the root

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 Consists

Entirely of enamel

Enamel, dentin and pulp tissue.

 Arise from localized bulging in the

odontoblastic layer with prolonged contact
between HERS and dentin leading to enamel
formation.

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 Anodontia

True anodontia congenital absence of teeth

 True total anodontia

 Deciduous and permanent dentition

 Hereditary ectodermal dysplasia

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 True partial anodontia

 Hypodontia

 Oligodontia

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 Missing third molars- common

 Maxillary lateral incisor and maxillary and

mandibular second premolars – bilaterally

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Syndromes associated

•Down syndrome

•Ectodermal dysplasia

•Turners syndrome

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Supernumerary teeth

 By splitting of the permanent bud itself

 Hyperactivity theory- local, independent,

conditioned hyperactivity of dental lamina

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 Hereditary tendency

 Males affected more

 Associated with
 Cleft lip and palate

 Cleido‐cranial dysplasia

 Gardner’s syndrome

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Mesiodens

 Most common

 It is situated between the maxillary central

incisors.

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Fourth molar

 Second most common

 Distal to the third molar

 Small rudimentary tooth but may be of normal

size

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Pre‐deciduous dentition

 Natal teeth

Infants born with structures appearing to be

erupted teeth in the mandibular incisor region.

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 Hornified, epithelial structures without roots

An accessory bud of the dental lamina ahead

of the deciduous tooth bud

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Post‐permanent dentition
 All permanent teeth extracted and yet
subsequently erupted several more teeth

 Due to delayed eruption of retained or

embedded teeth

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 Developmental disturbances in
structure of teeth

 Amelogenesis imperfecta

 Enamel hypoplasia

 Dentinogenesis imperfecta

 Dentin dysplasia

 Regional odontodysplasia

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Amelogenesis imperfecta

 Hereditary enamel dysplasia

 Hereditary brown enamel

 Hereditary brown opalescent teeth

 Yellow, brown or grey colour

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 Hypoplastic amelogenesis imperfecta

 Theenamel is not formed to full normal

thickness

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 Hypocalcified amelogenesis imperfecta

 Defects in matrix structure and mineral

deposition
 Coronal enamel is lost by function

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 Hypomature amelogenesis imperfecta

 Enamel lost by chipping

 Snow capped pattern

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 Enamel hypoplasia

 Incomplete of defective formation of the

organic enamel matrix.

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 Hypoplasia due to congenital syphilis

 Anteriors – Hutchinson’s teeth

 Posteriors – Mulberry molars (Moon’s molars,

Fournier’s molars)

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 Hypoplasia due to hypocalcemia

 Tetany

 Calcium level falls to 6‐8mg/dl and affects

the devloping tooth.

 Pitting variety

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Hypoplasia due to birth injuries

 Neonatal line or ring in deciduous teeth and

first permanent molars.

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Hypoplasia due to local trauma or infection

 Permanent maxillary incisors or

maxillary/mandibular premolar
 Turner’s teeth
 Mild, brownish discoloration to severe
pitting.
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Hypoplasia due to Intrinsic stains

Tetracycline stain

Congenital
erythropoietic porphyria

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 Alkaptonuria

Hyperbilirubinemia

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Hypoplasia due to fluoride –Mottled enamel

 Disturbance in the formative stage of enamel

 High levels of fluoride interferes with

calcification of the matrix

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 Questionable changes

 Mild changes

 Moderate changes

 Severe changes

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Dentinogenesis imperfecta

 Hereditary opalescent dentin

 Discolored- blue-gray or yellow-brown color

 Translucent

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 Type I: Occures with osteogenesis
imperfecta

 Type II: Hereditary opalescent dentin

 Type III: Brandywine type

A shell-like appearance and

Multiple pulp exposures

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 Dentin dysplasia

 Rootless teeth
 Normal enamel
 Atypical dentin formation with abnormal
pulp morphology

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Regional odontodysplasia (Ghost teeth)

 Delayed or total failure of eruption

 Irregular in shape with defective mineralization

 Ghost appearance

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Conclusion
Since development of tooth forms the base
of dentistry, a thorough understanding and a
sound knowledge is required by a dentist
regarding the development stages of tooth &
the anomalies related to it, so as to identify
& treat them in a proper fashion.

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References

 Orban’s Oral Histology & Embryology, 13th

Edition.
 Shafer’s Textbook of Oral Pathology, 7th Edition.
 Manual of Oral Histology & Oral Pathology, Maji
Jose.
 Oral and maxillofacial pathology,by Neville 2nd
edition.
 Human embryology by I B singh 8th edition.

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