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The document discusses the complex process of tooth development, including the formation of neural crest cells, stages of tooth development, and the roles of various tissues such as the enamel organ, dental papilla, and dental sac. It emphasizes the importance of genetic factors and clinical implications related to defects in tooth formation. The document concludes with a focus on clinical considerations and the significance of understanding tooth development for pediatric dentistry.

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0% found this document useful (0 votes)
7 views67 pages

Final Presentation

The document discusses the complex process of tooth development, including the formation of neural crest cells, stages of tooth development, and the roles of various tissues such as the enamel organ, dental papilla, and dental sac. It emphasizes the importance of genetic factors and clinical implications related to defects in tooth formation. The document concludes with a focus on clinical considerations and the significance of understanding tooth development for pediatric dentistry.

Uploaded by

Mohd Irfaan
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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You are on page 1/ 67

Development of tooth and it’s

clinical implications

BY-
DR. MOHAMMED IRFAAN
MDS- 1st Year
Dept of Pediatrics & Preventive Dentistry.
CONTENTS
❑ Introduction
❑ Formation of neural crest cells
❑ Origin of tooth
❑ Tooth development
❑ Stages of tooth development
❑ Root formation
❑ Dentinogenesis
❑ Amelogenesis
❑ Genes expressed during tooth development
❑ Clinical considerations
❑ Conclusion
❑ References
INTRODUCTION
❖ Development of tooth is a complex process initiated, mediated and controlled by the
interaction between ectoderm and supporting ectomesenchyme.

❖ For human teeth to have healthy oral environment, enamel, dentin, cementum & the
periodontium all must develop during appropriate stages of foetal development.

❖ Entire primary dentition is initiated between 6th and 7th weeks of embryonic
development.
Formation of neural crest cells
Tooth

Pulp

Enamel
Dentine Cementum

Ectomesenchyme
Ectoderm
Ectomesenchyme
ORIGIN OF TOOTH
The primitive oral cavity aka stomodeum, is lined by
stratified squamous epithelium called the oral
ectoderm or primitive oral epithelium.

The oral ectoderm + endoderm of the foregut


forms

buccopharyngeal membrane.

At 27th day IUL

membrane ruptures and the primitive oral cavity


establishes a connection with the foregut.
Fate of Dental Lamina

• Dental lamina 6 weeks IUL - 5 years of age.

• After tooth development is initiated at a


particular site, it degenerates at that location.

• The remnants may persist within the jaw or in


the gingiva as clusters of epithelial cells known as
epithelial pearls or epithelial cell rests of Serres.

• Significance of Cell Rests of Serres - Due to


unknown stimuli,the cell rests of Serres may start
proliferating and odontogenic cysts may develop
from them.
Tooth development
At certain points along the dental lamina, which represent the sites of the
future 20 deciduous teeth, the induction process is seen.

The ectomesenchyme induces the cells of the overlying ectoderm to start


dividing.

Thus small bud like or knob like structures are formed, which grow into the
underlying ectomesenchyme. (First ones to appear are of anterior
mandibular region)

This epithelial bud will give rise to the ectodermal part of the tooth, known as
Enamel Organ. Each bud or enamel organ represents the beginning of a
deciduous tooth.

As the enamel organ increases in size, it changes in shape due to differential


growth.
Takes shape that resembles a cap, with an outer
convex surface facing the oral cavity and an
inner concavity.

On the inside of the cap (i.e., inside the


depression of the enamel organ), the
ectomesenchymal cells increase in number.

Tissue appears more dense than the surrounding


mesenchyme and represents the beginning of
the dental papilla.

Surrounding the combined enamel organ and


dental papilla, the third part of the tooth bud
forms. It is the dental sac or dental follicle,
and it consists of ectomesenchymal cells and
fibers that surround the dental papilla and the
enamel organ.
❖Enamel organ + dental papilla+ dental
sac= Tooth germ

❖Enamel Organ Enamel

❖Dental Papilla Dentin and Pulp

❖Dental follicle cementum, PDL


Stages of tooth development

• MORPHOLOGICAL STAGES PHYSIOLOGICAL PROCESS

Dental lamina Initiation

Bud stage
Cap Stage Proliferation

Early Bell stage Histodifferentiation

Advanced Bell Stage Morphodifferentiation

Formation of enamel and dental matrix Apposition


Stages of tooth development
Bud Stage
The epithelium of the dental lamina is separated from the underlying ectomesenchyme
by a basement membrane.

The buds or primordia for the deciduous teeth are formed at 10 different points,
corresponding to the positions of the future deciduous teeth.

Primordia of Enamel organ develops, cells proliferate faster than adjacent cells.

Enamel organ consists of peripherally located low columnar cells and centrally located
polygonal cells

As a result of the increased mitotic activity and the migration of neural crest cells into
the area the ectomesenchymal cells surrounding the tooth bud condense.

The area of condensation immediately below the enamel organ is the dental papilla.
The ecto-mesenchymal condensation that surrounds the tooth bud & the dental papilla
is the tooth sac.
Cap Stage.
1. OUTER & INNER ENAMEL
EPITHELIUM:

❖Peripheral cells : cuboidal,


cover the convexity of the
cap-outer enamel epithelium

❖cells in the concavity of the


cap: columnar cells-inner
enamel epithelium
2. STELLATE RETICULUM:

❖ The ground substance in the centre of


the enamel organ is rich in GAG.

❖ Water is drawn into the enamel organ


from dental papilla.

❖ Polygonal cells get pushed apart from


each other.

❖ Increase in the intercellular spaces.

❖ The cells are connected to each other at


the desmosomal contacts and appear
star shaped and form a network.

❖ Acts as shock absorber; support and


protects enamel forming cells.
3. DENTAL PAPILLA:
• In the organizing influence of
proliferating epithelium of the enamel
organ, the ectomesenchyme proliferates.

• It condenses to form the dental papilla,


which is the formative organ of the
dentin and the primordium of the pulp.
The changes in the dental papilla occur
concomitantly with the development of
the epithelial enamel organ.

• The dental papilla shows active budding


of capillaries and mitotic figures, and its
peripheral cells adjacent to the inner
enamel epithelium enlarge and later
differentiate into the odontoblasts.
4. DENTAL SAC:
• There is condensation of ectomesenchyme around the enamel organ
and dental papilla.
• This condensation around the enamel organ and dental papilla is
called dental sac or dental follicle.
Difference between dental sac
and dental papilla
• Ectomesenchymal tissue is made up of cells
and fibres suspended in a ground substance,
along with supporting elements like blood
vessels and nerves etc.
• Dental papilla contains proportionately more
cells and less fibres.
• Dental sac contains proportionately more
fibres and less cells.
Bell stage
❖The bell stage, so called
because the enamel organ
comes to resemble a bell as
the undersurface of the
epithelial cap deepens.

❖ By the start of this stage


the shape of the tooth has
already been decided
(morpho differentiation).
Cell Types in Bell Stage
Four cell types are
seen-
1.Inner enamel
epithelium.
2.Stratum
intermedium.
3.Stellate reticulum.
4.Outer enamel
epithelium.
Inner enamel epithelium
❖ Tall columnar cells-40 micrometres high and 4-5 micrometres in diameter.
❖ Attached to each other laterally by junctional complexes and to cells of
stratum intermedium by desmosomes.
❖ These cells differentiate into ameloblasts prior to enamel
formation.(amelogenesis)

Stratum intermedium

❖ 3-4 layers of squamous cells between the inner enamel epithelium and the
stellate reticulum.
❖ Attached by desmosomes and gap junctions.
❖ There are abundant cell organelles ,acid mucopolysaccharides and glycogen
deposits in these cells, which indicate a high metabolic activity.
❖ Essential for enamel formation.
❖ It is absent in that part of the tooth germ that forms the root.
Stellate Reticulum
❖ The amount for intercellular fluid between the cells increases.
❖ The width of the stellate reticulum increases.
❖ This layer acts as a cushion or shock absorber for the cells of inner enamel
epithelium.
❖ Just before enamel formation begins, it collapses and becomes similar in
appearance to those of stratum intermedium.
❖ This change begins at the tips of the cusps and progresses cervically.

Outer Enamel Epithelium


❖ A single layer of very low cuboidal cells, lining the convexity of the bell.
❖ At the end of this stage, just before enamel formation, the smooth surface of
outer enamel epithelium gets thrown into folds.
➢ DENTAL LAMINA:

❖ Extends lingually; forms succesional lamina


❖ Forms enamel organ of permanent teeth.

➢ DENTAL PAPILLA:

❖ Peripheral cells of the dental papilla differentiate


into odontoblasts, which are initially cuboidal
and later become columnar and acquire the
potential to produce dentine.

❖ The basement membrane which separates the


enamel organ and the dental papilla just before
the formation of enamel and dentine is called
membrana preformativa.

➢ DENTAL SAC:

❖ The fibres of the dental sac form the


periodontal ligament fibres that span between the
root & the bone
APPOSITION ( Formation of
enamel and dentin matrix)
❖ It is the process by which the hard dental tissues,i.e enamel,dentine
and cementum are deposited.
❖ This takes place in an incremental pattern.
❖ This means that the organic matrix of these tissues are deposited in
form of layers.
❖ Periods of activity and rest alternate at definite intervals during
formation of these tissues.
Changes before enamel formation-
❖ The stellate reticulum collapses

❖ The formerly smooth surface of the outer enamel epithelium


is thrown into folds.

Breakup of dental lamina and crown pattern determination


❖ The dental lamina (and the lateral lamina) joining the tooth
germ to the oral epithelium fragments, eventually separating
the developing tooth from the oral epithelium.
❖ The inner enamel epithelium completes its folding, making it
possible to recognize the shape of the future crown pattern
of the tooth.
Reciprocal Induction
• The inner enamel epithelium induces. the
peripheral cells of dental papilla to
differentiate into odontoblasts.
• The odontoblasts start secreting the organic
matrix of dentine.
• After the first layer of dentine matrix is
formed,the ameloblasts in that area
differentiate fully and start secreting the
enamel matrix.
• This interdependence of the two tissues is an
example of reciprocal induction.
Root formation
❖ Once crown formation is completed, epithelial cells of the inner and outer
enamel epithelium proliferate from the cervical loop of the enamel organ to
form a double layer of cells known as Hertwig's epithelial root sheath

❖ The rim of this root sheath, the epithelial diaphragm, encloses the primary
apical foramen. As epithelial cells of the root sheath progressively enclose
more and more of the expanding dental pulp, they initiate the differentiation
of odontoblasts from ectomesenchymal cells at the periphery of the pulp,
facing the root sheath.

❖These cells eventually form the dentin of the root. In this way a single-rooted
tooth is formed.
• As the root sheath
fragments, it leaves behind
a number of discrete
clusters of epithelial cells,
separated from the
surrounding connective
tissue by a basal lamina,
known as the epithelial
cell rests of Malassez
DENTINOGENESIS
❖ Dentinogenesis, starts before
amelogenesis.
❖ Dentin is formed by odontoblast
cells.

It takes place in two phases:


❖ First, the formation of organic
collagen matrix and
❖ Second, the deposition of
hydroxyapatite crystals
❖ At the beginning of
dentinogenesis, the odontoblast
elongate resulting in the
formation of Tomes fibres or
odontoblastic processes.
AMELOGENESIS

Life Cycle of
Ameloblasts
❖ Morphogenic stage
❖ Organizing Stage
❖ Formative Stage
❖ Maturative Stage
❖ Protective Stage
❖ Desmolytic Stage
MORPHOGENIC PHASE ORGANIZING PHASE

❑ Cells become Longer


❑ Cell –Short, Columnar. ❑ Reversal of Polarity occurs by
migration of Golgi apparatus and
❑ Large oval nucleus. centrioles to distal parts of the cell.
❑ Nuclei shifts to the proximal part of
the cell.
❑ Golgi apparatus and
mitochondria are located at ❑ Amount of Rough endoplasmic
proximal end. reticulum increases.
❑ Basal lamina supporting ameloblasts
disintegrates after dentin formation.
❑ Change in nutritional supply of
ameloblasts occurs.
FORMATIVE STAGE MATURATIVE STAGE

❑ Enamel maturation occurs after


❑ This stage starts after first
most of enamel matrix in occlusal
layer of dentin is laid down. or incisal areas is laid down.

❑Development of blunt ❑ Ameloblasts are slightly reduced in


length with appearance of
surfaces processes occurs on microvilli at their distal surface.
ameloblast formation.
❑ Most of the organelles associated
with formation of enamel are
❑It penetrates basal lamina to enclosed in phagocytic vacuoles
enter predentin. and are digested by lysosomal
enzymes
PROTECTIVE STAGE DESMOLYTIC STAGE

❑ After mineralization of
enamel is complete, ❑ The reduced enamel
ameloblasts loose their epithelium induces atrophy
striated boarder and also of connective tissue
the shape. separating it from oral
epithelium and helps in
❑ These cells form the tooth eruption.
reduced enamel epithelium
over the newly formed ❑ Premature degeneration of
enamel. It prevents REE can lead to soft tissue
connective tissue from impaction of tooth due to
coming in contact of failure of desmolysis of
enamel till eruption occurs. connective tissue between
tooth and oral epithelium.
Nerve supply Vascular supply
➢ Nerve fibres enter the dental
papilla at a late stage. ➢ Clusters of blood vessels are
found ramifying around the
➢ First fibres to enter the papilla tooth germ in the dental
are from the trigeminal nerve follicle and entering the dental
close to blood vessels. papilla during cap stage.

➢ The nerve growth factors


neurotrophin, glial cell line ➢ With age, the volume of pulpal
derived growth factor and tissue diminishes and the blood
semaphorin are among the supply becomes progressively
few nerve related signaling reduced, affecting the viability
molecules.
of the tissue.
Important markers for tooth formation
❖ Initiation of tooth occurs at E11.

❖ Earliest markers for tooth formation are Lhx-6 and Lhx-7.

❖ Prime inductor of Lhx genes is Fgf-8 which is expressed at a proper time in first arch epithelium only.

Determinants of position and type of tooth

❖ The Pax- 9 gene is the earliest mesenchymal gene that localizes the tooth germs.

❖ This is also induced by Fgf -8.

❖ The expression of Pax-9 is downregulated by BMP-2, BMP-4.

❖ Tooth type determination is known as Patterning of the dentition.

❖ Seen in heterodont species.


Clinical considerations
➢ Initiation defects

➢ Proliferation defects

➢ Histodifferentiation defects

➢ Morphodifferentiation defects

➢ Apposition defects

➢ Root formation defects


Initiation defects

❖Anodontia

❖Fusion

❖Gemination
ANODONTIA
➢ Anodontia also called anodontia vera is
characterized by the congenital absence of all
primary or permanent teeth
➢ Types-
I. Complete anodontia /True anodontia
(refers to total absence of teeth)
II. Partial anodontia/subtotal anodontia (is the
congenital absence of one to six permanent
teeth excluding the 3rd molars due to the
failure of those teeth to develop, known as
tooth agenesis)
III. Oligodontia ( refers to absence of more than 6
teeth)
➢ Often associated with Hereditary ectodermal
dysplasia.
FUSION
❖ Fused teeth arise through union of two normally separated
tooth germs.
❖ Depending upon the stage of the teeth at the time of union,
fusion may be either complete/ incomplete.
❖ If this contact occurs early at least before calcification begins
two teeth may be completely united to form a single large
tooth.
❖ If this contact occurs later when a portion of tooth crown has
completed its formation there may be union of roots only.

❖ The possible clinical problems are- spacing, periodontal


condition.

❖ Syndrome – SOLITARY MEDIAN MAXILLARY


CENTRAL INCISOR SYNDROME
(The development of only one maxillary central incisor is an
indication for further evaluation for other anomalies such as
short stature with or without growth hormone deficiency,
microcephaly, choanal atresia, midnasal stenosis, and
congenital nasal pyriform aperture stenosis).
GEMINATION
❖ . Geminated teeth are anomalies which arise from an attempt
at division of a single tooth germ by an invagination with
resultant incomplete formation of two teeth.
❖ The structure is usually one with two completely or
incompletely separated crowns that have a single root and
root canal.
❖ It is seen in deciduous as well as permanent dentition
❖ Treatment of a permanent anterior geminated tooth
may involve reduction of the mesiodistal width of the
tooth to allow for normal development of the
occlusion. Periodic “disking” of the tooth is
recommended when the crown is not excessively large,
as is eventual preparation of the tooth for restoration if
dentin is exposed.
PROLIFERATION DEFECT

❖ Supernumerary teeth

❖ Odontoma
SUPERNUMERARY TEETH
➢ Results from continued proliferation of
permanent or primary dental lamina to
form extra tooth germ.

➢ Teeth may have- normal morphology,


rudimentary, miniature.

➢ Supernumerary teeth are common more


often in permanent dentition than primary
dentition.

➢ They are more common in maxilla than in


mandible.

➢ They may be impacted or partially erupted.

➢ Because of additional tooth bulk it causes-


malposition of adjacent teeth, prevent their
eruption.
➢ The most common supernumerary teeth are-
I. Mesiodens
II. Fourth molar- maxillary paramolar, distomolar/ distodens
III. Mandibular premolar
IV. Maxillary lateral incisor
V. Mandibular central incisor
VI. Maxillary premolars

➢ Most common supernumerary tooth is mesiodens, situated


between maxillary central incisor.
➢ Second most common tooth is fourth molar, situated distal
to 3rd molar
HISTODIFFERENTIATION
DEFECTS

❖Dentinogenesis imperfecta
❖Amelogenesis imperfecta
Amelogenesis imperfecta
➢ The other names are- Hereditary enamel dysplasia, hereditary brown enamel,
hereditary brown opalescent teeth.
➢ Types –
I. Hypocalcified
II. Hypoplastic
III. Hypomature

➢ Analysis of X linked AI has shown the defective gene for specific AI type to be
closely linked to the locus DXS85 at Xp22.

➢ The enamel may appear totally absent on the radiograph or when present may
appear as a very thin layer chiefly over the tips of the cusps and on the
interproximal surfaces.

➢ SYNDROME- NEPHROCALCINOSIS SYNDROME, ALSO CALLED


ENAMEL-RENAL SYNDROME OR LUBINSKY SYNDROME.
Dentinogenesis imperfecta
➢ It is an autosomal dominant condition affecting
both permanent and primary teeth.

➢ Affected teeth are gray to yellowish brown and


have broad crowns with constriction of the
cervical area resulting in a TULIP shape..

➢ Classification-

A. Dentinogenesis imperfecta I (Opalescent dentin,


dentinogenesis imperfecta without osteogenesis
imperfecta, opalescent teeth without osteogenesis
imperfecta, dentinogenesis imperfecta, Shields type
II, Capdepont teeth)

B. Dentinogenesis imperfecta II(Shields type III,


Brandywine type dentinogenesis imperfecta)
DENTINOGENESIS IMPERFECTA I DENTINOGENESIS IMPERFECTA II

❖ Dentinogenesis imperfecta is an entity ❖ The crowns of the deciduous and


clearly distinct from osteogenesis permanent teeth wear rapidly after
imperfecta with opalescent teeth, and eruption and multiple pulp exposures
affects only the teeth. may occur. The dentin is amber and
smooth.
❖ The teeth are blue-gray or amber brown
and opalescent. On dental radiographs, ❖ Radiographs of the deciduous dentition
the teeth have bulbous crowns, roots that show very large pulp chambers and root
are narrower than normal, and pulp canals, at least during the first few
chambers and root canals that are years, although they may become
smaller than normal or completely reduced in size with age. The permanent
obliterated. teeth have pulpal spaces that are either
smaller than normal or completely
❖ The enamel may split readily from the obliterated.
dentin when subjected to occlusal stress.
Sauk et al (1976) noted an increase in ❖ The amber discoloration of the teeth,
glyco saminoglycans in EDTA soluble attrition, and fractured enamel, as well
dentin in the teeth from patients with this as the classic ‘shell teeth’ appearance
disorder as compared to controls, and less on radiographs.
glycosaminoglycan in EDTA insoluble
residue.
MORPHODIFFERENTIATION
DEFECTS
❖Dens in dente
❖Dens evaginatus
❖Talons cusp
❖Hutchinson’s incisors
❖Mulberry molars
Dens in dente(dens
invaginatus, dilated composite Dens evaginatus(Tuberculated
odontome) cusp, accessory tubercle, Leong’s
premolar, occlusal pearl,
➢ Developmental variation
evaginatus odontoma)
➢ The permanent maxillary lateral ➢ The other names are- Occlusal
incisor most frequently involved. tuberculated premolar, Leong’s
Premolar, Evaginated odontome,
➢ In the mild form there is a deep Occlusal enamel pearl.
invagination in the lingual pit area.
➢ This is a developmental condition that
appears clinically as an accessory cusp or
➢ Radiographically it is recognized globule of enamel on the occlusal surface
between the buccal and lingual cusps of
as a PEAR shaped invagination of premolars.
enamel dentin with a narrow
constriction at the opening on the ➢ The pathogenesis of the lesion is thought
to be the proliferation and evagination of
surface of the tooth and closely an area of the inner enamel epithelium
approximating the pulp in its and subjacent odontogenic mesenchyme
into the dental organ during early tooth
depth. development.
Talons cusp (eagle’s talon, supernumerary cusp,
interstitial cusp, evaginated odontoma)

➢ An anomalous structure resembling an Eagle’s talon, projects lingually


from the cingulum areas of a maxillary or mandibular permanent incisor.

➢ It is composed of normal enamel and dentin, and contains a horn of pulp


tissue.

➢ If there is any occlusal interference it should be removed but exposure of


pulp horn necessitating endodontic therapy is almost certain to occur.

➢ SYNDROMES ASSOCIATED-
•RUBINSTEIN -TAYBI- SYNDROME
•STURGE WEBBER SYNDROME
•ELLIS – VAN CREVELD SYNDROME
HUTCHINSON’S INCISOR MULBERRY MOLAR( Fournier molars)
(Hutchinson’s sign, Hutchinson-
Boeck teeth) ➢ Dental condition usually associated with
congenital syphilis.
➢ Characterized in congenital syphilis.
➢ Characterized by multiple rounded
rudimentary enamel cusps on permanent 1st
➢ Lateral incisors are peg shaped or molar.
screwdriver shaped.
➢ Dwarfed molars with cusps covered with
➢ Widely spaced. globular enamel growths.

➢ Notched at the end. ➢ Giving the appearance of a mulberry.

➢ With a crescent deformity.


APPOSITION DEFECTS

❖Enamel hypoplasia

❖Concresence
ENAMEL HYPOPLASIA
➢ It is defined as an incomplete or defective formation of the organic
enamel matrix of the teeth.

➢ Two basic types of enamel hypoplasia exists


- Hereditary and the other type caused by environmental factors

➢ Factors that may give rise to this condition including-

❖ Nutritional deficiency( vit A,C,D)


❖ Exanthematous diseases
❖ Congenital syphilis
❖ Hypocalcemia
❖ Birth injury, prematurity, Rh hemolytic disease
❖ Local infection or trauma
CONCRESENCE
➢ It is actually a form of fusion which occurs
after root formation has been completed. In
this condition, teeth are united by cementum
only.

➢ It is thought to arise as a result of traumatic


injury or crowding of teeth with resorption
of the interdental bone so that the two
roots are in approximate contact and
become fused by the deposition of
cementum between them.

➢ Concrescence may occur before or after the


teeth have erupted, and although it usually
involves only two teeth.

➢ Diagnosis can be frequently made by the use


of radiograph.
CONCLUSION
❖ The developmental anomalies of teeth show variations
and no two anomalies of the same type are alike.

❖ Anomalies in the primary dentition are important


because of their effect on the underlying permanent
dentition.

❖ Early identification of these anomalies and intervention


at the appropriate time would minimize complicated
treatments in future.
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