Title Author & journal Aim Material and Method Result Conclusion
Epithelial
rests of
Malassez:
from latent
cells to active
participation
in
orthodontic
movement
Bianca Silva e
Silva
,1
Nathalia Caro
lina Fernand
es Fagundes
,1
Bárbara Cata
rina Lima No
gueira
,1
José Valladar
es, Neto
,2
David Norma
ndo
,3
and
Rafael Rodrig
ues Lima
1
The present
literature
review aims
at presenting
the potential
functions of
ERM, with
emphasis on
orthodontic
movement
and the
functional
structure of
the
periodontiu
m.
epithelial rests of Malassez (ERM)
represent a group of cells in the
periodontal ligament classically
consisting of latent or quiescent
structures associated with
pathological processes.
ERM cells
have a
functional
activity in
modulation
of
orthodontic
movement,
trough
their
potential
for
differentiati
on,
maintenanc
e functions
and the
capacity of
repairing
periodontiu
ERM cells
have a
functional
activity in
modulation
of
orthodontic
movement,
trough their
potential for
differentiatio
n,
maintenance
functions
and the
capacity of
repairing
periodontiu
m.
DEVELOPMENT OF
TEETH
Dr. Vidula MDS 1st
year
20XX
CONTENTS
 INTRODUCTION
 TOOTH DEVELOPMENT STAGES-
• A) MORPHOLOGICAL- BUD STAGE
CAP STAGE
EARLY BELL STAGE
ADVANCED BELL STAGE
ROOT DEVELOPMENT
• B) PHYSIOLOGIC- INITIATION
PROLIFERATION
HISTODIFFERENTIATION
MORPHODIFFERENTIATION
APPOSITION
 MOLECULAR INSIGHTS IN TOOTH
MORPHOGENESIS
20XX
INTRODUCTION
• The primitive oral cavity or
stomodeum lined by stratified
squamous epithelium is called oral
ectoderm or primitive oral epithelium.
• The oral ectoderm contacts the
foregut to form the buccopharyngeal
membrane.
• At 27th
day of gestation; the
membrane ruptures and stomodeum
ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH
EDITION
20XX
PRIMARY EPITHELIAL BAND
• 2-3 weeks after the rupture of
buccopharyngeal membrane, certain
areas develop more rapidly than the
adjacent cells
• This leads to formation of primary
epithelial band which appears in the
space of future horse-shaped dental
arches. ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH
EDITION
20XX
• Each band of primary
epithelium divides by 7th
week that quicky in- grows to
form
Dental lamina
Vestibular lamina
• The dental lamina arises
early from the inner lingual
process while the vestibular
lamina arises from outer
buccal aspect.
ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH
EDITION
20XX
CLINICAL SIGNIFICANCE OF
PRIMARY
EPITHELIAL BAND
• Initiation of tooth
development starts with
formation of placodes in the
epithelial band
• Dental placodes usually
result in formation of
different dental families ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH
EDITION
20XX
• The balance between stimulatory factors
(FGFs,WnTs) and inhibitory factors(BMP)
must be maintained.
Imbalance in these pathways may lead to
Ectodermal Dysplasia characterized by
oligodontia and misshapen teeth.
ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH
EDITION
20XX
DENTAL LAMINA
• Primordium for the ectodermal portion of the
deciduous teeth
Decidious Dental lamina
• 1st
tooth to be initiated is deciduous mandibular central
incisor( 6th
week in utero)
Successional Dental lamina
• It is the lingual extension of dental lamina.
• It develops from 5th
month in utero (permanent central
incior) upto 10th
month of age( 2nd
premolar)
ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH
EDITION
20XX
20XX
20XX
FATE OF DENTAL LAMINA
Dental lamina functions for a short period of time at any particular location.
It degenerates rapidly once the tooth development starts.
The total activity usually extends upto 5 years of age however it may still be active in
3rd
molar region.
Remnants of dental lamina persist as epithelial pearls or islands within jaw or
gingiva.
They are referred to as ”cell rest of serres”
ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH
EDITION
20XX
VESTIBULAR LAMINA
• Labial or buccal to dental
lamina
• Also termed as “lip-furrow
band”
• Usually forms by around 6th
week of development
• It forms the vestibule.
ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH
EDITION
20XX
FORMATION OF VESTIBULE
Vestibular lamina
Proliferates into the
ectomesenchyme
Cells rapidly enlarge &
degenerate
Cleft – vestibule formation
[Between alveolar portion of
jaws and the lips / cheeks]
ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH
EDITION
20XX
INITIATION OF THE TOOTH
• Initiation of tooth development usually
begins by interaction of epithelium of 1st
arch with ectomesenchymal cells derived
from neural crest cells.
• However, by 12th
day, 1st
arch epithelium
loses this potential and thereafter
ectomesenchyme can elicit tooth formation
from a variety of epithelia.
ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH
EDITION
20XX
•LHX-HOMEOBOX are the earliest
mesenchymal markers for tooth
development
•The domain genes LH-6 and LH-7
appear as earliest by 9th
day of
gestation.
•The expression of these genes
result from signaling
molecule ,Fibroblast growth
factor-8 (FGF-8) derived from
epithelium of 1st
branchial arch
ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH
EDITION
20XX
DEVELOPMENTAL STAGES
 Morphologic Stages
1. Dental lamina
2. Bud stage
3. Cap stage
4. Bell stage –
Early bell stage
Late / advanced bell stage
5. Root formation
ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH
EDITION
PHYSIOLOGIC STAGES
1.Initiation
2.Proliferation
3.Morphodifferentiatio
n
4.Histodifferentiation
5.Apposition
Click icon to add picture
20XX
ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH
EDITION
20XX
BUD STAGE
• Dental lamina is separated from underlying
ectomesenchyme- basement membrane.
• With differentiation of dental lamina- round/
ovoid swellings- basement membrane at 10
points corresponding to future position of
deciduous teeth- Primordia of Enamel organ
(tooth bud)
ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH
EDITION
20XX
•Condensation of
ectomesenchyme just beneath
the enamel organ- dental
papilla.
•Condensed ectomesenchyme
that surrounds enamel organ
& dental papilla- dental sac.
• Both Dental papilla and
Dental sac become more
prominent in the subsequent
stages of tooth development
ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH
EDITION
20XX
CAP STAGE
• Tooth bud continues to
proliferate- does not expand
uniformly- larger sphere.
• Unequal growth- cap stage-
shallow invagination on deep
surface of bud.
• Consist of:
Outer enamel epithelium
Stellate reticulum
Inner enamel epithelium
ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH
EDITION
20XX
OUTER & INNER ENAMEL
EPITHELIUM
• Inner enamel epithelial cells
Seen in the concavity of the
cap
Tall columnar cells
• Outer enamel epithelial cells
Seen in the convexity of the
cap
Cuboidal cells
ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH
EDITION
20XX
ENAMEL ORGAN -
- Composed of
Peripheral low columnar
cells
Central polygonal cells
ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH
EDITION
20XX
• Hemidesmosomes anchor
cells to basal lamina.
Enamel organ- double
attachment of dental lamina to
overlying epithelium enclosing
ectomesenchyme- Enamel
Niche
• Appearance- funnel shaped
depression of the dental
lamina. ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH
EDITION
20XX
STELLATE RETICULUM
• Polygonal cells begin to separate due to
water being drawn into the enamel organ
from surrounding dental papilla.
• Due to osmotic force exerted by
glycosaminoglycans contained in the
ground substance.
• Cells separate but maintain contact with
each other by their cytoplasmic process.
• Star shape cells- cellular network- stellate
ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH
EDITIO
20XX
• Functions
Cushion like consistency
Acts as a shock absorber
Supports and protects
delicate enamel forming
cells
ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH
EDITION
20XX
TRANSITORY STRUCTURES
ENAMEL KNOT
• It is formed by the cells in the centre
of enamel organ which are densely
packed.
• It acts as a reservoir of cells for the
growing enamel organ.
ENAMEL CORD
• It is the vertical extension of the
enamel knot
ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH
EDITION
20XX
ENAMEL KNOT –SIGNALLING CENTRE FOR TOOTH
MORPHOGENESIS
•It consists of cells that do not divide but promote the
division of adjacent epithelial cells that form cervical
loop and dental papilla.
ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH
EDITION
20XX
•BMP4 induces dental papilla cells to form
odontoblasts.
ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH
EDITION
•Although BMP-4 is the earliest marker
to start signalling of enamel knot
formation, it is not sufficient to induce
other markers, i.e bmp-2, fgf-4.
20XX
ENAMEL SEPTUM
• When the enamel cord extends to meet
the outer enamel epithelium, it divides
the stellate reticulum in 2 parts. Hence,
Enamel septum.
ENAMEL NAVEL
• The outer enamel epithelium shows a
small depression at the point of meeting
which resembles umbilicus .Hence,
enamel navel
• These structures disappear before
enamel formation begins
ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH
EDITION
20XX
DENTAL PAPILLA
• Present under the concavity of the
enamel organ.
• Is the condensed ectomesenchyme.
• Formative organ of dentin and pulp.
• Shows active budding of capillaries
and mitotic figures.
ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH
EDITION
20XX
• Peripheral cells of dental
papilla- differentiates into
odontoblast.
• Basement membrane that
separates enamel organ &
dental papilla- membrana
performativa
20XX
DENTAL SAC (Dental follicle)
• Marginal condensation in
the ectomesenchyme
surrounding enamel organ
and dental papilla.
• Gradually a denser and more
fibrous layer develops.
• It forms the supporting
structures namely
periodontal ligament, ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH
EDITION
20XX
EARLY BELL STAGE
Invagination of epithelium deepens, margins continue to grow- bell shape.
Crown shape is determined.
It was thought that the shape of crown is because of pressure exerted by
Dental papilla on IEE. This pressure was shown to be opposed equally by
fluid in stellate reticulum.
Folding of enamel organ- different crown shape- differential rate of mitosis
and differences in cell differentiation time.
ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH
EDITION
20XX
20XX
The IEE cells which lie in the region of future cusp tip or
incisor region stop dividing earlier and differentiate first.
The pressure exerted by continuous cell division on
these cells from other areas cause these cells to be
pushed in form of cusp-tip.
The area between two cusps tips i.e. cuspal slopes
extend and cusp height develops due to cell
proliferation and differentiation .
Cell differentiation progresses from incisor region to
cervically.
20XX
• Bell stage can be
distinguished by 4 cell layers
Inner enamel epithelium
Stratum intermedium
Stellate Reticulum
Outer enamel epithelium
• The junction between inner
and outer enamel epithelium
is called cervical loop and it
is the area of intense mitotic
activity.
20XX
INNER ENAMEL EPITHELIUM
• Single layer of cell- differentiate prior to
amelogenesis- tall columnar cells- ameloblasts.
• These cells- 4-5μm in diameter & 40μm high.
• These cells are attached to one another by junctional
complexes and to stratum intermedium-
desmosomes.
• These cells exert an organized influence on the
underlying mesenchymal cells which later
differentiate into odontoblasts.
ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH
EDITION
20XX
STRATUM INTERMEDIUM
• Few layers of squamous cells- between inner
enamel epithelium and stellate reticulum.
• Closely attached by desmosomes and gap
junctions.
• Well developed cytoplasmic organelles, acid
mucopolysaccharides and glycogen deposits
– indicate high metabolic activity.
This layer is essential-enamel formation.
ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH
EDITION
20XX
OUTER ENAMEL EPITHELIUM
• Cells flatten to low cuboidal.
• At end of bell stage- initially smooth
surface of OEE-laid in folds.
• Rich nutritional supply to enamel
organ
• This would compensate for loss of
nutritional supply owing to
formation of mineralized dentin. ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH
EDITION
20XX
DENTAL FOLLICLE
• Before formation of dental
tissues- circular arrangement
& resembles capsular
structure.
• With development of root-
fibers differentiate into PDL
fibers- embedded in
developing cementum &
alveolar bone.
ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH
EDITION
20XX
ADVANCED/LATE BELL STAGE
• Characterized by: mineralization & root formation.
• Boundary between IEE & odontoblast- DEJ.
• Formation of dentin- first- in region of future cusp
& proceeds pulpally & apically.
ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH
EDITION
20XX
•After 1st
layer of dentin formation-
ameloblast which has already
differentiated from IEE – lay enamel
over dentin.
• Cervical portion of enamel organ-
Hertwig’s epithelial root sheath.
ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH
EDITION
20XX
HERTWIG’S EPITHELIAL ROOT
SHEATH
• Outlines future root.
• Responsible for the shape, length, size
and number of roots.
• Consists of inner and outer enamel
epithelia only.
ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH
EDITION
20XX
• Does not include stellate reticulum and stratum
intermedium.
• The development of root begins only after
enamel and dentin formation has reached future
cementoenamel junction
• Initiates root dentin formation.
• Cells of inner enamel epithelia remain short and
do not produce enamel.
ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH
EDITION
20XX
• Inner enamel epithelial cells induce differentiation of
dental papilla cells into odontoblasts
Odontoblasts form dentin
Once dentin is laid down, HERS breaks down
Remnants of HERS – cell rests of Malassez
These are found in periodontal ligament of erupted teeth
(network of strands/ clumps)
ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH
EDITION
SINGLE ROOTED TOOTH
• Prior to root formation- root
sheath forms epithelial
diaphragm.
• Before root formation
begins, outer and inner
enamel epithelia bend at
future CEJ in a horizontal
plane. ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH
EDITION
20XX
• The plane of this diaphragm remains fixed during
development and growth of root.
• Free end of diaphragm does not grow. Inner enamel
epithelial cells of HERS have an organizing influence on
dental papilla cells.
Orban’s Oral Histology and Embryology- 14th
edition, Ten Cate’s Oral Histology- 7th
Edition
• These differentiate into odontoblasts which lay down
dentin.
• Once dentin is laid down, the dental sac proliferates and
invades into HERS.
• HERS breakdown into a network of epithelial strands.
• Epithelium moves away from the dentinal surface.
ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH
EDITION
20XX
• Ectomesenchymal cells of the dental sac come in
contact with the freshly laid dentin.
• They differentiate into cementoblasts, fibroblasts
and osteoblasts to give rise to cementum,
periodontal ligament and alveolar bone
respectively.
• Last stages - proliferation of epithelium of
diaphragm lags behind that of pulpal connective
tissue.
• Apical foramen is further narrowed by apposition
ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH
EDITION
20XX
MULTI-ROOTED TEETH
• Differential growth of the epithelial diaphragm.
• The number and position of these extensions
depend on the number and type of root to be
formed.
• each extension develops as normal root.
ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH
EDITION
20XX
• Two extensions-Germ of lower molar
• and three extensions – Germ of upper molar.
• On the pulpal aspect- dentin formation starts and on
the outer extension develops as normal root.
ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH
EDITION
• Enamel pearl
• Accessory canal
03/29/2025 55
CLINICAL SIGNIFICANCE OF
HERS
20XX
ENAMEL PEARL
• After dentin is formed -HERS does not
breakdown.
• The inner enamel epithelial cells of HERS
may differentiate into fully functional
ameloblasts and form enamel.
• Found in area of furcation of roots of
permanent molars.
ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH
EDITION
20XX
ACCESSORY CANAL
• HERS breaks down before
dentin is formed.
• There is a defect in the
dentinal wall of the pulp.
• Any point on the root.
ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH
EDITION
20XX
DEVELOPMENT OF
TEETH
Dr. Vidula MDS 1st
year
20XX
PREVIOUSLY ASKED
QUESTIONS
WHY DOES EACH TOOTH HAVE A
PARTICULAR SHAPE
20XX
• 8 Incisors.
These flat, thin teeth designed for cutting and biting food
• 4 Canines
to grip, tear, and rip food.
• 8 Molars
These large teeth have broad, flat surfaces that make them the
main teeth used for chewing and grinding food.
• 8 Premolars
Their flat surface and position allow you to grip, tear, chew, and
grind the food.
https://waldensquaredentalny.com/blog/teeth-shapes/
FACTORS WHICH REGULATE DENTIN
FORMATION
• IGFs, TGFs, and BMPs
These factors play a crucial role in dentin formation. The BMP family regulates processes
like cell proliferation, migration, differentiation, and extracellular matrix remodeling.
• Dentin sialoprotein and dentin phosphoprotein
These proteins have different roles in dentin mineralization.
• Dentin sialophosphoprotein (DSPP)
This is a key non-collagenous protein (NCP) involved in tooth development and
mineralization.
• Cell junction related genes
These genes include occludin (OCLN), claudin-1 (CLDN1), and zonula occludens-1/2
(Zo1/2). They play important roles in odontoblast differentiation.
20XX
• Sclerostin
This is secreted by odontoblasts and pulp cells and acts as a
negative regulator of reparative dentin formation.
• WNT signaling
This is involved in the signaling pathway and also has an
essential role in odontogenesis and dentin repair.
• Fibroblast growth factor (FGF)
This plays key roles in cell migration, proliferation, and
differentiation during embryonic development and wound
healing. These are critical drivers of the repair process and
stimulate reparative dentin formation by odontoblasts.
Odontoblasts are also called as Tomes's fibers
20XX
STRUCTURES FORMED FROM THE
ENAMEL KNOT
• The enamel knot is a signaling center of the tooth
that provides positional information for tooth
morphogenesis and regulates the growth of
tooth cusps.
• The enamel knot produces a range of molecular
signals from all the major signaling families, such as
Fibroblast Growth Factors (FGF), Bone morphogenetic
proteins (BMP), Hedgehog (Hh) and Wnt signals.
• These molecular signals direct the growth of the
surrounding epithelium and ectomesenchyme.
20XX
BLOOD SUPPLY OF AMELOBLASTS
• As long as the ameloblasts are in contact with the dental papilla,
they receive nutrient material from the blood vessels of the
tissue, but due to formation of this dentin the original source of
nutrition is cut off and the ameloblasts are supplied by capillaries
penetrating the outer enamel epithelium.
• This change in nutrition source is referred to as "reversal of
nutrition".
20XX
20XX
CLINICAL SIGNIFICANCE OF
CELL RESTS OF MALASEZZ
RADIX ENTOMOLARIS AND
PARAMOLARIS
If extra root on mandibular molars is located lingually called radix
entomolaris (RE) or located buccally called radix paramolaris (RP).
De Moor et al classified RE-based on the curvature in buccolingual
orientation into three types.

Type I – Refers to a straight root/root canal.

Type II – Refers to an initially curved entrance which continues as
a straight root/root canal.

Type III – Refers to an initial curve in the coronal third of the root
canal and a second buccally oriented curve starting from middle
to apical third.
20XX
The Radix Entomolaris and Radix Paramolaris: An Endodontic Challenge
Carlsen and Alexanderson
describes two different types
of RP
• Type A – Refers to an RP in
which the cervical part is
located on the mesial root
complex
• Type B – Refers to an RP in
which the cervical part is
located centrally, between
the mesial and distal root
complexes.
20XX
The Radix Entomolaris and Radix Paramolaris: An Endodontic Challenge
ODONTOMES
• Odontomas are the most common type of
odontogenic tumors. They are included
under the benign calcified odontogenic
tumors.
• The etiology behind odontomes remains
unknown.5
It has been related to various
pathological conditions, like local trauma,
inflammatory and/or infectious processes,
mature ameloblasts, cell rests of serres
(dental lamina remnants)
• There are two main types: compound and
complex.
20XX
ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH
EDITION
• A compound odontoma consists of the four separate
dental tissues (enamel, dentine, cementum and pulp)
embedded in fibrous connective tissue and
surrounded by a fibrous capsule. It may present a
lobulated appearance where there is no definitive
demarcation of separate tissues between the
individual "toothlets" (or denticles). Compound
odontomas are usually found in the anterior maxilla
and are less than 20mm in diameter.
• The complex type is unrecognizable as dental hard
and soft tissues, usually presenting as a radioopaque
area with varying densities indicating presence of
enamel. It generally appears in the posterior
20XX
ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH
EDITION
GLOBODONTIA
• Globodontia is a rare dental
condition that causes enlarged,
bulbous crowns on primary canine
and molar teeth.
• It can occur in both primary and
secondary teeth, but not incisors,
which are normally the same size
and shape.
20XX
NERVE SUPPLY
• Cluster of blood vessels starts ramifying around the tooth germ
around the dental follicle and entering papilla during the cap stage.
• Interestingly the vessels entering the papilla usually occupy the
space where future root develops.
• Pioneer nerve fibers approach the developing tooth during the
bud-to cap stage of development.
• These nerve fibres develop in dental follicle and they don’t encroach
the enamel organ until dentinogenesis begins.
• The pioneer nerve fibres are sensory in nature.
20XX
Ten Cate’s Oral Histology- 7th
Edition
20XX
INITIATION
• It is a momentary event.
• Potential for tooth formation lies in the
dental lamina and associated tooth buds.
• Different teeth are initiated at different
times.
• Initiation induction requires
ectomesenchymal epithelial interaction.
ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH
EDITION
Anomalies corresponding to
Initiation/Bud stage of tooth
development
• Anodontia
• Supernumerary teeth
• Microdontia
• Macrodontia
20XX
Anomalies corresponding to Cap
stage of tooth development
• Gemination
• Fusion
• Dens Invaginatus
• Dens Evaginatus
• Talon’s Cusp
20XX
Anomalies corresponding to
Apposition
• Enamel hypoplasia
• Concrescence
• Enamel Pearl
20XX
Anomalies corresponding to
Histodifferentiation
• Amelogenesis Imperfecta
• Dentinogenesis Imperfecta
20XX
CLINICAL SIGNIFICANCE
Lack of initiation.
Single tooth
(upper lateral incisors, lower second
premolars & third molars)- commonly
involved
20XX
20XX
Partial Anodontia
Anodontia
TYPES OF ANODONTIA
• True Anodontia: Rare condition where all teeth
are missing
• Induced or False Anodontia: Result of
extracting all teeth.
• Pseudo Anodontia: Multiple unerupted teeth.
ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH
EDITION
Etiology and Genetics:
• Familial tendency for missing teeth is common.
• Likely result of one or more point mutations in a polygenic
system, often transmitted in an autosomal dominant
pattern.
• Other Factors: Cases of missing third molars might be an
evolutionary trend.
• X-ray radiation at an early age can cause teeth to be
missing or deformed.
20XX
ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH
EDITION
PROLIFERATION STAGE
• Enhanced proliferative activity starts at the points of
initiation.
• Causes regular changes in size and proportions of the
growing tooth germ.
• Even during early part of this stage, the tooth shows
potential to be highly developed.
ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH
EDITION
20XX
Histodifferentiation
• Cells become restricted in their function.
• The cells differentiate and give up their capacity
to multiply- they assume new function.
• Differentiation of epithelial cells is essential for
differentiation of odontoblasts & initiation of dentin
formation.
ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH
EDITION
20XX
CLINICAL SIGNIFICANCE
• Vitamin A deficiency- Ameloblast fails to
differentiate- adjacent mesenchymal cells are
disturbed- osteodentin.
ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH
EDITION
• With the formation of dentin, IEE cells
differentiate into ameloblasts and lay down
enamel matrix.
20XX
• Dentinogenesis imperfecta
(Hereditary opalescent
dentin) is a genetic disorder
of tooth development
• They cause teeth to appear
discoloured as blue-green or
yellow-brown and
translucent.
DENTINOGENESIS IMPERFECTA
20XX
MORPHODIFFERENTIATION
• Basic form and relative size of future tooth is
established - differential growth.
• Morphodifferentiation is thus impossible
without proliferation.
• DEJ and CDJ are different and characteristic
for each type of tooth
ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH
EDITION
20XX
APPOSITION
• In this stage there is deposition of matrix
of dental hard tissues.
• Appositional growth of enamel and
dentin occurs by layer like deposition of
an extracellular matrix.
• Periods of activity and rest alternate at
definite intervals during tooth formation.
ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH
EDITION
20XX
CLINICAL SIGNIFICANCE
ENAMEL HYPOPLASIA
• It may be defined as an
incomplete or defective
formation of the organic
enamel matrix of teeth.
• Two basic types of enamel
hypoplasia exist:
• (1) a hereditary type (2) a
type induced by
20XX
AMELOGENESIS IMPERFECTA
HYPOPLASTIC HYPOCALCIFIED HYPOMATURATION
GEMINATION
• Partial cleavage of a single tooth germ
• Anomalous tooth
• 2 partially Separated crowns and one root
• Deciduous mandibular incisors and permanent
maxillary incisors
• Full Compliment number of teeth
• Twinning is complete equal division of single
tooth germ that results in one normal and one
supernumerary tooth
20XX
•SHAEFER’S TEXTOOK OF ORAL PATHOLOGY,R RAJENDRA,7TH
EDITION,CHP- DEVELOPMENTAL DISTURBANCES OF ORAL AND
PERIORAL STRUCTURES, PG NO 180-242
FUSION
• Union of two Adjacent normally separated
tooth germs at the level of dentin during
development.
• It could be hereditary, trauma during
development of teeth or physical force or
pressure.
• More in the primary dentition Affecting the
incisors
• Fusion can be complete or incomplete
20XX
•SHAEFER’S TEXTOOK OF ORAL PATHOLOGY,R RAJENDRA,7TH
EDITION,CHP- DEVELOPMENTAL DISTURBANCES OF ORAL AND
PERIORAL STRUCTURES, PG NO 180-242
CONCRESCENCE
• Union of roots of two or more completely
formed teeth along the line of cementum
• Deposition of Cementum after the root
formation is complete
• Limited only to roots
• It could be due to traumatic injury, crowding of
teeth, hypercementosis, which is associated
with chronic inflammation
• Clinical significance -difficulty in extraction in
undiagnosed cases
20XX
•SHAEFER’S TEXTOOK OF ORAL PATHOLOGY,R RAJENDRA,7TH
EDITION,CHP- DEVELOPMENTAL DISTURBANCES OF ORAL AND
PERIORAL STRUCTURES, PG NO 180-242
TAURODONTISM
• Crown portion is end up at the expanse of its
root
• This results in a large crown,short rudimentary
root and an elongated pulp chamber
• Multirooted permanent molars
• Associated with Down syndrome, Klinefilter
syndrome, amelogenesis imperfecta and
hypodontia.
• No treatment required but there is difficulty
during root canal treatment.
20XX
•SHAEFER’S TEXTOOK OF ORAL PATHOLOGY,R RAJENDRA,7TH
EDITION,CHP- DEVELOPMENTAL DISTURBANCES OF ORAL AND
PERIORAL STRUCTURES, PG NO 180-242
20XX
DENS-IN-DENTE (DENS-
INVAGINATUS)
• Represents a defect of tooth in
which a focal area on the
surface is folded or
invaginated pulpally to a
variable extent.
• Defect is generally localised to
a single tooth & interestingly
maxillary lateral incisors are
the most commonly affected.
•SHAEFER’S TEXTOOK OF ORAL PATHOLOGY,R RAJENDRA,7TH
EDITION,CHP- DEVELOPMENTAL DISTURBANCES OF ORAL AND
PERIORAL STRUCTURES, PG NO 180-242
Histological changes of dens invaginatus
include:
• No irregularities in the dentin below
invagination[10]
• Strains of vital tissue or fine canals that
communicates with the pulp could be found[10]
• Enamel lining irregularly structured
20XX
20XX
DENS EVAGINATUS
• It is a condition found in teeth
where the outer surface
appears to form an extra
bump or cusp.
• Most affected tooth- lower
premolar
• There is a risk of dens
evaginatus chipping off in
normal function.
• Hence this condition requires
monitoring and it may need
•SHAEFER’S TEXTOOK OF ORAL PATHOLOGY,R RAJENDRA,7TH
EDITION,CHP- DEVELOPMENTAL DISTURBANCES OF ORAL AND
PERIORAL STRUCTURES, PG NO 180-242
20XX
Talon’s cusp
• Talon cusp also known as an “eagle’s
talon” is an extra cusp on an anterior
teeth.
• Of all cases 55% occur on the
permanent maxillary lateral incisor and
33% on permanent maxillary central
incisor. •SHAEFER’S TEXTOOK OF ORAL PATHOLOGY,R RAJENDRA,7TH
EDITION,CHP- DEVELOPMENTAL DISTURBANCES OF ORAL AND
PERIORAL STRUCTURES, PG NO 180-242
20XX
• Whenever there are deep
developmental grooves
present restorative
treatment should be done to
prevent the dental caries.
• When talon cusp interferes
with normal occlusion
preventive care should be
taken by performing
endodontic treatment.
•SHAEFER’S TEXTOOK OF ORAL PATHOLOGY,R RAJENDRA,7TH
EDITION,CHP- DEVELOPMENTAL DISTURBANCES OF ORAL AND
PERIORAL STRUCTURES, PG NO 180-242
20XX
DILACERATION
• Dilaceration refers to an
angulation or a sharp bend
or curve anywhere along the
root portion of tooth
•SHAEFER’S TEXTOOK OF ORAL PATHOLOGY,R RAJENDRA,7TH
EDITION,CHP- DEVELOPMENTAL DISTURBANCES OF ORAL AND
PERIORAL STRUCTURES, PG NO 180-242
20XX
• Care should be taken during extraction
as these teeth are more prone to
fracture.
• It usually occurs because of trauma or
any other defect of development which
alter the angulation of tooth germ
during root formation.
20XX
CONCLUSION
A thorough understanding and sound knowledge of
development of teeth is essential for a dentist since it
forms the basis of dentistry
Although there has been significant progress in
understanding the tooth crown formation, the molecular
biology of root development lags behind.
Progress in this areas is fundamental for achieving tooth
regeneration
ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH
EDITION
20XX
 Abnormalities of Morphodifferentiation:
Abnormalities in the differentiation of dental lamina & tooth germ
causes abnormalities in the
# Size
# Shape
# Number of teeth.
 Abnormalities of Histodifferentiation:
Abnormalities in the formation of dental hard
structure, results in disturbances in tooth
# Structure
Clinical significance of Bud stage of
tooth development
Macrodontia
Microdontia
105
MICRODONTIA

Smaller than normal

Boyle 1955 “ in general microdontia teeth are small,
crowns are short and normal contacts between teeth are
frequently misssing.

Ufomata 1988 it can be of whole crown , only crown or only roots
 Types:
(a) true
(b) relative generalized
(c) Involving single tooth - is common
 Maxillary laterals and third molars commonly affected
 Maxillary laterals – “peg laterals”
 Prevalence : 0.8 – 8.4% Neville 2005
1% - S. Patil 2013 ,
4.3% - MD Kathariya 2013
 Etiology : pitutary dwarfism ,
fanconi’s anemia ,
ulrich-turner’s sydrome ,
Occulo – mandibulo-facial
syndrome
 All teeth are smaller than
normal
 Occur in some cases of
pituitary dwarfism
 Exceedingly rare
 Teeth are well formed
(1) True Generalized
Microdontia
 Normal or slightly smaller than
normal teeth
 Are present in jaws that are
somewhat larger than normal
(2) Relative Generalized
Microdontia
 Common condition
 Affects most often maxillary
lateral incisior + 3rd
molar
 These 2 teeth are most often
congenitally missing
(3) Focal/Localized
Microdontia
 Sides converge or taper
together incisally
 Forms cone-shaped crown
 Root is frequently shorter
than usual
Clinical significance:
1) Spacing due to microdontia is disturbing cosmetically
2) Crown and bridge prosthetic work is required for esthetic
rehabilitation
3) If shapes are altered (peg laterals), immediate correction is
needed
4) Midline shift
5) Reduced overjet
6) Mesial movement of upper molars
MACRODONTIA
o Teeth which are larger than
normal.
o Also known as
MEGADONTIA.
o 3 types:
1. True Generalized
2. Relatively Generalized
3. Localized
113
Prevalence : 0.2 % Altug-Atac 2007 , Uslu O 2009
1.3% MD Kathariya 2013
0.2% S. Patil 2013
Etiology : Hereditary
klinefelter syndrome
Pitutary gigantism
Insulin resistant diabetis
Hemifacial hypertrophy
 All teeth are larger than
normal
 Associated with
pituitary gigantism
 Exceedingly rare
(1) True Generalized
Macrodontia
 Normal or slightly larger than
normal teeth in small jaws
 Results in crowding of teeth
 Insufficient arch space
(2) Relative Generalized
Macrodontia
 Uncommon condition
 Unknown etiology
 Usually seen with
mandibular 3rd
molars
(3) Focal/Localized
Macrodontia
Management
• Extraction
• Due to problems of eruption and tooth size
discrepancy
Case report
Isolated bilateral macrodontia of mandibular second
premolars :Acase report
Ebru Canoglu,harun Canoglu,AlperAktas,Zafer C.
Cehreli ; European Journal of Dentistry; July 2012 ; vol:6
Clinical significance of Initiation
and proliferation
120
Anodontia
Supernumerary
teeth
ANODONTIA
o Congenital absence of teeth
o Prevalence
1.6-9.6 Graber 1978
4.8% MD Kathariya 2013
4.9% S. Patil 2013
Female > male
o .
121
Etiology:
a. Hereditary factors.
b. Environmental factors.
c. Familial factors.
d. Syndrome associated.
e. Radiation injury to the developing tooth germ.
ANODONTIA
True Induced or false Pseudo
anodontia
anodontia anodontia
Total Partial
Hypodontia Oligodontia
TRUE ANODONTIA
o Congenital absence of teeth.
123
Total Anodontia
All teeth are missing.
Both deciduous &
permanent dentition.
Rare condition
Hereditary ectodermal
dysplasia.
Partial Anodontia
One or few teeth missing.
 Relatively common
condition
PARTIAL ANODONTIA
o Involves one or more teeth.
o Common condition.
o Maxillary lateral incisors, maxillary or mandibular 2nd
premolars, third molars.
124
Hypodontia
Lack of development of
one or more teeth
Oligodontia
Lack of development of
six or more teeth
 when teeth are absent
clinically because of
impaction or delayed
eruption
when teeth have been
exfoliated or extracted
Pseudoanodontia
False anodontia
 Prevalence of each teeth:-
 Congenitally missing teeth (% of affected cause)
Central Lateral Cuspids 1st
2nd
1st
2nd
total
incisor incisor premolar premolar molar molar
Maxilla 0.0 12.3 1.8 5.5 25.3 0.0 0.8 45.7
Mandible 2.2 1.1 0.0 3.0 47.3 0.0 0.7 54.3
- Out of 10000 children ( 6 to 15 years of age) examined, 340 exhibited
congenital absence of 709 teeth or tooth germs. 3rd
molars were not
studied.
- E Dolder : Deficient dentition. Dent Record, 57:142,1937.
Management:
- Partial dentures
- Fixed dental prosthesis
- Implants
Implant age selection
- Must be carefully selected
- Implant placement should postponed till permanent dentition
period ( Guckes 1991)
- Implants acts as ankylosed teeth and can affect growth of jaws
and change position accordingly. ( Imirzalioglu 2002 )
- Due to frequency of congenitally missing teeth it has been
postulated that humans are in intermediate stage of dentitional
evaluation.
- A dental formula of one incisor, one canine, one premolar & two
molars per quadrant has been proposed for the future.
( Dahlberg, A.A: The changing dentition in man. J.am Dent.
Assso. 32:676, 1945.)
SUPERNUMERARY TEETH
- A supernumerary tooth is one that is addition to the normal series
and can be found in almost any region of dental arch.
Prevalence: 0.8% primary dentition
2.1% permanent dentition ( brook 1974)
1.2 % S. Patil 2013
5.3% MD Kathariya 2013
Supernumerary deciduous teeth- male> female, maxillary anterior> mandibular
anterior.
Supernumerary permanent dentition- male> female, maxilla>mandible.
Etiology
1) Supernumerary teeth develop from a third tooth bud
2) Hyperactivity theory
3) Hereditary tendency
Supernumerary teeth may be :
- Single or multiple.
- Unilateral or bilateral.
- Erupted or impacted.
- One or both jaws.
Multiple supernumerary teeth are associated with condition like
Cleft lip and palate
Cleidocranial dysplasia
Gardner syndrome
Occasionally orofacialdigital syndrome
- Supernumerary teeth associated with cleft lip and palate result from
fragmentation of the dental lamina during cleft formation and not commonly
seen in the maxillary lateral incisor area.
Classification of supernumeraries.
Single Multiple
Conical Composite Tuberculate
Supplement
odontoma
Complex Compound
Non-syndrome syndrome
- Cleft lip & palate
- Cleidocranial
dysplasia
- Gardner
syndrome
Gravey , Barry , Blake J can Dent Assoc1999 ;65;612-6
CONICAL ( MESIODENS)
Rarely it can be present in between mandibular central
incisiors. ( Seema D bagle, shital DP Kiran non-syndromic
occurrence of true generalized microdontia with mandibular
mesiodens- a name case Head face medicine 2011; 7 ; 19.)
TUBERCULATE
- Often paired
- Commonly located on the palatal
aspect of central incisors.
-
SUPPLEMENTAL
- Duplication of teeth
- Maxillary lateral incisors >
Premolars & molars
- Primary dentition
FOURTH MOLAR
- Common in maxillary molar area.
-
DISOMOLAR/ DISTODENSE
Molar located distal to molar
PARAMOLARS
Clinical significance of Cap stage
of tooth development
 Crown
 Fusion
 Gemination
 Taurodontism
 Talon’s Cusp
 Dens evaginatus 136
 Crown
 Dens Invaginatus
 Peg-shaped Lateral
 Hutchinson Incisor
 Mulberry Molar
FUSION
 Fused teeth arise from union of
two normally separated tooth
germs
 If union occurs before
calcification – teeth completely
united
 If union occurs after calcification
– roots get fused
 Prevalence : Primary (2-3%) >
Permanent (1-2%)
(Graham & Granath)
Can occur between same
dentition or primary to
permanent dentition ( Caceda
1994)
 Fusion of primary teeth may lead to congenital
absence of permanent teeth
 Associated syndrome:
Solitary median maxillary central incisor syndrome
Management :
- Cause problems with spacing, alignment and
function.
- Mesiodistal disking
- Surgical extraction
Solitary median maxillary central incisor syndrome
 Very rare condition
 Present as single midline symmetrical maxillary
central incisor
 Due to mutation in SHH gene
Clinical implications:
1. Spacing or diastema
2. Periodontal complications
3. Crowding
4. Esthetic problems
CASE REPORT
Unilateral fusion of primary molars with the presence
of a succedenous supernumerary tooth : case report
Jorge Caceda; Curtis creath; Joe p Thomas; Pediatric
dentistry; Jan-Feb 1994; Volume: 16; num :1
GEMINATION
 Arise from attempt at division of single
tooth germ by invagination, resulting
incomplete formation of two teeth
 One structure with two completely /
incompletely separated crowns having
single root or root canal
 More in primary dentition
 “Twinning” – coined by Levitas 1965
“Production of equivalent structures
by division resulting in one normal &
one supernumerary tooth”.
Case Report
Twins on either side :Acase report of bilateral
Gemination
Prasanna kumar rao, Veena KM, Laxmikanth Chatra;
Scientific reports; 2012, vo :1;issue : 6
TAURODONTISM
o Originated by Sir Arthur Keith in 1913.
o Body of the tooth is enlarged at the expense of the
roots.
o ‘Bull- like’ teeth.
145
o Shaw classified into:
146
Hypotaurodont Mesotaurodont Hypertaurodont
Mildest form Moderate form • Extreme form
• Furcation occurs
near the apices of
the roots.
o Causes: (enumerated by Mangion)
a) Specialized or retrograde character.
b) Primitive pattern.
c) Mendelian recessive trait.
d) Atavistic feature.
e) Mutation resulting from odontoblastic deficiency
during dentinogenesis of roots.
 Failure of hertwig’s epithelial sheath to invaginate at
proper horizontal level. (Hammer & his associates)
147
o Clinical Features:
a) Either deciduous or permanent
dentition.
b) Molars
c) Unilateral or bilateral.
o Radiographic Features:
a) Involved teeth–- rectangular shape.
b) Pulp chamber–- extremely large–- much
greater apico-occlusal height.
c) Pulp lacks usual constriction
at cervical of tooth.
d) Roots–- exceedingly short
e) Furcation–- only few mm above the
apices of roots. 148
TALONS CUSP
o Anomalous structure.
o Resembles eagle’s talon.
o Projects lingually from the cingulum
area.
o Maxillary or Mandibular permanent
incisor.
o Composed of normal enamel &
dentin & contains a horn of pulp
tissue.
o Clinical problems include: esthetics,
caries control, occlusal 149
Prevalence : 0.06 - 7.7 % Maya S. 2007
- Three types :
Type 1 : Additional cusp from incisal edge to half
to CEJ
Type 2 : Semi talon, extends from incisal edge to
1mm past half of the CEJ.
Type 3 : Prominent enlarged cingulum.
- Clinical problems include esthetics, caries
control, occlusal accommodation.
o Treatment:
* Prophylactically restoring groove–- to
prevent caries.
* Occlusal interference–- it should be
removed, but exposure of pulp horn—endodontic
treatment.
Case report
 Talon’s cusp of anterior teeth : A Case report
Moksha Nayak,Jitendra kumar,Krishna
Prasad; Journal of Endodontology
SHOVEL-SHAPED TEETH
 Characterstic shape on lingual side
 Lingual side is deeply concave giving tooth appearance
of shovel
 Seen in chinese, japanese, eskimos, north/south american
indians
 Anterior maxilla
PARAMOLAR TUBERCLES / BOLK CUSP
 Genetic basis.
 Seen on buccal surface of mesiobuccal cusp in
permanent and deciduous teeth
 Vary in populations, never seen in negroes
 Observed in 31% of a group of Pima Indians.
( Dahlberg 1950)
DENS EVAGINATUS
o Occlusal Tuberculated Premolar
o Leong’s Premolar
o Evaginated Odontome
o Occlusal Enamel Pearl
o Prevalence : 2.2 % Yip 1974
o Appears clinically as an accessory
cusp or a globule of enamel.
o Occlusal surface between buccal &
lingual cusps of premolars.
o Unilaterally or bilaterally.
154
o Pathogenesis: proliferation & evagination of an area
of inner enamel epithelium & subjacent odontogenic
mesenchyme into dental organ during early tooth
development.
o Can cause:
* Incomplete eruption
* Displacement of teeth
* Pulp exposure
* Occlusal wear
* Fracture
155
DENS INVAGINATUS
o Dens In Dente
o Dilated Composite Odontome
o Developmental variation-- Invagination in the surface
of tooth crown before calcification has occurred.
o Etiology-
• Increased localized external pressure
• Focal growth retardation
• Focal growth stimulation in certain areas of tooth bud.
156
 depth varies from slight
enlargement of cingulum
to a deep infolding that
extends to apex
 historically, it has been
classified into 3 major types:
 Type I
 Type II
 Type III
 Type I
• confined to the crown
 Type II
• extends below cemento
enamel junction
• ends in a blind sac
• may or may not
communicate with
adjacent dental pulp
 Type III
• extends through the root
• perforates in the apical or
lateral radicular area
without any immediate
communication with pulp
o Permanent maxillary lateral incisor.
o Bilateral.
o Mild form: deep invagination in the
lingual pit area–- not evident
clinically.
o Radiographically- pear shaped
invagination of enamel & dentin.
o Severe form: invagination extends
nearly to the apex of the root.
o Can cause: caries, pulp infection,
premature loss of tooth.
o Treatment: prophylactic restoration.
160
 undersized lateral incisor
 smaller than normal
 occurs when permanent lateral
incisors do not fully develop
PEG SHAPED LATERALS
 characteristic of congenital
syphilis
 lateral incisors are peg-shaped
or screwdriver-shaped
 widely spaced
 notched at the end
 with a crescent-shaped
deformity
HUTCHINSON’S INCIORS
 notches on their biting
surfaces
 named after Sir Jonathan
Hutchinson
 English surgeon +
pathologist who 1st
described it
 Dental condition usually
associated with congenital
syphilis
 Characterized by multiple
rounded rudimentary enamel
cusps on permanent 1st
molars
MULBERRY MOLARS
 dwarfed molars with cusps
covered with globular enamel
growths
 giving the appearance of a
mulberry
 Root
 Concresence
 Enamel Pearl
 Dilaceration
 Flexion
 Ankylosis
Supernumerary roots
Shape and Form
 2 fully formed teeth
 Joined along the root surfaces
by cementum
 Noted more frequently in
posterior and maxillary regions
CONCRESCENCE
 Often involves a 2nd
molar
tooth in which its roots
closely approximate the
adjacent impacted 3rd
molar
 May occur before or after the
teeth have erupted
 Usually involves only 2 teeth
 Diagnosis can frequently be
established by
roentgenographic examination
 Often requires no therapy
unless union interferes with
eruption; then surgical
removal may be warranted
Since with fused teeth,
extraction of one may result in
extraction of the other
Case report
Concrescence in primary dentition:Acase report
Zakirulla Meer, N Rakesh;International journal of
clinical dental science;May 2011;2(2)
 Angulation or a sharp
bend or curve in root
or crown of a formed tooth
 Trauma to a developing
tooth can cause root to form
at an angle to normal
axis of tooth
 Rare deformity
DILACERATION
 Movement of crown or
of the crown and part of root
from remaining developing
root may result in sharp
angulation after tooth
completes development
 Hereditary factors are
believed to be involved
in small number of cases
 Eruption generally continues
without problems
Clinical significance:
 Radiographic examination is needed before
extraction as there are chances of root
fracture during extraction.
 Orthodontic tooth movement is affected
Clinical significance of Advanced bell stage of tooth
development
 Amelogenesis Imperfecta
 Enamel hypoplasia
 droplets of ectopic enamel
 or so called enamel pearls
 may occasionally be found on
roots of teeth
 uncommon, minor abnormalities,
which are formed on normal
teeth
ENAMEL PEARLS
 Occur most commonly in
bifurcation or trifurcation
of teeth
 May occur on single-rooted
premolar as well
 Maxillary molars are
commonly affected than
mandibular molars
 Consist of only a nodule
of enamel attached to dentin
 May have a core of dentin
containing pulp horn
 May be detected on
radiographic examination
 May cause stagnation at
gingival margin but, if they
contain pulp, this will
be exposed when pearl is
removed
Thank you
180
20XX
References
•ORBAN’S TEXTBOOK OF ORAL HISTOLOGY &
EMBRYOLOGY,GS KUMAR,13TH
EDITION, PG NO 45-68
•TEN CATES,TEXTBOOK OF ORAL HISTOLOGY,ANTONIO
NANCI,9TH
EDITION,CHP-DEVELOPMENT OF TOOTH AND
IT’S SUPPORTING STRUCTURES,PG NO 178-231
•SHAEFER’S TEXTOOK OF ORAL PATHOLOGY,R
RAJENDRA,7TH
EDITION,CHP- DEVELOPMENTAL
DISTURBANCES OF ORAL AND PERIORAL STRUCTURES,
PG NO 180-242
Thank you

dev of toothnvhgfghvgvgvgvnvnbnvbvn fin.pptx

  • 1.
    Title Author &journal Aim Material and Method Result Conclusion Epithelial rests of Malassez: from latent cells to active participation in orthodontic movement Bianca Silva e Silva ,1 Nathalia Caro lina Fernand es Fagundes ,1 Bárbara Cata rina Lima No gueira ,1 José Valladar es, Neto ,2 David Norma ndo ,3 and Rafael Rodrig ues Lima 1 The present literature review aims at presenting the potential functions of ERM, with emphasis on orthodontic movement and the functional structure of the periodontiu m. epithelial rests of Malassez (ERM) represent a group of cells in the periodontal ligament classically consisting of latent or quiescent structures associated with pathological processes. ERM cells have a functional activity in modulation of orthodontic movement, trough their potential for differentiati on, maintenanc e functions and the capacity of repairing periodontiu ERM cells have a functional activity in modulation of orthodontic movement, trough their potential for differentiatio n, maintenance functions and the capacity of repairing periodontiu m.
  • 3.
  • 4.
    20XX CONTENTS  INTRODUCTION  TOOTHDEVELOPMENT STAGES- • A) MORPHOLOGICAL- BUD STAGE CAP STAGE EARLY BELL STAGE ADVANCED BELL STAGE ROOT DEVELOPMENT • B) PHYSIOLOGIC- INITIATION PROLIFERATION HISTODIFFERENTIATION MORPHODIFFERENTIATION APPOSITION  MOLECULAR INSIGHTS IN TOOTH MORPHOGENESIS
  • 5.
    20XX INTRODUCTION • The primitiveoral cavity or stomodeum lined by stratified squamous epithelium is called oral ectoderm or primitive oral epithelium. • The oral ectoderm contacts the foregut to form the buccopharyngeal membrane. • At 27th day of gestation; the membrane ruptures and stomodeum ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH EDITION
  • 6.
    20XX PRIMARY EPITHELIAL BAND •2-3 weeks after the rupture of buccopharyngeal membrane, certain areas develop more rapidly than the adjacent cells • This leads to formation of primary epithelial band which appears in the space of future horse-shaped dental arches. ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH EDITION
  • 7.
    20XX • Each bandof primary epithelium divides by 7th week that quicky in- grows to form Dental lamina Vestibular lamina • The dental lamina arises early from the inner lingual process while the vestibular lamina arises from outer buccal aspect. ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH EDITION
  • 8.
    20XX CLINICAL SIGNIFICANCE OF PRIMARY EPITHELIALBAND • Initiation of tooth development starts with formation of placodes in the epithelial band • Dental placodes usually result in formation of different dental families ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH EDITION
  • 9.
    20XX • The balancebetween stimulatory factors (FGFs,WnTs) and inhibitory factors(BMP) must be maintained. Imbalance in these pathways may lead to Ectodermal Dysplasia characterized by oligodontia and misshapen teeth. ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH EDITION
  • 10.
    20XX DENTAL LAMINA • Primordiumfor the ectodermal portion of the deciduous teeth Decidious Dental lamina • 1st tooth to be initiated is deciduous mandibular central incisor( 6th week in utero) Successional Dental lamina • It is the lingual extension of dental lamina. • It develops from 5th month in utero (permanent central incior) upto 10th month of age( 2nd premolar) ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH EDITION
  • 11.
  • 12.
  • 14.
    20XX FATE OF DENTALLAMINA Dental lamina functions for a short period of time at any particular location. It degenerates rapidly once the tooth development starts. The total activity usually extends upto 5 years of age however it may still be active in 3rd molar region. Remnants of dental lamina persist as epithelial pearls or islands within jaw or gingiva. They are referred to as ”cell rest of serres” ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH EDITION
  • 15.
    20XX VESTIBULAR LAMINA • Labialor buccal to dental lamina • Also termed as “lip-furrow band” • Usually forms by around 6th week of development • It forms the vestibule. ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH EDITION
  • 16.
    20XX FORMATION OF VESTIBULE Vestibularlamina Proliferates into the ectomesenchyme Cells rapidly enlarge & degenerate Cleft – vestibule formation [Between alveolar portion of jaws and the lips / cheeks] ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH EDITION
  • 17.
    20XX INITIATION OF THETOOTH • Initiation of tooth development usually begins by interaction of epithelium of 1st arch with ectomesenchymal cells derived from neural crest cells. • However, by 12th day, 1st arch epithelium loses this potential and thereafter ectomesenchyme can elicit tooth formation from a variety of epithelia. ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH EDITION
  • 18.
    20XX •LHX-HOMEOBOX are theearliest mesenchymal markers for tooth development •The domain genes LH-6 and LH-7 appear as earliest by 9th day of gestation. •The expression of these genes result from signaling molecule ,Fibroblast growth factor-8 (FGF-8) derived from epithelium of 1st branchial arch ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH EDITION
  • 19.
    20XX DEVELOPMENTAL STAGES  MorphologicStages 1. Dental lamina 2. Bud stage 3. Cap stage 4. Bell stage – Early bell stage Late / advanced bell stage 5. Root formation ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH EDITION
  • 20.
    PHYSIOLOGIC STAGES 1.Initiation 2.Proliferation 3.Morphodifferentiatio n 4.Histodifferentiation 5.Apposition Click iconto add picture 20XX ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH EDITION
  • 21.
    20XX BUD STAGE • Dentallamina is separated from underlying ectomesenchyme- basement membrane. • With differentiation of dental lamina- round/ ovoid swellings- basement membrane at 10 points corresponding to future position of deciduous teeth- Primordia of Enamel organ (tooth bud) ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH EDITION
  • 22.
    20XX •Condensation of ectomesenchyme justbeneath the enamel organ- dental papilla. •Condensed ectomesenchyme that surrounds enamel organ & dental papilla- dental sac. • Both Dental papilla and Dental sac become more prominent in the subsequent stages of tooth development ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH EDITION
  • 23.
    20XX CAP STAGE • Toothbud continues to proliferate- does not expand uniformly- larger sphere. • Unequal growth- cap stage- shallow invagination on deep surface of bud. • Consist of: Outer enamel epithelium Stellate reticulum Inner enamel epithelium ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH EDITION
  • 24.
    20XX OUTER & INNERENAMEL EPITHELIUM • Inner enamel epithelial cells Seen in the concavity of the cap Tall columnar cells • Outer enamel epithelial cells Seen in the convexity of the cap Cuboidal cells ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH EDITION
  • 25.
    20XX ENAMEL ORGAN - -Composed of Peripheral low columnar cells Central polygonal cells ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH EDITION
  • 26.
    20XX • Hemidesmosomes anchor cellsto basal lamina. Enamel organ- double attachment of dental lamina to overlying epithelium enclosing ectomesenchyme- Enamel Niche • Appearance- funnel shaped depression of the dental lamina. ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH EDITION
  • 27.
    20XX STELLATE RETICULUM • Polygonalcells begin to separate due to water being drawn into the enamel organ from surrounding dental papilla. • Due to osmotic force exerted by glycosaminoglycans contained in the ground substance. • Cells separate but maintain contact with each other by their cytoplasmic process. • Star shape cells- cellular network- stellate ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH EDITIO
  • 28.
    20XX • Functions Cushion likeconsistency Acts as a shock absorber Supports and protects delicate enamel forming cells ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH EDITION
  • 29.
    20XX TRANSITORY STRUCTURES ENAMEL KNOT •It is formed by the cells in the centre of enamel organ which are densely packed. • It acts as a reservoir of cells for the growing enamel organ. ENAMEL CORD • It is the vertical extension of the enamel knot ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH EDITION
  • 30.
    20XX ENAMEL KNOT –SIGNALLINGCENTRE FOR TOOTH MORPHOGENESIS •It consists of cells that do not divide but promote the division of adjacent epithelial cells that form cervical loop and dental papilla. ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH EDITION
  • 31.
    20XX •BMP4 induces dentalpapilla cells to form odontoblasts. ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH EDITION •Although BMP-4 is the earliest marker to start signalling of enamel knot formation, it is not sufficient to induce other markers, i.e bmp-2, fgf-4.
  • 32.
    20XX ENAMEL SEPTUM • Whenthe enamel cord extends to meet the outer enamel epithelium, it divides the stellate reticulum in 2 parts. Hence, Enamel septum. ENAMEL NAVEL • The outer enamel epithelium shows a small depression at the point of meeting which resembles umbilicus .Hence, enamel navel • These structures disappear before enamel formation begins ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH EDITION
  • 33.
    20XX DENTAL PAPILLA • Presentunder the concavity of the enamel organ. • Is the condensed ectomesenchyme. • Formative organ of dentin and pulp. • Shows active budding of capillaries and mitotic figures. ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH EDITION
  • 34.
    20XX • Peripheral cellsof dental papilla- differentiates into odontoblast. • Basement membrane that separates enamel organ & dental papilla- membrana performativa
  • 35.
    20XX DENTAL SAC (Dentalfollicle) • Marginal condensation in the ectomesenchyme surrounding enamel organ and dental papilla. • Gradually a denser and more fibrous layer develops. • It forms the supporting structures namely periodontal ligament, ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH EDITION
  • 36.
    20XX EARLY BELL STAGE Invaginationof epithelium deepens, margins continue to grow- bell shape. Crown shape is determined. It was thought that the shape of crown is because of pressure exerted by Dental papilla on IEE. This pressure was shown to be opposed equally by fluid in stellate reticulum. Folding of enamel organ- different crown shape- differential rate of mitosis and differences in cell differentiation time. ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH EDITION
  • 37.
  • 38.
    20XX The IEE cellswhich lie in the region of future cusp tip or incisor region stop dividing earlier and differentiate first. The pressure exerted by continuous cell division on these cells from other areas cause these cells to be pushed in form of cusp-tip. The area between two cusps tips i.e. cuspal slopes extend and cusp height develops due to cell proliferation and differentiation . Cell differentiation progresses from incisor region to cervically.
  • 39.
    20XX • Bell stagecan be distinguished by 4 cell layers Inner enamel epithelium Stratum intermedium Stellate Reticulum Outer enamel epithelium • The junction between inner and outer enamel epithelium is called cervical loop and it is the area of intense mitotic activity.
  • 40.
    20XX INNER ENAMEL EPITHELIUM •Single layer of cell- differentiate prior to amelogenesis- tall columnar cells- ameloblasts. • These cells- 4-5μm in diameter & 40μm high. • These cells are attached to one another by junctional complexes and to stratum intermedium- desmosomes. • These cells exert an organized influence on the underlying mesenchymal cells which later differentiate into odontoblasts. ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH EDITION
  • 41.
    20XX STRATUM INTERMEDIUM • Fewlayers of squamous cells- between inner enamel epithelium and stellate reticulum. • Closely attached by desmosomes and gap junctions. • Well developed cytoplasmic organelles, acid mucopolysaccharides and glycogen deposits – indicate high metabolic activity. This layer is essential-enamel formation. ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH EDITION
  • 42.
    20XX OUTER ENAMEL EPITHELIUM •Cells flatten to low cuboidal. • At end of bell stage- initially smooth surface of OEE-laid in folds. • Rich nutritional supply to enamel organ • This would compensate for loss of nutritional supply owing to formation of mineralized dentin. ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH EDITION
  • 43.
    20XX DENTAL FOLLICLE • Beforeformation of dental tissues- circular arrangement & resembles capsular structure. • With development of root- fibers differentiate into PDL fibers- embedded in developing cementum & alveolar bone. ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH EDITION
  • 44.
    20XX ADVANCED/LATE BELL STAGE •Characterized by: mineralization & root formation. • Boundary between IEE & odontoblast- DEJ. • Formation of dentin- first- in region of future cusp & proceeds pulpally & apically. ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH EDITION
  • 45.
    20XX •After 1st layer ofdentin formation- ameloblast which has already differentiated from IEE – lay enamel over dentin. • Cervical portion of enamel organ- Hertwig’s epithelial root sheath. ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH EDITION
  • 46.
    20XX HERTWIG’S EPITHELIAL ROOT SHEATH •Outlines future root. • Responsible for the shape, length, size and number of roots. • Consists of inner and outer enamel epithelia only. ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH EDITION
  • 47.
    20XX • Does notinclude stellate reticulum and stratum intermedium. • The development of root begins only after enamel and dentin formation has reached future cementoenamel junction • Initiates root dentin formation. • Cells of inner enamel epithelia remain short and do not produce enamel. ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH EDITION
  • 48.
    20XX • Inner enamelepithelial cells induce differentiation of dental papilla cells into odontoblasts Odontoblasts form dentin Once dentin is laid down, HERS breaks down Remnants of HERS – cell rests of Malassez These are found in periodontal ligament of erupted teeth (network of strands/ clumps) ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH EDITION
  • 49.
    SINGLE ROOTED TOOTH •Prior to root formation- root sheath forms epithelial diaphragm. • Before root formation begins, outer and inner enamel epithelia bend at future CEJ in a horizontal plane. ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH EDITION
  • 50.
    20XX • The planeof this diaphragm remains fixed during development and growth of root. • Free end of diaphragm does not grow. Inner enamel epithelial cells of HERS have an organizing influence on dental papilla cells. Orban’s Oral Histology and Embryology- 14th edition, Ten Cate’s Oral Histology- 7th Edition
  • 51.
    • These differentiateinto odontoblasts which lay down dentin. • Once dentin is laid down, the dental sac proliferates and invades into HERS. • HERS breakdown into a network of epithelial strands. • Epithelium moves away from the dentinal surface. ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH EDITION
  • 52.
    20XX • Ectomesenchymal cellsof the dental sac come in contact with the freshly laid dentin. • They differentiate into cementoblasts, fibroblasts and osteoblasts to give rise to cementum, periodontal ligament and alveolar bone respectively. • Last stages - proliferation of epithelium of diaphragm lags behind that of pulpal connective tissue. • Apical foramen is further narrowed by apposition ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH EDITION
  • 53.
    20XX MULTI-ROOTED TEETH • Differentialgrowth of the epithelial diaphragm. • The number and position of these extensions depend on the number and type of root to be formed. • each extension develops as normal root. ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH EDITION
  • 54.
    20XX • Two extensions-Germof lower molar • and three extensions – Germ of upper molar. • On the pulpal aspect- dentin formation starts and on the outer extension develops as normal root. ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH EDITION
  • 55.
    • Enamel pearl •Accessory canal 03/29/2025 55 CLINICAL SIGNIFICANCE OF HERS
  • 56.
    20XX ENAMEL PEARL • Afterdentin is formed -HERS does not breakdown. • The inner enamel epithelial cells of HERS may differentiate into fully functional ameloblasts and form enamel. • Found in area of furcation of roots of permanent molars. ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH EDITION
  • 57.
    20XX ACCESSORY CANAL • HERSbreaks down before dentin is formed. • There is a defect in the dentinal wall of the pulp. • Any point on the root. ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH EDITION
  • 58.
  • 60.
  • 61.
  • 62.
    WHY DOES EACHTOOTH HAVE A PARTICULAR SHAPE 20XX • 8 Incisors. These flat, thin teeth designed for cutting and biting food • 4 Canines to grip, tear, and rip food. • 8 Molars These large teeth have broad, flat surfaces that make them the main teeth used for chewing and grinding food. • 8 Premolars Their flat surface and position allow you to grip, tear, chew, and grind the food. https://waldensquaredentalny.com/blog/teeth-shapes/
  • 63.
    FACTORS WHICH REGULATEDENTIN FORMATION • IGFs, TGFs, and BMPs These factors play a crucial role in dentin formation. The BMP family regulates processes like cell proliferation, migration, differentiation, and extracellular matrix remodeling. • Dentin sialoprotein and dentin phosphoprotein These proteins have different roles in dentin mineralization. • Dentin sialophosphoprotein (DSPP) This is a key non-collagenous protein (NCP) involved in tooth development and mineralization. • Cell junction related genes These genes include occludin (OCLN), claudin-1 (CLDN1), and zonula occludens-1/2 (Zo1/2). They play important roles in odontoblast differentiation. 20XX
  • 64.
    • Sclerostin This issecreted by odontoblasts and pulp cells and acts as a negative regulator of reparative dentin formation. • WNT signaling This is involved in the signaling pathway and also has an essential role in odontogenesis and dentin repair. • Fibroblast growth factor (FGF) This plays key roles in cell migration, proliferation, and differentiation during embryonic development and wound healing. These are critical drivers of the repair process and stimulate reparative dentin formation by odontoblasts. Odontoblasts are also called as Tomes's fibers 20XX
  • 65.
    STRUCTURES FORMED FROMTHE ENAMEL KNOT • The enamel knot is a signaling center of the tooth that provides positional information for tooth morphogenesis and regulates the growth of tooth cusps. • The enamel knot produces a range of molecular signals from all the major signaling families, such as Fibroblast Growth Factors (FGF), Bone morphogenetic proteins (BMP), Hedgehog (Hh) and Wnt signals. • These molecular signals direct the growth of the surrounding epithelium and ectomesenchyme. 20XX
  • 66.
    BLOOD SUPPLY OFAMELOBLASTS • As long as the ameloblasts are in contact with the dental papilla, they receive nutrient material from the blood vessels of the tissue, but due to formation of this dentin the original source of nutrition is cut off and the ameloblasts are supplied by capillaries penetrating the outer enamel epithelium. • This change in nutrition source is referred to as "reversal of nutrition". 20XX
  • 67.
  • 68.
    RADIX ENTOMOLARIS AND PARAMOLARIS Ifextra root on mandibular molars is located lingually called radix entomolaris (RE) or located buccally called radix paramolaris (RP). De Moor et al classified RE-based on the curvature in buccolingual orientation into three types.  Type I – Refers to a straight root/root canal.  Type II – Refers to an initially curved entrance which continues as a straight root/root canal.  Type III – Refers to an initial curve in the coronal third of the root canal and a second buccally oriented curve starting from middle to apical third. 20XX The Radix Entomolaris and Radix Paramolaris: An Endodontic Challenge
  • 69.
    Carlsen and Alexanderson describestwo different types of RP • Type A – Refers to an RP in which the cervical part is located on the mesial root complex • Type B – Refers to an RP in which the cervical part is located centrally, between the mesial and distal root complexes. 20XX The Radix Entomolaris and Radix Paramolaris: An Endodontic Challenge
  • 70.
    ODONTOMES • Odontomas arethe most common type of odontogenic tumors. They are included under the benign calcified odontogenic tumors. • The etiology behind odontomes remains unknown.5 It has been related to various pathological conditions, like local trauma, inflammatory and/or infectious processes, mature ameloblasts, cell rests of serres (dental lamina remnants) • There are two main types: compound and complex. 20XX ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH EDITION
  • 71.
    • A compoundodontoma consists of the four separate dental tissues (enamel, dentine, cementum and pulp) embedded in fibrous connective tissue and surrounded by a fibrous capsule. It may present a lobulated appearance where there is no definitive demarcation of separate tissues between the individual "toothlets" (or denticles). Compound odontomas are usually found in the anterior maxilla and are less than 20mm in diameter. • The complex type is unrecognizable as dental hard and soft tissues, usually presenting as a radioopaque area with varying densities indicating presence of enamel. It generally appears in the posterior 20XX ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH EDITION
  • 72.
    GLOBODONTIA • Globodontia isa rare dental condition that causes enlarged, bulbous crowns on primary canine and molar teeth. • It can occur in both primary and secondary teeth, but not incisors, which are normally the same size and shape. 20XX
  • 73.
    NERVE SUPPLY • Clusterof blood vessels starts ramifying around the tooth germ around the dental follicle and entering papilla during the cap stage. • Interestingly the vessels entering the papilla usually occupy the space where future root develops. • Pioneer nerve fibers approach the developing tooth during the bud-to cap stage of development. • These nerve fibres develop in dental follicle and they don’t encroach the enamel organ until dentinogenesis begins. • The pioneer nerve fibres are sensory in nature. 20XX Ten Cate’s Oral Histology- 7th Edition
  • 74.
    20XX INITIATION • It isa momentary event. • Potential for tooth formation lies in the dental lamina and associated tooth buds. • Different teeth are initiated at different times. • Initiation induction requires ectomesenchymal epithelial interaction. ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH EDITION
  • 75.
    Anomalies corresponding to Initiation/Budstage of tooth development • Anodontia • Supernumerary teeth • Microdontia • Macrodontia 20XX
  • 76.
    Anomalies corresponding toCap stage of tooth development • Gemination • Fusion • Dens Invaginatus • Dens Evaginatus • Talon’s Cusp 20XX
  • 77.
    Anomalies corresponding to Apposition •Enamel hypoplasia • Concrescence • Enamel Pearl 20XX
  • 78.
    Anomalies corresponding to Histodifferentiation •Amelogenesis Imperfecta • Dentinogenesis Imperfecta 20XX
  • 79.
    CLINICAL SIGNIFICANCE Lack ofinitiation. Single tooth (upper lateral incisors, lower second premolars & third molars)- commonly involved 20XX
  • 80.
  • 81.
    TYPES OF ANODONTIA •True Anodontia: Rare condition where all teeth are missing • Induced or False Anodontia: Result of extracting all teeth. • Pseudo Anodontia: Multiple unerupted teeth. ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH EDITION
  • 82.
    Etiology and Genetics: •Familial tendency for missing teeth is common. • Likely result of one or more point mutations in a polygenic system, often transmitted in an autosomal dominant pattern. • Other Factors: Cases of missing third molars might be an evolutionary trend. • X-ray radiation at an early age can cause teeth to be missing or deformed. 20XX ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH EDITION
  • 83.
    PROLIFERATION STAGE • Enhancedproliferative activity starts at the points of initiation. • Causes regular changes in size and proportions of the growing tooth germ. • Even during early part of this stage, the tooth shows potential to be highly developed. ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH EDITION
  • 84.
    20XX Histodifferentiation • Cells becomerestricted in their function. • The cells differentiate and give up their capacity to multiply- they assume new function. • Differentiation of epithelial cells is essential for differentiation of odontoblasts & initiation of dentin formation. ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH EDITION
  • 85.
    20XX CLINICAL SIGNIFICANCE • VitaminA deficiency- Ameloblast fails to differentiate- adjacent mesenchymal cells are disturbed- osteodentin. ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH EDITION • With the formation of dentin, IEE cells differentiate into ameloblasts and lay down enamel matrix.
  • 86.
    20XX • Dentinogenesis imperfecta (Hereditaryopalescent dentin) is a genetic disorder of tooth development • They cause teeth to appear discoloured as blue-green or yellow-brown and translucent. DENTINOGENESIS IMPERFECTA
  • 87.
    20XX MORPHODIFFERENTIATION • Basic formand relative size of future tooth is established - differential growth. • Morphodifferentiation is thus impossible without proliferation. • DEJ and CDJ are different and characteristic for each type of tooth ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH EDITION
  • 88.
    20XX APPOSITION • In thisstage there is deposition of matrix of dental hard tissues. • Appositional growth of enamel and dentin occurs by layer like deposition of an extracellular matrix. • Periods of activity and rest alternate at definite intervals during tooth formation. ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH EDITION
  • 89.
    20XX CLINICAL SIGNIFICANCE ENAMEL HYPOPLASIA •It may be defined as an incomplete or defective formation of the organic enamel matrix of teeth. • Two basic types of enamel hypoplasia exist: • (1) a hereditary type (2) a type induced by
  • 90.
  • 91.
    GEMINATION • Partial cleavageof a single tooth germ • Anomalous tooth • 2 partially Separated crowns and one root • Deciduous mandibular incisors and permanent maxillary incisors • Full Compliment number of teeth • Twinning is complete equal division of single tooth germ that results in one normal and one supernumerary tooth 20XX •SHAEFER’S TEXTOOK OF ORAL PATHOLOGY,R RAJENDRA,7TH EDITION,CHP- DEVELOPMENTAL DISTURBANCES OF ORAL AND PERIORAL STRUCTURES, PG NO 180-242
  • 92.
    FUSION • Union oftwo Adjacent normally separated tooth germs at the level of dentin during development. • It could be hereditary, trauma during development of teeth or physical force or pressure. • More in the primary dentition Affecting the incisors • Fusion can be complete or incomplete 20XX •SHAEFER’S TEXTOOK OF ORAL PATHOLOGY,R RAJENDRA,7TH EDITION,CHP- DEVELOPMENTAL DISTURBANCES OF ORAL AND PERIORAL STRUCTURES, PG NO 180-242
  • 93.
    CONCRESCENCE • Union ofroots of two or more completely formed teeth along the line of cementum • Deposition of Cementum after the root formation is complete • Limited only to roots • It could be due to traumatic injury, crowding of teeth, hypercementosis, which is associated with chronic inflammation • Clinical significance -difficulty in extraction in undiagnosed cases 20XX •SHAEFER’S TEXTOOK OF ORAL PATHOLOGY,R RAJENDRA,7TH EDITION,CHP- DEVELOPMENTAL DISTURBANCES OF ORAL AND PERIORAL STRUCTURES, PG NO 180-242
  • 94.
    TAURODONTISM • Crown portionis end up at the expanse of its root • This results in a large crown,short rudimentary root and an elongated pulp chamber • Multirooted permanent molars • Associated with Down syndrome, Klinefilter syndrome, amelogenesis imperfecta and hypodontia. • No treatment required but there is difficulty during root canal treatment. 20XX •SHAEFER’S TEXTOOK OF ORAL PATHOLOGY,R RAJENDRA,7TH EDITION,CHP- DEVELOPMENTAL DISTURBANCES OF ORAL AND PERIORAL STRUCTURES, PG NO 180-242
  • 95.
    20XX DENS-IN-DENTE (DENS- INVAGINATUS) • Representsa defect of tooth in which a focal area on the surface is folded or invaginated pulpally to a variable extent. • Defect is generally localised to a single tooth & interestingly maxillary lateral incisors are the most commonly affected. •SHAEFER’S TEXTOOK OF ORAL PATHOLOGY,R RAJENDRA,7TH EDITION,CHP- DEVELOPMENTAL DISTURBANCES OF ORAL AND PERIORAL STRUCTURES, PG NO 180-242
  • 96.
    Histological changes ofdens invaginatus include: • No irregularities in the dentin below invagination[10] • Strains of vital tissue or fine canals that communicates with the pulp could be found[10] • Enamel lining irregularly structured 20XX
  • 97.
    20XX DENS EVAGINATUS • Itis a condition found in teeth where the outer surface appears to form an extra bump or cusp. • Most affected tooth- lower premolar • There is a risk of dens evaginatus chipping off in normal function. • Hence this condition requires monitoring and it may need •SHAEFER’S TEXTOOK OF ORAL PATHOLOGY,R RAJENDRA,7TH EDITION,CHP- DEVELOPMENTAL DISTURBANCES OF ORAL AND PERIORAL STRUCTURES, PG NO 180-242
  • 98.
    20XX Talon’s cusp • Taloncusp also known as an “eagle’s talon” is an extra cusp on an anterior teeth. • Of all cases 55% occur on the permanent maxillary lateral incisor and 33% on permanent maxillary central incisor. •SHAEFER’S TEXTOOK OF ORAL PATHOLOGY,R RAJENDRA,7TH EDITION,CHP- DEVELOPMENTAL DISTURBANCES OF ORAL AND PERIORAL STRUCTURES, PG NO 180-242
  • 99.
    20XX • Whenever thereare deep developmental grooves present restorative treatment should be done to prevent the dental caries. • When talon cusp interferes with normal occlusion preventive care should be taken by performing endodontic treatment. •SHAEFER’S TEXTOOK OF ORAL PATHOLOGY,R RAJENDRA,7TH EDITION,CHP- DEVELOPMENTAL DISTURBANCES OF ORAL AND PERIORAL STRUCTURES, PG NO 180-242
  • 100.
    20XX DILACERATION • Dilaceration refersto an angulation or a sharp bend or curve anywhere along the root portion of tooth •SHAEFER’S TEXTOOK OF ORAL PATHOLOGY,R RAJENDRA,7TH EDITION,CHP- DEVELOPMENTAL DISTURBANCES OF ORAL AND PERIORAL STRUCTURES, PG NO 180-242
  • 101.
    20XX • Care shouldbe taken during extraction as these teeth are more prone to fracture. • It usually occurs because of trauma or any other defect of development which alter the angulation of tooth germ during root formation.
  • 102.
    20XX CONCLUSION A thorough understandingand sound knowledge of development of teeth is essential for a dentist since it forms the basis of dentistry Although there has been significant progress in understanding the tooth crown formation, the molecular biology of root development lags behind. Progress in this areas is fundamental for achieving tooth regeneration ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH EDITION
  • 103.
  • 104.
     Abnormalities ofMorphodifferentiation: Abnormalities in the differentiation of dental lamina & tooth germ causes abnormalities in the # Size # Shape # Number of teeth.  Abnormalities of Histodifferentiation: Abnormalities in the formation of dental hard structure, results in disturbances in tooth # Structure
  • 105.
    Clinical significance ofBud stage of tooth development Macrodontia Microdontia 105
  • 106.
    MICRODONTIA  Smaller than normal  Boyle1955 “ in general microdontia teeth are small, crowns are short and normal contacts between teeth are frequently misssing.  Ufomata 1988 it can be of whole crown , only crown or only roots  Types: (a) true (b) relative generalized (c) Involving single tooth - is common  Maxillary laterals and third molars commonly affected  Maxillary laterals – “peg laterals”
  • 107.
     Prevalence :0.8 – 8.4% Neville 2005 1% - S. Patil 2013 , 4.3% - MD Kathariya 2013  Etiology : pitutary dwarfism , fanconi’s anemia , ulrich-turner’s sydrome , Occulo – mandibulo-facial syndrome
  • 108.
     All teethare smaller than normal  Occur in some cases of pituitary dwarfism  Exceedingly rare  Teeth are well formed (1) True Generalized Microdontia
  • 109.
     Normal orslightly smaller than normal teeth  Are present in jaws that are somewhat larger than normal (2) Relative Generalized Microdontia
  • 110.
     Common condition Affects most often maxillary lateral incisior + 3rd molar  These 2 teeth are most often congenitally missing (3) Focal/Localized Microdontia
  • 111.
     Sides convergeor taper together incisally  Forms cone-shaped crown  Root is frequently shorter than usual
  • 112.
    Clinical significance: 1) Spacingdue to microdontia is disturbing cosmetically 2) Crown and bridge prosthetic work is required for esthetic rehabilitation 3) If shapes are altered (peg laterals), immediate correction is needed 4) Midline shift 5) Reduced overjet 6) Mesial movement of upper molars
  • 113.
    MACRODONTIA o Teeth whichare larger than normal. o Also known as MEGADONTIA. o 3 types: 1. True Generalized 2. Relatively Generalized 3. Localized 113
  • 114.
    Prevalence : 0.2% Altug-Atac 2007 , Uslu O 2009 1.3% MD Kathariya 2013 0.2% S. Patil 2013 Etiology : Hereditary klinefelter syndrome Pitutary gigantism Insulin resistant diabetis Hemifacial hypertrophy
  • 115.
     All teethare larger than normal  Associated with pituitary gigantism  Exceedingly rare (1) True Generalized Macrodontia
  • 116.
     Normal orslightly larger than normal teeth in small jaws  Results in crowding of teeth  Insufficient arch space (2) Relative Generalized Macrodontia
  • 117.
     Uncommon condition Unknown etiology  Usually seen with mandibular 3rd molars (3) Focal/Localized Macrodontia
  • 118.
    Management • Extraction • Dueto problems of eruption and tooth size discrepancy
  • 119.
    Case report Isolated bilateralmacrodontia of mandibular second premolars :Acase report Ebru Canoglu,harun Canoglu,AlperAktas,Zafer C. Cehreli ; European Journal of Dentistry; July 2012 ; vol:6
  • 120.
    Clinical significance ofInitiation and proliferation 120 Anodontia Supernumerary teeth
  • 121.
    ANODONTIA o Congenital absenceof teeth o Prevalence 1.6-9.6 Graber 1978 4.8% MD Kathariya 2013 4.9% S. Patil 2013 Female > male o . 121 Etiology: a. Hereditary factors. b. Environmental factors. c. Familial factors. d. Syndrome associated. e. Radiation injury to the developing tooth germ.
  • 122.
    ANODONTIA True Induced orfalse Pseudo anodontia anodontia anodontia Total Partial Hypodontia Oligodontia
  • 123.
    TRUE ANODONTIA o Congenitalabsence of teeth. 123 Total Anodontia All teeth are missing. Both deciduous & permanent dentition. Rare condition Hereditary ectodermal dysplasia. Partial Anodontia One or few teeth missing.  Relatively common condition
  • 124.
    PARTIAL ANODONTIA o Involvesone or more teeth. o Common condition. o Maxillary lateral incisors, maxillary or mandibular 2nd premolars, third molars. 124 Hypodontia Lack of development of one or more teeth Oligodontia Lack of development of six or more teeth
  • 125.
     when teethare absent clinically because of impaction or delayed eruption when teeth have been exfoliated or extracted Pseudoanodontia False anodontia
  • 126.
     Prevalence ofeach teeth:-  Congenitally missing teeth (% of affected cause) Central Lateral Cuspids 1st 2nd 1st 2nd total incisor incisor premolar premolar molar molar Maxilla 0.0 12.3 1.8 5.5 25.3 0.0 0.8 45.7 Mandible 2.2 1.1 0.0 3.0 47.3 0.0 0.7 54.3 - Out of 10000 children ( 6 to 15 years of age) examined, 340 exhibited congenital absence of 709 teeth or tooth germs. 3rd molars were not studied. - E Dolder : Deficient dentition. Dent Record, 57:142,1937.
  • 127.
    Management: - Partial dentures -Fixed dental prosthesis - Implants Implant age selection - Must be carefully selected - Implant placement should postponed till permanent dentition period ( Guckes 1991) - Implants acts as ankylosed teeth and can affect growth of jaws and change position accordingly. ( Imirzalioglu 2002 )
  • 128.
    - Due tofrequency of congenitally missing teeth it has been postulated that humans are in intermediate stage of dentitional evaluation. - A dental formula of one incisor, one canine, one premolar & two molars per quadrant has been proposed for the future. ( Dahlberg, A.A: The changing dentition in man. J.am Dent. Assso. 32:676, 1945.)
  • 129.
    SUPERNUMERARY TEETH - Asupernumerary tooth is one that is addition to the normal series and can be found in almost any region of dental arch. Prevalence: 0.8% primary dentition 2.1% permanent dentition ( brook 1974) 1.2 % S. Patil 2013 5.3% MD Kathariya 2013 Supernumerary deciduous teeth- male> female, maxillary anterior> mandibular anterior. Supernumerary permanent dentition- male> female, maxilla>mandible.
  • 130.
    Etiology 1) Supernumerary teethdevelop from a third tooth bud 2) Hyperactivity theory 3) Hereditary tendency Supernumerary teeth may be : - Single or multiple. - Unilateral or bilateral. - Erupted or impacted. - One or both jaws.
  • 131.
    Multiple supernumerary teethare associated with condition like Cleft lip and palate Cleidocranial dysplasia Gardner syndrome Occasionally orofacialdigital syndrome - Supernumerary teeth associated with cleft lip and palate result from fragmentation of the dental lamina during cleft formation and not commonly seen in the maxillary lateral incisor area.
  • 132.
    Classification of supernumeraries. SingleMultiple Conical Composite Tuberculate Supplement odontoma Complex Compound Non-syndrome syndrome - Cleft lip & palate - Cleidocranial dysplasia - Gardner syndrome Gravey , Barry , Blake J can Dent Assoc1999 ;65;612-6
  • 133.
    CONICAL ( MESIODENS) Rarelyit can be present in between mandibular central incisiors. ( Seema D bagle, shital DP Kiran non-syndromic occurrence of true generalized microdontia with mandibular mesiodens- a name case Head face medicine 2011; 7 ; 19.) TUBERCULATE - Often paired - Commonly located on the palatal aspect of central incisors.
  • 134.
    - SUPPLEMENTAL - Duplication ofteeth - Maxillary lateral incisors > Premolars & molars - Primary dentition FOURTH MOLAR - Common in maxillary molar area. -
  • 135.
    DISOMOLAR/ DISTODENSE Molar locateddistal to molar PARAMOLARS
  • 136.
    Clinical significance ofCap stage of tooth development  Crown  Fusion  Gemination  Taurodontism  Talon’s Cusp  Dens evaginatus 136
  • 137.
     Crown  DensInvaginatus  Peg-shaped Lateral  Hutchinson Incisor  Mulberry Molar
  • 138.
    FUSION  Fused teetharise from union of two normally separated tooth germs  If union occurs before calcification – teeth completely united  If union occurs after calcification – roots get fused  Prevalence : Primary (2-3%) > Permanent (1-2%) (Graham & Granath) Can occur between same dentition or primary to permanent dentition ( Caceda 1994)
  • 139.
     Fusion ofprimary teeth may lead to congenital absence of permanent teeth  Associated syndrome: Solitary median maxillary central incisor syndrome Management : - Cause problems with spacing, alignment and function. - Mesiodistal disking - Surgical extraction
  • 140.
    Solitary median maxillarycentral incisor syndrome  Very rare condition  Present as single midline symmetrical maxillary central incisor  Due to mutation in SHH gene
  • 141.
    Clinical implications: 1. Spacingor diastema 2. Periodontal complications 3. Crowding 4. Esthetic problems
  • 142.
    CASE REPORT Unilateral fusionof primary molars with the presence of a succedenous supernumerary tooth : case report Jorge Caceda; Curtis creath; Joe p Thomas; Pediatric dentistry; Jan-Feb 1994; Volume: 16; num :1
  • 143.
    GEMINATION  Arise fromattempt at division of single tooth germ by invagination, resulting incomplete formation of two teeth  One structure with two completely / incompletely separated crowns having single root or root canal  More in primary dentition  “Twinning” – coined by Levitas 1965 “Production of equivalent structures by division resulting in one normal & one supernumerary tooth”.
  • 144.
    Case Report Twins oneither side :Acase report of bilateral Gemination Prasanna kumar rao, Veena KM, Laxmikanth Chatra; Scientific reports; 2012, vo :1;issue : 6
  • 145.
    TAURODONTISM o Originated bySir Arthur Keith in 1913. o Body of the tooth is enlarged at the expense of the roots. o ‘Bull- like’ teeth. 145
  • 146.
    o Shaw classifiedinto: 146 Hypotaurodont Mesotaurodont Hypertaurodont Mildest form Moderate form • Extreme form • Furcation occurs near the apices of the roots.
  • 147.
    o Causes: (enumeratedby Mangion) a) Specialized or retrograde character. b) Primitive pattern. c) Mendelian recessive trait. d) Atavistic feature. e) Mutation resulting from odontoblastic deficiency during dentinogenesis of roots.  Failure of hertwig’s epithelial sheath to invaginate at proper horizontal level. (Hammer & his associates) 147
  • 148.
    o Clinical Features: a)Either deciduous or permanent dentition. b) Molars c) Unilateral or bilateral. o Radiographic Features: a) Involved teeth–- rectangular shape. b) Pulp chamber–- extremely large–- much greater apico-occlusal height. c) Pulp lacks usual constriction at cervical of tooth. d) Roots–- exceedingly short e) Furcation–- only few mm above the apices of roots. 148
  • 149.
    TALONS CUSP o Anomalousstructure. o Resembles eagle’s talon. o Projects lingually from the cingulum area. o Maxillary or Mandibular permanent incisor. o Composed of normal enamel & dentin & contains a horn of pulp tissue. o Clinical problems include: esthetics, caries control, occlusal 149
  • 150.
    Prevalence : 0.06- 7.7 % Maya S. 2007 - Three types : Type 1 : Additional cusp from incisal edge to half to CEJ Type 2 : Semi talon, extends from incisal edge to 1mm past half of the CEJ. Type 3 : Prominent enlarged cingulum. - Clinical problems include esthetics, caries control, occlusal accommodation. o Treatment: * Prophylactically restoring groove–- to prevent caries. * Occlusal interference–- it should be removed, but exposure of pulp horn—endodontic treatment.
  • 151.
    Case report  Talon’scusp of anterior teeth : A Case report Moksha Nayak,Jitendra kumar,Krishna Prasad; Journal of Endodontology
  • 152.
    SHOVEL-SHAPED TEETH  Charactersticshape on lingual side  Lingual side is deeply concave giving tooth appearance of shovel  Seen in chinese, japanese, eskimos, north/south american indians  Anterior maxilla
  • 153.
    PARAMOLAR TUBERCLES /BOLK CUSP  Genetic basis.  Seen on buccal surface of mesiobuccal cusp in permanent and deciduous teeth  Vary in populations, never seen in negroes  Observed in 31% of a group of Pima Indians. ( Dahlberg 1950)
  • 154.
    DENS EVAGINATUS o OcclusalTuberculated Premolar o Leong’s Premolar o Evaginated Odontome o Occlusal Enamel Pearl o Prevalence : 2.2 % Yip 1974 o Appears clinically as an accessory cusp or a globule of enamel. o Occlusal surface between buccal & lingual cusps of premolars. o Unilaterally or bilaterally. 154
  • 155.
    o Pathogenesis: proliferation& evagination of an area of inner enamel epithelium & subjacent odontogenic mesenchyme into dental organ during early tooth development. o Can cause: * Incomplete eruption * Displacement of teeth * Pulp exposure * Occlusal wear * Fracture 155
  • 156.
    DENS INVAGINATUS o DensIn Dente o Dilated Composite Odontome o Developmental variation-- Invagination in the surface of tooth crown before calcification has occurred. o Etiology- • Increased localized external pressure • Focal growth retardation • Focal growth stimulation in certain areas of tooth bud. 156
  • 157.
     depth variesfrom slight enlargement of cingulum to a deep infolding that extends to apex  historically, it has been classified into 3 major types:  Type I  Type II  Type III
  • 158.
     Type I •confined to the crown  Type II • extends below cemento enamel junction • ends in a blind sac • may or may not communicate with adjacent dental pulp
  • 159.
     Type III •extends through the root • perforates in the apical or lateral radicular area without any immediate communication with pulp
  • 160.
    o Permanent maxillarylateral incisor. o Bilateral. o Mild form: deep invagination in the lingual pit area–- not evident clinically. o Radiographically- pear shaped invagination of enamel & dentin. o Severe form: invagination extends nearly to the apex of the root. o Can cause: caries, pulp infection, premature loss of tooth. o Treatment: prophylactic restoration. 160
  • 161.
     undersized lateralincisor  smaller than normal  occurs when permanent lateral incisors do not fully develop PEG SHAPED LATERALS
  • 162.
     characteristic ofcongenital syphilis  lateral incisors are peg-shaped or screwdriver-shaped  widely spaced  notched at the end  with a crescent-shaped deformity HUTCHINSON’S INCIORS
  • 163.
     notches ontheir biting surfaces  named after Sir Jonathan Hutchinson  English surgeon + pathologist who 1st described it
  • 164.
     Dental conditionusually associated with congenital syphilis  Characterized by multiple rounded rudimentary enamel cusps on permanent 1st molars MULBERRY MOLARS
  • 165.
     dwarfed molarswith cusps covered with globular enamel growths  giving the appearance of a mulberry
  • 166.
     Root  Concresence Enamel Pearl  Dilaceration  Flexion  Ankylosis Supernumerary roots Shape and Form
  • 167.
     2 fullyformed teeth  Joined along the root surfaces by cementum  Noted more frequently in posterior and maxillary regions CONCRESCENCE
  • 168.
     Often involvesa 2nd molar tooth in which its roots closely approximate the adjacent impacted 3rd molar  May occur before or after the teeth have erupted  Usually involves only 2 teeth
  • 169.
     Diagnosis canfrequently be established by roentgenographic examination  Often requires no therapy unless union interferes with eruption; then surgical removal may be warranted Since with fused teeth, extraction of one may result in extraction of the other
  • 170.
    Case report Concrescence inprimary dentition:Acase report Zakirulla Meer, N Rakesh;International journal of clinical dental science;May 2011;2(2)
  • 171.
     Angulation ora sharp bend or curve in root or crown of a formed tooth  Trauma to a developing tooth can cause root to form at an angle to normal axis of tooth  Rare deformity DILACERATION
  • 172.
     Movement ofcrown or of the crown and part of root from remaining developing root may result in sharp angulation after tooth completes development
  • 173.
     Hereditary factorsare believed to be involved in small number of cases  Eruption generally continues without problems
  • 174.
    Clinical significance:  Radiographicexamination is needed before extraction as there are chances of root fracture during extraction.  Orthodontic tooth movement is affected
  • 175.
    Clinical significance ofAdvanced bell stage of tooth development  Amelogenesis Imperfecta  Enamel hypoplasia
  • 176.
     droplets ofectopic enamel  or so called enamel pearls  may occasionally be found on roots of teeth  uncommon, minor abnormalities, which are formed on normal teeth ENAMEL PEARLS
  • 177.
     Occur mostcommonly in bifurcation or trifurcation of teeth  May occur on single-rooted premolar as well  Maxillary molars are commonly affected than mandibular molars
  • 178.
     Consist ofonly a nodule of enamel attached to dentin  May have a core of dentin containing pulp horn  May be detected on radiographic examination
  • 179.
     May causestagnation at gingival margin but, if they contain pulp, this will be exposed when pearl is removed
  • 180.
  • 181.
    20XX References •ORBAN’S TEXTBOOK OFORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH EDITION, PG NO 45-68 •TEN CATES,TEXTBOOK OF ORAL HISTOLOGY,ANTONIO NANCI,9TH EDITION,CHP-DEVELOPMENT OF TOOTH AND IT’S SUPPORTING STRUCTURES,PG NO 178-231 •SHAEFER’S TEXTOOK OF ORAL PATHOLOGY,R RAJENDRA,7TH EDITION,CHP- DEVELOPMENTAL DISTURBANCES OF ORAL AND PERIORAL STRUCTURES, PG NO 180-242
  • 182.

Editor's Notes

  • #121 Ectodermal dysplasia
  • #123 Hereditary ectodermal dysplasia
  • #145 Klinefelters syndrome Ectodermal dysplasia Tricho-dento osseous syndrome
  • #148 Permanent tooth involvement is more Rather than taper toward the roots. No special treatment
  • #149 Developmental groove * developmental retardation, broad thumbs, great toes, characteristic facial features.
  • #156 Tooth within a tooth