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.
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.
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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
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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.
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• 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
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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.
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• 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
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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
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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
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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
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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
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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
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•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
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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
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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
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•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
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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
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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
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ENAMEL ORGAN -
-Composed of
Peripheral low columnar
cells
Central polygonal cells
ORBAN’S TEXTBOOK OF ORAL HISTOLOGY & EMBRYOLOGY,GS KUMAR,13TH
EDITION
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• 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
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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
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• 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
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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
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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
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•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.
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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
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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
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• 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
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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
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
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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
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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.
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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
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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
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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
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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
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• 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.
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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.
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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
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
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
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.
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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
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
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
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”
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
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
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
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.
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.
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.
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
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
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