Growth&development of tooth / orthodontics courses

GROWTH
AND
DEVELOPMENT OF TOOTH
INDIAN DENTAL ACADEMY
Leader in continuing Dental Education
www.indiandentalacademy.com

CONTENTS
• Introduction.
• Definition of Growth & Development.
• Formation of Dental lamina.
• Developmental stages of tooth.
• Factors affecting growth & development.
• Developmental anomalies.
• Refrences.

According to Todd.
Growth refers to an increase in number and size.
Development refers to an increase in complexity and maturity.
Growth may be defined as an increase in weight and spatial
dimensions that an organism or organ goes through.
For growth to occur, three things must happen:
(1) increase in number of cells,
(2) increase in size of cells,
(3) increase in the product of the cells.
Development is an organism or organ going toward maturity.

GROWTH DEVELOPMENT
It is a part of developmental
process. Development in its
quantitative aspect is termed as
growth.
Growth is cellular . It takes place
due to the multiplication of cells.
Growth does not continue
throughout life. It stops when
maturity has been attained.
Growth may or may not bring
development
It is a comprehensive and wider
term and refers to overall changes
in the individual.
Development is organizational.
It is organization of all the parts
which growth and differentiation
have produced.
Development is a wider and
comprehensive term and refers to
overall changes in the individual. It
continues throughout life and is
progressive
 Development is also possible
without growth.www.indiandentalacademy.com

Stages in tooth development
Histo physiology & clinical
considerations
PHYSIOLOGICAL STAGES
• Initiation.
• Proliferation.
• Histo differentiation
• Morpho differentiation
• Apposition
MORPHOLOGICAL STAGES
•Dental lamina
•Bud stage.
•Cap stage:
•Bell Stage:
early.
advanced.

Tooth Development
• Initiation of tooth Development.
• Stages of Tooth Development.

Primary epithelial band formation:
• After about 37th days of gestation, continuous horse
shoe shaped bands around mouth in presumptive
upper & lower jaw are formed known as primary
epithelial band.

• The formation of these thickened epithelial bands is
result of increased proliferation activity within
epithelium as of a change in orientation of mitotic
spindle & cleavage of dividing cells.

Dental lamina & vestibule formation:
• Primary epithelial band quickly divides into subdivisions
Dental lamina just behind vestibular.A
Vestibular lamina or lip furrow band.B

Vestibular lamina:
• It proliferates into underlying mesenchyme.
• The cells enlarge ,then degenerate to form cleft
that becomes vestibule between cheek & tooth
bearing area.

• In Primary epithelial band, certain
areas of the basal cells proliferate
more rapidly than the cells of the
adjacent areas resulting in
formation of Dental lamina.
• It is seen at the site of future
deciduous teeth.
• Serves as primodium for
ectodermal component of
deciduous tooth.
Dental lamina :

• Later during development of
jaws ,permanent molars arise
directly from distal extension
of dental lamina.
1st permanent molar at
about 4th month in utero.
2nd permanent molar
initiated at about 1st year after
birth.
3rd permanent molar at
about 4th or 5th year.

• The other permanent teeth
develop from lingual
extension of free end of
dental lamina (known as
succesional lamina)
opposite to the enamel
organ of deciduous tooth.
• They develop from 5th
month in utero
(permanent central incisor)
to 10th month of age (2nd
premolar).

• Total activity of dental lamina
extends over a period of 5 yrs.
After which it begins to
degenerate .
• Dental lamina may be still active
in 3rd molar region after it has
disappeared elsewhere.
• Remnants of dental lamina
persist as epithelial pearls or
islands within the jaw as well as
in gingiva (Epithelial rests of
serre).
Fate of dental lamina:

STAGES OF DEVELOPMENT
• At certain point along
dental lamina,ectodermal
cells multiply still more
rapidly to form knob like
structures that grow into
underlying mesenchyme
called enamel organ.
ENAMEL ORGAN

As cell proliferation continues, each enamel
organ increases in size & change in shape. On
the basis of change in shape ,tooth
development is further divided into following
stages:
1. Bud Stage
2. Cap stage
3. Bell stage

STAGES OF DEVELOPMENT

Bud stage
• Enamel organ
differentiate into round or
ovoid swelling called
tooth bud.
• Enamel organ at this stage
consists of:
1.Peripherally located low
columnar cells.
2.Centrally located
polygonal cells
• Epithelium of dental
lamina is separated from
underlying mesenchyme
by a basement
membrane.
TOOTH BUD
TOOTH BUD

• A Ectomesnchymal condensation just below enamel organ
is known as dental papilla. It forms future dentin & pulp.
• B Ectomesnchymal condensation that surrounds tooth
bud & dental papilla is known as dental sac. It forms future
cementum & periodontal ligament.
Dental papilla & dental sac are not well defined in this
stage.
Ectomesnchymal condensation
A B

As the tooth bud continues to proliferates, it
does not expand uniformly into a large sphere.
Instead tooth bud leads to the cap shape which
is characterised by shallow invagination on
deeper surface of the bud.
Cap Stage

At this stage , tooth
germ consists of:
 Outer Enamel
epithelium,
 Inner enamel
epithelium,
 Stellate Reticulum,
 Dental papilla,
 Dental sac,

Outer Enamel epithelium cover convexity of cap. These cells
are cuboidal in shape. They are separated from dental sac &
inner enamel epithelium from dental papilla by a delicate
basement membrane.
Inner enamel epithelium covers concavity & are columnar in
shape.
Stellate reticulum consists of polygonal cells located
between inner & outer enamel epithelium which separate
from one another as more & more intracellular fluid
accumulates to form branched reticular pattern.
They give a cushioning consistency that may support &
protect delicate enamel forming cells.www.indiandentalacademy.com

Enamel Niche:
• Apparent structure created
during histological preparation
due to the sheet like structure
of dental lamina.
• Appears like a concavity
filled with connective tissue
and gives a impression of that
the tooth-germ has a double
attachment to the oral
epithelium.
Enamel Niche
Enamel Niche

Dental papilla:
• Under the influence of proliferating
epithelium of enamel organ &
ectomesenchyme (to a less
extent), gets enclosed by
invaginated portion of inner
enamel epithelium & condense to
form dental papilla.
• The papilla shows active budding of
capillaries & mitotic figures.
Dental sac :
•Formed by ectomesnchymal
condensation surrounding enamel
organ & dental papilla.
•Gradually this zone becomes dense
& more fibrous.
Dental sac

BELL STAGE
• As the invagination of epithelium deepens & its
margins continue to grow ,enamel organ
assumes bell shape .
• Early bell stage
• Advanced bell stage

• Inner enamel epithelium
• Outer enamel epithelium
• Stratum Intermedium
• Stellate reticulum
• Cervical loop or zone of
reflexion
• Dental Papilla
• Dental Sac
Early Bell Stage:

Inner enamel epithelium:
• Consists tall columnar cells about 4 to 5 microns in
diameter & about 40 microns .
• Contains nucleus away from basement membrane.
• Nucleus/cytoplasmic ratio is high.
• Characterised by high glycogen content.
• Cytoplasm contains free ribosomes ,a few RER ,some
mitochondria & few scattered tonofilaments.
• Separated from dental papilla by basement membrane.

Inner enamel epitheliumwww.indiandentalacademy.com

Stratum Intermedium:
• A few layers of sqamous cells form stratum
intermedium between inner enamel epithelium &
stellate reticulum.
• The well developed cytoplasmic organelles, acid
mucopolysacharides, alkaline phosphatase & glycogen
deposits indicate a high degree of metabolic activity.
• This layer seems to be essential for enamel formation.

Stratum
Intermedium
Stellate reticulum
Inner enamel
epithelium
Dental Papilla

• Expand further mainly by an
increase in amount of
intracellular fluid.
• Cells are star shaped &
attached to one another & to
outer enamel epithelium and
stratum intermedium by
desmosomes.
• Contains sparsely distributed
organelle in cytoplasm.
Stellate Reticulum :

• Consists of low cuboidal
epithelial cells.
• Supported by basement
membrane around its
periphery.
• Rich glycogen and
cytoplasmic organelle.
• High nuclear cytoplasmic
ratio.
Outer Enamel Epithelium:

• Dental papilla consists of undifferentiated
mesenchymal cells & fine scattered collagen
fibrils scattered throughout extracellular space.
• Nerves & vessels are also seen.
• It is separated from dental organ by a basement
membrane.
Dental Papilla:

•Consists of undifferentiated mesenchymal
cells & circularly arranged collagen fibrils
around enamel organ & dental papilla.
•Collagen fibrils are more in dental sac than
dental papilla.
•Nerves & vessels are also seen.
Dental Sac:

• Consists of only outer & inner enamel
epithelium.
• This is the point where cells continue to
divide until tooth attains its full size &
which after crown formation gives rise to
epithelial component of root formation.
Cervical loop or zone of reflexion :

Advanced Bell Stage:
• Separation of tooth germ from Dental Lamina.
• Root formation.
• Morphogenesis of crown.

Dental lamina joined tooth
germ to oral epithelium,
breaks into discrete
islands of epithelial cells,
and separate developing
tooth germ from oral
epithelium.
Separation of tooth germ from Dental Lamina:
Dental Lamina
Enamel Organ

Morphogenesis of crown:
• When tooth germ is growing rapidly during cap to bell
stage, cell division occurs throughout inner enamel
epithelium.
• As division continues, division ceases at a particular point
because cells are beginning to differentiate & assume their
eventual functioning of producing enamel.
• The point at which inner enamel epithelium
differentiation occurs first represent the site of future cusp
or growth center.

• Because inner enamel epithelium is constrained between
cervical loop & cusp tips ,continued proliferation causes the
inner dental epithelium to buckle & form cuspal outline.
• Thus future cusp is pushed towards outer dental
epithelium
• Inner dental epithelium completes its folding making it
possible to recognize shape of future crown pattern of tooth.
• Eventually differentiation of inner enamel epithelium &
dental papilla seeps down & is followed by dentin & enamel
formation. www.indiandentalacademy.com

Root Formation
• It begins after enamel &
dentin formation has
reached cemento enamel
junction.
• The enamel organ plays
important role by forming
Hertwig’s epithelial root
sheath.
• It is formed by proliferation
of cervical loop cells .
• It consists of only inner &
outer enamel epithelium.
• It molds the shape of root &
initiate radicular dentin
formation.

• When dentin is formed ,it
looses its structural integrity.
• This loss of structural integrity
is as a result of invasion of
surrounding connective tissue
of dental sac.
• The epithelium is moved away
from surface of dentin so that
connective tissue cells come
into contact with outer surface
dentin & differentiate into
cementoblasts that deposit a
layer of cementum onto surface
of dentin.

• Remnants of Hertwig’s
epithelial root sheath
are found in
periodontal ligament &
are called Cell Rests of
Malassez .
Cell Rests
of
Malassez

• Prior to the beginning of root formation ,epithelial root
sheath forms epithelial diaphragm by bending at future
cemento enamel junction into horizontal plane ,narrowing
the wide cervical opening of tooth.
• Proliferation of cells of epithelial diaphragm is
accompanied by ectomesenchymal cell proliferation
adjacent to diaphragm.

• In last stages of root development ,the
proliferation of epithelium in diaphragm lags
behind that of pulpal connective tissue.
• Thus wide apical foramen is first reduced to
width of diaphragmatic opening itself , later
by apposition of dentin & cementum at the
apex of root.

• In case of multirooted
teeth, there is differential
growth of epithelial
diaphragm in the form of
tongue like extensions
which grow towards each
other & fuse causing
division of trunk into two
or three roots.

Time Line of Human Tooth Development
Age Developmental Characteristics
• 42 to 48 days Dental lamina formation
• 55 to 56 days Bud stage for deciduous teeth
• 14 weeks Bell stage for deciduous teeth;
Bud stage for permanent teeth
• 18 weeks Dentin & functional
ameloblasts in deciduous teeth
• 32 weeks Dentin & functional ameloblasts in
permanent teeth.

Histophysiological & Clinical Considerations
1. Initiation
2. Proliferation
3. Histodifferentiation
4. Morphodifferentiation
5. Apposition

Initiation:
• A lack of initiation results in absence of either single tooth
or multiple teeth.
• Most frequently the permanent upper lateral incisor ,third
molar, and lower second premolars.
• Abnormal initiation may result in development of single or
multiple supernumerary teeth.www.indiandentalacademy.com

Proliferation:
• Proliferative growth causes regular changes
in the size and proportions of the growing
tooth germ.

Histo-differentiation:
This phase reaches its peak in the Bell stage, just
before hard tissue formation.
In vitamin deficiency ameloblasts fail to
differentiate ,as a result of which adjacent
mesenchyme fails to differentiate & an atypical
dentin known as osteodentin is formed

Morphodifferentiation:
Disturbance in this phase may result in
supernumerary cusps or roots or suppression of
parts may be there (loss of cusps or roots)
or may result in peg or malformed teeth ( e.g.
Hutchinson’s incisors) with normal enamel &
dentin.

Apposition:
Genetic & environmental factors may disturb
the normal synthesis & secretion of organic
matrix of enamel leading to condition called
enamel hypoplasia.
If organic matter is defective, then enamel or
dentin is said to be hypocalcified or
hypomineralised. www.indiandentalacademy.com

Factors affecting growth &
development
BROADLY CLASSIFIED AS
1. Genetic:
i. Inherited
ii. Mutagenic
2. Environmental Factors:
a. Infections :
i. Systemic:
- Rubella
- Influenza
ii. Local: periapical infection affecting
deciduous tooth

b. Exanthematous diseases: measles ,chickenpox ,scarlet fever.
c. Physical injuries: trauma , radiation,extra temperature.
d. Hormonal disturbances: parathyroid ,thyroid ,growth
hormone, pituitary hormone .
e. Nutritional deficiency : vitamin A,Vit B complex Vit C,Vit D,
proteins, aminoacides.
f. Hypocalcemia
g. Birth injury-premature birth ,traumatic birth,RH hemolytic
disease.
h. Congenital syphilis:
i. Ingestion of chemicals
j. Idiopathic
k. Miscellaneous drugs & chemicals:teratogenic
l. Maternal disease & defects
m. Embryonic defects

Developmental
Disturbances of the
Teeth

 (1) Size
 (2) Number and Eruption
 (3) Shape/Form
 (4) Defects of Enamel and Dentin
Developmental Disturbances

SIZE
Microdontia Macrodontia
(1) True Generalized
Microdontia
(2) Relative Generalized
Microdontia
(3) Focal or Localized
Microdontia
1) True Generalized
Macrodontia
(2) Relative Generalized
Macrodontia
(3) Focal or Localized
Macrodontia

Number and Eruption
Supernumerary
Anodontia
Impaction

Supernumerary
In addition to the regular number of teeth.
Supernumerary teeth develop from a second tooth bud arising
from the dental lamina near the regular tooth bud.
Gardner's syndrome and cleidocranial dysostosis.

Supernumerary teeth can be classified by shape
and by position.
• Supplemental,
• Tuberculate,
• Conical,
• Compound odontoma,
• Complex odontoma.
Shape
•Mesiodens,
• Paramolar,
• Distomolar.
Position

Anodontia
A congenital anomaly in which some or all of the
teeth are missing.
Types
▪ Complete anodontia—
The absence of permanent dentition, often associa
ted with ectodermal dysplasia.
▪ Partial anodontia, hypodontia—
Missing at least one tooth.

Impaction
Do not fully erupt into the oral cavity
distoangular impaction
mesioangular impaction horizontal impaction
vertical impaction

Shape and Form
Crown
Root

Crown
• Fusion
• Gemination
• Taurodontism
• Talon’s Cusp
• Leong’s Cusp
•Dens Invaginatus
• Peg-shaped Lateral
• Hutchinson Incisor
• Mulberry Molar

Root
•Concresence
• Enamel Pearl
• Dilaceration
• Flexion
• Ankylosis

Fusion
Joining of 2 developing
tooth germs
Resulting in a single
large tooth structure
May involve entire length of teeth
Fusion of 2 teeth from a
single enamel organ
Partial cleavage
Appearance of 2 crowns
that share same root canal
Gemination

Taurodontism
Variation in tooth form:
1. elongated crowns
2. apically displaced
furcations
3. resulting in pulp chambers
that have increase apical
occlusal height
Associated with syndromes
such as
Down syndrome
Klinefelter’s syndrome

Dens Evaginatus
Talon’s Cusp
Leung’s Premolar
1. Well-delineated additional cusp
2. Located on the lingual surface of
anterior tooth
1. Clinically as an accessory cusp
or a globule
2. Located on occlusal surface
between buccal and lingual
cusps of premolars

 deep surface invagination
of crown or root that is lined
by enamel
 2 forms:
 coronal
 radicular
Dens Invaginatus
(Dens in Dente)

 undersized lateral incisor
 smaller than normal
 occurs when permanent lateral
incisors do not fully develop
Peg-Shaped Lateral

 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 Incisor

 dental condition usually
associated with congenital
syphilis
 characterized by multiple
rounded rudimentary enamel
cusps on permanent 1st molars.
 giving the appearance of a
mulberry
Mulberry Molar

Concresence
Enamel Pearl
Dilaceration
Flexion
Ankylosis
Root

 2 fully formed teeth
 joined along the root surfaces
by cementum.
frequently in
posterior and maxillary regions.
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.
Concrescence

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.
Maxillary molars are
commonly affected than
mandibular molars

 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.
Dilaceration

Hereditary factors are believed
to be involved
in small number of cases.
Eruption generally continues
without problems, rare
deformity

• Deviation or bend restricted just to the root
portion.
• Usually bend is less than 90 degrees.
• May be a result of trauma to the developing
tooth.
Flexion

Ankylosis
1. Also known as “submerged teeth.”
2. Fusion of a tooth to surrounding
bone.
3. Deciduous teeth most commonly
mandibular 2nd molars.
4. Become ankylose to bone.
5. This process prevents their
exfoliation + subsequent replacement
by permanent teeth.

Defects of Enamel and Dentin

 also known as:
 Hereditary Enamel Dysplasia
 Hereditary Brown Enamel
 Hereditary Brown Opalescent
Teeth
Amelogenesis Imperfecta

 group of conditions caused by
defects in the genes encoding
enamel matrix proteins
 genes that encode for enamel
proteins:
 amelogenin mutated in
 enamelin in patients
 others with this
condition

 Reduced enamel thickness
 abnormal contour
 absent interproximal
contact points
 Radio graphically:
 enamel reduced in bulk
 shows thin layer over occlusal
+ interproximal surfaces
Hypoplastic Amelogenesis Imperfecta

 enamel is normal in form on
eruption but:
 opaque
 white to brownish-yellow
 softer than normal
 tends to chip from
underlying
dentin
Hypomaturation Amelogenesis Imperfecta

 enamel matrix is formed in
normal quantity
 poorly calcified
 when newly erupted:
 enamel is normal in thickness
 normal form
 but weak
 opaque or chalky in appearance
Hypocalcified Amelogenesis Imperfecta

 with years of function:
 coronal enamel is removed
 except for cervical portion
that is occasionally calcified
better
 Radio graphically:
 density of enamel and dentin are
similar

 also known as “Hereditary
Opalascent Dentin”
 due to clinical discoloration
of teeth
 mutation in the dentin
sialophosphoprotein
 affects both primary and permanent
dentition
Dentinogenesis Imperfecta

 have blue to brown
discoloration.
 with distinctive translucency.
 enamel frequently separates
easily from underlying defective
dentin.

 Radiographically:
 bulbous crowns
 cervical constriction
 thin roots
 early obliteration of roots
canals + pulp chambers

 Classification:
 Type I
 Type II
 Type III
Dentinogenesis Imperfecta

 Occurs in families with
Osteogenesis Imperfecta
 Primary teeth are more severely
affected than permanent teeth
Type I Dentinogenesis Imperfecta

 partial or total obliteration of pulp chambers and root
canals.
 by continued formation of dentin.
 roots may be short and blunted.
 cementum, periodontal membrane and bone appear
normal.

 Never occurs in association with osteogenesis
imperfecta unless by chance
 Most frequently referred to as hereditary
opalascent dentin
 Only have dentin abnormalities and no bone
disease
Type II Dentinogenesis Imperfecta

• Partial or total obliteration of pulp
chambers and root canals.
• Continued formation of dentin.
• Roots may be short and blunted.
• Cementum, periodontal membrane and
bone appear normal.

•“Bradwine type”.
• Racial isolate in Maryland.
• Multiple pulp exposures in deciduous not seen in
type I or II.
• Periapical radiolucencies.
• Enamel appears normal.
• Large size of pulp chamber is due to insufficient and
defective dentin formation.
Type III Dentinogenesis Imperfecta

DENTIN DYSPLASIA
• Also known as “Rootless Teeth”,
• Rare disturbance of dentin formation
• Normal enamel
• Atypical dentin formation
• Abnormal pulpal morphology
• Hereditary disease

Classification:
• Type I ( Radicular Type)
• Type II (Coronal Type)

•Both dentitions are of normal color
• Periapical lesion
• Premature tooth loss may occur because of short
roots or periapical inflammatory lesions
Type I (Radicular Type)

• Roots are extremely short
• Pulps almost completely
obliterated
• Periapical radiolucencies.
Radiographically:

• Color of primary dentition is
opalescent.
•Permanent dentition is
normal.
• Coronal pulps are usually
large (thistle tube
appearance)
• Filled with globules of
abnormal dentin.
Type II (Coronal Type)

Abnormally large pulp
chambers in coronal
portion of tooth
Radiographically:
Deciduous Permanent
• Roots are extremely
short
• Pulps almost completely
obliterated.

Also known as:
Odontogenic Dysplasia
Odontogenesis Imperfecta
Ghost Teeth
Regional Odontodysplasia

• One or several teeth in a
localized area are affected
• Maxillary teeth are involved
more frequent
• Etiology is unknown
• Teeth affected may exhibit a
delay or total failure in eruption
• Shape is altered, irregular in
appearance.

Radiographically:
• Marked reduction in radiodensity.
• Teeth assume a “ghost” appearance.
• Both enamel + dentin appear very thin.
• Pulp chamber is exceedingly large.

Recent research
related to
development

Tooth regeneration: a revolution in stomatology and
evolution in regenerative medicine.
One of the pivotal issues in tooth regeneration is to devise
clinically translatable approaches that are not cost-prohibitive and
can translate into therapies for patients who cannot afford or do
not have access to dental implants. Costs for development of cell
homing approaches for tooth regeneration are anticipated not as
substantial as for tooth regeneration by cell transplantation.
Thus, tooth regeneration by cell homing may provide tangible
pathways towards clinical translation.
Int J Oral Sci (2011) 3:107-116

Amelogenin is also expressed transiently in differentiating
odontoblasts during predentin formation, but was absent in mature
functional odontoblasts. In intact adult teeth, amelogenin was not
present in dental pulp, odontoblasts, and dentin. However, in
injured and carious adult human teeth amelogenin is strongly re
expressed in newly differentiated odontoblasts and is distributed in
the dentinal tubuli under the lesion site. In an invitro culture system,
amelogenin is expressed preferentially in human dental pulp cells
that start differentiating in to odontoblast like cells and form
mineralization nodules. These data suggest that amelogenin plays
important roles not only during cytodifferentiation, but also during
tooth repair processes in humans.
Distribution of the amelogenin protein in developing
injured carious human teeth.
Frontier in physiology. 2014

Cell proliferation on the scaffolds was determined by
MTS assay and it was observed that all scaffolds
supported cell proliferation. Immunostaining was
carried out for morphological and differentiation
analyses. Immunohistochemical analyses revealed
that the cells attached onto the scaffolds and
deposited cartilage-specific extracellular matrix (ECM)
Cartilage tissue engineering on macroporous
scaffolds using human tooth germ stem cells.
J Tissue Eng Regen Med. 2015 Jan 2

(1) The explant culture of DP led to harvesting of a
relatively pure cell population of DTSCs;
(2) DTSCs express pluripotent stem cell markers
(3) DTSCs are multipotent cells with high
differentiation potential that are able to contribute to
all embryonic germ lineage formation.
(4) DTSCs are almost unlimited source of young stem
cells with easy access.
Stem Cells in Dental Pulp of Deciduous Teeth
TISSUE ENGINEERING: Part B
Volume 18, Number 2, 2012

Dental Pulp Stem Cells isolated from laser pierced
cryopreserved teeth show mesenchymal stem cells
morphology, immunophenotype, viability and
proliferation rate similar to those of cells isolated
from fresh, non cryopreserved teeth, whereas
significant loss of cell viability and proliferation rate
was shown by cells isolated from teeth cryopreserved
without laser piercing.
A novel method for banking dental pulp
stem cells
Transfusion and apheresis science
October 2012 Volume 47, Issue 2,
Pages 199–206www.indiandentalacademy.com

It appears that dental stem cells have the potential for
continued cell division and regeneration to replace dental
tissues lost through trauma or disease. Clinical applications
using these cells for apexogenesis and apexification will be
dependent on a greater understanding of the environment at
the immature root end and what stimulates dental stem cells
to begin dividing and then express a certain phenotype
Dental stem cells and their potential role in
apexogenesis and apexification.
Int Endod J. 2009 Nov;42(11):955-62.

REFRENCES
1) TEN CATE’S Oral histology
2) NEVILLE, et al: Oral and Maxillofacial Pathology
3) G S KUMAR et al: Oral histology and embryology
4) SHAFER, et al: A textbook of Oral Pathology.

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Growth&development of tooth / orthodontics courses