Contents:

 Introduction
 Coronal and radicularpulp
 Apical foramen
 Accessory canal
 Functions of dental pulp
 Components of dental pulp
 Functions of pulpal extracellularmatrix
 Organization of cells in thepulp
 The principle cells of thepulp
 The pathways of collagen synthesis
 Matrix and ground substances
 Vasculature and lymphatic supply
 Innervation of Dentin- pulpcomplex
 Disorders of the dental pulp
 Advances in pulp vitalitytesting
 Conclusion
 Dental
Pulp
 Occupies the center of eachtooth.

 Soft connective tissue that supports the dentin.

 Total 52 pulp organs; 32: Permanent, 20: Primary

 Total Volume of all permanent teeth pulp organs is

0.38 cc.

 Mean volume of a single adult human pulp is 0.02 cc.

 Maxillary Mandibular
(Cubic Centimeter) (Cubic Centimeter)
Central Incisor 0.012 0.006
Lateral Incisor 0.011 0.007
Canine 0.015 0.014
First Premolar 0.018 0.015
Second Premolar 0.017 0.015
First Molar 0.068 0.053
Second Molar 0.044 0.032
Third Molar 0.023 0.031

Orban’s Oral histology & embryology: Pulp; Department of Oral Surgery,

Newcastle - Tyne, England
Coronal Pulp:

 Six surfaces

 Pulp horns, depends

on the cuspal
number.
 Radicular Pulp:

 The radicular portion of the pulp organs are

continuous with the periapical connective tissue
through the apical foramen or foramina.

 As growth proceeds, more dentin is formed, so that

when the root of teeth are matured the radicular pulp
is narrower.

 The apical pulp canal becomes smaller also becauseof

apical cementum deposition.
 Apical foramen:

 Average size of apical foramen of the maxillary teeth in

the adult is 0.4 mm

 Mandibular teeth 0.3 mm

 Sometimes it is found on the lateral side of the apex

although the root itself is notcurved.

 Frequently there are two or more foramina separated

by a portion of dentin and cementum or by cementum
only.
 Accessory canal:

 Leading from the radicular pulp laterally through the

root dentin to the periodontaltissue.

 May be seen anywhere along the root but are most

numerous in the apical third of the root.

 Clinically significant in spread of infection, either

from the pulp to the periodontal ligament or vice
versa.
 Occur in areas where there is premature loss of root
sheath cells; these cells induce the formation of
odontoblasts which formdentin.

 May also occur where the developing root encounters a

blood vessel.
Functions of dental pulp
 Inductive:
 Interact with the oral epithelialcells

 Differentiation of the dental lamina andenamel

organ formation.

 Cells of pulp + blood vessels & nerves

provides the toothvitality
 Formative:

 Produces dentin that surrounds and protects the pulp.

 Pulpal odontoblasts develop the organic matrix and

function in its calcification.
 Nutritive:

 Blood vascular system of the pulp; nourishes dentin

through the odontoblasts and their processes.

 Protective:
 Sensory nerve respond topain

 Nerves initiate reflexes that control circulation in the

pulp.
 Defensive or reparative:

 First line of defense to injuries and infection of

dentine
 Tertiary dentine
 Immuno-competent
 Clearance of toxic substances
 Components of dental pulp

Cells + (extracellular) Matrix

Fiber Ground substance

Structural Adhesive GAG Proteoglycan

• Collagen • Fibronectin • HS • Decorin
• Elastin • Laminin • DS • Versican
• CS
Components of dental pulp

 CELLS (odontoblast, fibroblast,

undifferentiated cell, macrophage,
dendritic cell)
 FIBERS AND GLYCOPROTEIN (collagen
type I, III, no elastic fiber,fibronectin)
 GROUND SUBSTANCES
(glycosaminoglycans, chondroitin sulfate
proteoglycan)
 BLOOD VESSELS, NERVES, LYMPH
VESSELS
Functions of pulpal
extracellular matrix
 Maintain tissue’s physical properties and integrity

 Control of growth and development and repairs

 Control of cell migration

 Control of diffusion of macromolecules

 Collagen in dental
pulp
Concentration varies from species to species, 32% inhuman
pulp.

Higher content in the middle and apical pulp.

 Total collagen decreases with age.

Interestingly high level of collagen type III. (43%) : vascular

content, tissue extensibility (cf. Elastin)

 Absence of elastin (except in b.v.).

 Adhesive glycoproteins in dental pulp

Fibronectin found in
predentine NOT mature
dentine.
Fibronectin present in
pulp and dental papilla.
Fibroblasts synthesize
pulpal fibronectin.
Fibronectin is expressed Immunoreactive fibronectin molecules detected
along the border of predentine and between
during reparative odontoblast (Yoshiba et al., 1994)
dentinogenesis.
 Glycosaminoglycans in
dental pulp
Chondroitin sulfate, dermatan sulfate, hyaluronic
acid present

 Amount of uronic acid decreases with age

 Total GAG decreases with reduced dentinogenic

activity

Decorin may involve in mineral nucleation at the

mineralization front
 Organization of cells in
the pulp
nerve terminals

tight junction
 Four distinct
zones:
1. The odontoblastic zone at the pulp periphery

2. A cell free zone of Weil beneath the odontoblast;

prominent in the coronal pulp

3. A cell rich zone; high celldensity

4. The pulp core; major vessels and nerves

 The principle cells of thepulp:

 Odontoblasts

 Fibroblast

 Undifferentiated mesenchymal cells

 Macrophages

 Immunocompetent cells
 Odontoblasts:

 The most distinctive cells of the dental pulp

 Form a layer lining the periphery of the pulp and have

a process extending into thedentin

 Arranged in palisade pattern of three to five cells deep

 59,000 to 76,000 per square milimeter in coronal

dentin, with a lesser number in root dentin.
 Active cells:

 Elongated, basal nucleus, much basophilic cytoplasm,

promonent golgi zone.

 Resting cell:

 Stubby, little cytoplasm, more hematoxophilic nucleus.

 Odontoblast process begins at the neck of the cells
just above the apical junctional complex where the cell
gradually begins to narrow as it enters predentin.

 The process is devoid of major organelles but does

display an abundance of microtubules and filaments
arranged in a linear pattern along itslength.
 The pathways of collagensynthesis:

 The spherical distensions contain free polypeptides

that assemble as a triple helix in the cylindrical
distensions to form the procollagenmolecule.

 The cylindrical distension bud off as secretory

granules.

 Secretory granules that are transported toward the

odontoblast process, where their content isreleased.
Synthesis of collagen and its assembly into fibrils and fiber
 Some types (of 15) of known collagen

Type Molecular Tissue distribution

Fibril-forming I [ 1(I)]2  2(I) bone, skin, tendon, ligaments

(90%) of body collagen

II [1(II)]3 cartilage, intervertebral disc,

notochord, vitreous humor of eye

III [1(III)]3 skin, blood vessels, internal organs

V [ 1(V]2  2(V) as type I
XI [ 1(XI]  2(XI)  3(XI) as type II

Fibril-associated IX [ 1(IX]  2(IX)  3(IX) cartilage (with type II)

XI [ 1(XII)]3 tendon, ligaments (with some type I)
I

Network-forming IV [ 1(IV)]2  2(IV) basal laminae

VI [ 1(VII)]3 anchoring fibrils beneath stratified
I squmous epithelia
The structure of a fibronectindimer.

RGD = cell-binding domain

Structure of a GAG

Structure of proteoglycans
 Some known
proteoglycans:
Aggrecan mechanical support
(cartilage)

Betaglycan binds TGF-beta

(cell surface*, matrix)

Decorin binds type I and (CNT)

TGF-beta
Perlecan basal laminae
(basal laminae)

Syndecan-1 binds FGF

(cell surface*)
* = Integral membrane proteoglycan
Junctions occur between adjacent odontoblasts
involving

 Gap junctions

 Occluding zones (Tight junctions)

 Desmosomes

The actin filaments inserting into the adherent

junction are prominent and form a terminal cell web.
This junctional complex does not form a zonula,
completely encircling the cell, as occurs in epithelia;

(it is focal, and there is some debate whether it can

restrict the passage of molecules and ions from the
pulp into the dentin layer)

Serum proteins seem to pass freely between

odontoblasts and are found indentin
 Fibrobla
sts:
 Greatest number in thepulp
 Numerous in coronal pulp where they form the cell-
rich zone.
 The function is to form and maintain pulp matrix.
 Undifferentiated
Ectomesenchymal
Cells:
 Represents the pool from which the connectivetissues
of the pulp arederived.

 Depending upon the stimulus these cells may give rise

to odontoblasts and fibroblasts.

 In older pulp they diminish, thereby reducing the

regenerative potential of the pulp.
 Macroph
ages
 Located throughout the pulpcenter.

 Involved in the elimination of dead cells, the presence

of which indicates that turnover of dental pulp
fibroblast occurs.
 Lymphoc
ytes
 In normal pulp T lymphocytes are found, but B
lymphocytes are scare.
 Dendritic
Cells
 Bone marrow derived, antigen presentingdendritic
cells.

 Beneath the odontoblastlayer.

 They capture and present foreign antigen to the T

cells.
 Cells participate in immunosurvillance and increase
in number in cariousteeth.

 Infiltrate odontoblast and project their processes into

the tubules.

 8% of total cell population.

 Matrix and Ground
Substance
 Principally Type I and Type IIIcollagen.

 Composed of glycosaminoglycans, glycoproteins, and

water.

 Overall collagen content increases with age.

 The greatest concentration of collagen generally
occurs in the most apical portion of the pulp.

 Significance:

 During pulpectomy; Engaging the pulp with a barbed

broach in the region of apex affords a better
opportunity to remove the tissueintact.
 Vasculature and
Lymphatic Supply
 Circulation establishes the tissue fluid pressure.

 One or sometimes two vessels of arteriolar size

(about 150µm) enter the apical foramen with the
sensory and sympathetic nervebundles.

 Smaller vessels, without any accompanying nerve

bundle, enter the pulp through the minor foramina.
Pulp
vasculat
ure
 The arterioles occupy a central position within the
pulp and, as they pass through the radicular portion of
pulp, give off smaller lateral branches.

 Occasionally U- looping of pulpal arterioles is seen,

and this anatomic configuration is thought to be
related to the regulation of blood flow.
Pulp tissue is highly
vascularized.

40-50 ml/min/100g

(Kim, 1985)
 Some terminal capillary loops extend upward between
the odontoblasts to abut the predentin if
dentinogenesis is occurring.

 Located on the periphery of the capillaries at random

intervals are pericytes.

 Pericytes are contractile cells capable of reducing the

size of the vessel lumen.
 Anastomosis are point of direct communication
between the arterial and venous sides of the
circulation.

 Lymphatic vessels also occur in the pulp tissue, they

exit via one or two large vessels through the apical
foramen.
 Sympathetic adrenergic nerves terminate in relation to
the smooth muscle cells of the arteriolar walls.

 Afferent free nerve endings terminate in relation to

arterioles, capillaries and veins and serve as effectors
by releasing various neuropeptides that exert an
effect on the vascular system.
 Hydrostatic
pressure
(20 mm Hg) in dental
pulp

(5.5-10.3 mm Hg*)

(35 mm Hg)

(43 mm Hg)

Dental pulp interstitial fluid (ISF) and exchange of substances betweenplasma

and ISF. (* values from Tonder and Kvinnsland, 1983; Ciucchi et al., 1995)
 Innervation of Dentin- Pulp Complex

 Nerve enter the pulp through

apical foramen, along the
afferent blood veessels, and
together from the
neurovascular bundle.

 Each nerve fiber has been

estimated to provide at least
eight terminal branches.
These branches ultimately
contribute to an
extensive plexus of
zone just below the cell bodies of the
nervesininthethe
odontoblasts cellportion offree
crown the
tooth.
Intradentinal nerves are mostly found in pulpal
horns.

Approx. 1800 non

myelinated +
400 myelinated
 This plexus of nerves, which is called the
subodontoblastic plexus of Raschkow, occupies the
cell- free zone of Weil and can be demonstrated in
silver nitrate stained sections under the light
microscope or by immunocytochemicaltechniques.
The nerve bundles that enter the tooth pulp consist
principally of :

Sensory afferent nerves of the trigeminal

nerve
and

Sympathetic branches from the superior

cervical ganglion.
As the nerve bundle ascendscoronally;

The myelinated axons gradually loose their

mylein coating,

So that a proportional increase in the number

of unmyelinated axons occurs in the more
coronal aspect of the tooth.
 Types and properties of pulpal sensory nervefibers
A-beta fibers
 Conduction velocity 30-70 m/s
 Very low threshold, non-noxious
sensation
 50% of myelinated fibers in pulp
 Functions not fully known
A-delta fibers
 Conduction velocity 2-30 m/s
 Lower threshold
 Involved in fast, sharp pain
 Stimulated by hydrodynamic
stimuli
 Sensitive to ischemia
 Sharp pain
C fibers
 Conduction velocity 0-2 m/s
 Higher threshold
 Involved in slow, dull pain
 Stimulated by direct pulp damage
 Sensitive toanesthetics
 Dull pain
Non-myelinated sympathetic
fibers
 Conduction velocity 0-2 m/s
 Post-ganglionic fibers of superior
cervical ganglion
 Vasoconstriction
A small number of axons pass between the
odontoblast cell bodies to enter the dentinal tubules
in proximity to the odontoblast process.
Possible mechanisms of
dentine sensitivity
Hydrodynamic mechanism
(Gysi, 1900; Brannstrom, 1963)
 Pulpal axonal reflex due to dentine
stimulation
Increased tubular
fluid flow
STIMULATION

Dentine
Increased A-V shunt
blood flow

Outward dentinal Increased pulp

Release of pressure Increased blood
fluid flow and
inf lammatory viscosity and rbc
aspiration of
agents? congestion incapillary
odontoblasts Increased pulp
bed
interstitial fluid

SP, CGRP
Pulpvenules
Axon
ref le
x
Without infection,
Vasodilation, Increased permeability
Vascular changescould
be resolved.
CNS, Pain, Reflexes
Disorders of the
Dental Pulp
 Pulp
Stones
 Pulp stones, or denticles, frequently are found in pulp
tissue.

 Discrete calcified masses that have calcium phosphorus

ratios comparable to that of dentin.

 More frequently at the orifice of the pulp chamber or

within the rootcanal.
 Concentric layers of mineralized tissue formed by
surface accretion around blood thrombi, dying or
dead cells, or collagen fibers.

 Occasionally a pulp stone may contain tubules and

be surrounded by cells resembling odontoblasts.
 Such stones are rare and, if seen, occur close to the
apex of the tooth. Such stones are referred to as ‘true’
pulp stones as opposed to ‘false’ stones having no cells
associated with them.
 If during the formation of a pulp stone, union occurs
between it and the dentin wall, or if secondary dentin
deposition surrounds the stone, the pulp stone is
called an attached stone.
 The presence of pulp stones is significant in that
They reduce the overall number of cells within
the pulp

and

Act as an impediment to debridement and

enlargement of the root canal system during
endodontic treatment.
 Age
Changes
 Decrease in the volume of pulp chamber and root
canal brought about by continued dentin deposition.

 On occasion can appear to be obliterated almost

completely.

 From about the age of 20 years, cells gradually

decrease in number until age 70, when the cell density
has decreased by about half.
 Fibrosis is due to aging &Injury.

 Increase in collagen fibers’

bundles which becomes more
evident with the decrease in pulp
size
 Lose and a degeneration of myelinated and
unmyelinated axons that correlate with an age-
related reduction in sensitivity.

Irregular areas of dystrophic calcification,

especially in central pulp.

 Gradual reduction of tubule diameter.

 The continued depositionoften leads to complete
closure of the tubule;
as can be seen readily in a ground section of
dentin, because the dentin becomes translucent
(or sclerotic).

Sclerotic dentin is found frequently near the root

apex in teeth from middle aged individuals.
 Pulpit
is
 Acute orchronic.

 Partial or total.

 Open orclosed.

 Exudative orsuppurative.

 Reversible or irreversible.
Pulpitis is a dynamic process and presents a
continuous spectrum of changes reflecting
interplay between cause and host
defenses.

Poor correlation between microscopic

changes & clinical symptoms.
 Pulpitis: Clinical
Features
Presents as pain which patient may have difficulty
in localizing to a particulartooth.

 Pain may radiate to adjacent jaw, face, ear, orneck.

May be continuous for several days or may occur

intermittently over a longerperiod.

Pulpitis is often described as acute or chronic

based on duration and severity of symptoms.
 Acute
pulpitis
Severe throbbing, lancinating pain on thermal
stimulation or lying down, keeps patientawake.

Generally lasts 10-15 minutes but may be more or

less continuous (reversible pulpitis).

With progression, may become spontaneous &

continuous (irreversible pulpitis).
 Chronic
pulpitis
 Bouts of dull aching which can last for an hour or
more.

 Pain on thermal stimulation or spontaneously.

 Pulpitis may be asymptomatic.

Most important decision clinically is whether

pulpitis is reversible orirreversible.

Decision is made based on many factors

including:

1. Severity of symptoms.
2. Duration of symptoms.
3. Size of carious lesion.
4. Pulp tests.
5. Direct observation during operativeprocedure.
6. Age of patient.
 Pulpitis: Etiology
 Microbial:

 Dental caries.

 Traumatic exposure.

 Marginal leakage.

 Cracked tooth

 Coronal fracture.

 Attrition.
 Abrasion.

 Traumatic restorative procedure.

 Invaginated odontome.

 Advanced periodontitis (periodontal-endodontic

lesion).
 Pulpitis starts before leading organisms in
carious dentin reach pulp.

 Pulpitis is not usually seen histologically

until organisms are within 1 mm of the
pulp in permanent teeth, or 2 mm in
deciduous teeth.
 Chemical and thermal injury

During restorative procedures: frictional heat,

irritant substances.

 May respond by reactionary dentinformation.

 Barotrauma (aerodontalgia)

Flying at high altitude in unpressurized aircraft,

or rapid decompression indivers.

Attributed to formation of nitrogen bubbles in

pulp tissue or vessels.

 Thought not to be a direct cause, but rather an

exacerbating cause in presence of caries.
 Pulpitis: Histopathology

 Poor correlation between microscopic changes &

clinical symptoms.

 Inf lammatory process may be modified by

several factors:
 Nature, severity and duration of insult.
 Efficiency of host defenses.
 Efficiency of pulpo-dentinal complexdefenses.
 Special anatomy of pulp: surrounded by hard
tissue and cannot tolerate edema.

85
Reactionary dentin may continue to form after
onset of pulpitis if odontoblasts and pulp have not
been irreversibly damaged, and may protectpulp.

Pulpitis caused by caries starts as a localized area,

but extends throughout pulp if caries is not
treated.

86
If inflammation is severe, local
microcirculation may be compromised,
leading to local necrosis and suppuration
of pulp (pulp abscess), or diffuse
suppuration and necrosis.
 Pulpitis: Chronic
Hyperplastic
Pulpitis (Pulp
Polyp)
Open pulpitis or chronic hyperplastic pulpitis (pulp
polyp):

Large carious cavities.

Young molar teeth with wide apices and good

blood supply.

88
 Usually devoid of sensation on gentleprobing.

 Polyp consists of chronically inf lame

hyperplastic granulation tissue d
from pulp cavity. protruding

May become epithelialized by spontaneous

grafting of desquamated oral epithelial cells from
saliva.
 Pulp Necrosis

May follow pulpitis or trauma to apicalblood

vessels.

 Coagulative necrosis after ischemia.

90
Liquefactive necrosis after pulpitis;

may become gangrenous with foul odorupon

infection by putrefactive bacteria fromcaries.

Pulp necrosis in sickling crisis of sickle cell

anemia.
Restorative factors contributing to
pulpal injury
 Effects of cavity
Preparation:
 Frictional heat

 Desiccation

 Exposure of dentinal tubules

 Direct damage to odontoblastprocesses

 Chemical treatment to exposed dentinalsurface

Cavity preparation: speed, heat, pressure &
coolant may all cause pulpirritation.

Aspiration or displacement of odontoblasts into

dentinal tubules, with reduction of numbers.

94
 Factors associated with the restorative material & its placement

 Material toxicity

 Insertion pressure

 Thermal effects

 Induced stresses
 Effects subsequent to
restoration
 Marginal leakage

 Cuspal fracture

 Effects of cavity preparation & restorative materials may

further complicate pulpitis caused by caries or other
causes.

 Thickness & nature of remaining dentine may affect pulp

response to dental material.
Advances in Pulp Vitality
testing
 Pulse Oximetry

 Dental sensor (a modified finger probe) that can be

successfully applied and adapted to the tooth and well
suited to detect pulsatile absorbance.

 The principle: relates the absorption of light, by a

solute to its concentration and optical properties at a
given light wavelength.
It also depends on the absorbance
characteristics of haemoglobin in the red
and infra-red range

In the red region, oxyhaemoglobin absorbs

less light than deoxyhaemoglobin and vice
versa in the infraredregion.
 Hence one wavelength was sensitive to
changes in oxygenation and the second was
insensitive to compensate for changes in
tissue thickness, haemoglobin content and
light intensity.
 The system consists of a probe containing a diode that
emits light in twowavelengths:

I. Red light of approximately 660 nm

II. Infra-red light of approximately 850 nm

 It is also useful in cases of impact injury where

the blood supply remains intact but the nerve
supply is damaged
 Dual Wavelength
Spectrophotometry

 Dual wavelength spectrophotometry (DWLS) is a

method independent of a pulsatilecirculation.

 The presence of arterioles rather than arteries in the

pulp and its rigid encapsulation by surrouding dentine
and enamel make it difficult to detect a pulse in the
pulpspace.
 This method measures oxygenation changes in
the capillary bed rather than in the supply vessels
and hence does not depend on a pulsatile blood
flow.

 A major advantage is that it uses visible light that

is filtered and guided to the tooth by fibreoptics

 The test is noninvasive and yields objective results.

 Laser doppler
flowmetry

 Laser Doppler Flowmetry (LDF) is a noninvasive,

electro optical technique,
• Which allows the semi-
quantitativerecording of pulpal
blood flow.
The Laser Doppler technique measures blood
flow in the very small blood vessels of the
microvasculature.
The technique dependson the Doppler principle;

whereby light from a laser diode incident on the

tissue is scattered by moving RBC's
and

As a consequence, the frequencybroadened.

 The primary issues in pulp-vitality testingas
follows:

A non-vital post-traumatized incisor has a better

long-term prognosis;

If root canal therapy is completed beforethe

necrotic pulp gets infected.
 The best outcome for the post
traumatized immature incisor is for it;

To revascularize and,

Continue normal root development, including

increased root wall thickness.

 Which is not possible to assess with conventional

electrical and thermal testing
 Conclusion

Thus the Preservation of Healthy Pulp during

operative procedures and successful management
in cases of disease are two of the most important
challenges.
 References:
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ed. of: The dental pulp / Samuel Seltzer, I.B. Bender. 3rd ed. c1984.
2. Oral histology; Development, Structure and Function: A.R. Ten Cate: 7th Edition
3. Orban’s Oral Histology and Embryology
4. Shafer’s Textbook of Oral Pathology; 5th Edition
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8. Seo, BM., Miura, M., Gronthos, S., Bartold, PM., Batouli, S., Brahim, J.,
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10.Morsczeck, C., Gotz, W., Schierholz, J., Zeilhofer, F., Kuhn, U., Mohl, C.,
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