“The pulp is a small tissue with a big issue” - I. B. Bender

DISEASES OF THE DENTAL PULP- Part I

DEEPTHI P.R.Ist YEAR MDSDEPT. OF CONSERVATIVE DENTISTRY AND ENDODONTICS

Introduction Development of pulp - disorders Pulp as a connective tissue - Cellular elements - Fibers - Ground substance - Vasculature - Nerve supply - Systemic factors affecting the pulp Dental pulp stem cells Conclusion

INTRODUCTION Unique tissue Soft tissue : mesenchymal origin Integral part of dentin – dentin pulp complex Rigid encasement: low compliance environment Incompressible: inflammation- increased tissue

pressure External communication: apical foramen & lateral

canals

DEFINITION‘A richly vascularized and innervated specialized connective tissue of ectomesenchymal origin; contained in the central space of a tooth, surrounded by the dentin, with inductive,formative, nutritive, sensory and protective functions’ - Glossary of Endodontic terms

FUNCTIONS PRIMARY: Formative

SECONDARY: tooth sensitivity, defense & hydration, nutrition

Odontoblasts:

Dentinogenesis

Interaction with dental epithelium:

Amelogenesis

DEVELOPMENT Downgrowths from dental lamina: Enamel organ Stages: Bud, Cap & Bell- deepening of

invagination Tissue within the invagination: ‘ Dental Papilla’

DEVELOPMENT 8th week IUL:

beginning of papilla Bell stage: inner layer

of papilla- odontoblasts dentin

Dental pulp: Cephalic neural crest cells

Blood supply Oval/ Circular reticulated plexus in

alveolar bone (Saunders-1966 & Cutright-1970)

Series of blood vessels- dental papilla: future pulpal vessels

Vessels in dental sac basal wall: course to papilla (Tobin 1972)

Pulpal artery: plexus of vessels at pulpodentinal junction

Byers (1980)

Nerve supply Early development: few axons enter

papilla- no peripheral nerve plexuses Eruptive stage: rapid development -

plexus of Raschkow & terminals in odontoblastic layer

Disorders: pulp development

Vitamin D deficiency Down’s syndrome: Jaspers -1981 Dens invaginatus Pulpal dysplasia : Witkop- 1973 Regional odontodysplasia Hypophosphatasia: Houpt et al (1970) Beumer et al (1973) Hereditary hypophosphatemia: Archard &

Witkop (1966) Hypophysectomy

Pulp as a Connective Tissue Cells, ground substance, fibers Cells: a fundamental matrix Site & precursor for the fiber complex Collagen & reticulin End product of the system

Cells of the Pulp Fibroblasts Odontoblasts Defense & other cells

Fibroblasts Basic cell type Baume: mesenchymal cells,

pulpoblasts, or pulpocytes- progressive levels of maturation

Active in collagen synthesis: fibers present on the cell body & processes

Galdames et al,Int. J. Morphol. vol.29 no.1 Temuco mar. 2011

Fibroblasts Synthesize 6

Glycoproteins: fibronectin

Fibronectin with Type III collagen: Reticulin fibers

faint metachromasia, phosphatase & ATP acitivity

Fibroblasts With age: more number & width of

fibers & cells reduce More fibrous pulp: less defensive than

young cellular pulp Responsible for increase in size of

denticles

Odontoblasts Highly differentiated cell in pulp Main function: dentin production Uniformly stained hyperchromatic in

tissue sections Cytoplasm: may or may not be evident

Marion D et al, 1991

Morphologic variations:

A, Pulp horn (pear shaped)B, coronal midpulp (spindle shape)C, coronal midroot level (elongated clubshape)D, mid-third of root (short club shape)E, apical third of root (globules).

Electron Microscope Findings

Large, closely aligned, multilayered sweet potato shaped cells

3 to 4 µm wide & 8 to 10 µm longNucleus:• Ellipsoidal – chromatin & nucleolus• Double membrane covered• Granules attached to outer membrane

Electron Microscope FindingsNucleolus: One to four in number ( Ivanyi 1972) Ring shaped: fully developed- inactive

RNA synthesis Compact: less developed- active RNA

synthesis

Electron Microscope FindingsCytoplasm: Extensive rER & numerous transitional

vesicles (Jesson-1968, Garant et al & Reith -1968, Takuma & Nagai- 1971)

Vesicles: fine fibrillar material Large Golgi apparatus : centre Membrane bound granules: lysosomes Secretory granules- abacus bodies: golgi

complex

Electron Microscope Findings

Mitochondria evenly distributed

Centrioles present : rudimentary cilium

Approx. 50 Ao diameter filaments

200 to 250 Ao diameter microtubules

Electron Microscope Findings Odontoblasts : 6-8 cells deep, palisade

formation along predentin border Organelles: extend to terminal bar

apparatus level Distal to this level: material constituting

odontoblastic process

Electron Microscope FindingsOdontoblastic process: Dentinal fibers/ Tomes’ fibers Traverses predentin, fills the lumen of

dentinal tubule Coated vesicles: pinocytic & ingest

material from predentin Numerous filaments: parallel to cell

membrane- characteristic

Electron Microscope FindingsIntercellular Junctions: Regions of plasma membranes between

cells 3 types:

Impermeable Adhering

Communicating

Electron Microscope FindingsImpermeable Junctions/ Tight Junctions: Helps: maintain a distinct internal

environment Plasma membranes appear to fuse &

offer a tight seal between cells

Electron Microscope FindingsAdhering Junctions: Maintained by desmosomes:

intercellular bridges 3 types: Belt, Spot & Hemidesmosomes Promote adhesion between cells

Electron Microscope FindingsCommunicating Junctions/ Gap Junctions: Mediate direct transfer of chemical

messages between cells Exchange nutrients & signal molecules

for coordination of function

Gap junction & Tight junction

Desmosome like junction

Sasaki T et al, 1982

Electron Microscope FindingsOdontoblastic Junctional Complexes: Surface epithelial cells: terminal bars at

apical extremities Consist of several components:

junctional complexes Components: Zonula occludens, Zonula

adherens & Macula adherens

Electron Microscope Findings Structures at border between odontoblastic

process & cell bodies: small gap junctions, tight junctions & desmosome like junctions

Tight adhesion between odontoblasts: not easily separated

Electron Microscope FindingsNerve endings: Presence of nerves in tubules:

controversial Nerve endings in juxtaposition to

odontoblastic processes: reported

Electron Microscope FindingsOdontoblastic Communications: Odontoblastic nuclei: inner border of

dentin Odontoblastic processes : adjacent

processes through extensive lateral branch system (Kaye & Herold, 1966)

Contact cells more centrally located: fine protoplasmic processes-

fibronectin: cell to cell adhesion

Electron Microscope Findings Odontoblasts: mesenchymal syncytium-

injury of one odontoblast affects others Continuity of cells lost: injury following

operative procedures Cytoplasm stains for: RNA, lipids,

ALP, ATPase, ACP, non specific esterases, protein

carbohydrate complex : present

Electron Microscope Findings Cell free Zone/ Layer

of Weil: under odontoblasts in coronal portion- nerve elements

Not observed in middle & apical portions (Gotjamanos,1969)

Cell rich Zone: Fibroblasts & undifferentiated mesenchyme cells

Defense cellsHistiocytes and Macrophages: Pericytes : differentiate into fixed or

wandering histiocytes under appropriate

stimulation. Highly phagocytic: remove bacteria,

foreign bodies, dead cells, debris. Pulpal macrophages & dendritic cells:

Langerhans’ cells

Defense cellsPolymorphonuclear Leukocytes: Commonest : pulpal inflammation Injury & cell death: rapidly migrate from

nearby vessels Microabscess formation Bacteria & dead cells. Develop wider zones of inflammation.

Silva et al, 2009

Defense cellsLymphocytes and Plasma Cells: Follows neutrophils. Injury & resultant immune responses Presence of a persistent irritant

Defense cellsMast Cells: Inflamed pulps Granules: histamine & heparin. Histamine: vasodilatation & increases

vessel permeability

Reserve Cells Descendants of undifferentiated cells in

the primitive dental papilla Multipotential cells : Fibroblast type Capable: dedifferentiate/redifferentiate-

mature cell types. Cell-rich zone: concentrations of such

cells.

Reserve Cells Produce little collagen: not mature

fibroblasts (Frank- 1970) Cytoplasmic connections: odontoblasts & subjacent mesenchymal cells (Baume-

1980) Near vessels: other mature cell types Mast cells and odontoclasts:

inflammation.

Reserve Cells Unique cells: calcified tissue - pulp cap/

pulpotomy[Ca(OH)2 ]

Along the calcified tissue: base of tubules involved with caries, restorations, attrition, abrasion

Not a true dentin; cells - not true odontoblasts

Fibers of the Pulp Reticular fibers: around blood vessels &

odontoblasts Collagen- 640 Ao

Type III collagen: 28% to 45%- histologically identified as reticulin

Type I also

Fibers of the Pulp 2 types of filaments Rel. straight, approx 200 Ao diameter &

200 Ao periodicity Coiled, branched & irregularly beaded,

100 Ao diamter

Bernick S

Fibers of the Pulpvon Korff fibers: Fine argyrophilic

fibers Spirally twisted

bundles- cork screw

Unmineralised dentin/ predentin

Fibrillar framework

Fibers of the Pulp Collagen deposition Diffuse: no definite orientation Bundle: large, coarse bundles run parallel

to nerves / independently (Stanley & Ranney, 1962)

Apical portion: more fibrous than coronal (van Amerongen et al, 1983)

Fibers of the Pulp Coronal pulp: more bundle collagen Type III collagen & proteoglycans:

arterial plexus & odontoblasts Extirpation of young cellular pulp:

difficult Aged pulp: like absorbent paper point

Ground substance Structureless mass, gel-like in consistency:

the bulk of the pulp Occupies the space between formed

elements Influences: Spread of infection Metabolic changes Stability of crystalloids Effects of metabolic substances

Ground substance Proteins with glycoproteins, acid

mucopolysaccharidesGAGs: Hyaluronic acid (Engfeldt & Hjerpe, 1972) Water retention Ion Binding Electrolyte distribution during

mineralization Collagen fibrillogenesis

Ground substance ‘Milieu interieur’: Engel (1958) Metabolites & breakdown products-

exchange Hyaluronic acid: metabolite transport

Ground substance Pulp tissue hydroatatic pressure: 15 mm

Hg increase- early stages of inflammation

Depolymerization: microbial enzymes change in ground substance

Hyaluronidases, chondroitin sulfatase Mucopolysaccharidase activity:

resorbing deciduous teeth

Circulation of the Pulp Systemic circulation Microcirculation Lymphatics Control of blood flow Transcapillary fluid exchange Circulation in the inflamed pulp Clinical correlations

Arterial blood supply to teethRight atrium

Right ventricle

Pulmonary artery

Lungs

Pulmonary vein

(left ventricle)

Aorta

CCA

ECA Internal Maxillary artery

Internal Maxillary artery

pterygopalatinepterygoidmandibular

Inferior alveolar

Dental branch

Lower Molars, premolars canines

Incisive branch

Lower Incisors

Infraorbital artery

ASA artery

PSA artery

Upper Incisors, canines

Upper molars

bicuspids

Venous drainageNasopalatine, infraorbital, descending palatine, PSA, pharyngeal, Deep temporal, masseteric, Inferior alveolar, Middle meningeal

Pterygoid venous plexus

Internal maxillary vein with superficial temporal vein

Retromandibular vein

EJV/ IJV Innominate vein(right side)

Superior venacava

Heart (Right atrium)

Microcirculation Arterioles, capillaries & venules Arterioles: 50μ diameter: enter

through apical foramen Branch : terminal arterioles capillary

plexus – subodontoblastic zone Young teeth: extend into odontoblastic

layer

Arteriovenous distribution of hemodynamics in rat dental pulp S. Kim et

al, 1984

Takahashi et al- 1982

Microcirculation Capillaries: 8 to

10μ Coronal portion:

capillary blood flow- twice that in the root

Pulp horns: greatest blood flow

Dr. K. Josephsen, Denmark

Microcirculation Fenestrations:

rapid transport of fluid & metabolites

Avg. capillary density: 1400/ mm3 : the greatest in the body

Microcirculation Capillary plexus

Postcapillary venules

Larger venules

Arteriovenous anastomosis: sympathetic innervation

Takahashi et al, 1982

Arteriole distribution Main arteriole- 2

groups Coronally – pulp

horn Between roof and

floor of pulp chamber

Microcirculation Pulpal venules: unusually thin walls,

discontinuous muscular layer Diameter maximum: central region-

200μ Resting pulpal blood flow: 0.15 to 0.6

ml/ min/g tissue Blood volume: 3% pulpal wet weight

Microcirculation Changes measured: Laser Doppler

flowmeters Detect revascularization: traumatized

teeth Ideal : pulp vitality Limited: sensitivity, specificity,

reproducibility & costs

Regulation of pulpal blood flow Neuronal, paracrine & endocrine

mechanisms Vasodilatation: neighboring tissues- drop

in pulpal blood flow & perfusion pressure

Pulp: vulnerable in gingivitis/ periodontitis

Neuronal regulation Little/ no sympathetic vasoconstrictor

tone Neuronal vasodilator tone: sensory

neuropeptides Cervical sympathetic trunk:

vasoconstriction Neuropeptide Y & norepinephrine

Neuronal regulation Blood flow sensory neuropeptides

Vasodilatation : CGRP release Muscarinic receptors: ACh & VIP –

vasodilatation (Yu CY et al- 2002) No parasympathetic vasodilatation: cat

pulp (Sassano et al- 1995)

Local control Local tissue demands: regulate

hemodynamics Endothelin-1 pulpal blood flow

Prostacyclin, NO : endothelium Adenosine: ischemic & hypoxic tissue-

low pulpal oxygen tension

Humoral control Angiotensin II : vasoconstrictive basal

tone Receptors: AT1, AT2- rat pulp (Souza PP

et al, 2007) DOPA, epinephrine: vasoconstriction ACh, Histamine, bradykinin : inhibit

vasoconstriction

Lymphatics Drains filtered fluids & proteins: returns

to blood Immune defense Lymphatic markers: extensive lymphatic

system in pulp Capillaries- pulp horns; leave via apical

foramen & lateral canals

From Berggreen E, Haug SR, Mkonyi LE, Bletsa A: Characterization of the dental lymphatic system and identification of cells immunopositive to specific lymphatic markers. Eur J Oral Sci 117(1):34–42, 2009

Lymphatics Arteriolar pulse pressure

High interstitial pulsatile pressure

Deformation of interstitial tissues

Propulsion of lymph

Lymphatic drainage of teethAll maxillary teeth, Mandibular canines, premolars & molars

Mandibular incisors

Submaxillary glands

Submental glands

Superficial & deep cervical glands

Thoracic duct (left)

Jugular duct (right)

Blood stream: junction of IJV & Subclavian veins

Transcapillary fluid exchange Regulated by : lymph flow & differences

in colloidal osmotic & hydrostatic pressures

Interstitial fluid volume: 0.6+ 0.03 ml/g

Interstitial fluid pressure: 6- 10 mm Hg COP: rel. high- 83% plasma COP

Wiig H, Rubin K, Reed RK: New and active role of the interstitium in control of interstitial fluid pressure: potential therapeutic consequences. Acta Anaesthesiol Scand 47:111–121, 2003.

Circulation in the inflamed pulp Inflammation: vasodilatation &

increased vascular permeability- interstitial fluid pressure

Reabsorption of tissue fluid: pressure- disproves Pulpal strangulation theory (Heyeraas & Berggreen- 1999, Heyeraas & Kvinnsland- 1992)

Circulation in the inflamed pulp PGE2, Bradykinin, SP, Histamine: pulpal

blood flow Serotonin: pulpal blood flow Acute inflammation: 200% of control flow &

increased vascular permeability (Heyeraas & Kvinnsland- 1992, Heyeraas et al- 1996)

LPS: circulatory dysfunction (Bletsa A et al, 2006)

Circulation in the inflamed pulp Endothelial perturbation: on

exposure to endotoxin/ cytokines Reduced perfusion, VEGF down

regulation & microvessel density : necrosis

Lymphangiogenesis : inflamed pulps(Pimenta et al, 2003)

Vascular permeability: Inflamed pulp Vascular leakage: Prostaglandin,

histamine, bradykinin, SP LPS, LTA, TNF-, IL-1: upregulate VEGF

vascular permeability protein Transport COP

Circulation in the inflamed pulp: Clinical aspect Reduced distractions at night Pulpal blood flow : supine Further pulpal tissue pressure:

activate sensitised nociceptors- spontaneous pain

Throbbing : pulsations in the pulp - systole

Clinical correlationsLOCAL ANESTHETICS: Blood flow infiltration : LA +

epinephrine

Pulp tissue pressure high conc. Vasoconstrictors (Van Hassel & Simard- Savoie et al 1973)

No serious/ permanent damage

Clinical correlationsGENERAL ANESTHETICS: Scott et al – 1972: rat study- pulpal

blood flow velocity: zero in 30 seconds Effects: disappear in 1 hourAGING: Decreased circulation Atherosclerotic changes: calcification Cells atrophy & die; fibrosis

Clinical correlationsTEMPERATURE CHANGESElevation: 100C to 150C increase: intrapulpal

pressure 2.5mm Hg/0C

Irreversible changes: heating to 450C- prolonged (Van Hassel & Brown- 1969)

Clinical correlations Tooth preparation: affect pulpal blood

flow Pulpal damage initiation: alteration in

microvasculature No water spray: reduced blood flow-

upto 1 hour (Kim et al, 1983)

Clinical correlationsReduction: Subfreezing temperatures: transient fall Intrapulpal pressure (Augsburger & Peters- 1981) < -20C: vascular engorgement &

necrosis H2O2 & CO2 : reduce capillary blood

flow

Clinical correlationsENDODONTIC THERAPY: Less hemorrhage: extirpation close to

apexDEVELOPMENT: Blood vessel density increased coronally Subodontoblastic capillary plexus- larger

: eruption Rich blood supply- floor of pulp chamber

Seltzer et al, 1963

Clinical correlationsPERIODONTAL DISEASE: Reduction- circulation:

degenerative changes Reparative processes

diminished: older pulps: operative procedures- necrosis

Excessive irradiation: necrosis

Clinical correlationsANTERIOR OSTEOTOMY: Blood flow: maximum decrease

immediate postop Apparently re established: normal

response to stimuli (Pepersack- 1973, Theisen & Guernsey- 1976)

Nerve supply of the pulp Innervation of the teeth Theories of tooth pain perception Modulation of nerve impulses

Innervation of the teethVth N

Ophthalmic Maxillary Mandibular

PSA Infraorbital

ASA Lingual Inferior alveolar

Maxillary molars

Maxillary premolars

Maxillary anteriors

Inferior dental Incisor

Mandibular molars and premolars

Mandibular cuspid and incisors

Convergence of sensory information : teeth to higher centres

Innervation Large no. of myelinated (A)&

unmyelinated (C) fibers Premolar: 2000 Not all are nociceptors Afferent: sensory Efferent: Sympathetic: circulation & eruption

Characteristics of sensory fibers

FiberMyelination

Location of Terminals

Pain Characteristics

Stimulation Threshold

A-delta YesPrincipally in region of pulp-dentin junction

Sharp, prickingRelatively low

C No

Probably distributed throughout pulp

Burning, aching, less bearable than A-delta fiber sensations

Relatively high, usually associated with tissue injury

Sensory fibers Aδ: 1-5μ; 6-30 m/s C: 0.4-1μ; 0.5-2 m/s Pain localization: Single neuron innervation Low density propioceptors Electrical stimulation: A fibers

Fiber location within pulp

Sensory fibersNerve bundles +blood vessels

Dr. Inge Fristad, Department of Clinical Dentistry, University of Bergen

Plexus of Raschkow

Mummery - 1919 Plexus of single nerve

axons Develop: final stages of

root formation Prolific branching:

overlapping receptor fields

A fibers: subodontoblastic plexus

Terminal axons: free nerve endings

Types of nerve endings: Gunji T- 1982

Odontoblasts: receptor?? No anatomic communication: nerve fibers Low membrane potential: -24 to -30 mV Disruption of layer: no sensitivity

Possibility: sodium channel activity/ factors release- neuromodulation

Nerve fibers: resist necrosis Noxious stimuli: periapical tissues

Pain in non vital

teeth

Tissue injury & deafferentiation Deafferentiation: regeneration/ neuronal

cell death V nuclei affected: pulp extirpation Phantom tooth pain Changes in gene expression: C-fos

(Byers et al, 1993) A fibers: thermal & electric tests C fibers: pulp injured

Theories of tooth pain perception Dentinal nerve

stimulation Dentinal receptor

theory Hydrodynamic

theory

Dentinal nerve stimulation Silver staining: controversial LM studies: variable penetration (Bernick-

1968) & termination (Rapp et al- 1957)

EM studies: difficult interpretation No connection: nerves & odontoblasts

(Fernehead – 1968)

Dentinal nerve stimulation Predentin:

associated cells- origin questioned (Arwill- 1967)

Arwill T

Dentinal nerve stimulation Axons: separated

by narrow cleft (Byers et al)

Nerves: beaded structures in SEM (Tidmarsh- 1981)

Frank RM

Dentinal nerve stimulation Frank et al- 1966

Nerve : concavity odontoblast(pic)

‘cork screw’ fibers Gap junctions: nerve

cell processes & odontoblasts (Holland- 1975)

Possible- no nerve connections

Dentinal receptor theory Odontoblasts & processes: receptor Inconclusive Evidence: recording electrical activity Heat, cold, touch receptors (Scott &

Tempel, Mumford- 1965) Electrical activity: nerves in pulp & not

dentin (Matthews- 1970)

Dentinal receptor theory Intradentinal receptor: connections

between odontoblastic process & nerve fiber (Frank- 1969)

Transducer mechanism AChE: demonstrated in several studies

(Avery and Rapp-1967); contrary too Adrenergic : pulpal blood vessel walls

Hydrodynamic theory Dentin pain & odontoblast

displacement: related BrӓnstrӦm et al (1966, 1967, 1969,

1972) and Lilja (1980): hydrodynamic mechanism

Hydrodynamic theory Stimuli:

expansion/ contraction – fluid

Pulpward/ outward movement: nerve stimulation

Hydrodynamic theoryMechanisms - reduce fluid flow in dentin: Pashley et al- 1982 Plaque/ saliva bacteria Mineralized deposits- tubules Salivary/plasma proteins

Hydrodynamic theory- hypersensitive dentin4 treatment modalities: Smear layer- burnishing root surface Oxalate compounds: insoluble ppts in

tubules Tubule occlusion: pptd. Plasma proteins-

HEMA + glutaraldehyde Dentin bonding agents applicationLASER : effects on pulp???

Pulpal tissue pressure & pain Blood flow, pressure changes, dental

pain hydrostatic pressure: nerve fiber stimulation (Nӓhri- 1978) Pulp: mechanoreceptor- pain

transmission

Polypeptides & NeurotransmittersPLASMA KININS: No pain: application to dentin

( Anderson and Naylor- 1972)0SUBSTANCE P: Pulp: rich in SP Vasodilatation , increased capillary

permeability (Pashley et al- 1982)

Polypeptides & NeurotransmittersPROSTAGLANDINS: Sensitize nociceptors: histamine,

bradykinin, SP CGRP, Neuropeptide Y, NKA, VIP: painful pulps/ beneath caries Vasodilatation SP, CGRP: wound healing, inflammation CGRP release: vasoconstrictors

Systemic factors Vitamin deficiency Hormones Protein deficiency Systemic virus infection Hereditary diseases Tumor metastases

Vitamin deficiency

Vitamin C- Fibroblasts- Odontoblasts: degenerate & lose

morphology

Hormones & hormonal imbalanceSteroids: Systemic corticosteroid Odontoblasts Inhibit reparative dentinogenesis Steroid :pulp therapy???

Hormones & hormonal imbalanceDiabetes mellitus: Glucose concentration rise in dentinal

pulp fluids Degenerative & inflammatory changes

in pulp Dentinogenesis affected Atrophic pulp: non carious teeth Acute inflamed pulp: carious teeth

Cohen et al, 1963

Hormones & hormonal imbalanceThyroid deficiency: Pulp vascularity Pulpal lumen Cellular elements

Protein deficiency No pulpal changes noted (Glickman &

Shklar- 1954) Larger areas of periapical rarefaction

( Stahl et al -1958)

Systemic virus infection Odontoblasts injured: lymphocytic

choriomeningitis (Hancock-1956) & Shope papilloma virus ( Fleming-1958)

Degenerative changes & eventual necrosis: rats with Polyoma virus

Hereditary diseases Blood: Sickle cell anemia, leukemia Reticulo endothelial system: Hand-

SchÜller- Christian disease Neurologic: Sturge- Weber disease Metachromatic leukodystrophy Krabbe’s leukodystrophy Fabry’s disease Niemann- Pick disease

Tumor transplantation Metastases: sparse reports Epitheliomas, sarcoma, Burkitt’s

lymphomas- human dental pulps (Stanley- 1973)

Dental Pulp Stem Cells (DPSCs) Gronthos et al – 2000 Osteo/ odontogenic, adipogenic,

neurogenic, chondrogenic, myogenic Tissue regeneration DPSCs: dentinal repair Appropriate carrier: dental implant

Courtesy:

DPSCs DPSCs+ collagen + DMP1: pulp like

tissue (Prescott et al, 2008) SHED: dental pulp tissue engg (Cordeiro

et al,2008) Serum free medium + Insulin-

transferrin- selenium- X & embryotrophic factor: suitable medium for culture (Hirata et al, 2010)

DPSCs Irreversible pulpitis: putative cells- stem

cell properties (Wang et al, 2010) Regeneration in canine teeth – Gelfoam

scaffold (Wang et al- 2013)

Conclusion Unique tissue Resembles embryonic connective tissue Dynamic response pattern

References Seltzer S, Bender J.B. Seltzer’s The

Dental Pulp. Biological considerations in dental procedures. 3rd Edition

Hargreaves KM, Cohen S. Cohen’s Pathways of the Pulp. 10th Edition

Ingle JI, Bakland LK. Ingle’s Endodontics. 5th Edition

References Gronthos S, Mankani M, Brahim J, Gehron

Roby P, Shi S. Postnatal human dental pulp stem cells (DPSCs) in vitro and in vivo. PNAS 2000; 97(25): 13625- 13630

In Vivo Generation of Dental Pulp-like Tissue by Using Dental Pulp Stem Cells, a Collagen Scaffold, and Dentin Matrix Protein 1 after SubcutaneousTransplantation in Mice. Prescott RS, Alsanea R, Fayad MI et al. J Endod 2008;34:421– 426

References Cordeiro MM, Dong Z, Kaneko T et al.

Dental Pulp Tissue Engineering with Stem Cells from Exfoliated Deciduous Teeth. J Endod 2008;34:962–969

Wang Z, Pan J, Wright JT et al. Putative Stem Cells in Human Dental Pulp with Irreversible Pulpitis: An Exploratory Study. J Endod 2010;36:820–825)

References Hirata TM, Ishkitiev N, Yaeigaki K et al.

Expression of Multiple Stem Cell Markers in Dental Pulp Cells Cultured in Serum-free Media. J Endod 2010;36:1139–1144

Wang Y, Zhao Y, Jia W, Yang J, Ge L. Preliminary Study on Dental Pulp Stem Cell–mediated Pulp Regeneration in Canine Immature Permanent Teeth. J Endod 2013;39:195–201

References

Kim S, Lipowsky HH, Usami S, Chien S. Arteriovenous Distribution of Hemodynamic Parameters in the Rat Dental Pulp. Microvasc Res 27, 28-38 (1984)

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