Diseases of the pulp:Part 1- Development, Physiology, Histology of Dental Pulp
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Diseases of the pulp:Part 1- Development, Physiology, Histology of Dental Pulp

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The development, physiology, histology of the dental pulp is briefly discussed. The features of the pulp as a connective tissue, its cells,fibers, innervation, vascularity are dealt with

The development, physiology, histology of the dental pulp is briefly discussed. The features of the pulp as a connective tissue, its cells,fibers, innervation, vascularity are dealt with

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Diseases of the pulp:Part 1- Development, Physiology, Histology of Dental Pulp Diseases of the pulp:Part 1- Development, Physiology, Histology of Dental Pulp Presentation Transcript

  • “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 MDS DEPT. 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 View slide
  • 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 View slide
  • 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
  • Nerve supply  Early development: few axons enter papilla- no peripheral nerve plexuses  Eruptive stage: rapid development - plexus of Raschkow & terminals in odontoblastic layer Byers (1980)
  • 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
  • Fibroblasts  Synthesize 6 Glycoproteins: fibronectin  Fibronectin with Type III collagen: Reticulin fibers  faint metachromasia, pho sphatase & ATP acitivity Galdames et al,Int. J. Morphol. vol.29 no.1 Temuco mar. 2011
  • 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
  • Morphologic variations: A, Pulp horn (pear shaped) B, coronal midpulp (spindle shape) C, coronal midroot level (elongated club shape) D, mid-third of root (short club shape) E, apical third of root (globules). Marion D et al, 1991
  • Electron Microscope Findings  Large, closely aligned, multilayered sweet potato shaped cells  3 to 4 µm wide & 8 to 10 µm long Nucleus: • Ellipsoidal – chromatin & nucleolus • Double membrane covered • Granules attached to outer membrane
  • Electron Microscope Findings Nucleolus:  One to four in number ( Ivanyi 1972)  Ring shaped: fully developed- inactive RNA synthesis  Compact: less developed- active RNA synthesis
  • Electron Microscope Findings Cytoplasm:  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 Findings Odontoblastic 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 Findings Intercellular Junctions:  Regions of plasma membranes between cells  3 types:  Impermeable  Adhering  Communicating
  • Electron Microscope Findings Impermeable Junctions/ Tight Junctions:  Helps: maintain a distinct internal environment  Plasma membranes appear to fuse & offer a tight seal between cells
  • Electron Microscope Findings Adhering Junctions:  Maintained by desmosomes: intercellular bridges  3 types: Belt, Spot & Hemidesmosomes  Promote adhesion between cells
  • Electron Microscope Findings Communicating 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 Findings Odontoblastic 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 Findings Nerve endings:  Presence of nerves in tubules: controversial  Nerve endings in juxtaposition to odontoblastic processes: reported
  • Electron Microscope Findings Odontoblastic 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 cells Histiocytes 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 cells Polymorphonuclear 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 cells Lymphocytes and Plasma Cells:  Follows neutrophils.  Injury & resultant immune responses  Presence of a persistent irritant
  • Defense cells Mast 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
  • Fibers of the Pulp von Korff fibers:  Fine argyrophilic fibers  Spirally twisted bundles- cork screw  Unmineralised dentin/ predentin  Fibrillar framework Bernick S
  • 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 mucopolysaccharides GAGs:  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 teeth Right 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 drainage Nasopalatine, 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
  • Microcirculation  Fenestrations: rapid transport of fluid & metabolites  Avg. capillary density: 1400/ mm3 : the greatest in the body Dr. K. Josephsen, Denmark
  • Microcirculation Capillary plexus Postcapillary venules Larger venules
  • Arteriovenous anastomosis: sympathetic innervation
  • Arteriole distribution  Main arteriole- 2 groups  Coronally – pulp horn  Between roof and floor of pulp chamber Takahashi et al, 1982
  • 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 teeth All 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 correlations LOCAL ANESTHETICS:  Blood flow infiltration : LA + epinephrine  Pulp tissue pressure high conc. Vasoconstrictors (Van Hassel & Simard- Savoie et al 1973)  No serious/ permanent damage
  • Clinical correlations GENERAL ANESTHETICS:  Scott et al – 1972: rat study- pulpal blood flow velocity: zero in 30 seconds  Effects: disappear in 1 hour AGING:  Decreased circulation  Atherosclerotic changes: calcification  Cells atrophy & die; fibrosis
  • Clinical correlations TEMPERATURE CHANGES Elevation:  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 correlations Reduction:  Subfreezing temperatures: transient fall Intrapulpal pressure (Augsburger & Peters- 1981)  < -20C: vascular engorgement & necrosis  H2O2 & CO2 : reduce capillary blood flow
  • Clinical correlations ENDODONTIC THERAPY:  Less hemorrhage: extirpation close to apex DEVELOPMENT:  Blood vessel density increased coronally  Subodontoblastic capillary plexus- larger : eruption  Rich blood supply- floor of pulp chamber
  • Clinical correlations PERIODONTAL DISEASE:  Reduction- circulation: degenerative changes  Reparative processes diminished: older pulps: operative procedures- necrosis  Excessive irradiation: necrosis Seltzer et al, 1963
  • Clinical correlations ANTERIOR 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 teeth Vth 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 Fiber Myelination Location of Terminals Pain Characteristics Stimulation Threshold A-delta Yes Principally in region of pulp- dentin junction Sharp, pricking Relatively 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 fibers Nerve 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)
  • 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 Frank RM
  • 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 theory Mechanisms - reduce fluid flow in dentin: Pashley et al- 1982  Plaque/ saliva bacteria  Mineralized deposits- tubules  Salivary/plasma proteins
  • Hydrodynamic theory- hypersensitive dentin 4 treatment modalities:  Smear layer- burnishing root surface  Oxalate compounds: insoluble ppts in tubules  Tubule occlusion: pptd. Plasma proteins- HEMA + glutaraldehyde  Dentin bonding agents application LASER : 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 & Neurotransmitters PLASMA KININS:  No pain: application to dentin ( Anderson and Naylor- 1972)0 SUBSTANCE P:  Pulp: rich in SP  Vasodilatation , increased capillary permeability (Pashley et al- 1982)
  • Polypeptides & Neurotransmitters PROSTAGLANDINS:  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 imbalance Steroids:  Systemic corticosteroid  Odontoblasts  Inhibit reparative dentinogenesis  Steroid :pulp therapy???
  • Hormones & hormonal imbalance Diabetes 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 imbalance Thyroid 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)