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

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

2. DISEASES OF THE DENTAL PULP-
Part I
DEEPTHI P.R.
Ist YEAR MDS
DEPT. OF CONSERVATIVE
DENTISTRY AND
ENDODONTICS

3.  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

4. 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

5. 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

6. FUNCTIONS
 PRIMARY: Formative
 SECONDARY: tooth sensitivity, defense &
hydration, nutrition
Odontoblasts:
Dentinogenesis
Interaction
with dental
epithelium:
Amelogenesis

7. DEVELOPMENT
 Downgrowths from dental lamina:
Enamel organ
 Stages: Bud, Cap & Bell- deepening of
invagination
 Tissue within the invagination:
‘ Dental Papilla’

8. DEVELOPMENT
 8th week IUL: beginning
of papilla
 Bell stage: inner layer of
papilla- odontoblasts
dentin
 Dental pulp: Cephalic
neural crest cells

9. 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

10. 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)

11. 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

12. 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

13. Cells of the Pulp
 Fibroblasts
 Odontoblasts
 Defense & other cells

14. 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

15. 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

16. 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

17. Odontoblasts
 Highly differentiated cell in pulp
 Main function: dentin production
 Uniformly stained hyperchromatic in tissue
sections
 Cytoplasm: may or may not be evident

18. 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

19. 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

20. Electron Microscope Findings
Nucleolus:
 One to four in number ( Ivanyi 1972)
 Ring shaped: fully developed- inactive
RNA synthesis
 Compact: less developed- active RNA
synthesis

21. 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

22. Electron Microscope Findings
 Mitochondria
evenly distributed
 Centrioles present :
rudimentary cilium
 Approx. 50 Ao
diameter filaments
 200 to 250 Ao
diameter
microtubules

23. 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

24. 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

26. Electron Microscope Findings
Intercellular Junctions:
 Regions of plasma membranes between
cells
 3 types:
 Impermeable
 Adhering
 Communicating

27. Electron Microscope Findings
Impermeable Junctions/ Tight Junctions:
 Helps: maintain a distinct internal
environment
 Plasma membranes appear to fuse &
offer a tight seal between cells

28. Electron Microscope Findings
Adhering Junctions:
 Maintained by desmosomes: intercellular
bridges
 3 types: Belt, Spot & Hemidesmosomes
 Promote adhesion between cells

29. Electron Microscope Findings
Communicating Junctions/ Gap Junctions:
 Mediate direct transfer of chemical
messages between cells
 Exchange nutrients & signal molecules for
coordination of function

30. Gap junction & Tight
junction
Desmosome like junction
Sasaki T et al, 1982

31. 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

32. 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

33. Electron Microscope Findings
Nerve endings:
 Presence of nerves in tubules:
controversial
 Nerve endings in juxtaposition to
odontoblastic processes: reported

34. 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

35. 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

36. 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

38. 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

39. 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

40. Defense cells
Lymphocytes and Plasma Cells:
 Follows neutrophils.
 Injury & resultant immune responses
 Presence of a persistent irritant

41. Defense cells
Mast Cells:
 Inflamed pulps
 Granules: histamine & heparin.
 Histamine: vasodilatation & increases
vessel permeability

42. 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.

43. 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.

44. 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

45. 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

46. Fibers of the Pulp
 2 types of filaments
 Rel. straight, approx 200 Ao diameter &
200 Ao periodicity
 Coiled, branched & irregularly
beaded, 100 Ao diamter

47. Fibers of the Pulp
von Korff fibers:
 Fine argyrophilic
fibers
 Spirally twisted
bundles- cork
screw
 Unmineralised
dentin/ predentin
 Fibrillar framework
Bernick S

48. 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)

49. 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

50. 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

51. Ground substance
 Proteins with glycoproteins, acid
mucopolysaccharides
GAGs:
 Hyaluronic acid (Engfeldt & Hjerpe, 1972)
 Water retention
 Ion Binding
 Electrolyte distribution during mineralization
 Collagen fibrillogenesis

52. Ground substance
 ‘Milieu interieur’: Engel (1958)
 Metabolites & breakdown products-
exchange
 Hyaluronic acid: metabolite transport

53. 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

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

55. Arterial blood supply to teeth
Right atrium
Right ventricle
Pulmonary artery
Lungs
Pulmonary vein
(left ventricle)
Aorta
CCA
ECA
Internal Maxillary artery

56. 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

57. 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)

58. Microcirculation
 Arterioles, capillaries & venules
 Arterioles: 50μ diameter: enter through
apical foramen
 Branch : terminal arterioles  capillary
plexus – subodontoblastic zone
 Young teeth: extend into odontoblastic
layer

59. Arteriovenous distribution of hemodynamics
in rat dental pulp S. Kim et al, 1984

60. Takahashi et al- 1982

61. Microcirculation
 Capillaries: 8 to 10μ
 Coronal portion:
capillary blood
flow- twice that in
the root
 Pulp horns:
greatest blood flow

62. Microcirculation
 Fenestrations:
rapid transport of
fluid & metabolites
 Avg. capillary
density: 1400/ mm3
: the greatest in the
body
Dr. K. Josephsen, Denmark

63. Microcirculation
Capillary plexus
Postcapillary venules
Larger venules

64. Arteriovenous anastomosis:
sympathetic innervation

65. Arteriole distribution
 Main arteriole- 2
groups
 Coronally – pulp
horn
 Between roof and
floor of pulp
chamber
Takahashi et al, 1982

66. 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

67. Microcirculation
 Changes measured: Laser Doppler
flowmeters
 Detect revascularization: traumatized
teeth
 Ideal : pulp vitality
 Limited: sensitivity, specificity,
reproducibility & costs

68. Regulation of pulpal blood
flow
 Neuronal, paracrine & endocrine
mechanisms
 Vasodilatation: neighboring tissues- drop
in pulpal blood flow & perfusion pressure
 Pulp: vulnerable in gingivitis/ periodontitis

69. Neuronal regulation
 Little/ no sympathetic vasoconstrictor tone
 Neuronal vasodilator tone: sensory
neuropeptides
 Cervical sympathetic trunk:
vasoconstriction
 Neuropeptide Y & norepinephrine

70. 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)

71. Local control
 Local tissue demands: regulate
hemodynamics
 Endothelin-1 pulpal blood flow
 Prostacyclin, NO : endothelium
 Adenosine: ischemic & hypoxic tissue- low
pulpal oxygen tension

72. 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

73. 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

74. 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

75. Lymphatics
Arteriolar pulse pressure
High interstitial pulsatile pressure
Deformation of interstitial tissues
Propulsion of lymph

76. 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

77. 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

78. 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.

79. 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)

80. 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)

81. 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)

82. Vascular permeability:
Inflamed pulp
 Vascular leakage:
Prostaglandin, histamine, bradykinin, SP
 LPS, LTA, TNF-, IL-1: upregulate VEGF
 vascular permeability protein
Transport COP

83. 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

84. 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

85. 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

86. 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)

87. 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)

88. Clinical correlations
Reduction:
 Subfreezing temperatures: transient fall
Intrapulpal pressure (Augsburger & Peters-
1981)
 < -20C: vascular engorgement & necrosis
 H2O2 & CO2 : reduce capillary blood flow

89. 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

90. Clinical correlations
PERIODONTAL DISEASE:
 Reduction-
circulation:
degenerative
changes
 Reparative processes
diminished: older
pulps: operative
procedures- necrosis
 Excessive irradiation:
necrosis Seltzer et al, 1963

91. Clinical correlations
ANTERIOR OSTEOTOMY:
 Blood flow: maximum decrease
immediate postop
 Apparently re established: normal
response to stimuli (Pepersack-
1973, Theisen & Guernsey- 1976)

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

93. 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

94. Convergence of sensory
information : teeth to higher
centres

95. Innervation
 Large no. of myelinated (A)&
unmyelinated (C) fibers
 Premolar: 2000
 Not all are nociceptors
 Afferent: sensory
 Efferent:
 Sympathetic: circulation & eruption

96. 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

97. 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

98. Fiber location within pulp

99. Sensory fibers
Nerve bundles +blood vessels
Dr. Inge Fristad,
Department of Clinical
Dentistry, University of
Bergen

100. 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

101. Types of nerve endings: Gunji
T- 1982

102. 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

103. 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

104. Theories of tooth pain
perception
 Dentinal nerve
stimulation
 Dentinal receptor
theory
 Hydrodynamic
theory

105. 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)

106. Dentinal nerve
stimulation
 Predentin:
associated cells-
origin questioned
(Arwill- 1967)
Arwill T

107. Dentinal nerve stimulation
 Axons: separated
by narrow cleft
(Byers et al)
 Nerves: beaded
structures in SEM
(Tidmarsh- 1981)

108. 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

109. 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)

110. 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

111. Hydrodynamic theory
 Dentin pain & odontoblast displacement:
related
 BrӓnstrӦm et al (1966, 1967, 1969, 1972)
and Lilja (1980): hydrodynamic
mechanism

112. Hydrodynamic theory
 Stimuli: expansion/
contraction – fluid
 Pulpward/ outward
movement: nerve
stimulation

113. Hydrodynamic theory
Mechanisms - reduce fluid flow in dentin:
Pashley et al- 1982
 Plaque/ saliva bacteria
 Mineralized deposits- tubules
 Salivary/plasma proteins

114. 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???

115. Pulpal tissue pressure & pain
 Blood flow, pressure changes, dental pain
 hydrostatic pressure:
nerve fiber stimulation (Nӓhri- 1978)
 Pulp: mechanoreceptor- pain transmission

116. 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)

117. 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

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

119. Vitamin deficiency
 Vitamin C
- Fibroblasts
- Odontoblasts: degenerate & lose
morphology

120. Hormones & hormonal
imbalance
Steroids:
 Systemic corticosteroid
 Odontoblasts
 Inhibit reparative dentinogenesis
 Steroid :pulp therapy???

121. 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

122. Hormones & hormonal
imbalance
Thyroid deficiency:
 Pulp vascularity
 Pulpal lumen
 Cellular elements

123. Protein deficiency
 No pulpal changes noted (Glickman &
Shklar- 1954)
 Larger areas of periapical rarefaction
( Stahl et al -1958)

124. Systemic virus infection
 Odontoblasts injured: lymphocytic
choriomeningitis (Hancock-1956) & Shope
papilloma virus ( Fleming-1958)
 Degenerative changes & eventual
necrosis: rats with Polyoma virus

125. 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

126. Tumor transplantation
 Metastases: sparse reports
 Epitheliomas, sarcoma, Burkitt’s
lymphomas- human dental pulps (Stanley-
1973)

127. 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:

128. 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)

129. DPSCs
 Irreversible pulpitis: putative cells- stem
cell properties (Wang et al, 2010)
 Regeneration in canine teeth – Gelfoam
scaffold (Wang et al- 2013)

130. Conclusion
 Unique tissue
 Resembles embryonic connective tissue
 Dynamic response pattern

131. 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

132. 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

133. 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)

134. 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

135. 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)