Dental Pulp: development, innervation, vascular functions, pathways of pain, sensitivity and sensibility tests, pulpal diagnosis as applied to pediatric dentistry.

1. PEDIATRIC ENDODONTICS
Pathophysiology of Pulp
Dr. Balraj Shukla

2. CONTENTS
• Development of Pulpodentin complex
• Change of vascular architecture of dental pulp with
growth
• Microvascular exchanges within the Pulp
• Pulpal organization
• Regulation of blood flow in the Dental Pulp
• Response of Pulpodentin complex to caries
• Response of Pulpodentin complex to restorative
treatment

3. CONTENTS
• Dental innervation
• Dental Pain: Detection, Processing & Perception
• Pain pathways of the dental pulp
• Pulp Vitality Tests
• Clinical Pulpal Diagnosis

4. DEVELOPMENT OF PULPODENTIN COMPLEX
6th week IU
Epithelium
thickens to form
dental lamina that
proliferates &
joins enamel
organ to form
permanent bud
Epithelium covers
embryonic tissue
derived from
neural crest cells
to form
ectomesenchyme
Ectomesenchymal
cells condense &
proliferate to form
enamel organ,
dental papilla &
dental sac

5. Enamel
Organ
Inner Enamel Epithelium  DEJ
Outer Enamel Epithelium
Stellate Reticulum
Stellate Intermedium  REE
Junction of outer & inner enamel
epithelium forms cervical loop which
later becomes the HERS
Dental
Papilla
Becomes
more
fibrous &
condenses
PULP
Dental
sac/follicle
Cementum, PDL,
Alveolar Bone

6. Inner Enamel
Epithelium
Preameloblasts
Ameloblasts
Enamel Matrix
Outer layer
of dental
papilla
Preodontoblas
ts
Odontoblasts
Odontoblastic
processes
Deposition of
organic matrix
Predentin
Dentinal tubules
Deposition of
von Korff
fibers
Mantle dentin
Circumpulpal
dentin
Secondary
dentin
DENTINOGENES
IS

7. Oval/Circulated Reticulated
Plexus
Encircles enamel organ & dental
papilla
Formation of
subodontoblastic plexus (SP)
during dentinogenesis
Atrophy of SP to form pulpal
vessels
Reappearance of SP after root
formation
This constricts the pulpal
vessels into a small apical
foramen
Nerve fibers can be
initially seen in the
dental follicle but
they do not
proliferate
After root formation,
nerve proliferation begins
and inferior & superior
alveolar nerves enter the
pulp through apical
Formation of
Subodontoblastic
Nerve Plexus of
Raschkow
PULPAL INNERVATION &
CIRCULATION

8. Apical Foramen
Opening at the apex of the tooth root whose
location & shape depends on
- Pressure exerted on the tooth
- Mesial Migration of the tooth
- Resorption due to tissues entering from the
foramen
- Deposition of apical cementum
Can be traditional single, tapering, multi-
constricted, parallel
Accessory Canals
- Clinically important in the spread of infection
- Can be formed by premature loss of HERS
cells OR if the developing root encounters a
blood vessel.
- According to Cohen, these are found: 73.5% in
the apical third, 11.4% in the middle third and
15.1% in the coronal third

9. THE PULP
Dental pulp can be defined as a richly
vascularized and innervated connective
tissue of mesodermal origin enclosed
by dentin with communications to the
periodontal ligament.
‘Pulpa’ is Latin for animal and plant
tissues that are moist and soft,
occurring in the form of cohering mass.

10. THE PULP
Volume of pulp of all teeth: 0.38 cm3
Mean volume of single human pulp:
0.02 cm3
Fanibunda KB et al

11. • The development of pulpal vasculature with growth can be seen
in four stages:
-Completion stage of crown formation
-Root formation stage
-Root completion stage
-Maturation stage
Change of Vascular Architecture of Dental Pulp
with Growth

12. Completion stage of crown formation
• Crown calcification is complete
• Branches from inferior alveolar artery
in the mandible and the superior
alveolar artery in the maxilla enter
from the base of the tooth bud and
distributes in the coronal pulp.
• Another group of blood vessels
distributes over the reduced enamel
epithelium. From here, two groups of
vasculature develop, that grows in:
- Epithelium of gingiva
- Periodontal membrane
• Terminal capillary network forms at

13. Root formation stage
• Capillary network in coronal pulp now
has a thickness of 400-500 micrometres
• Blood vessels are now less tortuous
• In the apical region, arterioles and
venules run parallel to each other.
• There is now a close association
between vessels of pulp and
periodontium.

14. Root completion stage
• Stage of root formation with open apex
• Arterioles: run from apical foramen to
coronal pulp
• Venules: Along side the root canal
• Three layers of pulp vasculature (fish-net
appearance):
-Terminal Capillary Network
-Second Capillary Network
-Venular Network
APEX

15. Maturation stage
• Completion of apex formation,
narrowing of pulp chamber,
progression of dentin formation
• Entire pulpal vasculature remodels
itself
• Decrease in total number of blood
vessels
• Only terminal capillary network is
prominent. It is characterized by
‘short hairpin loops’
• These loops also indicate the
formation of secondary dentin.

16. Primary vs Permanent Pulp
Pulp Horn
Pulp Horn
Pulp
Chambe
r
Pulp
Chamber
Accessor
y Canals
Accessor
y Canals
Apical
Foramen
Apical
Forame
n
Root
canal
shap
e
Root
canal
shap
e

17. Pulpal
Organization
(Zones of the
Pulp)

18. Zone 1: Odontoblastic Zone
• Odontoblasts present in palisading
arrangement at the periphery of the
pulp.
• Cells bodies lies in the pulp, Cell
processes in the dentinal tubules.
• Length: 25-40 micrometres
• Diameter: 5-7 micrometres
• Coronal Pulp: Odontoblasts are tall
columnar
• Apical region: Odontoblasts are
flattened
• Rough endoplasmic reticulum
• Golgi apparatus
• Terminal bar apparatus of the
Odontoblast: Located at the area
where the cell body ends near the
Predentin.

19. Zone 1: Odontoblastic Zone
• Odontoblasts are end cells
• If they are lost, they are
replaced by the cells from the
cell-rich zone.
• Role in pulpal inflammation:
Release IL-8, Nerve Growth
Factor and Nitric Oxide
synthetase for vasodilatation
and regulation of blood
pressure within the pulp
microvasculature.

20. Zone 1: Odontoblastic Zone
Odontoblastic/Tomes processes are
present through the thickness of the
dentin. The end of these processes
play an important role in sensory
transmission.
Predentin is deposited around the
odontoblastic processes. Calcium
and Phosphorous salts are deposited
in this matrix to produce the dentin.
Interglobular dentin are the
hypocalcified areas in mature dentin.
Surrounding of the dentinal tubules
is called the peritubular dentin.

21. Zone 2: Cell-Free Zone/Zone of Weil
• This zone is absolutely absent in
the period of dentinogenesis.
• After maturation, it is more
commonly seen in the coronal
pulp.
• It contains Type I and Type III
collagen fibers. These fibers are
present diffusely (coronal) or in
bundles (apically).
• A part of the Plexus of Raschkow is
also present in this region.
• This zone contains ground
substance (proteoglycans,
glycoproteins and water) that helps
in metabolic exchanges of cells
and limits the spread of infection.

22. Zone 3: Cell-Rich zone
Fibroblasts
• Formation of collagen and deposition
of calcified tissue.
• Stellate/Spindle in shape
• Become rounder as age progresses.
• Apical third houses more fibroblasts
compared to coronal pulp.
• The fibrous tissues at the apex protect
the neurovascular bundles from injury
and facilitates removal of pulp during
pulpectomy.
• Apart from releasing chemical
mediators of inflammation, they
release FGF-2 & VEGF which helps in
healing.

23. Zone 3: Cell-Rich zone
Undifferentiated Mesenchymal cells
• Pluripotent characteristics
• Derived from dental papilla.
• Polyhedral in shape.
• Found along the blood vessels.
• Decrease in number with
increasing age.
Macrophages, Lymphocytes,
Histiocytes & Plasma cells
contribute to immune surveillance
of the pulp.
Ground substance
Performs the same function as it
does in the cell-free zone and

24. Potency of Pulpal stem cells
• Totipotent: They are formed shortly after
fertilization of an egg cell by a sperm cell.
They can become any type of cell in the
human body.
• Pluripotent: Can develop into any cell type of
the three germ layers (embryonic stem cells).
• Multipotent: Can develop into cell types of a
particular class or category. Example:
Haematopoietic stem cells (into cells of
immune system), Mesenchymal stem cells
(into cells of bone, fat, muscle, cartilage,
dental tissues), Neural stem cells (into glia,
neurons)

25. Zone 4: Central Zone/Pulp Core
Consists of blood vessels and nerves
embedded in the pulp core together with
the fibroblasts.
The blood vessels and nerves send their
branches to the periphery of the pulp.
Function in the pulp: NUTRITION

26. - MICROcirculatory system
- Arterioles and venules are
arranged axially in the pulp
with capillary loops extending
out toward the dentin.
The pulpal microcirculation is a
dynamic system that regulates
blood and lymph flow in response
to nearby metabolic or
inflammatory stimuli.
Microvascular exchanges within the Pulp

27. Lymphatic Drainage of Pulp
REGION PRIMARY LYMPH
NODES
SECONDARY LYMPH
NODES
Maxillary incisors and
canines
Submandibular Superior Deep Cervical
Maxillary premolars,
Maxillary first & second
molars
Submandibular Superior Deep Cervical
Maxillary third molar Superior Deep Cervical Inferior Deep Cervical
Mandibular incisors Submental
Submandibular & Deep
Cervical
Mandibular canines,
premolars, molars
Submandibular Superior Deep Cervical

28. Pulpal Interstitial Pressure
• Initially it was believed that inflammation of pulp
would lead to a generalized collapse of pulp vascular
(Pulp Strangulation Theory).
• Now we understand that pulp circulatory responses to
pulp inflammation are localized in nature.
• This is because of the regulation of pulpal interstitial
pressure (5-6 mmHg). This level is maintained by
Starling’s forces, capillary permeability and lymphatic
outflow.
• Lymphatic vessels coexist with blood vessels in the
dental pulp.
• The lymphatic system is the dominant mechanism for
removal of high molecular weight solutes from
interstitial fluid. This reduces the interstitial colloidal

29. Microcirculation
• This process directs capillary blood flow to
local pulpal regions with the greatest
metabolic need.
• Alterations in capillary blood flow produce
changes in capillary hydrostatic pressure
(Pc); this in turn regulates fluid balance
between the vascular and interstitial
compartments.
• The terminal arterioles and precapillary
sphincters play major roles in the control of
capillary perfusion. In contrast, the major
sites of blood volume control and
postcapillary resistance are the muscular

30. Transcapillary Exchange
Several factors regulate the exchange of materials
between the vascular compartment and the
interstitial space.
- Composition/concentration of exchange material
- Fenestrated capillaries with junctional openings
- Capillary filtration (defined by the Starling forces)
Difference between capillary hydrostatic pressure (PC)
& interstitial hydrostatic pressure (PI): Outward
direction of fluid flow (filtration) at the arteriolar end
of capillaries.
Difference between capillary colloidal osmotic
pressure (COPC) and interstitial colloidal osmotic
pressure (COPI): Inward direction of fluid flow
(absorption) at the venular end of capillaries.
The clinical significance of the Starling forces is that
they are altered during inflammation, giving rise to

31. Regulation of Pulpal Blood Flow
Neuronal regulation
Sympathetic fibers present more near pulp horns and
less at the apical region.
Stimulation of sympathetic nerves releases
neurotransmitters like norepinephrine, adenosine
triphosphate and neuropeptide Y, that cause
vasoconstriction.

32. Regulation of Pulpal Blood Flow
Metabolic regulation
Adenosine, low interstitial pO2 levels, low pH, or elevated
pCO2 levels may increase pulpal blood flow via
vasodilatory effects.
Localized increases in pulpal activity (eg, dentinogenesis)
may lead to localized increases in pulpal blood flow.
The relatively low overall metabolic activity of the pulp
suggests that metabolic control of pulpal blood flow may

33. Regulation of Pulpal Blood Flow
Endocrine Regulation
Bradykinins, Endothelin I, Prostaglandins and Histamines
increase pulpal blood flow (elevated in irreversible
pulpitis). These factors are locally produced or released
at their site of action and do not circulate in the
bloodstream.

34. Response of Pulpodentin Complex to Caries
The response of Pulpodentin complex to caries
can be explained under 3 subheadings:
- Injury responses
- Defense responses
- Repair responses

35. INJURY RESPONSES
Acids found in carious dentin: Lactic, Acetic & Propionic
Dentin’s resistance against these acids: outward fluid flow,
hydrogen ions release
Thus, to initiate an injury in the Pulpodentin complex, the acids
have to diffuse within the 0.6 mm thick dentin.
When microbes exert their effect over a quarter of the enamel
thickness, the odontoblasts and subodontoblastic plexus get
activated.

36. INJURY RESPONSES
Odontoblasts are the first layer of cells that come into contact
with pathogens that penetrate dental tissues.
Odontoblasts have both secretory and sensory function.
• Secretory: Reactionary dentin formation
• Sensory: Release of VEGF and Release of Neuropeptides from
Fibroblasts
This leads to an increase in dentin permeability, causes oedema,
increase in intrapulpal pressure and eventual irreversible pulpal
damage.
Function in the pulp:
PROTECTIVE

37. DEFENSE RESPONSES
The innate immunity of the body can help in resisting
shallow caries initially. Pulpal responses are low grade
and chronic at this stage.
When the carious lesion is deep (2 mm away from
pulp) odontoblasts try to modify the permeability of
the dentinal matrix by forming tertiary dentin. The first
formed tertiary dentin is called interphase dentin.
The progression of caries reduces the amount of
peritubular dentin, as a result of which sclerotic dentin
is formed. Both sclerotic and tertiary dentin can have
trapped bacteria, which can further degrade these
dentinal layers and cause acute pulpal inflammation.
If the source of caries infection is not eliminated,
immune inflammation in pulp will cause its irreversible
Deep
Localized
microabscess
Clinically identifiable
abscess
Pulp Necrosis
Peri-radicular lesion

38. REPAIR RESPONSES
Reparative dentinogenesis is the secretion of dentin after the death of
odontoblasts. The loss of odontoblasts leads to the formation of dead tracts,
that allow microbes and noxious products to enter the pulp.
Reparative dentinogenesis is usually seen in caries lesion that are approaching
the pulp. This leads to the formation of dentin bridge.
If the remaining dentin thickness is less than 0.25 mm, reparative
dentinogenesis cannot take place as secretory potential of odontoblasts is
hampered.

39. Response of Pulpodentin Complex to Restorative
Treatment
The response of Pulpodentin complex to
restorative treatment can be explained under 2
subheadings:
- Response to cavity preparation
- Response to restorative materials

40. RESPONSE TO CAVITY PREPARATION
Dental pulp responds to irritation stresses (like heat generation by
Airotor) by producing heat shock proteins. Expression of these proteins
in odontoblasts and various cells of the pulp indicate that they are
involved in resisting injury during cellular stress.
TECHNIQUE
TEMPERATURE
CHANGE (ᵒC)
Absence of water coolant 5.5
High speed + High air pressure 20
Low water cooling + High air pressure + High
speed
5.9
Copious water cooling + Air pressure + Normal
speed
-1.8 to 3.1
*Critical increase in intrapulpal temperature by 5.5 –
Irreversible pulpal injury
*Critical increase in intrapulpal temperature by 11 – Pulpal
Necrosis

41. RESPONSE TO RESTORATIVE MATERIALS
Acid-etching can cause temporary dentin
permeability, until resin penetrates and
polymerizes.
Material toxicity of underlying pulp becomes an
issue only when remaining dentin thickness is less
than 0.5 mm.
Ingress of microbes and microbial products due to
marginal gaps and microleakage is often seen with
resin-based cements.
Odontoblasts survive best when the restorative
material is placed over a RDT of 0.5-3 mm.
Calcium hydroxide and MTA perform best when
placed in cavities with RDT of less than 0.5 mm

42. PULPAL INNERVATION
Nerve fibres contribute to tooth
survival by:
- Detecting dental stimuli
- Triggering dental reflexes
- Interacting with pulp cells
- Maintenance of healthy tooth
function
- Repair Based on sensory
perception
Sharp pain
Dull pain
Pre-pain
Based on stimulus
Mechanical
Thermal
Chemical
Noxious
Polymodal
Based on conduction
velocity
Aβ fibres
Aδ-fast fibres
Aδ-slow fibres
C-fibres

43. DEVELOPMENT OF THE INNERVATION WITHIN THE PULP
11th Week IU
18th Week IU
24th Week IU
Emergence
of
myelinated
nerves
No nerve fibers or
plexus are observed
near the dentin
during the foetal
period.
Nerves reach pulp
horns by following
blood vessels as the
pulp develops.
Pulp cells produce:
• Nerve growth
factor
• Semaphorin 7A
• Brain-derived
neurotrophic
factor

44. Nerve fibers in pulp and dentin are
components of a large somatosensory
system that also includes
• Gingiva: sensations of touch, pressure,
and temperature via activation of special
mechanoreceptors or thermoreceptors
• Junctional Epithelium: Regulates
vasodilation, transmigration of leukocytes
across the epithelium into the oral cavity,
and antimicrobial actions
• Periodontal ligament: contains large
Ruffini mechanoreceptors from the
trigeminal ganglion or mesencephalic
nucleus that give sensations of tooth

45. C-fibers Aδ-fibers
Unmyelinated Myelinated
Conduction
velocity: 0.4-2m/s
(slow)
Conduction
velocity: 6-30m/s
(fast)
Distributed
throughout pulp
tissue
Distributed in
odontoblastic and
subodontoblastic
zones
Lingering, dull,
poorly localized,
aching pain
Short, well-
localized, sharp
and pricking pain
Triggered when
chemical mediators
are released due to
Mechanism best
explained by
hydrodynamic
theory (fluid

46. Neural response after injury to pulpodentin complex
Stimuli that injure the pulpodentin complex have been classified at
four different levels.
Type I – Least damaging
Transient change in pulp, including reactive dentinogenesis
Changes in nerve fibres return from normal to within a few days to few
weeks
Example: shallow cavity preparations, scaling of cervical dentin, strong
orthodontic forces
Type II – Dentinal injury
Some loss of pulpal tissue, focal inflammation
Pulp can repair itself and form reparative dentin
Example: deep dentinal caries, small pulpal exposures, heat stimulation
of long duration/high intensity.

47. Neural response after injury to pulpodentin complex
Type III – Pulpal damage
Irreversible pulpitis
Progression to necrosis is faster
Example: Large infected pulpal exposures, bacterial invasion to failed
restorations, deep infected caries, coronal pulp destruction
Type IV – Injuries to other tissues apart from dentin and pulp
Affects the periradicular tissues
Example: dental fractures, tooth extractions damaging the ligament

48. Detection, Processing and Perception of Dental Pain
Dental pain can be stimulated because
of the stimulation of nociceptive fibres
by:
- Dentinal fluid movement
- Chemical mediators released by
inflammation
• Components of the pulpal
nociceptive stimuli:
- Peripheral afferent nerve fibres
- Local interneurons
- Projection neurons
- Descending neurons
- Glia

50. Hydrodynamic Theory
Dentinal sensitivity is characterized as
a sharp pain that occurs soon after a
provoking stimulus.
Anatomical relationship between nerve
fibers and odontoblasts may be the
physiologic basis for the hydrodynamic
theory of dentinal pain which was given
by M.Brannstrom in 1967.
It is not known how nerve fibers detect
fluid movement. But sharp quality of
the resulting pain suggests activation
of Aδ nociceptive fibers.

51. Peripheral Afferent Nerve Fibres
(DETECTION)
C-fibres and Aδ fibres receive the stimulus
Depolarization of nociceptors
Generation of action potentials
Opening of voltage-gated sodium channels
Release of proinflammatory neuropeptides like
Substance P
Calcitonin gene-related peptide
Neurokinins
Glutamate
Information sent to CNS
Odontoblasts act as receptor cells for noxious stimuli

52. Dual pathways for transmission of pain
signals
(PROCESSING)
• Responsible for slow-chronic pain signal transmission
• Maintains wakefulness of the CNS during pain signalling
• Activated descending neurons for pain-control

53. Dual pathways for transmission of pain
signals
(PROCESSING)
• Also known as anterolateral or ventrolateral tract
• Transmits fast-sharp pain signals
• Conveys pain caused by touching the face

54. Local, Projection, Descending neurons and Glia
(PROCESSING)
• Local neurons: Responsible for impulse transmission
and modulation of pain signal by release of
neurotransmitters like GABA. Act as bridge between
afferent nerve fibres and projection neurons.
• Projection neurons: Project pain information to
thalamus depending on type of stimulation (3 types)
- Low-threshold mechanoreceptive: Light tactile
stimulation
- Nociceptive-Specific: High-threshold noxious
stimulation
- Wide Dynamic Range: Both tactile and noxious stimuli
• Descending neurons: Help in modulating pain by
release of endogenous opiates and endorphins that
block neurotransmitters to the thalamus.

55. Trigeminal Pathway of Pain Transmission from Face
Pain
pathway
(generalized
)
Pain Pathway (face)
Nociceptive
receptors – First
order neurons
Nociceptive
receptors – First
order neurons
Dorsal horn –
Second order
neurons
Trigeminal, Facial,
Glossopharyngeal, Vagus
nerve
Spinal Trigeminal Nucleus
– Second order neurons
C2-S5 nerves
Spinothalamic tract
Trigeminothalamic tract

56. Trigeminal convergence
The overlap of the
trigeminal nerve
with the cervical
nerve occurs when
the spinothalamic
tract meets the
trigeminothalamic
tract.
This convergence is
responsible for
chronic headaches,
migraines, diffuse
pain,

57. Central Sensitization
Central sensitization is the
hyperexcitability of neurons that leads to
secondary effects of pain (Example:
Referred pain). Prolonged nociceptive
input can lead to functional changes in
the spinal dorsal horn, subnucleus
caudalis and the thalamus.
Central sensitization leads to a
dysfunctional hypersensitive system
where the discrimination between low-
intensity stimuli and noxious stimuli
(pain) is lost.
It occurs due to convergence mechanisms
or due to neuroplasticity (sensory

58. Central Sensitization
C-Fibers are activated upon tissue
inflammation and peripheral nerve injury.
Slow action potentials sum up with the
help of NMDA and Neurokinin receptors
that lead to alteration in
neurotransmission.
Increased excitability and synaptic
efficacy due to phosphorylation of ion
channels.
Central sensitization due to firing action
potentials.

59. Dental Pain caused by Inflammation (PROCESSING)
C-fibres
triggered
Sympathetic nerve
fibers of dental pulp
cause vasodilatation
upon pulpal
inflammation
Histamine, Bradykinin,
Capsaicin ,Prostaglandins
and Cytokines are
activated
Microbial
invasion
Release of
endotoxins/
lipopolysaccharides

60. Nature of Dental Pain (Perception)
Dental
pain
Odontogeni
c
Non-
Odontogenic
Nociceptiv
e
Inflammat
ory
Neuropathic Dysfunctio
nal
Referred
Periphera
l
Central
Allodyni
a
Hyperalgesi
a

61. Nociceptive Pain
No nervous system lesion or pulpal inflammation
Stimulus-dependent pain
Adaptive: Protects by signalling potential tissue
damage
Reversible: Resolves upon healing of damaged
tissue
Pulp test and Percussion tests are normal
Examples:
- Mechanical injury
- Chemical injury
- Thermal injury

62. Allodynia
It is defined as a reduction in pain threshold so
that previously non-noxious stimuli are
perceived as painful.
Pain due to stimulus that normally does not
evoke pain.
Involvement of Aβ fibers apart from C-fibers.
Percussion test is usually positive (mechanical allodynia).
Example: Mastication, Eating/Drinking hot or
cold foods
Hyperalgesia (Peripheral)
It is an increase in the perceived magnitude of a
painful stimulus. Primary hyperalgesia occurs only
in the area of inflammation and tissue injury.
Secondary hyperalgesia occurs in adjacent areas
too.
It is induced by heat and mechanical stimuli and is
• Active
inflammation
• Sensory
amplification
• Protects by
producing pain
hypersensitivity
after injury and
during healing

63. Hyperalgesia (Central)
Arises due to firing action potential of C-fibers in
central pulp. It is also called central sensitization. It
can occur due to inhibition of descending neurons,
sprouting of nerves into inflamed tissues,
heightened released of chemical mediators.
Examples:
Reversible pulpitis
Symptomatic irreversible pulpitis
Symptomatic apical periodontitis
Acute apical abscess
Post-pulpotomy

64. Neuropathic
High intensity, electric-shock like, lancinating,
stabbing pain
Underlying nervous system lesion or disease
Abnormal sensory amplification
Lack of response to anti-inflammatory drugs or
NSAIDs
Examples:
Trigeminal/Glossopharyngeal neuralgia
Nerve compression
Traumatic nerve injury
Stroke
Multiple sclerosis
Spinal cord injury

65. Dysfunctional
No known structural lesion or inflammation
Sensory amplification
Maladaptive and potentially persistent
Examples:
Fibromyalgia
Atypical odontalgia
Referred
Pain perceived in a region that is away from the nociception origin.
It is based on theory of convergence (dermatome rule), according to
which multiple sensory neurons project on the same centrally projecting
neuron. Example: Pain in inflamed mandibular molar radiates to
preauricular region.
Central sensitization can also cause referred pain. Example: Pain in the

66. Referred Pain from Teeth
Trigeminal convergence and
Central sensitization can explain
the mechanism of referred pain.
This is because follows a
dermatome pattern, where a
single nerve projects on a
centrally projecting neuron.

67. Hot Tooth
Hot tooth generally introduce to a pulp that has been
diagnosed with irreversible pulpitis, with
spontaneous, moderate-to-severe pain. Size of the nerve fibre
outweighs myelination in the
sequence in which they are
blocked.
Small myelinated fibers 
Small unmyelinated fibers 
Large myelinated fibers 
Large unmyelinated fibers
Order in which sensations are
lost:
Pain  Temperature  Touch
 Pressure
In hot tooth, anesthetic failures can occur because
of the following reasons:
- Conventional anesthetic techniques do not
necessarily cause pulpal anesthesia
- Inflamed tissue has a lower pH which brings down
the amount of base form of anesthetic that
invades the nerve membrane to cause anesthesia.
- Resting potential of nerves in the inflamed tissue
varies and thus transmission of nerve impulses
takes time to stop.

68. Hot Tooth
Hot tooth generally introduce to a pulp that has been
diagnosed with irreversible pulpitis, with
spontaneous, moderate-to-severe pain. Size of the nerve fibre
outweighs myelination in the
sequence in which they are
blocked.
Small myelinated fibers 
Small unmyelinated fibers 
Large myelinated fibers 
Large unmyelinated fibers
Order in which sensations are
lost:
Pain  Temperature  Touch
 Pressure
In hot tooth, anesthetic failures can occur because
of the following reasons:
- Tetrodotoxin resistant sodium channels are
resistant to local anesthesia. They are present in
the inflamed dental pulp and are sensitized by
prostaglandins. In such cases, pre-emptive
analgesia with NSAIDs can help in improving the
effect of local anesthetics.
- Increased production of prostaglandins due to
activation of nociceptors in inflamed tissues can
increase the sensitivity of nerve tissues.

69. Pulp Vitality Tests
Neural Sensibility Tests
Thermal tests: Heat and
Cold Tests
Electric Pulp Test
Anesthetic Test
Test Cavity
Pulp Vascularity Tests
Pulse Oximetry
Laser Doppler Flowmetry
Dual-wavelength
Spectrophotometry
Thermography
Photoplethysmography
Pulp Hemogram
Experimental Tests
(requiring further
evidence)
Ultraviolet Light
Photography
Transillumination
Hughes Probeye
Recent Developments
Detection of Interleukins
Gas Desaturation
Thermographic imaging
Optical Reflection
Vitalometry
Cholesteric Liquid Crystals
Color Power Doppler
Radiolabelled Microsphere

70. • HEAT TEST – Van Hassel’s
Theory
Heat application for <5
seconds (from
occlusobuccal third
towards the cervical
margin)
Increased intrapulpal pressure
Reduced neuronal excitation
threshold
Immediate
Excruciating Pain
OR Lingering Pain
Response
similar to
control tooth
No response
Irreversible Pulpitis Healthy
state of the
pulp
Further diagnosis
with other tests to
confirm non-

71. • COLD TEST – Brannstrom’s
Theory
Cold application for <15
seconds (from occlusobuccal
third towards the cervical
margin)
Short sharp
pain that
disappears
after
removal of
stimulus
Respon
se
similar
to
control
tooth
No response
Reversib
le
Pulpitis
Healthy
state of
the
pulp
Further
diagnosis
with other
tests to
confirm
non-
vitality
Lingerin
g Pain
after
stimulu
s
removal
Irreversi
ble
Pulpitis

72. • Electric Pulp Test
Same
neural
excitation
threshold
as control
tooth
Negativ
e
respons
e
False
positive
response
Normal
Non-
vital
tooth
Gangrenous
necrotic pulp,
Partially
necrotic pulp
in multi-
Early/
Delayed
Respon
se
Diseased
state of
the pulp
False
negative
response
Calcified teeth, Fibrotic
Pulp, Traumatized teeth,
Diminishing pulp with
greater reparative dentin,
Restored teeth, Incomplete
root formation, Patient on
Principle: Stimulation of pulpal response by
subjecting the tooth to increased degrees of
electric current
Procedure: Following isolation of teeth, prophy
paste is applied to the tooth & the probe of EPT
is placed on occlusobuccal third (for anteriors)
or middle third of mesiobuccal cusp (for
posteriors). The circuit is completed by placing a
lip clip or by asking the patient to hold the
metal sheath of the EPT.

73. • Anesthetic Test
Infiltration or intraligamentary
injection is given in the posterior
tooth in the area where pain is
suspected. If pain persists,
anesthetize the next tooth
mesial to it until pain
disappears.
If source of pain (maxillary or
mandibular) is unidentifiable, an
IANB can be given. Localization
of specific tooth can later be
done by intraligamentary
injection.
• Test Cavity
Prepared by drilling through DEJ
of unanaesthetised tooth.
Sensitivity or pain felt by the
patient is indicative of pulp
vitality. No endodontic treatment
is needed.
If drilling continues till the pulp
chamber is reached, necrotic
pulp is suspected and
endodontic treatment can be
carried out without anesthesia.

74. Pulse Oximetry
Principle: To assess the
relationship between
pulsatile change in the
absorption of light of
different wavelengths
and its analysis with the
pulse oximeter to
determine saturation of
arterial blood.
Red light  660 nm
Infrared light  940 nm
Finger, ear or foot
probes can be used for
measuring oxygen

75. Principle: Laser light transmitted through
a fibre-optic source is absorbed by the
RBCs which leads to change in the
frequency of scattered light. This is
based on Doppler’s frequency where the
light wave’s frequency changes with the
movement of the blood cells. This
movement helps us in knowing that
blood is present within the pulp space.
This technique takes at least 30 minutes
to produce recordings making it
impractical for routine dental use.
Laser Doppler Flowmetry

76. • Dual wavelength
spectrophotometry
This method is independent of
pulsatile circulation. It measures
oxygenation changes in pulp
space by passing an incident
light of 850 nm and 760 nm. It
requires strict isolation and is
also highly technique sensitive.
• Thermography
In this method, the teeth of
concern are cooled down for 15
seconds. Teeth with a vital pulp
will rise to surface temperature.
Teeth with necrotic pulp will
rise to surface temperature
much slower.
This technique is non-invasive
and highly accurate but
requires the patient to be at
rest for 1 hour prior to testing.

77. • Photoplethysmography
Involves passing light on the
tooth and measuring existing
wavelengths using a photocell
and galvanometer.
If tooth has an intact blood
supply, there should be vascular
vasodilatation, which records as
a current from the photocell.
• Pulp Hemogram
It was suggested in 1966 by
Guthrie and Baume that taking
a drop from exposed pulp and
subjecting it to differential WBC
count can help in diagnosis of
pulpal conditions.

78. • Transillumination
Utilizes strong light source
which identifies color changes
that indicate pulp pathosis.
Cannot be useful in teeth with
large restorations.
• Ultraviolet Light Photography
Examines different fluorescence
patterns that may allow
additional contrast of otherwise
more difficult to observe visible
changes.
• Hughes Probeye Camera
Was sensitive enough to detect
changes as small as 0.1◦C. It is a
thermographic/infrared camera
utilizing wavelength of 14000
nm.

79. • Detection of Interleukins
IL-1 beta has been shown to be active
during bone resorption. Periapical
samples when put under organ culture
exhibit significant activity of IL-1 beta
whereas normal pulp had no activity.
• Gas Desaturation
In 1999, Goho carried out a study in
permanent and deciduous teeth where
they found out the spO2 to be in the
range of 93-94%.
• Optical Reflection Vitalometry
In 1997, Oikarinen et al reported
another method where one can see the
pulse of the pulp of oral mucosa. The
device for this is yet to be clinically
accepted.
• Cholesteric Liquid Crystals
Non-vital teeth have lower
temperature than vital teeth.
Cholesteric liquid crystals when
applied to tooth surface changed
colours which helped in detecting the
vitality of the tooth.
• Radiolabelled Microsphere
Pulpal blood flow through radiolabelled
microsphere has been estimated to be
20-60 mL/min/100g tissue. In exposed
pulp, fluid pressure is high and
• Xenon 133
Xenon 133 in saline when injected as
a buccal intraligamentary injection.
Radiation counts were higher for vital
teeth and less for non-vital teeth.

80. • Limitation of Pulp Neural Sensitivity Tests
- Do not measure vascular flow of the pulp
- Cannot be used in elderly as these tests require the dentinal
tubules to be open to allow fluid movement. In elderly, more
secondary dentin results in closed tubules.
- They cannot be used in immature teeth as Plexus of Raschkow
does not completely develop till root apices close.
- Does not correlate with histological status of the pulp
- Inconclusive when used in children as their response to sensitivity
test varies
- Cannot be a reliable indicator in traumatized and restored teeth
- Patient response may also vary with reference to the time of the
day

81. • Accuracy of Pulp Vitality Tests
(Permanent teeth)
Gopikrishna V et al (2006)
Cold Test: 86%
EPT: 81%
Heat Test: 71%
Abd-Elmeguid and Yu (2009)
Pulse Oximetry: 100%
Cold Test: 81%
EPT: 71%

82. • Accuracy of Pulp Vitality Tests (Primary
teeth)

83. • Accuracy of Pulp Vitality Tests (Primary
teeth)

84. Clinical Pulpal Diagnosis
Clinical pulpal diagnosis process:
- History taking
- Clinical examination
- Clinical tests
- Radiographs
- Diagnosis
Acute—rapid onset and a short, severe course; moderate to severe pain
(symptomatic) ; patient is seeking urgent relief of the symptoms.
Chronic—long-standing; no pain (asymptomatic) or only mild and
occasional pain; patient not seeking urgent relief.
Reversible - pulp is capable of healing following conservative
management.
Irreversible - pulp is not capable of healing following conservative
management and therefore the pulp or the tooth needs to be removed.

85. Clinical Pulpal Diagnosis
CLINICALLY NORMAL
PULP
- No symptoms
- Normal reaction
to pulp tests
- Normal
percussion and
palpation
- Normal periapical
tissues
CHRONIC REVERSIBLE PULPITIS
- Long standing pain, mild in
nature, present for short
duration
- Percussion test may or may
not be positive
- Pain only occurs in extreme
temperature changes
- Thermal tests are positive
- Slight widening of the PDL
space
- Previously restored tooth
ACUTE REVERSIBLE PULPITIS
- Sharp pain present since a
few days upon application
of stimulus
- Percussion test may or
may not be positive
- Pain only occurs in
extreme temperature
changes
- Thermal tests are positive
- Slight widening of the PDL
space
- Previously restored tooth

86. Clinical Pulpal Diagnosis
CHRONIC IRREVERSIBLE
PULPITIS
- Pain present since a
long time (months)
- Pain occurs due to
minor temperature
changes (tap water)
- Pain is initially sharp
and severe  dull
aching  lingering
(more than 5 minutes)
- Pulp testing can
reproduce the pain
caused by the hot or
cold stimuli
- May or may not be
accompanied by apical
ACUTE IRREVERSIBLE
PULPITIS
- Pain present since a
short time
- Pain is sharp, severe
and lingering (more
than 5 minutes)
- Pain occurs due to
minor temperature
changes (tap water)
- Pain can occur while
lying down, maybe
spontaneous.
- Pulp testing can
reproduce the pain
caused by the hot or
cold stimuli
PULP NECROBIOSIS/PARTIAL
NECROSIS
- Presence of necrotic tissue
with the inflamed tissue
- Different conditions may
exist with different canals
in the same tooth
- Patient presents with a
mixture of symptoms which
can include spontaneous,
lingering pain due to minor
temperature changes
- Pulp testing results are
inconclusive
- Swishing the mouth with
cold water can temporarily
relieve pain.

87. Clinical Pulpal Diagnosis
PULP NECROSIS
- No pulp-related
symptoms
- No response to pulp
testing
- Discoloration of teeth
is often seen and
history of trauma is
taken
- No signs of apical
periodontitis
NECROTIC AND INFECTED
PULP
- Transient condition
that occurs following
necrosis.
- Initially there is no
periapical finding.
- Primary apical
periodontitis maybe
present
- Occasional pain with
positive percussion
test maybe present
- No response to pulp
testing
PULPLESS AND INFECTED
CANAL
- Symptoms depend on
periapical status as there
are no pulp-related
symptoms
- Occasional dull aches
accompanying apical
periodontitis maybe
present
- Mobility and tooth
discoloration must be
assessed
- Abscess, Sinus tracts and
facial cellulitis may develop

90. • The utmost goals of modern pediatric dentistry are to bring children
into the permanent dentition after natural exfoliation of their healthy
and/or properly treated primary teeth and instill a positive attitude
toward keeping habits of optimal dental and oral health.
• Studying the endodontium can help in understanding the various ways
the tooth responds to different stimuli.
• Diagnosis of the condition that a patient presents with should be
methodical with proper history taking, assessing the nature of pain,
pulp testing and radiographic appearance.
CONCLUSION

91. • Hargreaves, K., Goodis, H., Tay, F., & Seltzer, S. (2012). Seltzer
and Bender's dental pulp (2nd ed.). Quintessence Publishing.
• Inoki, R., Kudo, T., & Olgart, L. (1990). Dynamic Aspects of
Dental Pulp. Dordrecht: Springer Netherlands.
• Kumar G.S. (2019). Orban’s Oral Histology and Embryology
(15th ed.). Elsevier India.
• Chandra, B., Gopikrishna, V., & Grossman, L.
(2014). Grossman's Endodontic Practice (13th ed.). Gurgaon:
Wolters Kluwer (India).
• Goldberg, M. (2014). The Dental Pulp. Springer.
• Fuks, A., & Peretz, B. (2016). Pediatric Endodontics. Springer
International Publishing Switzerland.
REFERENCES

92. • Pashley, D. (1996). Dynamics of the Pulpo-Dentin
Complex. Critical Reviews In Oral Biology & Medicine, 7(2),
104-133. doi: 10.1177/10454411960070020101
• BERGGREEN, E., BLETSA, A., & HEYERAAS, K. (2007). Circulation
in normal and inflamed dental pulp. Endodontic Topics, 17(1),
2-11. doi: 10.1111/j.1601-1546.2010.00249.x
• Jafarzadeh, H., & Abbott, P. (2010). Review of pulp sensibility
tests. Part I: general information and thermal
tests. International Endodontic Journal, 43(9), 738-762. doi:
10.1111/j.1365-2591.2010.01754.x
• GOPIKRISHNA, V., PRADEEP, G., & VENKATESHBABU, N. (2009).
Assessment of pulp vitality: a review. International Journal Of
Paediatric Dentistry, 19(1), 3-15. doi: 10.1111/j.1365-
263x.2008.00955.x
REFERENCES

93. • Sahu, Somya & Kabra, Pooja & Choudhary, Ekta. (2019). Hot
Tooth -A Challenge to Endodontists. International Journal of
Science and Research (IJSR). 8. 106-109.
10.21275/ART20195849.
• Hall, J., Guyton, A., & Hall, M. (2015). Guyton and Hall textbook
of medical physiology (3rd ed.). Saunders.
• Piovesan, Elcio & Kowacs, Pedro & Oshinsky, Michael. (2003).
Convergence of cervical and trigeminal sensory afferents.
Current pain and headache reports. 7. 377-83.
10.1007/s11916-003-0037-x.
• Latremoliere, A., & Woolf, C. J. (2009). Central sensitization: a
generator of pain hypersensitivity by central neural
plasticity. The journal of pain, 10(9), 895–926.
REFERENCES