Pulp & pulpal diseases from intro to diseases

1. DEPT. OF
CONSERVATIVE DENTISTRY
&
ENDODONTICS
9/26/2013 1

2. DENTAL PULP & PULPAL
DISEASES
Presented By:- Dr Nishant Khurana
PG Student
Guided By:- Dr M.P. Singh
&
Dr Hemant Chourasia
9/26/2013 2

3. CONTENTS
DENTAL PULP
• INTRODUCTION
• DEVELOPMENT
• ANATOMY
• CELLS OF PULP
• FUNCTIONS OF PULP
• BLOOD FLOW
• METABOLISM
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4. • INNERVATION & NERVE SUPPLY
• CLINICAL CORELATION
• REGRESSIVE CHANGES
• FACTORS TO BE CONSIDERED
CLINICALLY
• EFFECT OF DENTAL MATERIAL ON
PULP9/26/2013
4

5. PULPAL DISEASES
CLASSIFICATION
CAUSES
ACUTE REVERSIBLE PULPITIS
ACUTE PROGRESSIVE PULPITIS
CHRONIC PULPITIS
CHRONIC OPEN HYPERPLASTIC
PULPITIS
PULP CALCIFICATION
PULP NECROSIS
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6. DIFFERENTIAL DIAGNOSIS
PULP INSULTS
PROGRESSION OF DISEASES
DYNAMICS OF PULPAL RESPONSE
CLINICAL CLASSIFICATION OF PULP
DISEASES
REFERENCES9/26/2013 6

7. DENTAL PULP
9/26/2013 7

8. WHY STUDY PULP?
• From many perspective, dental
health is directly related to the
health of unique tissue that is –
DENTAL PULP
• However, the study of dental pulp is
not restricted to this tissue alone,
but extends to its interactions with
many other tissues in health and
disease
9/26/2013 8

9. INTRODUCTION
• Pulp is a soft connective tissue of
mesenchymal origin occupying the central
position in the tooth.
• It is similar to other connective tissues
present in the body except that it has
highly sophisticated cell layer of
odontoblasts.
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10. Definition
• Dental pulp is the soft tissue located in
the center of the tooth ,enclosed in a
rigid chamber comprising dentine,
enamel & cementum which provides
strong mechanical support &protection
from the microbial rich oral flora.
» Acc. To Shafer’s
9/26/2013 10

11. Acc. To Cohen
The pulp is a soft tissue of
mesenchymal origin residing within the
pulp chamber and root canals of teeth.
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12. DEVELOPMENT
• Genesis begins in 7th week of IUL
during initiation of tooth development.
• Origin:- Ectomesenchymal cells of
dental papilla.
• Initially called the Dental Papilla & is
designated as “pulp” only after dentin
forms around it.
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13.  At 7th week of intrauterine life – primary epithelial
bands divides into vestibular / lip band and inner dental
lamina.
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14.  8th week of intrauterine life – dental lamina
shows ten areas of thickening called tooth
buds.
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15. DETAILS OF TOOTH GERM
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16. A9/26/2013 16

17. Fig:-A the bud; B the cap, and
C the bell stage9/26/2013 17

18. 9/26/2013 18

19. S.No Morphologic Stages
Histogenetic or physiologic
phases
1. Dental lamina Initiation
2. Bud stage Proliferation
3. Cap stage Histo-differentiation
4. Bell stage Morpho-differentiation
5.
Formation of enamel and
dentin matrix
Apposition
9/26/2013 19

20. 9/26/2013 20

21. 9/26/2013 21

22. • It is a soft connective tissue which is
vital & occupies centre of tooth
surrounded by dentin.
• Total of 52 pulp organs are present
– 32 in permanent teeth
– 20 in the primary teeth
• Average volume of pulp 0.024 ml
9/26/2013 22

23. PULP VOLUME FOR THE PERMANENT
HUMAN TEETH
Maxillary (cc) Mandibular (cc)
Central incisor 0.012 0.006
Lateral incisor 0.011 0.007
Canine 0.015 0.014
First premolar 0.018 0.015
Second premolar 0.017 0.015
First molar 0.068 0.053
Second molar 0.044 0.032
Third molar 0.023 0.0319/26/2013 23

24. Anatomically pulp is divided into
• Coronal pulp
• Radicular pulp
• Accessory canals
• Apical foramen
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25. Coronal pulp
• Its Centrally situated shows following
surfaces:
–Roof or the occlusal portion
–Mesial surface
–Distal surface
–Buccal surface
–Lingual surface
• Deposition of secondary dentin leads in the
change in shape and size of coronal pulp.9/26/2013 25

26. RADICULAR PULP
• This is continuous with a Periapical
connective tissue through the apical
foramen.
• The shape of the radicular pulp is
tubular or funnel shaped
• The caliber of the canal is greatest
during development and decreases as
life increases.9/26/2013 26

27. APICAL FORAMEN
• Average size
Maxillary – 4mm
Mandibular – 3mm
• Location may change
• Can be lateral in position or it may
branch at the tip to form 2 foramina.
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28. Accessory canals
• May be seen any where from floor
along the length of root.
• Most commonly seen in the apical third
9/26/2013 28

29. CELLS OF PULP
The principle cells of pulp are the
odontoblasts, fibroblasts and
undifferentiated mesenchymal cells
When pulp is examined microscopically four
distinct zones can be distinguished.
1. Odontoblastic zone
2. Cell free zone of Weil
3. Cell rich zone
4. Pulp core9/26/2013 29

30. 9/26/2013 30

31. PULP
CENTRAL PERIPHERAL
BLOOD
VESSELS
NERVES
ODONTOBL
ASTIC
ZONE
CELL
FREE
ZONE
CELL
RICH
ZONE
9/26/2013 31

32. DEFENCE
CELLS
F
I
B
R
O
B
L
A
S
T
UNDIFFERENTIA
-TED
MESENCHYMAL
CELLS
CELL RICH ZONE
9/26/2013 32

33. 9/26/2013 33

34. Functions of the pulp
• Inductive
• Formative
• Nutritive
• Protective
• Defensive
9/26/2013 34

35. Inductive
• The pulp also induces the enamel
organ to become a particular type of
tooth.
• The pulp Odontoblasts develop the
organic matrix and function in its
calcification
9/26/2013 35

36. Nutritive
• The pulp nourishes the dentin through
the Odontoblasts and their processes.
9/26/2013 36

37. Formative
• Through the development of the
Odontoblast processes dentin is
formed along the tubule wall as well
as at the pulp predentin front.
9/26/2013 37

38. Protective
• The sensory nerves in the tooth
respond with pain to all stimuli such as
-heat
-cold
-pressure
9/26/2013 38

39. Defensive
• The pulp is an organ with remarkable
restorative abilities
• It responds to irritation whether
mechanical,Thermal, Chemical or
bacterial by producing reparative
dentin and mineralizing any affected
dentinal tubules.
9/26/2013 39

40. Blood flow
• Blood flow in the pulp is more rapid than
any other tissue in the body
• The largest arteries in pulp are 50-100μm
in diameter equal to the arterioles found
in other places in the body.
Function :-
• To provide nutrition and elimination
of waste products.
9/26/2013 40

41. ( Longitudinal section of coronal pulp
showing large blood vessels)
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42. Aorta
Left side Right side
Innominate Artery
Common Corotid Artery
External Carotid Artery
Internal Carotid Artery
First portion
(Mandibular)
Second portion
(Pterygoid)
Third portion
(Pterygo-palatine)
Inferior Alvolar (Dental)
(Traverses Mandibular
Foramen and enters
Mand Canal)
Infraorbital Artery Posterior
Superior Alveolar
Artery
Dental Branch Mental Artery
Lower Lip and
Chin
Molars,
Premolars,
Canines Incisive Artery
Incisors
Incisors and
Cuspids
Molars and
Bicuspids
Anterior
Superior
Alveolar Artery
BLOOD SUPPLY OF TEETH9/26/2013 42

43. CONTROL OF BLOOD SUPPLY
• Nerve impulses, humoral mechanism e.g. epinephrine
causing vasoconstriction and parasympathetic nerve
fibres (cholinergic) causing vasodilation.
• Blood vessels of pulp – contains  & ß
adrenoreceptors.  for contraction ß for relaxation (Kim &
Chien --1983).
• Diameter of arterioles is about 50µm, capillary is 8-
10µm.
9/26/2013 43

44. RATE OF PULPAL BLOOD FLOW
• Higher as compared to other organs of the body,
however in kidney and spleen it is substantially higher.
• Values of intrapulpal pressure
- Normal pulp - 5.5mmHg
- Inflamed pulp - 16.3mmHg
- 1mm away from inflammation site - 7mmHg
9/26/2013 44

45. METABOLSIM
Metabolism has been studied by
measuring the rate of O2 consumption &
production of CO2 lactic acid by pulp
tissue.
During dentinogenesis, rate of O2
consumption is high than after crown
completion.
Greatest metabolic activity is seen in the
odontoblast layer.
9/26/2013 45

46. Reduced pH of pulp causes decreases in
O2 consumption as in pulp abscess.
Several dental materials have shown to
inhibit O2 consumption Eg. ZOE , Ca(OH)2
& silver amalgam
Pulpal irritation causes increases in
cycloxygenase products, which is inhibited
by ZOE
9/26/2013 46

47. INNERVATION
o Dental pulp is richly innervated
o Principles role is to help in conscious
recognition of irritants to the pulp.
o To have the problem corrected before
irreversible effects can occur.
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48. • Nerve follow the same course as the afferent
vessels, beginning as large nerve bundles
that arborize peripherally as they extend
occlusally through the pulp core.
• This plexus of nerve is called the
SUBODOTOBLASTIC PLEXUS, or PLEXUS
OF RASHKOW.
9/26/2013 48

49. NERVE SUPPLY OF TEETH
9/26/2013 49

50. NERVES
Two types
1.Myelinated
2.Non-myelinated
SILVER STAINTOLUIDINE BLUE STAIN X200
DEMONSTRATING MYELINATED NERVE FIBRES9/26/2013 50

51. Table 3.2 Classification and function of fibers in peripheral nerves
Fiber
Diameter
(m)
Conduction velocity
(speed of impulse,
m/sec)
Function
A-alpha ()
A-beta()
6-20
5-12
15-80 (myelinated)
30-70
Afferent fibers for touch, pressure
proprioception, vibration
(mechanorecptors)
A-gamma()
A-delta ()
B
1-5
1-3
2-30 (myelinated)
3-15 (myelinated)
Afferent fibers for pain and temperature
Visceral afferent fibers preganglionic
visceral efferent fibres
C 04-1.0 0.4-2(unmyelinated) Afferent fibers for pain and tempature;
post ganglionic visceral efferent fibers
 Majority of nerves of pulp falls
into two categories A-delta and
C-fibres.
9/26/2013 51

52. A-delta & C fibres
Fiber Myelination Location of terminals Pain
characteristics
Stimulation
threshold
1. A-delta Yes Principally in region of
pulp-dentin junction
Sharp,
pricking
Relatively
low
2. C No Probably distributed
throughout pulp
Burning,
aching, less
bearable than
A-delta fiber
sensations
Relatively
high,
usually
associated
with tissue
injury
9/26/2013 52

53. 9/26/2013 53

54. PERCENTAGE OF DENTINAL TUBULES
INNERVATED
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55. THEORIES OF TOOTH PAIN
PERCEPTION
a.Dentinal nerve stimulation
b.Dentinal receptor theory
c.Hydrodynamic theory9/26/2013 55

56. Hydrodynamic is widely excepted theory of impulse
conduction.
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57. 9/26/2013 57

58. CLINICAL CORRELATION
 Local anesthesia
Local anesthesia with epinephrine decrease blood
flow upto 30% (Meyer et al).
 Temperature Changes
 10-15°C increase in temperature leads to arterial
dilation and increase in intrapulpal pressure by
2-5mmHg per degree centigrade.
 Irreversible changes occurs by heating pulp to
45°C for a long period. (Van Hassel and Brown)
 At -2°C pulp exhibit immediate pathology.
9/26/2013 58

59.  Restorative Procedure :-
 Stimulate inflammatory responses.
 Cumulative effect of thermal changes with
irritating dental cements or metallic restoration 
degenerative changes and necrosis.
 Care should be taken to protect the vitality of the
underlying pulp while performing any restorative
procedures.
9/26/2013 59

60. REGRESSIVE CHANGES
( AGING )
• A.k.a :-
DEGENERATIVE
AGING
DYSTROPIC
CATABOLIC
PULPOSIS
9/26/2013 60

61. CELL CHANGES
• The size and number of cells decrease
with aging.
• Fibrolasts in young pulp exibit prominent
orgenelles where as aging fibroblasts
show less perinuclear cytoplasm and long
thin cytoplasmic processes.
9/26/2013 61

62. RETROGRESSIVE
PULP
CHANGES
ATROPHY AND
FIBROSIS
CACLIFICATIONS
9/26/2013 62

63. • Increase in collages fibers decrease in the
size of the pulp
• External trauma such as dental caries (or)
deep restorations cause a localized
fibrosis (or) scarring effect
(Fig:- H&E section of
Pulp Fibrosis)
9/26/2013 64

64. CALCIFICATIONS
• LARGER MINERALIZATIONS ARE
CALLED DENTICLES.
• THESE ARE LARGER MINERALIZED
BODIES SOMETIMES RESULTING
FROM FUSION OF SEVERAL
SMALLER ONES.
9/26/2013 65

65. DENTICLES
a.k.a
PULP STONES
9/26/2013 66
CLASSIFICATION
STRUCTURE SIZE LOCATION

66. 9/26/2013 67
DENTICLES
STRUCTURE
TRUE
DENTICLE
FALSE
DENTICLES
SIZE
FINE
DIFFUSED
LOCATION
EMBEDED
ADHERENT
FREE
Pulp Stones:-Hard mineralized
bodies found in the pulp or the
dentin

67. P
U
L
P
TWO TYPES:
1 TRUE - Made of dentin by
ectopic odontoblasts & showing
dentinal tubules
2 FALSE - mineralized connective
tissue, etc, (not made of dentin)
Both may show layering/lamellar patterns
from incremental growth
Acc. To Structure

68. P
U
L
P
1 FREE - in the pulp
2 IMBEDDED - enclosed in the
dentine as this has slowly grown
inwards
3 ATTACHED - partly imbedded
IT HAS THREE SUBTYPES:

69. TRUE DENTICLE
• H&E section
of true
denticle
• Higher
magnification

70. FALSE DENTICLE
False calcification seen along the walls
of the blood vessel
www.rxdentistry.blogspot.com

71. DIFFUSE CALCIFICATION
Diffuse calcification of the pulp, seen
along with pulp fibrosis

72. AGE CHANGES
• Formation of secondary dentin through
out life, reduces the size of the pulp
chamber and root canals
• Decrease in cellularity
• Odontoblast decrease in size & number,
& may disappear in certain areas.
Especially on pulpal floor over bifurcation
& trifurca

73. • Increase in number & thickness in
collagen fibers particularly radicular pulp
• Reduction in the nerve fibers & blood
vessels
• Increase resistance of pulp against action
of enzymes
• In dentin
–Increase in peritulular dentin
–Dentinal sclerosis, reduces
permeability
–Increase in dead tracts

74. FACTORS INFULENCING TERTIARY
DENTINOGENESIS
Reactionary Dentinogenesis:
• Shallow cavity- RDT > 0.5mmRD
• Deep cavity - RDT 0.25mm - RD
• Very deep cavity- RDT 0.008 –0.25mm
RD
Reparative Dentinogenesis:
• Pulp exposure – RDT< 0.008mm-
Reparative dentin formation.

75. TERTIARY
DENTINOGENESIS

76. INTERNAL RESORPTION
• Idiopathic slow or fast progressive
resorptive process.
• Cause is unknown – may be due to
trauma.
• The tooth is asymptomatic and is often
referred as “PINK TOOTH”.

77. FACTORS TO BE CONSIDERED
CONSIDERATIONS DURING OPERATIVE
PROCEDURES
1) Shape of the pulp chamber and its
extensions into the cusps pulpal horns is
important.
2) Wide pulp chamber into tooth of young
person will make a deep cavity
preparation hazardous

78. 3) The pulpal horns project high into the
cusps exposure of pulp can occur
4) If opening a pulp chamber for treatment
its size and variation in shape must be
taken into consideration

79. CONSIDERATIONS DURING ENTODONTIC
TREATMENT
5) Age advance , the pulp chamber
becomes smaller difficult to locate the
root canals.
6) Shape of the apical foramen and its
location may play an important part in
treatment of root canals.
7) Accessory canals, and multiple canals
are rarely seen in roentgenograms.

80. 8) The pulp is highly responsive to stimuli,
even slight stimulus cause inflammatory
cell infiltration.
9) Dehydration causes pulpal damage
operative procedures producing this
condition should be avoided.

81. EFFECT OF DENTAL MATERIALS ON
PULP
GIC – Well tolerated by pulp
Calcium hydroxide – Helps in dentin
bridge formation.
Zine Oxide Eugenol- has an anti-bacterial
effect.
Formocresol – Cause chronic
inflammation of the pulp.
Dentin bonding agent – can irritate the
pulp causing inflammation

82. PULPAL DISEASES
9/26/2013 83

83. PULPAL DISEASES
• It is an inflammation of pulp tissue.
• The vitality of the tooth depends on
defence response of pulp dentine
complex.
9/26/2013 84

84. • The Term “PULPALGIA” was coined by
Cohen.
• PULPALGIA IS A CLINICALLY
DETECTABLE INFLAMMATORY
RESPONSE OF PULPAL CONNECTIVE
TISSUE TO AN IRRITANT
9/26/2013 85

85. CAUSES OF PULP DISEASE
1. PHYSICAL CAUSE
a) Mechanical
i) Trauma
ii) Iatrogenic
iii)Cracked tooth syndrome
iv)Barodontalgia
9/26/2013 86

86. b) Thermal
i) Heat from cavity preparation
ii) Heat from setting of cement
iii) Conduction of heat through deep
filling without base
iv) Frictional heat due to polishing
c) Electrical
i) Galvanic current
9/26/2013 87

87. 2. CHEMICAL CAUSE
i) Toxic chemical of restorative
materials
ii) Erosion
3. BACTERIAL CAUSE
i) Toxins associated with caries
ii) Direct invasion of pulp from caries &
trauma
iii) Anachoresis
9/26/2013 88

88. CLASSIFICATION
1. Intact un inflamed pulp
2. Atrophic pulp
3. Acute pulpitis
4. Intact pulp with scattered chronic
inflammatory cell
1. with partial liquefaction necrosis
2. with partial coagulation necrosis
5. Total pulp necrosis
9/26/2013 89
SELTZER’ S CLASSIFICATION

89. GROSSMAN’S
CLASSIFICATION
1. Pulpitis ( inflammation)
A. Reversible pulpitis
i) Acute
ii) Chronic
B. Irreversible pulpitis
i) Acute
- abnormal response to cold
- abnormal response to heat

90. 2.Chronic
A. asymptomatic with pulp exposure
B. Hyper plastic pulpitis
C. Internal resoption
3. Pulp degeneration
4. necrosis
9/26/2013 91

91. WEINE’S CLASSIFICATION
1. Inflammatory diseases of dental pulp
a. hyperalgesia
* Hypersensitivity dentin
* Hyperemia
b. Painful pulpitis
* Acute pulpitis
* Chronic pulpitis
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92. c. No painful pulpitis
* Chronic ulcerative
* Chronic pulpitis
* chronic hyperplastic
2. Additional pulp change
a. Necrosis
b. Retrogressive changes
c. Internal resorption
9/26/2013 93

93. INGLE’S CLASSIFICATION
1. HYPERREACTIVE PULPALGIA.
A. DENTINAL HYPERSENSTIVITY.
B. HYPEREMIA.
2. ACUTE PULPALGIA.
A. INCEPIENT.
B. MODERATE.
C. ADVANCED.
9/26/2013 94

94. 3. CHRONIC PILPALGIA
BARODONTALGIA.
4. HYPERPLASTIC PULPITIS.
5. NECROTIC PULP.
5. INTERNAL RESORPTION.
6. TRAUMATIC OCCLUSION.
7. INCOMPLETE FRACTURE.9/26/2013 95

95. • Necrobiosis
(Part infected and part
inflamed)
• Pulp Necrosis
( Nonvital Pulp)
• Clinically Normal Pulp
(Based on examination and
test results)
• Reversible Pulpitis
• Irreversible Pulpitis
– Symptomatic
– Asymptomatic
CLINICAL CLASSIFICATION OF
PULPAL DISEASES ( Acc. To Cohen)

96. • Previous Endodontic
Treatment
– No sign of infection
– Infected
– Technical standard
(based on radiographs)
• Inadequate
• Adequate
– Other problems
• e.g. Perforation,
fractured file, missed
canal, etc.
• Previous Initiated
Threapy
(partial endodontic therapy)
– Previously trated
• Pulpotomy
• pulpectomy
– Other Partial t/t in cases
• e.g. Traumatic tooth
injuries,Apexification ,
Apexogenesis

97. • Other Conditions
– Atrophy
– Pulp Canal
Obliteration (PCO)
– Hyperplasia
– Internal Resorption

99. PULP DISEASE IS A DYNAMIC
PROCESS
Reversible
Normal Inflammation
Irreversible
Infection Total Partial
Necrosis Necrosis
Pulpless
(loss of tissue)
Progression of Pulp Disease

100.  SIGNS & SYMPTOMS will depend on the stage
of the disease at the time of examination
Reversible
Normal Inflammation
Irreversible
Infection Total Partial
Necrosis Necrosis
Pulpless
(loss of tissue)
Progression of Pulp Disease
PULP DISEASE IS A DYNAMIC
PROCESS

101.  TREATMENT REQUIRED will depend on the stage
of the disease at the time of examination
Reversible
Normal Inflammation
Irreversible
Infection Total Partial
Necrosis Necrosis
Pulpless
(loss of tissue)
Progression of Pulp Disease

102. ACUTE REVERSIBLE
PULPITIS
(FOCAL REVERSIBLE PULPITIS, PULP HYPERAEMIA)

103. DEFINITION
Reversible pulpitis is a mild-to
moderate inflammatory condition of
the pulp caused by noxious stimuli in
which the pulp is capable of returning
to the uninflamed state following
removal of the stimuli.
AETIOLOGY: -
 Any mild irritants

104. CLINICAL FEATURES: -
Signs and symptoms: painful ; Sharp
pain lasts for a moment. Doesn’t occur
spontaneously & doesn’t continue when
the cause has been removed.
Duration: LASTs FOR A MOMENT, severe
and short
Precipitating factors of pain: hot and
cold agents More often cause by cold
than hot food.

105.  Nature of pain:
• Pain stops when precipitating
factors are removed
The pain depends on -
• The size of exposed pulp (size of
dental caries)
• Severity of pulp inflammation
• Age of patient
• Nature of covering dentine

106. DIFFERENTIAL
DIAGNOSIS
• Clinically Reversible & Irreversible
pulpitis is, that, in Reversible pulpitis
pain is sharp & short duration where
as in Irreversible pulpitis is sever & long
lasting.
9/26/2013 107

107. DIFFERENTIAL DIAGNOSIS
• REVERSIBLE PULPITIS
PAIN LASTS FOR FEW
SECONDS.(A$ FIBERS)
SHARP PAIN.
PAIN SUBSIDES WHEN
STIMULUS IS REMOVED.
• IRREVERSIBLE PULPITIS
PAIN LASTS FOR SEVERAL
MINUTES OR LONGER(C
FIBERS)
SHARP SHOOTING AND
PIERCING PAIN
LATER PAIN IS BORING OR
GNAWING
SEVERE PAIN
PAIN ON BENDING OR
LYING.

108. HISTOLOGICAL
FEATURES: -
• Inflamed pulp tissue
contains dilated
blood vessels of
various sizes and
are lined by
endothelial cells
• Presence of normal
odontoblasts
indicate vitality of
the pulp tissue.

109. PROGNOSIS-:
• It is a reversible condition.
• If it is treated , pulp will return
back to its normal status.
• If it is left untreated , it will not
return back to its normal status
but it will enter the next
phase....

110. ACUTE PROGRESSIVE
PULPITIS

111. CLINICAL FEATURES: -
Duration : - more than 10-15 minutes,
severe and continuous, especially at
night
Precipitating factors of pain : -
spontaneously as well as hot and cold
agents
Nature of pain : -
• Throbbing continuous and radiating pain
• The pain does not stop even when
precipitating factors are removed.

112. PROGNOSIS: -
• If it is left untreated, it will
change to chronic pulpitis or
pulp necrosis

116. CHRONIC PULPITIS

117. DEFINITION
IT IS A PERSISTANT INFLAMATORY
CONDITION OF THE PULP,
SYMPTOMATIC OR ASYMPTOMATIC,
CAUSED BY NOXIOUS STIMULI.
 The pulp has been damaged beyond
repair & even with removal of irritant it
will not go. The pulp will progressively
degenerate, causing necrosis & reactive
destruction.

118. CLINICAL FEATURES: -
Signs and symptoms: - painful ; it exhibits
pain by hot or cold stimuli, or pain that
occurs spontaneously.
Duration: - several minutes to hours ,
lingering after removal of stimulus.
Precipitating factors of pain: - hot, cold
agents and during biting.
9/26/2013 119

119. Nature of pain: -
 PAIN IS BORING GNAWING
OR THROBBING
 Intermittent pain to severe pain
 patient have sleepless nights
 pain increases by hot application; pain
is relieved by cold but it may intensify
by continous cold application

120. HISTOPATHOLOGICAL FEATURES: -
 The pulp tissue
contains dilated
blood vessels with
varying sizes.
 Degenerated
odontoblasts
seen.
 Areas of chronic
inflammatory cells
and fibrosis can
be seen around
inflamed areas

121. PROGNOSIS: -
• It is dependant on the
success of pulpectomy or
complete removal of pulp.

122. PULPITIS
Symptoms Reversible
 Nature Sharp, mild  mod.
 Thermal sensitivity Extreme temp’s
 Duration Short
(sec’s  min’s)
 Biting pain +
 Percussion +
 Spontaneous _
 Wakes at night _
 Worse lying down _
 Radiographic changes _
 History previous problems _ _

123. Symptoms Reversible Irreversible
 Nature Sharp, mild  mod. Sharp & aching
 Thermal sensitivity Extreme temp’s Mild changes
 Duration Short Lingers
(sec’s  min’s) (? > 5-10 min’s)
 Biting pain + +
 Percussion + +
 Spontaneous _ +
 Wakes at night _ +
 Worse lying down _ +
 Radiographic changes _ +
 History previous problems _ +
PULPITIS

124. CHRONIC OPEN
HYPERPLASTIC
PULPITIS
( PULP POLYP )

125. • It is a chronic inflammation of pulp
tissue characterized by hyperplasia of
connective tissue of pulp in the form of
polypoid mass which originates from
exposed pulp chamber

126. CLINICAL FEATURES : -
Site:
• A grossly carious molar
(permanent/deciduous) where pulp
chambers are wide, having multiple
roots with highly vascular pulp tissue
Shape : nodular fungated mass fills pulp
chamber

127. Size : variable
Colour : reddish, bleeds readily
Covering surface : intact or
ulcerated

130. HISTOLOGICAL FEATURES: -
• Proliferation of granulation tissue with
newly formed, dilated blood vessels of
varying sizes, chronic inflammatory cells
and fibrosis
• Generalized degenerated odontoblasts
also called “Wheat Sheaving” of
Odontoblasts
• The mass is covered by hyperplastic
stratified squamous epithelium.

134. PULP CALCIFICATION
(PULP STONE OR DENTICLES)

135. It is a localized / generalized condition of
pulp tissue characterized by formation of
pulp stone in the form of calcified bodies
CLINICAL FEATURES : -
Site: coronal or radicular pulp
Size: variable
Signs and symptoms : painless

136. • RADIOGRAPHIC
FEATURES: -
Radiopaque mass /
masses with variable
sizes inside the pulp
chamber or pulp
canals.

137. HISTOLOGICAL TYPES: -
True pulp stone - consists of dentinal
tubules.
False pulp stone - consists of concentric
calcified rings
Free pulp stone - is freely located within
the pulp tissue
Attached pulp stone - is adherent to
dentin wall
Embedded pulp stone - is surrounded by
secondary dentin

141. COMPLICATIONS: -
• It interferes with root canal treatment.
• Can cause pain if it impinges on
major pulp nerves.

143. PULP NECROSIS

144. Necrosis Or Death Of A Pulp Tissue Is
A Sequel Of Acute And Chronic
Inflammation Of The Pulp Or An
Immediate Arrest Of Circulation By
Traumatic Injury. It May Be Partial Or
Total Depending On Extent Of Pulp
Tissue Involvement
AETIOLOGY : -Severely irritant agents.
CLINICAL FEATURES : -
Signs and symptoms : pain is absent with
total necrosis
• SWELLING -Negative.
• MOBILITY - Negative.
• TENDERNESS TO PERCUSION - Negative

145. Symptoms:
Discoloration of tooth.
The dull or opaque appearance of crown.
Partial necrosis can respond to thermal
changes.
 Mostly Necrotic tooth doesn’t respond to
electric & thermal test
Necrosis is of two type:-
Coagulation necrosis
Liquefaction necrosis

146. TREATMENT
• Preparation And Obturation Of Root
Canals.
PROGNOSIS
Good If Proper Endodontic Therapy Is
Done.
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149. Necrobiosis
(Louis Grossman 1985)
Partial necrosis with pulpitis
 Pulp chamber -v- root canals
 One canal -v- other canal(s)

150. REVISING & CONCLUDING
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151. Main Cause of Pulp Disease
Bacteria
Caries
Cracks
Leaking restorations
Fractures - tooth, restorations
Trauma - luxations, etc
Periodontal disease

152. • Short term
– Cutting & drying
Acute
inflammation
PULP INSULTS

153. • Short term
– Cutting & drying
• Trauma
– Blood supply
lost or reduced
– Bacteria
Acute
inflammation
Necrosis
PULP INSULTS

154. • Short term
– Cutting & drying
• Trauma
– Blood supply
lost or reduced
– Bacteria
• Long term
– Caries
– Bacteria
– Chemical
Acute
inflammation
Necrosis
Chronic
inflammation
PULP INSULTS
Necrosis

155. REFERECES
• Shafer’s; Textbook of Oral Pathology
• ORAL HISTOLOGY AND
EMBROLOGY; Orban
• Cohen’s; Pathways of Pulp
• ENDODONTIC PRACTICE; Grossman
• Seltzer & Bender; The Dental Pulp
• Ingle’s Endodontics 6
• ENDODONTIC PRACTICE;Weine
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156. THANK YOU
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