Classification and description of each diagnosis

1. DISEASES OF
THE DENTAL
PULP- Part II
Deepthi P.R.
1st year MDS
Dept of Conservative
Dentistry & Endodontics

2. CONTENTS
 Introduction
 Irritants
 Inflammatory process
 Immunologic responses
 Lesion progression
 Classification of diseases

3. INTRODUCTION
 Etiologic factors causing pulp
inflammation
 Mechanism of spread of inflammation
 Mediators of pulpal inflammation
 Classification & features of diseases

4. IRRITANTS
Living
• Micro organisms
• Viruses
Non Living
• Mechanical
• Thermal
• Chemical

5. Microbial irritants
 Main source
 Numerous species: S. mutans, Lactobacilli,
Actinomyces
 Toxins: deep penetration to pulp
 Local infiltration of pulp- chronic
inflammatory cells
 Progression: intensity & character
changes

6. Microbial irritants
 Actual exposure: PMN infiltration &
liquefaction necrosis
 Long periods of inflammation/ necrosis-
• Virulence
• Release of inflammatory fluid: avoiding
intrapulpal pressure
• Host resistance
• Circulation
• Lymphatic drainage

7. Microbial irritants
 Yamasaki et al : pulpal necrosis in rats
 Exposed pulp: bacteria & by products
 Temporary impeding of spread &
destruction
 Persistence: extensive destruction –
spread throughout pulp- periapical
spread & inflammatory lesions

8. Microbial irritants
 Kakehashi et al : pulp exposures in
conventional & germ free rats
 Mӧller et al: sealed infected & non
infected canals in monkeys
 Sundqvist et al: traumatised teeth with
and without apical pathosis

9. Microbial irritants
 Viruses: symptomatic apical pathoses
 Periapical lesions: CMV & EBV-
symptomatic

10. Mechanical irritants
 Deep cavity preparations
 Removal of tooth structure without proper
cooling
 Impact trauma
 Occlusal trauma
 Deep periodontal curettage
 Orthodontic movement

11. Mechanical irritants
 Extensive restorative procedures: pulpal
inflammation
 Dentin permeability closer to pulp
 𝑃𝑢𝑙𝑝 𝑑𝑎𝑚𝑎𝑔𝑒 ∝
𝑎𝑚𝑜𝑢𝑛𝑡 𝑜𝑓 𝑡𝑜𝑜𝑡ℎ 𝑠𝑡𝑟𝑢𝑐𝑡𝑢𝑟𝑒 𝑟𝑒𝑚𝑜𝑣𝑒𝑑 +
𝑑𝑒𝑝𝑡ℎ 𝑜𝑓 𝑟𝑒𝑚𝑜𝑣𝑎𝑙
 Operative procedures without coolant-
more pulpal irritation

12. Mechanical irritants
 Impact injuries : severity of trauma &
degree of apical closure – pulpal
recovery
 Orthodontic forces beyond physiologic
tolerance: cellular atrophy, alteration of
nerve axons, apical resorption
 Deep scaling & curettage

13. 48 hours after crown
preparation through enamel &
1mm into dentin
Aspiration of
odontoblasts into
tubules & pulpal
infiltration by PMNs &
Lymphocytes
M Torabinejd. Endodontics

14. Chemical irritants
 Dentin sterilizing :
Silver nitrate, phenol,
eugenol &
desensitizing
substances
 Cleansers: Alcohol,
chloroform, H2O2,
various acids
 Restorative materials
& liners
Periapical extrusion of filling materials
causing periapical inflammation
M Torabinejd. Endodontics

15. Pulpal pathosis
 Injury: cell death & inflammation
 Slight: little or no inflammation
 Incipient caries, shallow cavity
preparations
 More damaging: severe inflammation
 Deep caries, extensive operative
procedures, persistent irritants

16. Pulpal pathosis
 Severity & duration of illness
 Host capacity
Reversible
pulpitis
Irreversible
pulpitis
Total
necrosis

17. Inflammatory process
 Irritation of dental pulp – mediators:
Histamine, Bradykinin, Arachidonic acid
metabolites
 Lysosomal granule products: Elastase,
Cathepsin G, Lactoferrin
 Protease inhibitors: Antitrypsin, CGRP,
Substance P

18. Inflammatory process
 Mast cells: Histamine, Leukotrienes, PAF
 Released: Physical injury to mast cells or
bridging of IgE
 Bradykinin, Substance P, Neurokinin A
Plasma/
Tissue
kallikreins
Kininogens Kinins

19. Inflammatory process
 iCGRP release : PGE2
 Pulpal nerve fibers: SP, CGRP- protective
 Mild- moderate injuries: iCGRP
 Severe: iCGRP
Cellular
damage
Arachidonic
acid

20. Immunologic Responses
 Bacteria & by products: Antigen
 Immunocompetent cells – Normal pulp
 Ig levels in inflamed pulps
 Arthus reaction
 Delayed hypersensitivity reactions
 Necrotic foci & pulpal necrosis

21. Healthy pulp
 Pulp : vital; free of inflammation
 Prosthetic reasons
 First hours after traumatic pulp exposure

22. Pulpitis
 Vital & inflamed
 No info on:
 Degree of inflammation
 Reversible/ irreversible
 Two clinical diagnoses for inflamed pulp
 Symptomatic pulpitis
 Asymptomatic pulpitis

23. Pulpitis
Symptomatic
 Vital, inflamed
 Symptoms of
pulpitis
 Exacerbation of
chronic pulpitis
 Acute
Asymptomatic
 Vital, inflamed &
no symptoms
 Knowledge of
etiology of pulpitis
& reaction pattern
of pulp

24. Lesion Progression
 Moderate to severe injuries: localized
inflammation & mediators
 Increase in protease inhibitors: natural
modifiers
 Increased vascular permeability, vascular
stasis, migration of WBCs- injury site
 CGRP: increased blood flow during
inflammation

25. Accumulation of inflammatory cells
within the pulp horn
Beer. Pocket Atlas of Endodontics

26. Neutrophilic granulocytes in Predentin
layer & Dentin tubules
Beer. Pocket Atlas of Endodontics

27. Lesion Progression
 capillary pressure & permeability
 Exudation
 tissue pressure: passive compression &
complete collapse of venules
 Increased pressure
 Inablity to expand
 Lack of collateral circulation
Pulpal
necrosis

28. Lesion Progression
Inflammatory
mediators
IndirectDirect

29. PULPITIS
 Acute/ Chronic: Clinical differentiation
 Partial/ Total
 Infected/ Sterile: smear or culture
 Acute: Precipitous short course
Violently painful
 Chronic: Practically symptomless
Slightly painful
Longer duration
Exposed pulp:
caries/
trauma
Hyperplastic
pulpitis
Ulcerative
pulpitis

30. CLASSIFICATION
OF PULPAL
DISEASES

31. CONTENTS
 Introduction
 Different classifications
 Normal pulp
 Reversible pulpitis
 Irreversible pulpitis
 Chronic hyperplastic pulpitis
 Necrotic pulp
 Pulp degeneration
 Previously treated pulp
 Previously initiated therapy

32. CLASSIFICATION OF PULPAL
DISEASES
 *No correlation between histologic
findings & symptoms
 Clinical classification: Signs & symptoms
 Helps: appropriate treatment, prognosis,
restorative needs
 Indistinct demarcation between the
classes
Garfunkel et al: direct correlation -49%, partial correlation- 46%.
Wegner & Knorr: Correlation- 40%

33. CLASSIFICATION OF PULPAL
DISEASES
 Grossman
 Baume
 Seltzer & Bender
 Wiliam T. Johnson
 American Board of Endodontics (ABE)- 2007
 Reit, Petersson & Molven
 Walton & Torabionejad
 Torabinejad & Shabahang
 Tronstad
 Ingle & Beveridge
 Castelucci
 Beer & Baumann
 Abbott
 WHO- 1995

34. Grossman
1. Inflammatory diseases of the dental pulp
a. Reversible pulpitis
(i) Symptomatic (acute)
(ii) Asymptomatic (chronic)
b. Irreversible pulpitis
(i) Acute
- Abnormally responsive to cold
- Abnormally responsive to heat

35. Grossman
(ii) Chronic
- Asymptomatic with pulp exposure
- Hyperplastic pulpitis
- Internal resorption
2. Pulp degeneration
a. Calcific (radiographic diagnosis)
b. Others (histopathologic diagnosis)
3.Necrosis

36. Baume
 Symptomless vital pulp: Deep caries- pulp
capping done
 History of pain: Amenable to
pharmacotherapy & restorative
rehabilitation
 Infected pulps: Extirpation & immediate
RCT
 Infected & necrosed pulps: Intracanal
serous drainage- medicament prior to
RCT

37. Seltzer & Bender
(a) Treatable without
pulp extirpation
and RCT:
 Intact, uninflamed
pulp
 Transitional stage
 Atrophic pulp
 Acute pulpitis
 Chronic partial
pulpitis without
necrosis
(b) Untreatable without
pulp extirpation and
RCT:
 Chronic partial
pulpitis with necrosis
 Chronic total pulpitis
 Total pulp necrosis

38. William T.Johnson
 Normal
 Reversible pulpitis
 Irreversible pulpitis

39. American Board of
Endodontics (ABE)- 2007
 Normal pulp
 Reversible pulpitis
 Irreversible pulpitis
 Symtomatic
 Asymptomatic
 Pulp necrosis
 Previously treated
 Previously initiated therapy

40. Reit, Petersson & Molven
 Pulpa sana
 Pulpitis
 Necrosis pulpae
 Periodontitis apicalis chronica/ acuta

41. Walton & Torabinejad
 Normal
 Reversible pulpitis
 Irreversible pulpitis
 Hyperplastic pulpitis
 Necrosis

42. Torabinejad & Shabahang
 Normal pulp
 Reversible pulpitis
 Irreversible pulpitis
 Hyperplastic pulpitis
 Necrosis
 Previously treated pulp

43. Tronstad
 Healthy pulp
 Asymptomatic pulpitis
 Symptomatic pulpitis
 Necrotic pulp

44. Ingle & Beveridge
 Incipient acute pulpalgia
 Moderate & advanced acute pulpalgia
 Chronic pulpalgia
 Hyperplastic pulposis
 Necrosis

45. Castelucci
 Healthy pulp
 Hyperemia
 Pulpitis
 Necrosis

46. Beer & Baumann
 Asymptomatic pulp pathology
 Reversible pulpitis
 Irreversible pulpitis
 Pulpal necrosis

47. Abbott
a.Clinically normal pulp
b.Reversible pulpitis
Types: Acute, Chronic
c. Irreversible pulpitis
Types: Acute Chronic, Necrobiosis
d. Pulp necrosis
Types: Necrosis without infection, Necrosis
with infection

48. Abbott
e. Pulpless Canals
Types: Pulpless and no signs of infection
Pulpless and infected
f. Degenerative Changes
Types: Atrophy,
Pulp canal obliteration(calcification)-
Partial, Total
Hyperplasia
Internal resorption- Inflammatory,
Replacement

49. Abbott
g. Previous Root Canal Treatment
Types : Satisfactory – No signs of infection
- Infected
Technically inadequate
- No signs of infection
- Infected
h. Endodontic- Periodontal Lesions

50. Abbott
h. Endodontic- Periodontal Lesions
Classification based on the origin of the
periodontal defect:
- Lesion of endodontic origin
- Lesion of Periodontal origin
- Combined Endo- Perio Lesions
Types: Separate endo & perio lesions that
do NOT communicate
endodontic and periodontal lesions
that DO communicate

51. Application of the International Classification of
Diseases to Dentistry and Stomatology (3rd ed), World
Health Organization (WHO), Geneva, 1995
K04 DISEASES OF PULP AND PERIAPICAL TISSUES
 K04.0 Pulpitis
 K04.00 Initial (hyperaemia)
 K04.01 Acute
 K04.02 Suppurative [pulpal abscess]
 K04.03 Chronic
 K04.04 Chronic, ulcerative
 K04.05 Chronic, hyperplastic [pulpal polyp]
 K04.08 Other specified pulpitis
 K04.09 Pulpitis, unspecified
Gutmann et al. JOE — Volume 35, Number 12, December 2009

52. Application of the International Classification of
diseases to Dentistry and Stomatology (3rd ed), World
Health Organization (WHO), Geneva, 1995
 K04.1 Necrosis of pulp
 Pulpal gangrene
 K04.2 Pulp degeneration
 Denticles
 Pulpal calcification
 Pulpal stones
 K04.3 Abnormal hard tissue formation in pulp
 K04.3X Secondary or irregular dentine
Excludes: pulpal calcifications (K04.2)
pulpal stones (K04.2
Gutmann et al. JOE — Volume 35, Number 12, December 2009

53. Application of the International Classification of
diseases to Dentistry and Stomatology (3rd ed), World
Health Organization (WHO), Geneva, 1995
 K04.4 Acute apical periodontitis of pulpal origin
Acute apical periodontitis
 K04.5 Chronic apical periodontitis
Apical granuloma
 K04.6 Periapical abscess with sinus
Includes: dental abscess with sinus
dentoalveolar abscess with sinus
periodontal abscess of pulpal origin
 K04.60 Sinus to maxillary antrum
 K04.61 Sinus to nasal cavity
 K04.62 Sinus to oral cavity
 K04.63 Sinus to skin
 K04.69 Periapical abscess with sinus, unspecified
Gutmann et al. JOE — Volume 35, Number 12, December 2009

54.  K04.7 Periapical abscess without sinus
 Dental abscess }
 Dentoalveolar abscess } without sinus
 Periodontal abscess of pulpal origin }
 K04.8 Radicular cyst
Includes: cyst
 apical periodontal
 periapical
 K04.80 Apical and lateral
 K04.81 Residual
 K04.82 Inflammatory paradental
Excludes: developmental lateral periodontal cyst (K09.04)
 K04.89 Radicular cyst, unspecified
 K04.9 Other and unspecified diseases of pulp and periapical
tissues
Gutmann et al. JOE — Volume 35, Number 12, December 2009

55. Normal pulp
 A clinical diagnostic category in which
the pulp is symptom-free and normally
responsive to pulp testing*.
 Asymptomatic
 Mild to moderate response: stimuli
 Subside immediately on removal
AAE Consensus Conference.JOE — Volume 35, Number 12, December 2009

56.  No painful response: palpation &
percussion
 Radiographs: clearly delineated canal-
tapers to apex, intact lamina dura, no
calcification/ resorption.

57. Reversible Pulpitis
 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
 *Pulpal inflammation which should resolve
once the etiology is removed (defective
restorations or caries).
Dabuleanu M. J Can Dent Assoc 2013;79:d90

58. Reversible Pulpitis
 Clinical condition associated with
subjective & objective findings indicating
presence of mild inflammation in pulp
tissue
 A clinical diagnosis based on subjective
and objective findings indicating that the
inflammation should resolve and the pulp
return to normal*.
*AAE Consensus Conference.JOE — Volume 35, Number 12, December 2009

59. Reversible Pulpitis - Causes
 Incipient caries
 Cervical erosion
 Occlusal attrition
 Thermal shock: Operative procedures
 Deep periodontal curettage
 Enamel fracture

60. Causes
 Trauma: Occlusal / Blow
 Fresh amalgam filling: contact with cast
restoration
 Circulatory disturbances
 Local vascular congestion

61. Reversible Pulpitis-
Histopathology
 Reparative dentin
 Disruption of odontoblast layer
 Dilated blood vessels
 Extravasation of oedema fluid
 Immunologically competent chronic
inflammatory cells & occasional acute
cells

62. Reversible Pulpitis- Symptoms
 Thermal stimuli: quick, sharp hypersensitive
response- subsides on removal of stimulus
 More often by cold than hot
 Asymptomatic- incipient caries
 No spontaneous pain

63. Diagnosis
Patient’s symptoms
 Momentary sharp
pain, disappearing
on removal of
stimulus
 Cold, sweet, sour
 Chronic pain-
paroxysm of short or
long duration
 Complete recovery
or shorter relief
Clinical tests
 Application of cold
 Normal reaction to
percussion,
palpation, mobility
 Normal on
radiographic
examination

64. Treatment
Prevention
 Early restoration
 Desensitization – marked gingival
recession
 Cavity varnish/ cement base
 Care in cavity preparation & polishing
 Sedative dressing- ZOE dressing
 Vitality tests

65. Treatment & Prognosis
 Sealing & insulating exposed dentin/ vital
pulp
Continuous / increased irritation- moderate
to severe inflammation
 Irreversible pulpitis
 Pulpal necrosis
 Favorable: irritant removed early enough
 Persistence: irreversible pulpitis

66. Irreversible Pulpitis
 Persistent, inflammatory condition of the
pulp, symptomatic or asymptomatic,
caused by a noxious stimulus
 Clinical condition associated with
subjective and objective findings
indicating presence of severe
inflammation in the pulp tissue
 *Pulpal inflammation which will not resolve
once the etiology is removed
*Dabuleanu M. J Can Dent Assoc 2013;79:d90

67. Irreversible Pulpitis
 Acute/ Subacute/ Chronic
 Partial/ Total
 Infected/ Sterile
 Acute: pain by hot/ cold stimulus or
spontaneous
 Lingering pain
 Chronic quiescent to Acute symptomatic-
hours/ years
 Exudate: vented- quiescent, confined- painful

68. Irreversible Pulpitis-
Histopathology
 Chronic & acute inflammatory features
 Congestion of postcapillary venules
 Affect pulpal circulation : necrosis
 PMNs: acute inflammatory reaction
 Lysosomal enzymes + cellular debris of
PMNs: pus

69.  Areas of microabscesses: necrotic tissue +
micro organisms+ lymphocyte, plasma
cells, macrophages
 Walled off by fibrous connective tissue
 No micro organisms in the centre of
abscess
 On pulpal penetration: area of ulceration
 Necrotic tissue+ PMN zone+ proliferating
fibroblasts: calcific masses

70. Symptomatic Irreversible
Pulpitis
 A clinical diagnosis based on subjective
and objective findings indicating that the
vital inflamed pulp is incapable of
healing. Additional descriptors: lingering
thermal pain, spontaneous pain, referred
pain*.
 Spontaneous intermittent or continuous
paroxysms of pain.

71. Symptomatic Irreversible
Pulpitis
 Prolonged painful response to cold:
relieved by heat
 Prolonged painful response to heat :
relieved by cold.
 Painful response to both
 Moderate/ severe
 Sharp/ dull

72.  Localized/ referred
 Continuous/ intermittent
 Later: ‘boring, gnawing, throbbing’
 Triggered by change in posture
 Cavity with no outlet: intense pain
 Kept awake at night

73. Asymptomatic Irreversible
Pulpitis
 A clinical diagnosis based on subjective
and objective findings indicating that the
vital inflamed pulp is incapable of
healing. Additional descriptors: no clinical
symptoms but inflammation produced by
caries, caries excavation, trauma*
 Progress to symptomatic/ necrotic
 Treatment as soon as possible
*AAE Consensus Conference.JOE — Volume 35, Number 12, December 2009

74. Diagnosis
 Grayish scum like layer: exposed pulp
 Odor of decomposition
 Probing painful & hemorrhage : deeper
areas of pulp
 Drop of pus: gaining access

75. Diagnosis
Radiographs
 Little use
 Helps identification of suspect teeth
 Advanced stages: thickening of PDL
 Mobility, percussion & palpation: Negative

76. Diagnosis
Thermal tests
 Early: Persistent pain after removal of
stimulus
 Late: normal response, feeble
 EPT: marked variation from normal

77. Differential diagnosis
Reversible
 Pain disappears on
removal of thermal
stimulus
 EPT: responds with
less current than on
control
Irreversible
 Lingering/
spontaneous pain
 Asymptomatic:
little/ no pain
 EPT: more current
required

78. Differential diagnosis
Irreversible
 Early symptomatic:
less current with EPT
 Abnormal response
to cold- sharp,
piercing
 Later stage: diffuse
dull constant pain
 Abnormal severe
response to heat
Acute alveolar
abscess
 Swelling
 Tenderness on
palpation,
percussion
 Mobility
 Lack of response to
vitality tests

79. Differential diagnosis
Pain of non-odontogenic origin:
 Musculoskeletal pain
 Neurovascular pain
 Neuropathic pain
 Pain caused by a distant pathology
(cardiovascular, cranial, throat, neck)
 Psychogenic pain
*Dabuleanu M. J Can Dent Assoc 2013;79:d90

80. Treatment & Prognosis
 Pulpectomy
 Pulpotomy: emergency procedure
 Surgical removal: not restorable
 Favorable prognosis: Proper endodontic
therapy & post endodontic restoration

82. Chronic Hyperplastic Pulpitis
 ‘Pulp polyp’
 Productive pulpal inflammation due to an
extensive carious exposure of a young
pulp
 A form of irreversible pulpitis that
originates from overgrowth of a
chronically inflamed young pulp onto the
occlusal surface
 Granulation tissue – epithelial covering
 Long standing, low grade irritation

83. Causes & Symptoms
 Slow progressive carious exposure
 Large open cavity
 Young resistant pulp
 Chronic low grade stimulus
 Symptomless: discomfort during
mastication

84. Chronic Hyperplastic Pulpitis-
Histopathology
 Surface covering: Stratified squamous
epithelium (deciduous)
 Gingiva/ mucosa/ tongue
 Young vascular connective tissue+ PMNs+
lymphocytes+ plasma cells
 Nerve fibers

85. Diagnosis
 Fleshy, reddish pulpal mass filling chamber
& beyond confines of the tooth
 Size of a pin or upto interfering with
comfortable closure
 Sensitivity : < pulp, > gingiva
 No pain, easy bleeding
 Stalk traced back to pulp chamber

86. Diagnosis
 Radiographs: Large, open cavity: direct
access to the pulp chamber
 Thermal test: no or feeble response
 EPT: more current than normal
 Distinguished from proliferating gingival
tissue

87. Treatment & Prognosis
 Elimination of polypoid tissue; pulp
extirpation
 Bleeding controlled after tissue removal
 Temporary dressing after pulpotomy
 Radicular pulp extirpation later
 Favorable after adequate endodontic
treatment & restoration

89. Necrotic pulp
 Clinical condition associated with subjective
and objective fndings indicating death of the
dental pulp
 A clinical diagnostic category indicating
death of the dental pulp. The pulp is usually
nonresponsive to pulp testing*.
 Exudate: absorbed / drained- necrosis
delayed & radicular pulp vital for long periods
 Closure/ sealing of inflamed pulp- rapid &
total necrosis & periradicular pathosis
*AAE Consensus Conference.JOE — Volume 35, Number 12, December 2009

90. Necrotic pulp
 Non vital/ necrotic
 Suspected on negative reaction to
sensitivity tests
 Confirmed on inspection of root canal
space only
 Total/ Partial
 Sequel to inflammation/ trauma- before
inflammation: Dry gangrenous necrotic
pulp

91. Necrosis- Types
 Coagulation : soluble portion precipitated/
converted to solid material
 Caseation : form of coagulation necrosis-
tissue converted to cheesy mass: coagulated
proteins+ fat+ water
 Liquefaction : softened mass/ liquid/
amorphous debris by proteolytic enzymes.
Follows irrevrsible pulpitis
 Ischemic : traumatic injury, disruption of blood
supply

92. Necrotic pulp
Intermediate
products- unpleasant
odor
 Indole
 Skatole
 Putrecine
 Cadaverine
End products
 H2S
 NH3
 Fatty substances
 Indican
 Protamines
 Water
 CO2

93. Necrotic pulp
Histopathology
 Necrotic pulp tissue
 Cellular debris
 Microorganisms
 Normal/ slight
evidence of
inflammation:
peripaically
Cause
 Bacteria
 Trauma
 Chemical irritation

94. Necrotic pulp- Symptoms
 No painful symptoms if otherwise normal
 Discoloration: first symptom
 Dull/ Opaque: lack of normal
translucency
 Grayish/ Brownish discoloration
 By chance discovery

95. Symptoms
 Usually asymptomatic
 Episodes of spontaneous pain/
discomfort, pain on pressurePartial
necrosis: Vital nerve fibers- positive
thermal tests
 Pain on heat application- thermal
expansion of gases present in RC space
 Unlikely
 Cold, heat, electric stimuli: no response

96. Diagnosis
 Non responsive to vitality testing
 Presence of various degrees of
inflammatory response- teeth with
multiple canals: confusion
 Minimal response-EPT: conduction
through moisture

97. Diagnosis
 Spread of inflammatory reactions to
periradicular tissues: sensitive to
percussion & palpation
 Radiographs: large cavity/ filling , open
approach to RC, thickening of PDL

98. Treatment & Prognosis
 RCT
 Surgical removal
 Favorable: proper endodontic therapy

100. Pulp Degeneration
 Seldom recognized clinically
 Generally: old; persistent mild irritation:
young
 Not infected/ restored always
 Early: no definite symptoms
 Late: discolored, no response to
stimulation
 Types: Calcific, Atrophic, Fibrous

101. Calcific Degeneration/Hard
tissue changes
 Pulp calcification
 Resorption

102. Pulp Calcification
Extensive- pulp stones/ diffuse
 Trauma
 Caries
 Periodontal disease
 Other irritants
 Sources: Thrombi in vessels & collagen
sheaths around vessel walls

103. Pulp stones
 Pulp chamber generally
 Laminated structure: Skin of an onion
 Source: True/ False
 Position: canal wall- Free
- Attached/ Adherent
- Embedded/ Interstitial

104. Pulp Calcification
Calcific Metamorphosis:
 Extensive formation of hard tissue on
dentin walls
 Irritation/ death & replacement of
odontoblasts
 Partial/ complete radiographic
obliteration of pulp chamber & root canal
 Yellowish discoloration of the crown

105. Pulp Calcification
 Increased pain threshold to stimuli; often
unresponsive
 Palpation & percussion : WNL
 Various degrees of pulp space
obliteration- radiographic
 Reduction in coronal pulp space &
gradual narrowing of root canal
 Not pathologic, no treatment

106. Internal/ Intracanal resorption
 Idiopathic slow or fast progressive
resorptive process occurring in the dentin
of the pulp chamber or root canals of
teeth
 Resorption of dentin walls, advancing
from centre to periphery
 Asymptomatic mostly
 Advanced cases:
pink spots in the crown

107. Internal resorption-
Histopathology
 Osteoclastic activity
 Lacunae- filled by osteoid tissue
 Granulation tissue
 MNGCs/ Dentinoclasts
 Chronic inflammation
 Metaplasia of pulp: Bone/ Cementum

108. Internal/ Intracanal resorption
 Pulpal & periapical tests: WNL
 Radiographs: Radiolucency with irregular
enlargement of root canal compartment;
round/ ovoid radiolucent area
 Immediate removal of inflamed tissue, RCT
 Progression & perforation to lateral
periodontium-
necrosis & treatment difficult

109. Treatment & Prognosis
 Routine endodontic therapy
 Obturation: Plasticized GP method
 Root perforation: MTA repair
 Prognosis: Best before perforation
 Guarded: perforation
 Surgical repair

110. Atrophic Degenration
 Histopathological diagnosis
 Older people
 Fewer stellate cells, increased intracellular
fluid
 Less sensitive pulp tissue
 ‘Reticular atrophy’- delay of fixative
agent reaching pulp: artifact

111. Fibrous degeneration
 Cellular elements replaced by fibrous
connective tissue
 Leathery fiber appearance on extirpation
 No clinical diagnosis
Kouros et al Eur J Dent 2013;7 Suppl 1:s26-32

112. Pulp artifacts
 Unsatisfactory
fixation:
 Fatty degeneration
of pulp
 Vacoulization
Tumor metastasis
 Rare
 Terminal stages
 Direct local
extension from jaw

113. PREVIOUSLY TREATED PULP
 A clinical diagnostic category in which
the tooth had had either partial or
complete endodontic therapy
 A clinical diagnostic category indicating
that the tooth has been endodontically
treated and the canals are obturated
with various filling materials other than
intracanal medicaments*
*AAE Consensus Conference.JOE — Volume 35, Number 12, December 2009

114. PREVIOUSLY TREATED PULP
 Symptomatic/ asymptomatic
 Completion of partial RCT
 Retreatment of failed RCT
 Endodontic surgery
 Extraction

115. Previously Initiated Therapy
 A clinical diagnostic category indicating that
the tooth has been previously treated by
partial endodontic therapy (eg, pulpotomy,
pulpectomy)*
 Pulpotomy/ Pulpectomy performed before
presenting for RCT
 Emergency procedure: Irreversible pupitis
 Vital pulp therapy
 Traumatic injuries
 Accurate pulpal diagnosis: Impossible
*AAE Consensus Conference.JOE — Volume 35, Number 12, December 2009

116. Dental pulp in Systemic
diseases
 Systemic viral infections
 Genetic & developmental disorders
 Endocrine disorders
 Cancer

117. Genetic disorders
 Hypophosphatemic rickets
 Taurodontism
 Dens invaginatus
 Dentinogenesis imperfecta
 amelogenesis imperfecta
 Gaucher’s disease

118. Systemic viral infections
Glick et al
 HIV: dental pulp &
periradicular
tissues- reinforcing
universal
precautions
 HSV-I &II: pain,
pulpal necrosis &
internal resorption
Gregory et al- 1975
Solomon et al- 1986
Sigurdsson & Jacoway- 1995

119. Systemic viral infections
 Rubella:
cytopathic effects
on ameoblasts
 1st trimester
 Paget’s disease:
 Measles virus –
Paramyxovirus family
 Pulpal obliteration
 Internal resorption
 Dystrophic
calcification
 Apical ending:
difficult to localize in
treatment

120. Diabetes mellitus
 Presence of large-vessel and small-vessel
angiopathies and a thickened basement
membrane*
 Extensive amorphous calcifications**
 Larger & more prevalent periradicular
lesions of endodontic origin***
*Russel B.Acta Pathol Microbiol Scand 1967; 70: 319-320
**Bissada et al. Egypt Dent J 1970; 283-296
***falk et al. Scand J Dent Res 1989; 97:198-206

121. Diabetes mellitus
 Limited dental collateral circulation
 Impaired immune response
 Increased risk of acquiring pulp infection/
necrosis
 Hyperglycaemia- bone resorption,
inhibiting osteoblastic differentiation and
reducing bone recovery.
Lima et al .International Endodontic Journal, 46, 700–709, 2013

122. New investigation
 EphA7 genetic expression: marked in
inflamed human dental pulp
 Pathogenesis, diagnosis & therapy of
tumors: lymphoma & GIT
Dong Y et al. JOE — Volume 39, Number 2,
February 2013

123. References
 Chandra BS, Gopi Krishna V. Grossman’s
Endodontic Practice. 12th Edition
 Beer R, Baumann MA, Kielbassa AM.
Pocket Atlas of Endodontics
 Tronstad L. Cinical Endodontics. A
textbook. 2nd revised edition
 Abbott PV. Endodontics and Dental
Traumatology. An overview of Modern
Endodontics

124. References
 Castelucci A. Endodontics. Volume 1
 Hargreaves KM, Cohen S. Cohen’s Pathways
of the Pulp. 10th Edition
 Ingle JI, Bakland LK. Ingle’s Endodontics. 5th
Edition
 Hargreaves KM, Goodis HE. Seltzer and
Bender’s Dental Pulp.
 AAE Consensus Conference on Diagnostic
Terminology: Background and Perspectives.
J Endod .2009;35(12):1634

125. References
 Gutmann JL, Baumgartner GC, Gluskin AH,
Hartwell GR, Walton RE. Identify and Define All
Diagnostic Terms for Periapical/
Periradicular Health and Disease States. J
Endod 2009;35:1658–1674
 Dabuleanu M. Pulpitis (Reversible/
Irreversible). Can Dent Assoc 2013;79:d90
 Lima SMF, Grisi DC, Kogawa EM. et al.
Diabetes mellitus and inflammatory pulpal
and periapical disease: a review. Int End J. 46,
700–709, 2013

126.  Fernandes M, de Ataide I, Wagle R. Tooth
resorption part I - pathogenesis and case
series of internal resorption. J Conserv Dent
2013;16:4-8
 Kouros P, Koliniotou-Koumpia E, Koulaouzidou
E, Helvatjoglu-Antoniades M, Tziafas D. Pulp
response to dentine adhesives: A study on
mature human pulps. Eur J Dent 2013;7 Suppl
1:s26-32