1. DISEASES OF
THE PULP
Prepared by:
Dr. Rea Corpuz

2. Pulp
 formative organ of tooth
 builds primary dentin
during development of tooth
 secondary dentin after
tooth eruption
 reparative dentin in response
to stimulation as long as
odontoblast remain vital

3. Pulpitis
 most common cause of
dental pain
 loss of teeth in younger
persons
 usual cause is caries
penetrating the dentin

4. Pulpitis
UNTREATED
Death of pulp
Spread of Infection through
apical foramina into periapical
tissues
Causes Periapical Periodontitis

5. Causes of Pulpal
Inflammation
 (1) Mechanical Cause
 (2) Thermal Cause
 (3) Chemical Cause
 (4) Bacterial Cause

6. Causes of Pulpal
Inflammation
 (1) Mechanical Cause
 traumatic accident
 iatrogenic damage for
dental procedure
 atrrition
 abrasion

7. Causes of Pulpal
Inflammation
 (2) Thermal Cause
 uninsulated metallic
restoration
 during cavity preparation
 polishing

8. Causes of Pulpal
Inflammation
 (3) Chemical Cause
 arise from erosion
 or inappropriate use
of acidic dental material

9. Causes of Pulpal
Inflammation
 (4) Bacterial Cause
 can damage pulp
through toxins secreted
by bacteria from caries

10. Classification
 (1) Based on Severity of
Inflammation
 (2) According to Involvement

11. (1) Based on Severity
of Inflammation
 (1) Reversible Pulpitis
 (2) Irreversible Pulpitis
 (3) Pulp Degeneration
 (4) Pulp Necrosis

12. (1) Based on Severity
of Inflammation
 (1) Reversible Pulpitis
 Symptomatic (acute)
 Aysptomatic (chronic)
 (2) Irreversible Pulpitis
 Acute
• Abnormally responsive to cold
• Abnormally responsive to heat

13. (1) Based on Severity
of Inflammation
 (2) Irreversible Pulpitis
 Chronic
• Asymptomatic with
pulp exposure
• Hyperplastic
• Internal resorption

14. (1) Based on Severity
of Inflammation
 (3) Pulp Degeneration
 Calcific
 (4) Pulp Necrosis

15. (2) According to
Involvement
 (1) According to Involvement
 (2) According to Severity
 (3) According to presence or
absence of direct
communication
between dental pulp +
oral environment

16. (2) According to
Involvement
 (1) According to Involvement
 Focal or Subtotal or
Partial Pulpitis
 Total or Generalized
Pulpitis

17. (2) According to
Involvement
 (2) According to Severity
 Acute
 Chronic

18. (2) According to
Involvement
 (3) According to presence or
absence of direct
communication
between dental pulp +
oral environment
 Pulpitis Aperts (open pulpitis)
 Pulpitis Clausa (closed pulpitis)

19. Reversible Pulpitis
 mild to moderate inflammatory
condition of pulp
 caused by noxious stimuli
 pulp is capable of returning
to un-inflammed state
 following removal of stimuli

20. Reversible Pulpitis
 Causes
 agent capable of
injuring pulp like:
• trauma
• disturbed occlusal
relationship
• thermal shock

21. Reversible Pulpitis
 Clinical Features
 sharp pain lasting for
a moment
 often brought on by cold
than hot food or beverages
and by cold air

22. Reversible Pulpitis
 Clinical Features
 does not continue
when the cause has been
removed
 tooth responds to electric
pulp testing at lower
current

23. Reversible Pulpitis
 Management
 prevention
 periodic care
 early insertion of filling
if a cavity has developed
 removal of noxious
stimuli

24. Focal Reversible
Pulpitis
earliest form
 also known as pulp hyperemia
 excessive accumulation of
blood within pulp tissue
 leads to vascular congestion

25. Focal Reversible
Pulpitis
 Clinical Features
 sensitive to thermal
changes
 particularly to cold
 application of ice or cold
fluids to tooth result in pain

26. Focal Reversible
Pulpitis
 Clinical Features
 disappears upon removal
of thermal irritant or
restoration of normal
temperature
 responds to electrical test
stimulant at lower level
of current

27. Focal Reversible
Pulpitis
 Clinical Features
 indicates lower pain
threshold than that of
adjacent normal
teeth

28. Focal Reversible
Pulpitis
 Clinical Features
 teeth show:
• deep carious lesion
• large metallic restoration
• restoration with defective
margins

29. Focal Reversible
Pulpitis
 Management
 removal of irritants
before the pulp is
severely damaged

30. Irreversible Pulpitis
 persistent inflammatory
condition of pulp
 may be symptomatic or
asymptomatic
 caused by noxious stimulus

31. Irreversible Pulpitis
 Causes
 bacteria involvement of
pulp through caries
 chemical
 thermal
 mechanical injury

32. Irreversible Pulpitis
 Clinical Features
Early Stage
 paroxysm of pain
caused by:
• sudden temperature
changes like cold,
sweet, acid foodstuffs

33. Irreversible Pulpitis
 Clinical Features
Early Stage
 pain often continues
when cause has been
removed
 may come and go
spontaneously

34. Irreversible Pulpitis
 Clinical Features
Early Stage
 pain
• sharp
• piercing
• shooting
• generally severe

35. Irreversible Pulpitis
 Clinical Features
Early Stage
 pain
• bending over exacerbates pain which
• lying down is due to change in
• change of position intrapulpal pressure

36. Irreversible Pulpitis
 Clinical Features
Late Stage
 pain
• more severe as if tooth is under
• throbbing constant pressure

37. Irreversible Pulpitis
 Clinical Features
Late Stage
 pain
• patient is often awake
at night due to pain
• increased by heat and
sometimes relieved by cold,
although continued application
of cold may intensify pain

38. Irreversible Pulpitis
 Management
 complete removal of pulp
or pulpectomy
 placement of intracanal
medicament
 to act as disinfectant or
obtundent
• cresatin
• eugenol
• formocresol

39. Clinical Difference
Reversible Pulpitis Irreversible Pulpitis
 pain is generally traceable  more severe
to a stimulus  lasts longer
 cold water  pain may come
 air without
any apparent stimulus

40. Acute Pulpitis
 extensive acute inflammation
of pulp
 frequent sequel of focal
reversible pulpitis

41. Acute Pulpitis
 Causes
 tooth with large carious
lesion
 defective restoration
where there has been
recurrent caries
 pulp exposure due to
faulty cavity preparation

42. Acute Pulpitis
 Clinical Features
 severe pain is elicited by
thermal changes
 pain persists even after
thermal stimulus
disappears or been
removed

43. Acute Pulpitis
 Clinical Features
 may be continuous
 intensity may be increased
when patient lies down
 application of heat may
may cause acute
exacerbation of pain

44. Acute Pulpitis
 Clinical Features
 tooth reacts to electric
pulp vitality tester at a
lower level of current
than adjacent normal
teeth

45. Acute Pulpitis
 Clinical Features
 pressure increases
because of lack of
escape of inflammatory
exudate
 rapid spread of inflammation
through pulp with pain
+ necrosis

46. Acute Pulpitis
 Management
 early stages of pulpotomy
(removal of coronal pulp)
 placing material that
favors calcification such
as:
• calcium hydroxide
over entrance of
root canals

47. Acute Pulpitis
 Management
 root canal filing with
inert material like
gutta percha should be
done

48. Chronic Pulpitis
 may develop with or
without episodes of
acute pulpitis
 many pulps under large
carious cavities die painlessly
 1st indication is then
development of periapical
periodontitis, either with pain
or seen by chance in radiograph

49. Chronic Pulpitis
 Clinical Features
 dull aching type
 more often intermittent
than continuous

50. Chronic Pulpitis
 Management
 root canal therapy
 followed by crown
restoration

51. Chronic Hyperplastic
Pulpitis
 also called as pulp polyp
or pulpitis aperta
 essentially an excessive
exuberant proliferation
of chronically inflammed
dental pulp tissue

52. Chronic Hyperplastic
Pulpitis
 pulpal inflammation due
to an extensive carious
exposure of a young pulp
 development of granulation
tissue
 covered at times by epithelium
 resulting from long standing
low grade infection

53. Chronic Hyperplastic
Pulpitis
 Causes
 slow progressive
exposure of pulp
 bacterial infection

54. Chronic Hyperplastic
Pulpitis
 Clinical Features
 most commonly involved
are deciduous molars +
1st permanent molar
• excellent blood supply
• large root opening

55. Chronic Hyperplastic
Pulpitis
 Clinical Features
 asymptomatic
 seen only in teeth of children
+ young adults

56. Chronic Hyperplastic
Pulpitis
 Clinical Features
 polypoid tissue appears
• fleshy
• reddish pulpal mass filling
most of pulp chamber
or cavity
• or even extend beyond
confines of tooth

57. Chronic Hyperplastic
Pulpitis
 Clinical Features
 polypoid tissue appears
• sometimes, if mass is
large enough
• interferes with closure
of mouth

58. Chronic Hyperplastic
Pulpitis
 Clinical Features
 polypoid tissue appears
• may cause discomfort
during mastication
• due to pressure of food
bolus

59. Chronic Hyperplastic
Pulpitis
 Clinical Features
 polypoid tissue appears
• tissue easily bleeds
because of rich network
of blood vessels
• tooth may respond or
not at all to thermal test

60. Chronic Hyperplastic
Pulpitis
 Management
 elimination of polypoid tissue
 followed by extirpation of pulp
 hyperplastic tissue bleeeding
can be controlled by pressure
 extraction of tooth can also
be done

61. Necrosis
 death of pulp
 may be partial or total
depending on whether part
or the entire pulp is
involved

62. Necrosis
 Causes
 sequeala of inflammation
 can also occur following
trauma
• pulp is destroyed before
an inflammatory reaction

63. Necrosis
 Types
 (1) Coagulation Necrosis
 (2) Liquefaction Necrosis

64. Necrosis
 Types
 (1) Coagulation Necrosis
• soluble portion of
tissue is precipitated
• or converted into a solid
material

65. Necrosis
 Types
 (1) Coagulation Necrosis
• tissue is converted into
tissue mass consisting
chiefly of coagulated
 proteins
 fats
 water

66. Necrosis
 Types
 (2) Liquefaction Necrosis
• results when proteolytic
enzymes convert the
tissue into softened mass
liquid or amorphous debris

67. Necrosis
 Clinical Features
 no painful symptoms
 discoloration of tooth
• 1st indication that the pulp
is dead

68. Necrosis
 Clinical Features
 history of pain lasting from
a few minutes to a few
hours followed by
complete + sudden
cessation of pain

69. Necrosis
 Management
 preparation + obturation of
root canals

70. References:
 Books
 Cawson, R.A: Cawson’s Essentials of Oral
Oral Pathology and Oral Medicine,
8th Edition
• (page 60)
 Ghom, Ali & Mhaske, Shubhangi: Textbook of
Oral Pathology
• (pages 420-425)