for dental students

1. Diseases of The Pulp
Prepared by,
VISHAL KURIAN

2.  Pulpitis is the inflammation of the pulp tissue
 Usually caused by caries penetrating the dentin
 Most common manifestations are tooth ache
&increased sensitivity to hot & cold
 Pulp inflamed > pressure build ups on pulp cavity >
pressure on nerves & surrounding tissues > pain

3. Causes of Pulpal Inflammation
 (1) Mechanical Cause
 traumatic accident
 iatrogenic damage for
dental procedure
 attrition
 abrasion
 (2) Thermal Cause
 uninsulated metallic
restoration
 during cavity preparation
 polishing

4.  (3) Chemical Cause
 arise from erosion
 or inappropriate use
of acidic dental material
 (4) Bacterial Cause
 can damage pulp
through toxins secreted
by bacteria from caries

5. Classification
1) Based on Severity of Inflammation
(1) Reversible
-Symptomatic ( acute)
- Asymptomatic ( Chronic)
(2) Irreversible
a) Acute
- abnormally responsive to cold
-abnormally responsible to hot
b)Chronic
- Asymptomatic with
pulp exposure
- Hyperplastic
- Internal resorption
(3) Pulp Degeneration
- Calcific
(4) Pulp Necrosis

6. (2) According to Involvement
 Acc. To involvement:
1. Focal / subtotal /partial pulpitis (inf. Is confined to a portion of pulp)
2. Total / generalized pulpitis ( most part of the pulp is involved)
 Acc. To severity :
1.Acute
2.Chronic
 Acc. To presence or absence of direct communication b/w pulp & oral
evironment:
1.Pulpitis asperta (open)
2.Pulpitis clousa (closed)

7. Reversible pulpitis
 Pathogenesis:
 Stimuli of short duration
eg. Cutting dentin
 mild to moderate inflammatory
condition of pulp
 caused by noxious stimuli
 pulp is capable of returning
to un-inflammed state
 following removal of stimuli
 Causes:
 agent capable of
injuring pulp like:-
• trauma
• disturbed occlusal
relationship
• thermal shock

8. Clinical Features
 sharp pain lasting for
a moment
 often brought on by cold
than hot food or beverages
and by cold air
 does not continue
when the cause has been
removed
 tooth responds to electric
pulp testing at lower
current

9.  Ranges from hyperemia to mild to moderate inflammation of the affected area.
 Reperative dentine
 Dilated blood vessels
 Edema
 Presence of immunologic response
Histopathological features:

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

11. Focal reversible pulpitis
 earliest form
 also known as pulp hyperemia
 excessive accumulation of
 blood within pulp tissue
 leads to vascular congestion

12. Clinical Features
 sensitive to thermal
changes
 particularly to cold
 application of ice or cold
fluids to tooth result in pain
 disappears upon removal
of thermal irritant or
restoration of normal
temperature
 responds to electrical test
stimulant at lower level
of current
 indicates lower pain
threshold than that of
adjacent normal
teeth
 teeth show:
• deep carious lesion
• large metallic restoration
• restoration with defective
margins

13.  Management
 removal of irritants
before the pulp is
severely damaged
 Carious lesion should be
excised & restored or
defective filling is replaced.
 If primary cause is not
corrected, extensive pulpitis
may result in death of pulp.

14. Histopathologic features:
Dilation of pulp blood vessels.
Edema fluid collection due to damage of vessel wall & allowing extravasations
of RBC or diapedesis of WBC.
Slowing of blood flow & hemoconcentration due to transudation can cause
thrombosis.
Reparative or reactionary dentin in adjacent dentinal wall

15. Acute pulpitis
 extensive acute inflammation
of pulp
 frequent sequel of focal
reversible pulpitis
Usually occurs in a tooth with a large
carious lesion /restoration
Commonly a defective restoration
around whivh there has been recurrent
caries

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

17.  Clinical Features
 severe pain is elicited by
thermal changes
 pain persists even after
thermal stimulus
disappears or been
removed
 may be continuous
 intensity may be increased
when patient lies down
 application of heat may
may cause acute
exacerbation of pain
 tooth reacts to electric
pulp vitality tester at a
lower level of current
than adjacent normal
teeth

18. HISTOLOGICAL FEATURES
Edema in pulp with vasodilation.
Infiltration of polymorphonuclear leukocytes along
vascular channels & migrate through endothelium
lined structures.
Destruction of odontoblasts at pulp dentin border.
Rise in pressure due to inflammatory exudate
local collapse of venous part of circulation
Tissue hypoxia & anoxia Destruction of pulp &
abscess formation.
Abscess consists pus, leukocytes & bacteria.
Numerous abscess formation cause pulp liquefaction
& necrosis. (acute suppurative pulpitis)

19. TREATMENT & PROGNOSIS:
Drainage of exudates from pulp chamber.
Pulpotomy & placing calcium hydroxide over entrance of root
canal.
Root canal treatment.
Extraction of tooth.

20. CHRONIC PULPITIS
 may develop with or without episodes of acute pulpitis
 More frequewntly occurs as chronic type from the onset.
 CLINICAL FEATURES:
Pain is not prominent, mild, dull ache which is intermittent.
Reaction to thermal changes is reduced because of degeneration of nerves.
Response to pulp vitality tester is reduced.
Wide open carious lesion & with exposure of pulp cause relatively little
pain.
Manipulation with small instruments often elicits bleeding but with little
pain.

21. HISTOLOGIC FEATURES:
Infiltration of mononuclear cells, lymphocytes & plasma cells, with vigorous
connective tissue reaction.
Capillaries are prominent; fibroblastic activity & collagen fibers in bundles.
When granulation tissue formation occurs in wide open exposed pulp surface
– ulcerative pulpitis. (with bacterial stains & micro org. in carious lesion)
If pulpal reaction vacillates between an acute & chronic phase causes pulp
abscess formation, which is surrounded by fibrous CT wall.

22. TREATMENT & PROGNOSIS:
Root canal therapy
Extraction of tooth.

23. Chronic Hyperplastic pulpitis
 also called as pulp polyp or pulpitis aperta
 Overgrowth of pulp tissue outside the boundary of pulp
chamber as protruding mass.
 a form chronic pulpitis
 Occurs either as a chroniv lesion
from onset or as a chronic stage of
a previously ACUTE PULPITIS

24. Children & young adults with high
degree of tissue resistance &
reactivity & responds to proliferative
lesions.
Pulp - pinkish red globule of tissue
protruding from chamber & extend
beyond caries.
Most commonly affected are
deciduous molar & Ist permanent
molars.
Pulp is relatively insensitive because
few nerves in hyperplastic tissue.
Clinical feaures:

25. Lesion bleeds profusely upon provocation.
Due to excellent blood supply high tissue
resistance & reactivity in young persons leads to
unusual proliferative property of pulp.
Some cases, gingival tissue adjacent, may
proliferate into carious lesion & superficially
resemble hyperplastic pulpitisa

26. HISTOLOGIC FEATURES:
Hyperplastic tissue is basically
granulation tissue, consisting
delicate CT fibers & young blood
capillaries.
Inflammatory infiltrates –
lymphocytes, plasma cells &
polymorphs.
Stratified squamous type epithelial
lining resembles oral mucosa with
well formed rete pegs.

27.  TREATMENT & PROGNOSIS:
Extraction of tooth or RCT.
Grafted epithelial cells are believed
to be desquamated epith. Cells,
which carried by saliva.
Origin of these cells is unknown.
They are degenerated superficial
squames, which ’ve lost dividing
capacity.
When pulp polyp is present for a
long time, persistent rubbing of
buccal mucosa may help in grafting
of epith. cells

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

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

30.  Types
 (1) Coagulation Necrosis
• tissue is converted into
tissue mass consisting
chiefly of coagulated
 proteins
 fats
 water
 (2) Liquefaction Necrosis
• results when proteolytic
enzymes convert the
tissue into softened mass
liquid or amorphous debris

31.  Clinical Features
 no painful symptoms
 discoloration of tooth
• 1st indication that the
• pulp is dead
 history of pain lasting from
a few minutes to a few
hours followed by
complete + sudden
cessation of pain

32.  Management
 preparation + obturation of
root canals