This document discusses diseases of the dental pulp, including pulpitis and its causes and classifications. Pulpitis, or inflammation of the dental pulp, is most commonly caused by microorganisms entering through caries or trauma. It can be acute or chronic and partial or total. Acute pulpitis causes severe pain from thermal changes. Chronic pulpitis may be asymptomatic or cause dull pain. Left untreated, pulpitis can lead to pulp necrosis and spread of infection to the periapical area, potentially causing a periapical abscess.

1. Presentation by:Presentation by:
Dr. Prof. Fahmy Abd ElDr. Prof. Fahmy Abd El
SalamSalam
Oral PathologyOral Pathology
First TermFirst Term

2. The disease ofThe disease of
the dental pulpthe dental pulp

3.  Pulpitis or inflammation of the dental pulpPulpitis or inflammation of the dental pulp
is the most common disease of the pulp.is the most common disease of the pulp.
 If the pulpitis was not treated it leads toIf the pulpitis was not treated it leads to
pulp necrosis, the infection will spread topulp necrosis, the infection will spread to
the pertiapical areathe pertiapical area
 The pulp response against various typesThe pulp response against various types
of irritants like any other C.T byof irritants like any other C.T by
inflammation.inflammation.
 There are special anatomical featuresThere are special anatomical features
makes the response of the pulpalmakes the response of the pulpal
inflammation have a special way:inflammation have a special way:

4. 1. The pulp lies in rigid chamber, to decrease1. The pulp lies in rigid chamber, to decrease
the accommodation ion of the inflammatorythe accommodation ion of the inflammatory
fluid exudates, Rapid degeneration andfluid exudates, Rapid degeneration and
necrosis.necrosis.
2. Have constricted narrow apical formen,2. Have constricted narrow apical formen,
limits the blood supply.limits the blood supply.
3. No collateral circulation, low resistance of3. No collateral circulation, low resistance of
the pulp.the pulp.
4. Decrease below 20C and above 45C pulp4. Decrease below 20C and above 45C pulp
hyperaemiahyperaemia

5. Causes of pulpitis:Causes of pulpitis:
1. Living irritants: =Micro organism1. Living irritants: =Micro organism
 These are the most common for pulpitisThese are the most common for pulpitis
 The M.O enters the pulp throughThe M.O enters the pulp through
i) Cariesi) Caries
ii) Due to traumatic exposureii) Due to traumatic exposure
iii) During cavity preparationiii) During cavity preparation
iv) During crown and bridge preparationiv) During crown and bridge preparation
 Facture of a crown of the teethFacture of a crown of the teeth
 Cracked tooth syndrome. Lower premolar underCracked tooth syndrome. Lower premolar under
masticatory forces, split of the tooth, invisiblemasticatory forces, split of the tooth, invisible
crack, M.O enter the pulp.crack, M.O enter the pulp.
 Through the blood stream i.e. Hematogenous.Through the blood stream i.e. Hematogenous.

6. 2. Non living irritants:2. Non living irritants:
a) Thermal irritation:a) Thermal irritation:
Excessive heat generation during:Excessive heat generation during:
- Cavity preparation- Cavity preparation
- Large metallic restoration without- Large metallic restoration without
adequate insulation.adequate insulation.
b) Chemical irritation: Silicate or compositeb) Chemical irritation: Silicate or composite
without base, Pilp irritation + Necrosis.without base, Pilp irritation + Necrosis.

7. c) Aeronautical irritation:c) Aeronautical irritation:
- High altitude flying persons, tooth ache- High altitude flying persons, tooth ache
and called aerodontalyia.and called aerodontalyia.
- This condition occurs in cases of- This condition occurs in cases of
recently filled teeth, leads to pulprecently filled teeth, leads to pulp
hyperaemia.hyperaemia.

8. Classification of pulpitisClassification of pulpitis::
-- According to the degree of inflammationAccording to the degree of inflammation ::
1. Acute pulpitis1. Acute pulpitis
2. Chronic pulpitis2. Chronic pulpitis
-- According to the degree of pulp involvementAccording to the degree of pulp involvement ::
1. Partial pulpitis.1. Partial pulpitis.
2. Total pulpitis.2. Total pulpitis.
-- According to the communication with the oralAccording to the communication with the oral
environment:environment:
1. Open pulpitis.1. Open pulpitis.
2. Closed pulpitis2. Closed pulpitis

9. Focal reversible pulpitisFocal reversible pulpitis
= Pulp hyperaemia= Pulp hyperaemia..
 This is the earliest form of pulpitis.This is the earliest form of pulpitis.
 It was called pulp hyperemia.It was called pulp hyperemia.
 It is reversible i.e. the pulp returnIt is reversible i.e. the pulp return
normal when the irritant is removed.normal when the irritant is removed.

10. Clinical picture:Clinical picture:
It occurs in :-It occurs in :-
a) Deep carious lesionsa) Deep carious lesions
b) Large metallic restorations withoutb) Large metallic restorations without
adequate base.adequate base.
The tooth is sensitive to thermal changesThe tooth is sensitive to thermal changes
specially the coldspecially the cold
The pain is removed with the removal with theThe pain is removed with the removal with the
stimulus.stimulus.

11.  Histology:Histology:
 Dilation of the B.Dilation of the B.
vessels, High vascularvessels, High vascular
permeability, Formationpermeability, Formation
of inflammatory fluidof inflammatory fluid
exudates (edoma fluid),exudates (edoma fluid),
Hemoconsumtration,Hemoconsumtration,
Thromobosis.Thromobosis.

12. Acute PulpitisAcute Pulpitis
1. It is the direct and immediate sequlae1. It is the direct and immediate sequlae
of focal reversible pulpitis.of focal reversible pulpitis.
2. it occurs due to an acute exacerbation2. it occurs due to an acute exacerbation
of chronic pulpitis,of chronic pulpitis,
I.e. chronic pulpitis well change to acuteI.e. chronic pulpitis well change to acute
pulpitis.pulpitis.

14.  Clinical picture:Clinical picture:
 Severe intermittent pain produced by thermalSevere intermittent pain produced by thermal
changes specially the cold. Persistence of painchanges specially the cold. Persistence of pain
after removal of stimulus ( acute partial pulpitis)after removal of stimulus ( acute partial pulpitis)
 As greater part of the pulp is involved the painAs greater part of the pulp is involved the pain
becomes more severe. It is lancinating type ofbecomes more severe. It is lancinating type of
pain. (acute total pulpitis)pain. (acute total pulpitis)
 The tooth is not sensitive to percussion.The tooth is not sensitive to percussion.
 The electronic pulp tester gives lower readingsThe electronic pulp tester gives lower readings
than normal teeth.than normal teeth.

15. The histology picture:The histology picture:
 V. dilatation of B.V.,V. dilatation of B.V.,
edema formation,edema formation,
Inflammatory cellularInflammatory cellular
exudates i.e. P.N.L (ployexudates i.e. P.N.L (ploy
nuclear leucocysts).nuclear leucocysts).
 The P.N.L increase in no.The P.N.L increase in no.
which are directed towardwhich are directed toward
the site of bacterialthe site of bacterial
invasion, dense mass ofinvasion, dense mass of
P.N.L is collected, breakP.N.L is collected, break
down of some of P.N.L,down of some of P.N.L,
release of proteolyticrelease of proteolytic
enzymes, liquefaction ofenzymes, liquefaction of
the pulp tissue so pulpalthe pulp tissue so pulpal
abscess will be formed.abscess will be formed.

16. 3. The pulp abscess is formed of:3. The pulp abscess is formed of:
- Central pus- Central pus
- Surrounded by dense coat of P.N.L- Surrounded by dense coat of P.N.L
- At periphery there is plasma cells + Lymphocytes- At periphery there is plasma cells + Lymphocytes
- Collagen fibers at the periphery of the area.- Collagen fibers at the periphery of the area.
4. Partial destruction of the odontoblasts in the area.4. Partial destruction of the odontoblasts in the area.
5. The P.N.L evades the entire pulp, multiple pulp5. The P.N.L evades the entire pulp, multiple pulp
abscesses.abscesses.

17. 6. Eventually the pulp tissue undergoes6. Eventually the pulp tissue undergoes
necrosis and liquefactionnecrosis and liquefaction
= This is called acute suppurative= This is called acute suppurative
pulpitis.pulpitis.

19. Chronic pulpitisChronic pulpitis
 May be pulpitis, chronic pulpitisMay be pulpitis, chronic pulpitis
 May start chronic pulpitis from theMay start chronic pulpitis from the
beginningbeginning

20. Chronic pulpitis is classified into:Chronic pulpitis is classified into:
A) Chronic closed pulpitisA) Chronic closed pulpitis
b) Chronic open pulpitisb) Chronic open pulpitis
A) Chronic closed pulpitis:A) Chronic closed pulpitis:
Clinical Picture:Clinical Picture:
Intermittent pain dull aching type of painIntermittent pain dull aching type of pain
Sensitivity to thermal changes is lesser than acuteSensitivity to thermal changes is lesser than acute
pulpitis.pulpitis.
E. pulp tester gives higher readings than normal tooth.E. pulp tester gives higher readings than normal tooth.

21. Histopathology:Histopathology:
 Large no. of chronicLarge no. of chronic
inflammatory cellsinflammatory cells
( Lymphocytes, Plasma( Lymphocytes, Plasma
cells)cells)
 Capillary are prominent.Capillary are prominent.
 Collagen bundles areCollagen bundles are
present.present.

22. b) Chronic open pulpitisb) Chronic open pulpitis
Chronic open pulpitis is characterized by:Chronic open pulpitis is characterized by:
1. The pulp chamber is opened to the oral cavity1. The pulp chamber is opened to the oral cavity
by wide exposureby wide exposure
2. Large part of the crown is broken.2. Large part of the crown is broken.
There are 2 types of chronic open pulpitisThere are 2 types of chronic open pulpitis
i) Chronic open ulcerative pulpitisi) Chronic open ulcerative pulpitis
ii) Chronic open hyperplastic pulpitis = Pulpii) Chronic open hyperplastic pulpitis = Pulp
polyp.polyp.

23. i) Chronic open ulcerative pulpitis:i) Chronic open ulcerative pulpitis:
Histopathology:Histopathology:
1. The pulp tissue show:1. The pulp tissue show:
a) Chronic inflammation cells. ( plasma cells,a) Chronic inflammation cells. ( plasma cells,
Lymphocysts)Lymphocysts)
b) Prominent blood cap.b) Prominent blood cap.
c) Collagen bundles.c) Collagen bundles.
2. The surface at the exposure site: the pulp tissue is2. The surface at the exposure site: the pulp tissue is
replaced by:replaced by:
a) Inflamed granulation tissuea) Inflamed granulation tissue
b) Newly formed capb) Newly formed cap
c) Collagen fibers + fibroblastsc) Collagen fibers + fibroblasts
e)Plasma cells + lymphocysts + macrphagese)Plasma cells + lymphocysts + macrphages

24. ii) Chronic open Hyperplastic pulpitisii) Chronic open Hyperplastic pulpitis
= Chronic hyperplastic pulpitis.= Chronic hyperplastic pulpitis.
= Pulp polyp.= Pulp polyp.
Def:Def: It is hyperplasia of chronically inflamed pulpIt is hyperplasia of chronically inflamed pulp
tissue.tissue.
Age:Age: Children and young adults.Children and young adults.
SiteSite: 6<6 and E<E + wide exposure because:: 6<6 and E<E + wide exposure because:
Young age means high tissue reactivity.Young age means high tissue reactivity.
6<6 and E<E have wide apical formen, good6<6 and E<E have wide apical formen, good
blood supply.blood supply.

25. Appearance:Appearance:
- Red, pink globule of tissue protruding- Red, pink globule of tissue protruding
from the wide exposure.from the wide exposure.
- It is not painful and bleeds easily.- It is not painful and bleeds easily.

26. Histogenisis:Histogenisis:
 The coronal part of the pulp is replaced byThe coronal part of the pulp is replaced by
chronically inflamed granulation tissue.chronically inflamed granulation tissue.
 The granulation tissue proliferates and protrudesThe granulation tissue proliferates and protrudes
from the wide exposure and fill the wide exposure.from the wide exposure and fill the wide exposure.
 The desquamated epithelial cells from the oralThe desquamated epithelial cells from the oral
mucosa will be implanted upon the granulation.mucosa will be implanted upon the granulation.
 The epithelial cells will proliferate to form stratifiedThe epithelial cells will proliferate to form stratified
squemous epith which cover the granulation tissuesquemous epith which cover the granulation tissue
nodule.nodule.
 By time the granulation tissue is changed into fibrousBy time the granulation tissue is changed into fibrous
tissue.tissue.

28. Microscopic picture:Microscopic picture:
 Mass of chronically inflamedMass of chronically inflamed
granulation tissue + chronicgranulation tissue + chronic
inflammatory cells (plasma cells +inflammatory cells (plasma cells +
lymphocysts).lymphocysts).
 It is covered with st. sq. epith.It is covered with st. sq. epith.

29. The infection of theThe infection of the
peripical areaperipical area
 The pulp infections spread through the root canal to reachThe pulp infections spread through the root canal to reach
the periapical area.the periapical area.
 The periapical pathosis may be:The periapical pathosis may be:
i) Apial periodontitis: a) Acute b) Chronic.i) Apial periodontitis: a) Acute b) Chronic.
ii) Periapical abscess: a) Acute b) Chronic.ii) Periapical abscess: a) Acute b) Chronic.
iii) Periapical granuloma.iii) Periapical granuloma.
iv) Periapical cyst.iv) Periapical cyst.
This depends upon:This depends upon:
1. Severity of irritation.1. Severity of irritation.
2. Duration of condition.2. Duration of condition.
3. The host response.3. The host response.

30. Apial periodontitisApial periodontitis::
 It is the earliest signs of the periodontitis.It is the earliest signs of the periodontitis.
Clinical picture of acute periodontitis:Clinical picture of acute periodontitis:
1. Moderate to severe pain.1. Moderate to severe pain.
2. Severe pain on percussion.2. Severe pain on percussion.
Clinical picture of chronic periodontitis:Clinical picture of chronic periodontitis:
1. Asymptomatic or mild discomfort.1. Asymptomatic or mild discomfort.
2. Vertical percussion produces little or no2. Vertical percussion produces little or no
pain.pain.

31. Periapical abscessPeriapical abscess::
Acute or chronic suppuration in theAcute or chronic suppuration in the
periapical area.periapical area.
Etiology: -sequla of pulp infection.Etiology: -sequla of pulp infection.
- Other causes:- Other causes:
1. Trauma1. Trauma
2. Mechanical or chemical irritation2. Mechanical or chemical irritation
during root canal ttt.during root canal ttt.

32. Clinical picture of acute peripical abscess:Clinical picture of acute peripical abscess:
 The tooth is painful.The tooth is painful.
 Severe pain on vertical percussion.Severe pain on vertical percussion.
 The tooth is slightly extruded from the socket.The tooth is slightly extruded from the socket.
 Systematic manifestation as: Fever, malaise,Systematic manifestation as: Fever, malaise,
leucocytosis and lymphadenitis.leucocytosis and lymphadenitis.

34. Chronic periapicalChronic periapical
abscessabscess::
 Characterized byCharacterized by
sinus tractsinus tract
formation.formation.
 This sinus tractThis sinus tract
drains on: oraldrains on: oral
mucosa or to skinmucosa or to skin
( very rare)( very rare)
 It is asymptomaticIt is asymptomatic
because of thebecause of the
drainage.drainage.

35. Histological picture:Histological picture:
 Central area of pus.Central area of pus.
 Surrounded by: leukocysts and ch. Inf.Surrounded by: leukocysts and ch. Inf.
Cells.Cells.
 On the periphery there is granulationOn the periphery there is granulation
tissue.tissue.

36. The periapicalThe periapical
granulomagranuloma::
 It is a localized mass of chronically inflamedIt is a localized mass of chronically inflamed
granulation tissue.granulation tissue.
 It is formed in response to infection.It is formed in response to infection.
Etiology:Etiology:
 Most of the cases caused by spread ofMost of the cases caused by spread of
infection from pulp.infection from pulp.
 Faulty procedures in endodontic therapy.Faulty procedures in endodontic therapy.

37. Clinical picture:Clinical picture:
 Usually asymptomatic and discoveredUsually asymptomatic and discovered
during routine x-ray examination.during routine x-ray examination.
 Some cases mild sensitivity to verticalSome cases mild sensitivity to vertical
percussion or when biting on chewingpercussion or when biting on chewing
on solid food.on solid food.
 The tooth feel slightly enlarged in theirThe tooth feel slightly enlarged in their
socket.socket.

38. HistopathologyHistopathology::
A) Pathogenesis:A) Pathogenesis:
1. It begins as hyperaemia + edema + chronic1. It begins as hyperaemia + edema + chronic
inflamed in the peripical area.inflamed in the peripical area.
2. The inflammation process + high vascularity2. The inflammation process + high vascularity
will stimulates osteoclasts, Bone resorpation.will stimulates osteoclasts, Bone resorpation.

39. 3. The reserbed bone will be replaced by granulation3. The reserbed bone will be replaced by granulation
tissue.tissue.
 Endoth. cap + fibroblasts , Delicate fibrilis.Endoth. cap + fibroblasts , Delicate fibrilis.
b. The microscopic picture of the periapical granuloma:b. The microscopic picture of the periapical granuloma:
1. Mass of granulation tissue surround apex of root.1. Mass of granulation tissue surround apex of root.
2. Chronic inflammatory cells.2. Chronic inflammatory cells.
3. Large no. of phagocytes (Histocytes = Macrophages)3. Large no. of phagocytes (Histocytes = Macrophages)
These will digest the lipid forming sheets of foam cells.These will digest the lipid forming sheets of foam cells.

41.  4. Cholesterol:4. Cholesterol:
 Appears as needle shape.Appears as needle shape.
 The cholesterol crystals dissolve in zylol during preparationThe cholesterol crystals dissolve in zylol during preparation
so it appears empty and called coolest clefts.so it appears empty and called coolest clefts.
 The foreign body multinucleated giant cells may be seen inThe foreign body multinucleated giant cells may be seen in
relation to the cholesterol clefts.relation to the cholesterol clefts.

42. 5. Presence of Epithelial rests5. Presence of Epithelial rests
malasseze.malasseze.
6. Fibrous capsule encircle the6. Fibrous capsule encircle the
granuloma and separating it from thegranuloma and separating it from the
bone.bone.

43. Thank YouThank You
Best wishesBest wishes
& Good Luck& Good Luck
Dr. Fahmy Abd El SalamDr. Fahmy Abd El Salam