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1. RATIONALE OF ENDODONTICS
INDIAN DENTAL ACADEMY
Leader in Continuing Dental Education
www.indiandentalacademy.com

2. CONTENTS
• Introduction
• Inflammation
• Causes of pulpal Inflammation
• Pathways of pulpal & periapical infection
• Responses of the pulp and periradicular tissue
Cellular & Vascular Components
Chemical mediators.
• Syngcuk kim’s hypothetic mechanism of pathophysiology
of pulpal disorder
• Periradicular tissue changes following inflammation
• Endodontic implication
Fish theory of zones of inflammation
• Sequence of pulpo periapical pathoses
• Conclusion

3. INTRODUCTION
• Injury to the calcified structure of teeth and to the
supporting tissues by noxious stimuli may cause
changes in the pulp and the periradicular tissues.
• The inflammatory response of the connective tissue of
the dental pulp is modified because of its milieu.
Because the pulp is encased in hard tissues with
limited portals of entry, it is an organ of terminal and
limited circulation with no efficient collateral
circulation and with limited space to expand during
the inflammatory reaction. A clear concept is
necessary for the understanding or the diseases of the
pulp and their extension to the periradicular tissues.

4. INFLAMMATION
• Inflammation is a complex reaction to
injurious agents such as microbes and
damaged, usually necrotic cells that consists
of vascular responses, migration and
activation of leucocytes, and systemic
reactions.
Robbins et al 2004

5. CAUSES OF PULP INFLAMMATION
• Bacterial
Coronal ingress : caries, fracture,nonfracture tract, anomalous
tract.
Radicular ingress: caries, retrogenic infection, hematogenic
• Traumatic
Acute : Coronal #, radicular #, vascular stasis, luxation,
avulsion
Chronic: adolescent female bruxism,traumatism, attrition

6. Iatral causes:
• Cavity preparation: Heat of preparation, depth
of preparation, dehydration, pulp horn
extensions, pulp hemorrhage, pulp exposure, pin
insertion, impression taking
• Restoration: Insertion, Fracture, Force of
cementing, Heat of polishing.
• Intentional extirpation and root canal filling,
Orthodontic movement, Periodontal curettage,
Electrosurgery, Laser burn, Periradicular
curettage, Rhinoplasty, Osteotomy, Intubation for
general anesthesia

7. Chemical causes
Restorative materials: Cements, Plastics,Etching
agents, Cavity liners, Dentin bonding agents,
Tubule blockage agents
Disinfectants : Silver nitrate, Phenol, Sodium
fluoride
Desiccants : Alcohol, Ether, Others

8. Idiopathic causes
• Aging
• Internal resorption
• External resorption
• Hereditary hypophosphatemia
• Sickle cell anemia
• Herpes zoster infection
• Human immunodeficiency virus (HIV) and
acquired immune deficiency syndrome (AIDS)

9. PATHWAYS OF PULPAL &
PERIAPICAL INFECTIONS
• Dentinal tubules
• Pulp exposure
• Periodontal ligament
• Anachoresis

10. Dentinal tubules
• Position, size and number
• Dentinal tubules exposed due to loss of enamel
and cementum
• As per the size and number of the tubules
microorganisms enter, multiply and invade
exposed tubules
• Role of dental caries, dental procedures and
periodontal diseases.
• Bacterial strains involved

11. Pulp exposure
• Contamination of the pulp – truama, caries, and
others
• Depending on the virulence of the organism, host
resistance, amount of circulation and degree of
drianage ranges the pulpal inflammation.
• Microbiology involved.

12. Periodontal ligament
• Relation between root canal infection and
periradicular lesion ?
• Grossman found that periodontal ligament
provided pathways for passage of
microorganisms into the pulpal tissue.

13. Anachoresis
• Defined as a positive attraction of blood borne
microorganisms to inflamed or necrotic tissue during
bacteremia.
• Csernyei 1939 – demonstrated anachoretic effect of
periapical inflammation in dogs.
• Dental extractions,toothbrushing can produce
bacteremia during which circulating microorganisms
can be attracted to the inflamed or necrotic pulp.

14. • Depending on the level of oxygen tension & the
presence or absence of essential nutrients,specific
groups of bacteria colonize,multiply,contaminate
& establish the flora in the entire root canal
system including periradicular tissues.

16. SIGNS OF INFLAMMATION
Described in a Egyptian papyrus-in 3000BC by
Celsus as:
Rubor [redness]
Tumor [swelling]
Calor [heat]
Dolor [pain]
Functio laesa [virchow in 1793]

17. Components Of Inflammation
Cellular Vascular

18. Cellular Components of
Inflammation
• Polymorphonuclear neutrophils
• Eosinophils
• Basophils
• Mast cells
• Monocytes & Macrophages
• Lymphocytes
• Osteoclasts
• Epithelial cells

19. Polymorphonuclear
Neutrophils

20. Eosinophils,Basophils & Mast cells

21. Monocytes & Macrophages

22. Lymphocytes

23. Osteoclasts
&
Epithelial Cells

24. CHEMICAL MEDIATORS
DEFINITION
Inflammatory mediators are chemical
substances present in plasma or produced
by certain cells which mediate the
inflammatory reactions.

25. CLASSIFICATION

26. Plasma derived mediators
Complement System
The complement system consists of 20
component proteins and their cleavage products
found in greatest concentration in plasma.
The complement system is activated by two
pathways.
1.Classic pathway.
2.Alternate pathway.

27. Complement Cascade

28. Actions
1. vascular phenomenon:
-C3a, C5a- increases vascular permeability, vasodilation
-C5a- activates lipoxygenase pathway in neutrophil and
monocyte
2. Leukocyte adhesion and chemotaxis:
-C5a- powerful chemotactic agent for neutrophils,
monocytes, eosinophils, basophils
-Increased adhesion of leukocytes to endothelium
-Increases avidity of surface integrins to endothelial ligand

29. Hageman factor activated
kinin and coagulation system

31. Kinin system
• Bradykinin:is shortlived due to the activity of
kinase enzyme
• Kallikrien
Actions:
• Kallikrien converts High Molecular Weight
Kininogen (HMWK) into bradykinin, which in turn
converts plasminogen into plasmin
• Plasmin splits C3 into C3a
• Kallikrien also directly converts C5 into C5a and
has chemotactic activity

32. Clotting System:
Two components of activated coagulation system
links coagulation inflammation
1. Fibrinopeptides- increase vascular permeability,
chemotactic for leukocytes
2. Thrombin- increase leukocyte adhesion,
fibroblast proliferation

33. Cell derived mediators
Histamine
Histamine is released by mast cell degranulation in response
to variety of stimuli like:
• Physical injury - trauma, heat, cold.
• Immune reactions involving binding of antibody to
mast cell.
• Fragments of complement called anaphylatoxins -
C3a, C5a.
• Histamine releasing proteins derived from leucocytes.
• Neuropeptides e.g. substance P.
• Cytokines - IL1, IL8.

34. ACTIONS:
Acts on microcirculation mainly via H1
receptors. Histamine causes
1 Dilatation of arterioles, constriction of
large arteries.
2 Increased vascular permeability of venules.

35. SEROTONIN:(5 - hydroxytryptamine. )
• Present in platelets and enterochromaffin cells.
• Their release is stimulated by when platelets
aggregate after contact with collagen, thrombin,
ADP, antigen-antibody complexes.
• Platelet aggregation and release stimulated by
platelet activation factor(PAF)
• PAF derived from mast cells during IgE mediated
reactions
ACTIONS:
• Platelet aggregation.
• Increases vascular permeability.

36. Lysosomal enzymes
• Neutral proteases – elastase, collagenase, cathepsin
can mediate tissue injury by degrading elastin collagen and
other tissue proteins
• Proteases – cleave C3 and C5 directly to generate
anaphylotoxins.
• Kallikerin released from the lysosomes promotes the
generation of bradykinin
• Cationic proteins

37. Phospholipid metabolism & Arachidonic
acid metabolism

38. Neuropeptides
• Several neuropeptides have been detected in the dental pulp
of humans
• These include substance P (SP), calcitonin gene-related
peptide(CGRP), neurokinin A (NKA), neuropeptide K,
neuropeptide Y, somatostatin and vasoactive intestinal
peptide (VIP)
• Increased production and release of neuropeptides play an
important role in initiating and propagating pulpal
inflammation.
• SP, CGRP and VIP are potent vasodilators
• Neuropeptide Y is a vasoconstrictor

39. Cytokines
• Cytokines are polypeptides produced by many cell types that
modulate the function of other cell types
• Cytokines that appear to be important mediators of
inflammation are IL-1 and TNF and IL-8
• IL-1 and TNF are produced by activated macrophages, they
induce the synthesis and surface expression of the endothelial
achesion molecules that mediate leucocyte sticking and
increase surface thrombogenicity of the endothelium TNF
also causes aggregation and activation of neutrophils.
• IL-8 is a small polypeptide, produced by activated
macrophages and other cell types, that is a powerful
chemoattractant and activator of neutrophils

40. Nitric oxide
In macrophages nitric oxide acts as free radicals- cytotoxic to
certain microbes and tumor cells
Oxygen derived free radicals:
Released from leukocytes after exposure to chemotactic
agents, immune complexes or phagocytes.
Produce effects by:
• Generation of super –oxide
• Combining with nitric oxide to form toxic derivatives
Actions:
• Endothelial cell damage- vascular permeability increases
• Inactivation of anti-proteases
• Injury to other cells e.g. tumor cells, red cells

41. Vascular changes
Changes in vascular flow and caliber
a] Vasodialation
 induced by histamine and nitrous oxide
 follows a trasient constriction of arterioles
increased blood flow
 cause of heat & redness
b] Increased permeability of the microvasculature
 increased outflow of protein rich tissues into the extra vascular tissues
 increase in concentration of red cells in small vessels
 increase in viscosity of blood with slower blood flow
c] Leucocyte accumulation and migration accumulate along the
vascular endothelium

43. Increased vascular permeability
loss of protein from plasma
Decrease in intra vascularosmoticpressure
Increase in the osmotic pressure of the
interstitial Fluid&increased hydrostatic
pressure
Accumulation in the Interstitial Fluid
net increase of extra vascular fluid
Edema

44. Cellular Events
 Leukocyte extravasations and
 Phagocytosis
• Leukocyte extravasations:
• Delivery of leukocytes to the site of injury and activate
them to perform normal functions.
• The events are:
• Margination
• Rolling and adhesion
• Transmigration(diapedesis)
• Migration towards chemotaxic stimulus
• Opsonization

45. Margination
• In venules- erythrocytes occupy central column with
leukocytes displaced towards vessel wall. In
inflammation- stasis occurs with more leukocytes
assuming a peripheral position.
Rolling
• Rows of leukocytes adhere transiently to endothelium
Pavementing
• After adhesion leukocytes insert pseudopods between
endothelial cells and basement membrane.
• Traverse the basement membrane and escapes to tissue
space.

46. Leucocyte exudation &
Phagocytosis

47. Chemotaxis

48. Opsonization & Phagocytosis

49. To summarize
Vasodilatation:
• Prostaglandins
• Nitric oxide
Increase in vascular permeability
• Vasoactive amines
• C3a, C5a
• Bradykinin
• Leucotrienes C4,D4, E4
• Platelet activation factor

50. Chemotaxis
• C5a
• Leucotrienes B4
• IL8
• Bacterial products
Tissue damage
• Lysosomal enzymes
• Oxygen derived free radicals
• Nitric oxide

51. Syngcuk kim’s hypothetic mechanism of
pathophysiology of pulpal disorder

53. Periradicular tissue changes following
inflammation
Degenerative changes
• May be fibrotic, resorptive, or calcific.
• If degenerative changes continues necrosis will result.
• Another form – PMN are injured releasing proteolytic enzymes &
causing liquefaction of dead tissue - suppuration / formation of
pus.
3 requisites are necessary for pus :
– Necrosis of tissue cells
– Sufficient number of PMNs
– Digestion of dead material by proteolytic enzymes

54. • If the reaction is not great enough , when the irritant is weak,
an exudate consisting of serum, lymph, & fibrin will result.
• PMN liberate proteolytic enzymes which digest not only
leukocytes but also the adjacent dead tissue leading to
abscess formation.
• Microorganism are not necessary for development of an
abscess. eg : A sterile abscess may result from chemical or
physical irritation in the absence of microorganism.

55. Proliferative changes
• Irritant must be mild enough to act as stimulant to
produce proliferative changes.
• Within the same inflammatory area , a substance
can be both an irritant & a stimulant such as
calcium hydroxide.
• When it is strong in the center it may produce
degeneration or destruction whereas at the
periphery it may be mild enough to stimulate
proliferation.

56. • When the tissue is in apposition fibroblastic repair
will take place & when a gap is present repair is
made with granulation tissue which is resistant to
infection.
• Fibroblasts are the principle cells of repair which
lay down cellular fibrous tissue.
• In some cases when collagen fibres are laid down
dence acellular tissue is formed.
• Destroyed bone is not always replaced by new
bone but it may be replaced by fibrous tissue.

57. Endodontic implication
Fish theory of zones of inflammation
• The reaction of the periradicular tissues to
noxious products of tissue necrosis, bacterial
products, & antigenic agents from the root
canal has been described by Fish

58. Four well defined zones of reaction were found
• Zone of infection
Exudative(acute)zones
• Zone of contamination
Transitional area
• Zone of irritation
Proliferative(chronic)
zones
• Zone of stimulation

59. Zone of necrosis ( zone of infection)
Necrotic or infected root canal
contents are
1. Pus fluid contains dead cells,
destructive components
released from phagocytes, end
products of protein
decomposition ( proteolysis)
2. PMN
3. Microorganism, exotoxins,
endotoxins, antigens , bacterial
enzymes, chemotactic factors.

60. Zone of contamination ( exudative
inflammatory zone)
Immediate response to toxic
elements coming out of
root canal are
1. Principal exudative defense
response – vasodilatation,
fluid exudation, cellular
infiltration
2. Dilution of toxic elements
plus antibacterial action of
inflammatory fluid.
3. Principal defense cells –
PMN’s, macrophages

61. Zone of irritation ( granulomatous zone,
proliferative inflammatory zone)
Toxicity diminishing as distance
from canal foramina increases
1. Function – defense, healing ,
repair.
2. Principal proliferative response –
granulation tissue ( capillary
proliferation & fibroblastic
activity)
3. Granulomatous – granulation
tissue plus chronic defense cell
4. Principal Chronic defense cell –
lymphocytes, plasma cells, blood
derived macrophages,tissue
macrophages

62. Conti..
5. Cell derived mediators of inflammation –
antibodies from plasma cells, lymphokines from
sesitized T cells, histamine & serotonin from
basophils.
6. Russel bodies- enlarged plasma cells with
numerous antibody inclusion.
7. Eosinophils – attracted by mast cell ECF- A &
lymphokine ECF – A.. They modulate
inflammation & allergy by destroying certain
vasoactive substances like PAF & SRS – A
8. Foam cells , cholesterol crystals , epithelial
clusters & strands.
9. Favorable environment for osteoclast

63. Zone of stimulation ( zone of
encapsulation / productive fibrosis)
Toxicity reduced to a mild
stimulant
1. Peripheral orientation of
collagen ( fibroblastic
activity )
2. Favorable environment for
osteoblastic activity
3. Bone apposition &
reversal lines evident
4. Reactive hyperostosis
when lesion encroaches on
the cortical plate.

66. •

67. Sequence of pulp pathoses related to inflammation

68. CLINICAL CORRELATION
Hyperemia
• It is an initial & potentially reversible response that sets the
stage for inflammatory cycle.
• Caused by Pulpal reaction to external stimuli such as
caries , restorative procedures.
• Pain does not occur spontaneously & requires an external
stimulus, ceases when the irritant is removed.
• H/P: Increased blood volume, prolonged vasodilatation,
increased intrapulpal pressure , edema, with minimal
amount of WBC infiltration.
Treatment
• Preventive measures such as controlled operative
procedures and in deep cavities pulp capping procedures
may be performed.

69. Painful pulpitis
• Clinically detectable inflammatory response of the
pulpal connective tissue to an irritant.
• The exudative (acute) forces are hyperactive
• Acute pulpalgia ( acute pulpitis):
– Severely painful , irreversible acute inflammatory
response.
• Chronic pulpalgia( subacute pulpitis) :
– Mild exacerbation of a chronic pulpitis. sometime
described as “smouldering inflammatory response”

70. • C/F : pain varies from mild discomfort to severe,
even excruciating throbbing.
• Spontaneous because of the presence of necrotic
tissue & lingers even after the primary irritant has
been removed.
• H/P:
• Prolonged vasodilation, increased vascular
permeability, edema & increased intrapulpal
pressure, congestion & blood stasis producing
small zones of necrosis.
• PMN is the characteristic principal cell &
macrophages also appear.

71. • The disintegration of leukocytes release proteases
& liquefy the injured cells & tissue, resulting in
pus formation.
• The suppurative core (zone I ) may be referred to
as Zone of Necrosis or Infection.
• The inflamed connective tissue surrounding zone I
is termed as Zone of Contamination( zone II )
where the exudative activity has its greatest effect.
• As the inflammation persists chronic pulpitis
ensues.
• Treatment
– Root canal treatment is the definitive treatment
procedure.

72. Non painful pulpitis
Chronic pulpitis:
• Here the proliferative zones become
hyperactive and attempts to heal & repair.
• Pain is absent due to diminished exudative
activity & coresponding decrease in intra
pulpal pressure.

73. H/P :
• characterized by PMNs infiltration , inflammatory edema
leading to formation of abscess surrounded by
granulomatous tissue termed as pulpal chronic abscess/
pulpal granuloma.
• Young fibroblast & new capillaries develop & form
granulation tissue in attempt to replace the exudate in zone
II.
• This zone of repair & healing tissue is the Zone of
Proliferation ( zone III).
• Lymphocytes , Plasma cell & macrophages are
prominently present.
Treatment
• Root canal treatment is the definitive treatment procedure.

74. • If the conditions is not treated the persistant
chronic pulpitits may lead to the formation of
dentinoclasts by activating undifferentiated
reserve connective tissue cells of the pulp and may
lead to internal resorption.
• When the inflammatory process or the toxic
components of pulpal necrosis approach the
connective tissue of the pulpoperiapical junction,
an apical periodontitis ensues.

75. Sequence of pulpoperiapical pathoses
related to inflammation

76. Painful pulpoperiapical
pathosis
• They are inflammatory response of the
periapical connective tissues to pulpal
irritants in which exudative ( acute) forces
become hyperactive.
• Acute apical periodontitis:
– Is an incipient exudative reaction
– Caused by contaminants from the pulp canal
which produce vasodilation, fluid exudation,
WBC infiltration in the periapex.

77. • Acute periapical abscess
– It is an advanced exudative reaction
– Caused by contaminant from pulp canal that
produce increasing inflammatory exudate, edema,
WBC infiltration & suppuration.
• Recrudesscent abscess ( phoenix abscess)
– It is an acute excerbation of chronic apical
periodontitis

78. • H/P: vasodilation, edema & increased
intrapriapical pressure will activate osteoclast
formation to resorb the bone. This increase
pdl space.
• PMN s causes proteolysis & suppuration
occurs.
• Thus acute exudative zones (I & II ) develop
identical with those described for pulpal
inflammation.

79. NON PAINFUL PULPOPERIAPICAL
PATHOSIS
• Here the proliferative components are hyperactive.
• Pain is absent because of diminished
intraperiapical pressure.
Incipient Chronic apical periodontitis:
– Widened PDL space , with dilated blood vessel ,
edema& accumulation of chronic inflammatory cells.
Periapical Granuloma:
– This advanced form of chronic apical periodontitis is
characterized by growth of granulation tissue &
presence of chronic inflammatory cells.

80. • Chronic periapical abscess:
– Develops from chronic apical periodontitis
• Periapical cyst:
– Develops from chronic lesion with preexisting
granulomatous tissue .
– Characterized by a central fluid filled epithelium
lined cavity surrounded by granulomatous tissue
& peripheral fibrous encapsulation.

81. • H/P:
• Similar to histopathological features of non
painful pulpal pathosis.
• The zone of necrosis( zone I) is then ecrotic tissue
in the root canal.
• There is capilary dilation, PMNs infiltration
closest to the zone, surrounded by lymphocytes
and plasma cells.
• As the necrotic products diffuse into the periapex
they enter the zone of contamination (Zone II),
Where the toxicity is reduced by fluid and cellular
exudative activity.

82. • This stimulates the osteoclasts to resorb the
contaminated periapical bone.
• The gap surrounding the lesions is filled with the
granulomatous tissue to form the zone of irritation
(Zone III).
• It is important to note that viable microorganisms
are absent in this zone III.
• Here the periapical granuloma may be compared to
the pulpal granuloma.
• Unlike the chronic pulpal response here the zone of
stimulation (Zone IV) becomes well developed.

83. • In this zone the fibroblasts lay down a wall of
collagen fibres to encapsulate the entire
inflammatory complex and osteoblasts lay down
additional bone matrix over the surface of the older
resorbed bone.
• Treatment:
– Pulpectomy followed by adequate apical seal for healing
and repair to take place
– But if the periapical lesion does not resolve for prolonged
periods and patient is symptomatic then surgical
management may be considered where periapical
curettage is performed to completely remove the
granulation tissue and root resection done.

84. Kronfeld’s Mountain Pass Concept
• Kronfeld has pointed out that the granuloma is not an
environment in which bacteria live but one in which they
are destroyed.
• He compared the bacteria in the root canal (Zone I) with an
army entrenched “behind high and inaccessible
mountains” the foramina serving as mountain passes.
• The exudative and granulomatous tissues of the granuloma
represents a mobilized army defending the plains
(periapex) from the invaders.
• If only a few invaders enter the plain through the mountain
pass they are destroyed be the defenders (leukocytes)

85. • Only complete elimination of the invaders form their
mountainous entrenchment will eliminate the need for a
defense force in the “plains”.
• Once this is accomplished the defending army of
leukocytes withdraws the local destruction created is
repaired (granulation tissue of zone III) and the
environment returns to with normal pattern.
• Therefore the objective in non-surgical root canal therapy
of teeth with periapical pathoses is elimination of the
irritant from the canal and keeping it out by a “Three-
dimensional” filling of the canal. If the contents of the
zone of necrosis are eliminated the granuloma can complete
its function of healing and repair.

86. Conclusion
Removal of the irritants and their source by
debridement and proper obturation permits the
healing of periradicular tissues and is often
associated with formation and organization of a
fibrin clot, granulation tissue formation and
maturation, subsidence of inflammation and
finally restoration of normal architecture of the
periodontal ligament. Since the inflammatory
reactions are usually accompanied by microscopic
and macroscopic resorption of hard tissues bone
and cementum repair occur as well.