This document discusses the rationale for endodontic therapy and periradicular healing. It begins by explaining that the rationale for endodontic therapy is to completely debride and seal the root canal system through non-surgical or surgical means. This achieves a fluid-tight seal and removes the source of infection, allowing periradicular tissues to heal. Several theories are discussed relating to the spread of infection and zones of reaction in periradicular tissues. Complete elimination of irritants from the root canal through treatment is necessary for periradicular healing to occur over several months. Factors like technical quality of the root filling and ability to clean the entire root canal influence healing outcomes.

2. Contents
1. Rationale
2. Rationale of endodontics
3. Sequele of periapical infection
4. Pathways of pulpitis
5. Theories of spread of infection
6. Periradicular diseases
7. Histopathology of periradicular diseases
I. -apical granuloma
II. -apical abcess
III. Apical cyst
8. Mechanism of cyst formation
9. Zones of infection by fish
10. Kronfield’s mountain pass theory
11. The healing
12. Factors influencing healing.

3. rationale
ˌ/raʃəˈnɑːl/
Noun:
A set of reasons or a logical
basis for a course of action or belief.
The term Rationale

4. Rationale of endodontic therapy is complete
debridement of root canal system followed by three-dimensional
obturation

5. Endodontic pathology is caused by
Physical injury Chemical injury
Bacterial injury
These cause reversible or irreversible changes in the pulp
& periradicular tissues.

6. Changes depends on the
Intensity
Duration
Pathogenicity
Host defence mechanism

7. Changes are mediated by series of inflammatory & immunological
reactions.
These reactions are for eliminating the irritant & repair the damages
But certain conditions are beyond their ability to repair.
These need to be treated
endodontically for the survival of
the tooth.

8. The Rationale of endodontic therapy
Avascular non
vital pulp
_NO DEFENCE_
Autolysis of
damaged tissue
Breakdown
products
Diffuse down to
surrounding
tissues
Periapical
irritation
So SEAL THE
PORTAL OF EXITS
& ROOT CANAL 3
DIMENSIONALLY

9. Non
Surgical
endodontic
therapy
Shaping &
cleaning
Obturation
Access
preparation
Surgical
Endodontic
therapy to achieve
a fluid tight
seal.
METHOD of achieving this objective

10. Sequel of pulpal infection

11. Dental caries
Defensive reactionsDental caries with pulpitis
Bone reactions [osteomyelitis]
Soft tissue reaction [cellulitis]
Blood reaction
[septicaemia]

12. Pathway of Pulpitis

13. Pulpitis
Acute Pathway
Periapical abscess
Osteomyelitis
Cellulitis
Chronic Pathway
Chronic Apical Periodontitis
Periapical Granuloma
Periapical cyst

15. Focal Infection
Definition:
It is localized or general infection caused by the
dissemination of microorganisms or toxic products from a focus of
infection.

16. Focus of Infection
Definition:
This refers to a circumscribed area of tissue, which is
infected with exogenous pathogenic microorganisms and is usually
located near a mucous or cutaneous surface.

17. Theory Related to Focal Infection
William Hunter first suggested that oral
microorganisms and their products involved in number of
systemic diseases, are not always of infectious origin.
In year 1940, Reimann and Havens criticized the
theory of focal infection with their recent findings.

18. Periradicular diseases

19. PERIAPICAL LESIONS are produced by an inflammatory response at
the root apices of teeth with non vital pulp.
Apical granuloma
Apical cyst
Apical abcess

20. The root canal is the main source of infection
microorganisms present in root canal are rarely motile
they can proliferate sufficiently to grow out of the root canal
the microorganisms enter in the periradicular area, they are
destroyed by the polymorphonuclear leukocytes.

21. toxic bacterial products get diluted sufficiently to act as
stimulant.
As But if microorganisms are highly virulent, they overpower the
defensive mechanism and result in development of periradicular lesion
At the periphery of the destroyed area of osseous tissue
form a
granuloma

22. Toxic byproducts + necrotic pulp
Irritate and destroy the periradicular tissues.
Irritants + proteolytic enzymes
CHRONIC ABSCESS

24. fibroblasts come into play
build fibrous tissue
osteoblasts restrict the area by formation of sclerotic bone
these if epithelial rests of Malassez are also stimulated
formation of a cyst.

26. Histopathology of periradicular diseases

27. Apical Granuloma
 Dominated by- Macrophage ,lymphocyte and plasma cells
 Abundant capillaries + fibroblast +connective tissue fibers.
 Often encapsulated in collagenous connective tissue.
lymphocytes (green arrow) and
macrophages (yellow arrow), with
abundant fibroblasts (blue arrow).

28. Epithelial cell proliferation.
 Formed from the epithelial cell rest of malasez.
 Under the influence of cytokines and growth factors generated in
the granuloma.
 They are the source of the epithelial lining of cysts that may
develop in apical granulomas.

29. A chronic periapical lesion with a
polymorphonuclear leukocyte (PMN)
infiltrate (yellow arrow)
Epithelial strands in an apical
granuloma.
Epithelial strands form a network in an
apical granuloma.
-Observed in a longitudinal section (blue arrow) or
at cross section (yellow arrow and enlargement).

30. Apical abcess
• PUS present + an area with liquefied tissue.
• From a pre-existing granuloma
• Represent a shift in cellular dynamics.
• The influx of PMNs is dramatically increased.
• Thus tissue macrophages are no longer
able to effectively cope with the tissue
damage caused by hydrolytic enzymes
from a vast number of dying PMNs.

31. • Connective tissue constituents such as collagen
and hyaluronic acid are degraded
• The tissue in the center of the abscess is
liquefied.
• On the periphery of the abscess, the tissue of the
apical granuloma persists
• its adjacent layer is infiltrated with a large
number of PMNs that are migrating
from the nearest blood vessel to end their life
in the pus-containing center of the abscess.

32. Apical cyst
• An epithelium lined cavity
• With fluid / semisolid material
• Surrounded by dense connective tissue.
• Associated with necrotic pulp
• Develop within the granuloma.
• Cyst cavity- stratified squamous epithelium.
• From Epithelial cell rest of malasez.
• The epithelial lining can be continuous or disrupted
or completely missing.

33. Apical cyst.
A partial view of the wall of a space that was filled with liquid and lined with
stratified cuboidal epithelium (yellow arrow and enlargement), originating from the
epithelial rests of Malassez.

34. Periapical cyst is divided into
PERIAPICAL POCKET CYST
(BAY CYST)
• An apical inflammatory
cyst
• Sac-like
• Epithelium lined cavity.
• Open to and continuous
with the root canal space.
• Within the periapical
granuloma with no
connection between
their cavity and the
rootcanal space.
 >half of the apical cysts are true apical cyst
 Remaining are pocket cyst variety.
TRUE CYST

35. The mechanism of cyst formation in
periapical inflammatory lesions
‘‘Nutritional deficiency theory’’
epithelial proliferation results in
an epithelial mass that is too
large for nutrients to reach its
core
results in necrosis
and liquefaction
of the cells in its
center,
Forms
the
cystic
cavity.

36. The ‘‘Abscess theory’’ assumes that,
Tissue liquefaction occurred
first,
at the central part of an abscess
Due to the inherent
nature of epithelial
cells to cover the
exposed connective
tissue surfaces
Gets lined by
locally
proliferating
epithelium.

37. ENDODONTIC IMPLICATIONS
(PATHOGENESIS OF APICAL
PERIODONTITIS AS EXPLAINED BY FISH)
FISH in1939 theorised that the zones of infection are not an infection by
themselves but the reaction of the body to infection. Thus he concluded
that the removal of this nidus of infection will result in resolution of
infection.
Four well defined zones of reaction were found during the experiment:

38. Zone of infection or necrosis (PMNLs)
Zone of contamination(Round cell infiltrate – lymphocytes)
Zone of irritation (Histiocytes and osteoclasts)
Zone of stimulation(Fibroblasts, capillary buds and
Osteoblasts).
Zone of infection

39. Zone of Contamination
• Around the central zone, there is an area of
cellular destruction.
• not invaded by bacteria,
• the destruction was from toxins discharged
from the micro- organisms in the central
zone.
• characterized by round cell infiltration,
osteocyte necrosis and empty lacunae.
Lymphocytes were prevalent everywhere.
Zone of Infection
• Infection was confined to the center of the lesion.
• characterized by polymorphonuclear leukocytes and
microorganisms.
• along with the necrotic cells and destructive components
released from phagocytes.

40. Zone of Irritation
• FISH observed evidence of irritation further away from the
central lesion as the toxins became more diluted.
• This is characterized by macrophages, histocytes and osteoclasts.
• degradation of collagen framework by
phagocytic cells and macrophages was
observed while osteoclasts attack the bone
tissues.

41. Zone of Stimulation
• FISH noted that, at the periphery, the toxin was mild enough to
act as stimulant.
• This zone is characterized by fibroblasts and osteoblasts
• In response to this stimulatory irritant
fibroblasts result in secretion of collagen fibers,
which acted both as wall of defense around the
zone of irritation and as a scaffolding on
which the osteoblasts synthesize new bone.

42. KRONFELD’S MOUNTAIN PASS THEORY
Kronfeld explained that the granuloma does not provide a favorable
environment for the survival of the bacteria. He employed the FISH
concept so as to explain the tissue reaction in and around the
granulomatous area.
Micro organisms
Body’s defence

43.  Micro-organisms in root canal is the army in the mountain
 Enters the PLAINS through the foramina / MOUNTAIN PASS
 Smaller group of bacteria entered –gets destroyed by
the ARMY of leucocyte which stands in the front to
counter the attacks.
 Thorough cleaning and shaping will bring down the army
allowing the environment to return to normality

45. Zone A: Bacteria / invaders entrenched behind high and
inaccessible “mountains”, the foramina serving as mountain
passes.
Came up with 4 zones

46. Zone B: The exudative and granulomatous (proliferative) tissue of
the granuloma represents a mobilized army defending the plains
(periapex) from the invaders (bacteria). When a few invaders
enter the plain through the mountain pass, they are destroyed by
the defenders (leukocytes). A mass attack of invaders results in a
major battle, analogous to acute inflammation.

47. Zone C: Only complete elimination of the invaders from their
mountainous entrenchment will eliminate the need for a defense
forces in the “plains”. Once this is accomplished, the defending
army of leukocytes withdraws, the local destruction created by the
battle is repaired (granulation tissue) and the environment returns to
its normal pattern.

48. This explains the rationale for the non-surgical
endodontic treatment for teeth with periapical
infection.
The complete elimination of pathogenic
irritants from the canal followed by the
three-dimensional fluid impervious obturation will
result in complete healing of periapical area.

49. Indications for RCT based on rationale
• All teeth with irreversible damage to pulp from physical,chemical
or bacteria attack
• And are not contraindicated for treatment.
• Intentional RCT- for restorative / prosthetic restorations
• Elective endodontics :
-is done with crack or heavily restored tooth,
-to prevent premature loss of cusp during its
restoration(crown preparation)

50. • Inadequate restorations :
-cracked or carious teeth having crowns
repair of the crown margins.
-use of pre-existing crowns even after another
restoration
• Devitalization of tooth :
-severe attrited/ rampant caries / smooth
surface defects
-so that patient do not feel discomfort to cold
or sweet.
• Endodontic emergency :
acute dental pain

51. THE HEALING
Healing of the lesions may take many months .It may be argued
that if a given lesion eventually heals in 12, 24, or even
36months, there is no benefit in rushing the process.
Immune response
• It neutralizes and removes any foreign material
• allows and probably initiates the second part, recovery,
repair, and regeneration

52. When no cells are killed, the original
odontoblasts can form reactionary
(tertiary) dentin
When the odontoblasts are killed, new
dentin-forming cells develop from stem
cells (undifferentiated mesenchymal cells)
They form reparative (tertiary)
dentin
An example of extensive tissue
damage from which the pulp
recovers is the pulp polyp

53. • The repair of larger areas of damage is more variable
• It depends on the nature of any clinical intervention.
• It seems that normally organized pulp tissue does not re-form.
• Mineral trioxide aggregate may have some
stimulatory activity, but
its main property may be its high level of
biocompatibility and its success in preventing
recontamination.

54.  With the discovery of biologically active molecules such as
growth factors and matrix proteins, there is the possibility of
stimulating repair.
 The development of cultures of pulpal cells and supporting
scaffolds may allow tissue regeneration.

55. FACTORS INFLUENCING HEALING AFTER
ENDODONTIC TREATMENT

56. The technical standard of the root filling had no significant
influence on the prognosis of the treatment for roots with
pulp necrosis undergoing initial treatment.
for previously root-filled teeth which were retreated with
adequate seal, the success rate (67%) was significantly (p =
0.03) higher than for teeth inadequately sealed (31%).

57. The prognosis was slightly less favorable for roots with
preoperative pulp necrosis and periapical lesions when the
root was restored with a crown or acted as an abuntment
for a bridge

58. Age and sex of the patient
presence of deep
periodontal pockets
roots were provided with
posts or not or were used as abutments
the number of bacterial sampling done before
filling the root.
Had no influence on the outcome of
treatment

59. Thus, the
lower success rate
The inability to
instrument a
canal to its full
length :-
-due to a preexisting obstruction of the canal by
the
accumulation of tertiary dentin
-by branching of the canal
into an apical delta.
-obliteration of a previously patent apical portion
of the canal by dentin chips during debridement

60. Perforation of the lingual cortical bone
plate may occur because of inflammatory
changes, and first of all of large cysts.
When a cavity in the bone is walled by
periosteum vestibularly and palatally,
Normal bone regeneration may be
disturbed.
Whereas fibrous scar tissue is probably
being formed by the soft tissue walls, bone
regeneration will take place from the osseous
part of the cavity.

61. The outcome of the simultaneous regeneration of these two
types of tissue may be assumed to depend on the :-
rate of growth of bone and scar tissue,
the dimension of the cavity, i.e. the relation
between the distances between the soft tissue
walls and the bony walls.
If a firm fibrous scar tissue has been established first, between
the vestibular and the palatal soft tissues, this will probably
act as a barrier to further bone formation.

62. Shortening the healing time
(1)allows earlier decisions in regard to the restorative
treatment plan related to the treated teeth and
(1) limit the period for which temporary crowns and bridges
are used; temporary restorations that may leak and allow
recontamination of the treated root canal.

63. The prolonged healing process
Raises the possibility that the activated cells in the lesion
may maintain their state of activation long after the initial cause
of their activation has been eliminated.
 The activation state may outlive its useful purpose and
become a burden. .

64.  Macrophages are known to persist in tissues for many
months and if their state of activation persists, they may
 maintain osteoclastic activity,
 inhibit the fibroblasts
 inhibit osteogenesis,
 thus preventing both soft connective tissue and
bone repair from taking place.

65. Early surgical removal of the tissue containing activated
macrophages, allowed its replacement with fresh granulation
tissue that contains a fresh set of cells that will not delay
repair.

66. FACTORS LIMITING THE PULP’S
RESPONSE
• The only significant factor that limits the pulp’s ability to
respond to injury is age.
• The older pulp has a reduced
 number of cells,
 innervation, and
 vascularity,
but the immune response remains active.

67. CONCLUSION
Pulp tissue is compromised from the start, and dies for 3 reasons:
1. The tissue has a very small blood supply, making it very difficult to
regenerate on its own once it is injured.
2. 2. It lies inside the unyielding walls of dentin and, therefore, when
it becomes inflamed, it does not have room to swell.
3. 3. It is a terminal circulation, like the appendix, which once
diseased, needs to be removed.
4. The most common cause of pulpal pathology is caries,
5. with trauma being the second.
6. Add in parafunction, plus the inflammation that is created from
dental procedures.
And it is amazing that any pulps actually remain vital and
asymptomatic. Fortunately, many do, but the higher the frequency,
duration, and magnitude of the injury to tooth, the more likely the
pulp will succumb to an irreversible pathological change.

68. We have an ethical responsibility to provide patients with the most
conservative, cost effective, predictable treatment in order to restore
function, aesthetics, and oral health.
If the tooth is restorable; if the periodontal condition is stable or can
be made so; and, if the root is intact, saving the tooth should be
considered.
But, if there is a high risk that the site for a future implant would be
compromised, endodontic treatment should not be a first choice.

69. Vince Lombardi (American football player, coach, and
executive in the National Football League.) is quoted as having
said,
“We would accomplish many more things if we did not
think of them as impossible.”
And, while we can’t expect to put it through the
uprights on every offensive possession, it is important to know
what is possible.

70.  FactorsAffecting the Long-term Results ofEndodontic Treatment
 UIf Sjbgren, DDS, Bjorn H,'igglund, DSS, Goran Sundqvist, DDS, PhD, and
Kenneth Wing, DMD, PhD. JOURNAL OF ENDODONTICS, Printed in U.S.A.
 VOL. 16, NO. 10, OCTOBER 1990
 A multivariate analysis of the influence of various factors upon
healing after endodontic surgery
 JORGEN RUD, J. O. ANDREASEN AND J. E. Mt3LLER JENSEN.
 Int. J. oral Surg. 1972: 1:258-271
 Ingle’s Ingle’s ENDODONTICS6
 Textbook of endodontics –Nisha Gargh
 Step by step root canal treatment-Gurkeerat Singh
 Grossman’s endodontics
 https://www.dentalcetoday.com/courses/175%2FPDF%2FDT_Aug_14_NPR_Germain_fn
l1.pdf
 www.googlescholars.com
 www.pubmed.com