HISTO PHYSIOLOGY AND PATHOLOGY OF PERIAPEX-DR KRIPA

3.  The relationship between the pulpal and the
periapical pathosis is a very close one. Pulpal
involvement is almost always the forerunner of
periapical pathosis.
 Historically, when X-rays first began to reveal dark
areas at the apices of the teeth whole sole
extraction of these "bags of infection" was
recommended. This was the beginning of the focal
infection era.

4.  THEORY OF FOCAL INFECTION:
In 1890, the dentist and physician, WD Miller,
published his treatise: ‘The Micro-Organisms of the
Human Mouth: The Local and General Diseases
Which are Caused By Them’ and a year later in
Dental Cosmos first used the term: ‘focal infection’.
Miller did not mandate removal of teeth as a focus of
infection and also suggested ‘treating and filling root
canals’.
.

5.  THEORY OF FOCAL INFECTION:
This theory was described by Rosenow in 1909 as a
localised or generalised infection caused by bacteria
travelling through the blood stream from a distant
focus of infection.
In the 1930s, Dr Weston Price presented research
suggesting that bacteria trapped in dentinal tubules
during root canal treatment could cause almost any
type of degenerative systemic disease.

7.  The apical periodontium consists of root
cementum, periodontal ligament, and the bone of
the alveolar process – all interdependent tissues.
 CEMENTUM:
Coronal two thirds of root, cementum is thin and
lamellated; due to greater functional stresses
cementum in apical third is wider, irregularly
lamellated, and cellular

8.  Functions-
The basic function is to attach principal fibers of the
periodontal ligament to the tooth.
Othe functions that affect endodontic diagnosis and
treatment include:
1. The continuous deposition of cellular cementum
around the apical third of the root (passive eruption)
compensates for coronal attrition.
This deposition results in increased tooth length and
multiple constricted apical canals.
Excessive constriction of the apical canals can affect
the blood flow into the pulp and induce restrogressive or
age changes.

9. 2. The terminal area of intercanal preparation
is the cementodentinal junction, which is usually
estimated to be 1 mm from the apical foramen.
It is also referred to as the histologic foramen
because it represents the junction of pulpal
connective tissue with the interstitial loose
connective tissue of the periodontal ligament.

10. 3. Cementum repairs root resorption, which is
pathologically produced by a granuloma or
physiologically induced by the drifting
movement of teeth (migration).
As result of the resorption followed by
cementum replacement in migrating teeth, the
apical foramen may be changed to a more
lateral position.
4. The loss of cementum from the cervical position of
the tooth may render the tooth hypersensitive to
thermal change because of the exposed dentinal
tubules. This may complicate identification of an
approximating tooth requiring endodontic
treatment.

11. 5) Michanowicz et al and Andreason and Hjorting –
Hansen have shown evidence to support the
cementogenic theory of root repair .
Continuous deposition of cementum can occur at
the fractured ends of two segments of a horizontal
root fracture, joining them and effecting root
repair.

12. 6) Torneck et al . Heithersay, and others have shown
that cementum contributes significantly to the hard
tissue barrier formed at the root end as a result of
apexification procedures.

13.  The periodontal ligament consists of two different tissues, each with
separate and distinct functions (1) a suspensory ligament and (2) a periosteum.
The spaces (interstices) between the principal fiber bundles are occupied by
irregular loose connective tissue.
 This interstitial loose connective tissue performs the multiple functions of
periosteum: formative, nutritive, nervous and defense. The histologic makeup
of these tissues provides several endodontic considerations.

14.  Nervous Function :
Pressure receptors terminate in and around the bundles of principal fibers; thus the ligament portion
provides a sensory function of proprioception or position localization. The interstitial loose connective
tissue contains the free nerve ending that are the specific receptors for pain.
 Identifying a tooth with acute pulpalgia is difficult because only pain receptors are
evident in the pulp. Localization of the pain is facilitated by the extension of the
inflammatory response into the periapex (acute apical periodontitis), which
activates both pain and proprioceptive responses.

15.  Pulpoperiodontal junction:
Pulp tissue response to an irritant does not necessarily end at a
“magical” point of demarcation called the apical foramen.
The connective tissue of the pulp forms a continuum (coalescence)
with interstitial loose connective tissue of the periodontal ligament
at the juncture of rot canal foramina and continues into the marrow
spaces.
An inflamed vital pulp therefore may be accompanied by
tenderness to percussion with or without radiographic evidence of
periapical change.

16.  Periapical cyst formation
Remnants of Hertwig’s epithelial root sheath remain in the
interstitial loose connective tissue as clusters of cells called rests of
Malassez. These cells remain dormant until activated by periapical
inflammation to play a principal role in cyst formation.

17. Alveolar process consists of alveolar bone proper and supporting
bone. alveolar bone proper is thin layer of compact bone that lines
socket. It appears as a radiopaque line on radiograph and is referred to as
lamina dura (hard layer).
Alveolar bone proper made of lamellated bone. lamellae are arranged
parallel with surface of PDL space, and in small haversian systems.
 Sicher termed bundle bone to describe alveolar bone containing
attachment of principal fiber bundles (Sharpey's fibers).

18. cribriform plate is describe as alveolar bone proper because surface
view shows a sieve like appearance.
Alveolar bone proper have openings due to perforations by
interalveolar nerves, blood vessels as well as coalescence of interstitial
loose connective tissue of periodontal ligament with loose connective
tissue of the marrow spaces.
 During stress periods, osteoclastic cells are found to increase this
space. Persistent periapical inflammation will result in resorption of the
periapical lamina dura.

19.  Radiographic detection of loss in continuity of compact bone is an
effective diagnostic aid.
absence of break in lamina dura does not rule out presence of early
periradicular inflammatory lesion. radiographic evidence lags behind actual degree
of tissue destruction. It is estimated that at least 30% to 50% loss of minerals from
bone is needed to make lesions become visible on radiograph.
Supporting bone that surrounds and gives support to alveolar bone
proper of tooth socket consists of facial and lingual cortical plates of
compact bone and intervening spongy or trabecular bone

20. BENDER AND SELTZER demonstrated that:
1) If a lesion does not encroach on junction between cortical bone and cancellous bone,
its not visible on radiograph. lesion around mesial root of lower first molar is more
visible on radiograph than would a distal root because it is usually closer to cortical
plate.
2) The angulation of the x-rays will determine the accuracy of interpretation of the healing
or breakdown of clinical lesions.
Trabecular (cancellous) bone has a septal or labyrinthine arrangement of bone
lamellae, with its marrow forming a continuum with interstitial loose connective tissue of
PDL.
Since specific receptors for pain are not present in trabecular spaces, feeling associated
with extension of inflammatory response into marrow spaces is fullness or continuing
pressure

21. Pain receptors present in blood vessel sheaths or pressure on nerves
passing through area may give referred sensation.
Pain receptors are numerous in periosteum that covers cortical plates
and in specialized periosteum of periodontal ligament, which is
interstitial loose connective tissue. Pressure in these areas produces pain
of varying intensities

23. NOMENCLATURE AND CLASSIFICATION
World Health Organization (1995) classified apical periodontitis
under "diseases of Periapical tissues" and subdivided it into several
categories based on clinical signs .(cohen)
K04.4 -Acute apical periodontitis
K04.5 -Chronic apical periodontitis (apical Granuloma)
K04.6 -Periapical abscess with sinus (dentoalveolar abscess with sinus,
periodontal abscess of pulpal origin)
K04.60 -Periapical abscess with sinus to maxillary antrum
K04.61 - Periapical abscess with sinus to nasal cavity.
K04.62- Periapical abscess with sinus to oral cavity.
K04.63-Periapical abscess with sinus to skin

24. NOMENCLATURE AND CLASSIFICATION
K04.7-Periapical abscess without sinus (dental abscess without sinus,
Dento alveolar abscess without sinus, periodontal abscess of pulpal
origin without sinus)
K04.8-Radicular cyst (apical periodontal cyst, Periapical cyst)
K04.80-Apical and lateral cyst
K04.81-Residual cyst.
K04.82-Inflammatory paradental Cyst
This classification system does not take into account structural aspects
of diseased tissues. Because structural framework forms basis for an
understanding disease process, a histopathologic classification is used

25. NOMENCLATURE AND CLASSIFICATION
This system is based on four factors:
(1) Distribution of inflammatory cells in lesion;
(2) Whether epithelial cells are present or absent;
(3) Whether lesion has been transformed into a cyst; and
(4) Relationship of cyst cavity to root canal of affected tooth.
 Histopathologically lesions of apical periodontitis are classified as
acute, chronic, or cystic.
 Acute apical periodontitis characterized by distinct focus of
neutrophils it may be primary or secondary
Primary or initial when inflammation is short lived

26. NOMENCLATURE AND CLASSIFICATION
Acute apical periodontitis is an acute inflammation of the
periodontium of endodontic origin. It is characterized by distinct focus
of neutrophils. it may be primary or secondary
Primary or initial when inflammation is short lived and starts
in a healthy periodontium in response to irritants.
Secondary or exacerbating when acute response
occurs in already existing chronic apical periodontal lesion. This latter
form is referred as phoenix abscess or periapical flare up.
Established Chronic apical periodontitis- it is a long standing
inflammation of the periodontium of endodontic origin.
characterised by granulomatous tissue infiltrated with lymphocytes,
plasma cells, and macrophages.

27. NOMENCLATURE AND CLASSIFICATION
Periapical cysts are differentiated into
True cysts – apical inflammatory cyst with a distinct pathologic
cavity completely enclosed in an epithelial lining. No communication to
root canal.
Pocket cyst – apical inflammatory cyst with epithelium lined
cavity that is open to root canal.

28. NOMENCLATURE AND CLASSIFICATION
PNR Nair: Pathology of apical
periodontitis

29. NOMENCLATURE AND CLASSIFICATION
Classification used at Loyola University (weine)
Painful pulpoperiapica1 pathoses
 Incipient acute apical periodontitis (describes beginning stage only)
 Advanced acute apical periodontitis (describes advanced, more
symptomatic stages only)
Acute periapical abscess
Recrudescent abscess (acute exacerbation of prior existing
advanced chronic apical periodontitis)
Sub acute periapical abscess (painful phase of chronic
periapical abscess cycle)

30. NOMENCLATURE AND CLASSIFICATION
Classification used at Loyola University (weine)
Nonpainful pulpoperiapical pathoses
 Pulpoperiapical osteosclerosis
Incipient chronic apical periodontitis (describes beginning stage only)
Advanced chronic apical periodontitis (describes more extensive
stages)
(a) Periapical granuloma
(b) Periapical cyst
(c) Chronic periapical abscess (nonpainful
phase of chronic periapical abscess cycle)

31. NOMENCLATURE AND CLASSIFICATION
INGLE’S CLASSIFICATION (weine)
Painful pulpoperiapical pathoses
Acute apical periodontitis
 Terms listed below describe advanced stages of acute apical
periodontitis:
Acute apical abscess
Phoenix abscess (acute exacerbation of prior
existing chronic lesion)
Suppurative apical periodontitis (chronic apical
abscess) (terms used to describe both painful and nonpainful phases of
the chronic apical abscess cycle)

32. NOMENCLATURE AND CLASSIFICATION
INGLE’S CLASSIFICATION (weine)
Non-painful pulpoperiapical pathoses
Condensing osteitis
Chronic apical periodontitis (describes both incipient and advanced
stages)
 Chronic apical periodontitis (describes both incipient and advanced
stages)
Periapical granuloma
Apical cyst
Suppurative apical periodontitis (chronic apical
abscess) (terms used to describe both painful and nonpainful phases of
the chronic abscess cycle

33. NOMENCLATURE AND CLASSIFICATION
GROSSMANS CLASSIFICATION :
 According to Grossman
1. Acute Periradicular disease
a) Acute alveolar abscess
b) Acute Apical periodontitis(symptomatic periodontitis)
vital
Non Vital

34. NOMENCLATURE AND CLASSIFICATION
 According to Grossman
2. Chronic Periradicular disease with area of rarefaction
a) Chronic alveolar abscess
b) Granuloma
c) Cyst
3. Condensing osteitis
4. External Resorption
5. Diseases of periradicular tissues of Non Endodontic Origin

35. NOMENCLATURE AND CLASSIFICATION
 According to AAE:

36. SEQUENCE OF PULPAL PATHOSES RELATED
TO INFLAMMATION (WEINE)

38. SEQUENCE OF PULPOPERIAPICAL
PATHOSES RELATED TO INFLAMMATION
(WEINE)

40. PATHOGENESIS AND HISTO PATHOLOGY

41.  It is a general belief that the development of apical periodontitis
follows total pulp necrosis.
 This belief is based on:
1) Pulpal strangulation theory due to a generalized increase in pulpal
interstitial pressure inside the uncompromised pulp space during
pulpal inflammation that causes collapse of venules and cessation
of blood flow96 and
2) Animal and human studies that concluded that uncontaminated
necrotic pulps that are intentionally devitalized or accidentally
traumatized are generally incapable of inducing periapical
inflammation unless they are infected.1

42.  However, if the vital pulps become infected due
to caries or other pathways, periapical
inflammation can develop even when inflamed,
but vital tissue is still present in the apical
portion of the root canal.
 The biologic basis for these observations
appears to hinge on the apical development of
pulpal infection/inflammation leading to the
diffusion of many inflammatory mediators,
proinflammatorycytokines, chemokines, and
bacterial toxins into the periapical area154 prior to
total pulpal necrosis.

43. Acute Apical Periodontitis: / SYMPTOMATIC APICAL
PERIODONTITIS
Definition: -
It is an acute inflammation of periodontium of endodontic
origin; characterized by presence of a distinct focus of neutrophils in the
lesion. (AAE definition)
Etiology: -
Irritants diffusing from an inflamed or necrotic pulp
Egress of irritants such as bacteria, bacterial toxins
Disinfecting medications
Debris pushed into periradicular tissues
 Physical irritation of periapical tissues and trauma

44. Clinical features: -
Sensitivity to percussion is principal clinical feature
Pain is pathognomonic and varies from slight tenderness to
excruciating pain on contact of opposing teeth.
Firm pressure against mucosa over root end may initiate a positive
painful response
 involved tooth may or may not respond to vitality tests.

45. Clinical features: -
release of chemical mediators and their action on the nerve fibers in
periradicular tissues cause pain during acute apical periodontitis.
Pain is induced by sensitization and activation of nociceptive sensory
nerve fibers by inflammatory mediators, proinflammatory cytokines,
nerve growth factor, and pressure.
since there is little room for expansion of periodontal ligament,
increased interstitial tissue pressure cause physical pressure on nerve
endings, causing an intense, throbbing, periradicular pain.

46. Histopathology: -
Tissue changes are limited to apical periodontal ligament and
neighboring spongiosa.
changes are hyperemia,
vascular congestion,
edema of the periodontal ligament,
and extravasation of neutrophils.
Neutrophils are attracted to area by chemotaxis induced initially by
tissue injury, bacterial products (LPS) and Complement factor C5a.

47. When integrity of hard tissues (bone, cementum, and dentin) has not
been disturbed, periapical changes are undetectable radio graphically.
When infection is involved, neutrophils attack and kills
microorganisms releasing leukotrienes and prostaglandins,
 LTB4 attracts more neutrophils and macrophages into area,

48. Initial rapid bone resorption can be prevented by administration of
indomethacin, which inhibits cyclooxygenase and thus suppresses
prostaglandin synthesis.
Neutrophils die in great numbers at inflammatory site and release
enzymes from their "suicide bags" causing destruction of extra cellular
matrices and cells.
 Later stages of acute response, macrophages begin to appear at
periapex. macrophages activate osteoclasts.
 In few days bone surrounding periapex is resorbed, and a radiolucent
area may be detectable at the peri apex.

49. Macrophages produces a variety of mediators - proinflammatory (IL-l,
IL-6, and TNF-alpha) and chemotactic (IL-8) cytokines are particularly
important at this stage.
Cytokines intensify local vascular response, osteoclastic bone resorption, and
effector mediated degradation of extra cellular matrices
 Much of periapical tissue damage that occurs during acute
inflammation can be attributed to release of proteolytic
lysosomal enzymes and matrix metalloproteinases from
disintegrated neutrophilic leukocytes and macrophages rather
than to bacteria and their toxins

50. The fundamental purpose of the acute inflammatory response is to restore the
structural and functional integrity of damaged tissue by eliminating irritants as soon as
possible.
Acute early lesion may take any of several possible courses
Spontaneous healing may occur; ( if irritants are immediately eliminated by root canal
therapy,)
Infection may intensify and spread into the bone (alveolar abscess);(if massive
invasion of periapical
tissues by highly pyogenic bacteria occurs,)
Lesion may open to the exterior (fistulation or, sinus tract formation);
organisation by scarring ( if extensive destruction of periapical tissue occur )
chronic apical periodontitis ( if irritants continue to persist )
Radiographic features: -
Shows little variation, ranging from
normal to a “thickening” of periodontal
ligament space.

51. Chronic Apical Periodontitis/ ASYMPTOMATIC APICAL
PERIODONTITIS
Definition: -
 It is a long-standing inflammation of periodontium of endodontic
origin; it is characterized by presence of granulomatous tissue predominantly
infiltrated with lymphocytes, plasma cells, and macrophages. (AAE definition)
Etiology: -
Chronic apical periodontitis may be preceded by acute apical periodontitis or
by an apical abscess.

52. Inadequate root canal treatment may also cause development of
chronic lesions. Lesion frequently develops and enlarges without any
subjective signs and symptoms
Longstanding low-grade inflammatory reaction of periapical
connective tissue to pulpal irritants results in development of
chronic apical periodontitis.
 This pathosis is a long-standing, “smoldering” lesion and is
usually accompanied by radiographically visible periradicular bone
resorption.

53. Clinical features: -
Clinical features chronic apical periodontitis are unremarkable.
Patient usually reports no significant pain,
Tests reveal little or no pain on percussion.
Associated tooth has a necrotic pulp and doesn’t respond to
electrical or thermal stimuli.

54. Histo pathology:
Neutrophils-dominated by macrophage, lymphocyte, and plasma cell
rich lesion encapsulated in a collagenous connective tissue in chronic
apical periodontitis.
Activated T cells produce a variety of cytokines that down-regulate
output of proinflammatory cytokines, leading to suppression
of osteoclastic activity and reduced bone resorption.

55. T cell-derived cytokines may up-regulates production of connective tissue
growth factors (TGF -beta), with stimulatory and proliferative effects on
fibroblasts and microvasculature.
Option to down-regulate destructive process explains absence of retarded
bone resorption and rebuilding of collagenous connective tissue during
chronic phase of the disease.
Chronic lesions can remain "dormant" and symptom less for long periods
without major changes in radiographic status.
Delicate equilibrium prevailing at periapex can be disturbed by one or more
factors that may favor microbes in root canal.

56. Microbes advance into peri apex and lesion spontaneously becomes
acute with recurrence of symptoms (exacerbating apical periodontitis,
phoenix abscess)
Due to this microorganisms are found extra radicularly during these
acute episodes with possibly rapid enlargement of radiolucent area.
This characteristic radiographic feature is result of apical bone
resorption that occurs rapidly during acute phases, with relative
inactivity during chronic periods.

57. Radiographic features: -
Chronic apical periodontitis is usually
associated with periradicular radiolucency
Changes range from thickening of periodontal ligament and resorption
of lamina dura to destruction of apical bone resulting in a well-
demarcated radiolucency
Chronic periapical periodontitis, which if allowed to continue will
develop into a periapical granuloma or cyst. Chronic apical periodontitis
is classified histologically as either a periradicular granuloma or a
periradicular cyst.

58. Periapical granuloma: - ( WEINE 4th edition)
Definition
Is more advanced form of chronic apical periodontitis
characterized by growth of granulation tissue and presence of chronic
inflammatory cells (Granulomatous tissue) in response to continued
pulpal irritation. A peripheral collagenous fiber capsule is usually
present.
Etiology:
chronic apical periodontitis if allowed to continue, will
develop into a periapical granuloma or cyst.

59. Reaction of periradicular tissues to noxious products of tissue necrosis,
bacterial products and antigenic agents from root canal has been
described by FISH
Established experimental foci of infection in jaws of guinea pigs by
drilling opening in bone and packing in wool fibers saturated with a
broth culture of microorganisms. Described four zones of well
established granuloma.
zone of necrosis
zone of contamination
zone of irritation
zone of stimulation

60. Zone of necrosis (zone of infection)
Presence of necrotic pulp tissue in root canal (zone of
necrosis/infection) results in diffusion of toxic material into and slightly
beyond area of coalescence of pulpal and periodontal connective tissue.
This zone consists of Pus fluid containing
dead cells, destructive components
released from Phagocytes, intermediate
and end products of protein decomposition
(Proteolysis).
Polymorphonuclear leukocytes (neutrophils) surrounded by large mass
of lymphocytes and plasma cells present.

61. Zone of contamination (exudative inflammatory zone)
Toxicity of root canal irritant is reduced by fluid and cellular exudative
activity in zone of contamination.
 Principal exudative (acute) defense
response (vasodilation, fluid exudation,
cellular infiltration); dilution of toxic
elements plus antibacterial' action of
inflammatory fluid.
 Principal defense cells
Polymorph nuclear leukocytes (PMNs) (early)
Macrophages
Histiocytes

62. This reduction in toxicity stimulates undifferentiated cells to form
osteoclasts and resorb contaminated periapical bone.
Radiographic evidence –widening of periodontal space becomes
evident.gap that is created in bone is filled by granulomatous tissue to
form Zone III zone of irritation

63. Zone of irritation (Granulomatous, proliferative inflammatory zone)
Toxicity diminishing as distance from canal foramina increases
Functions: defense, healing, repair
Principal proliferative (chronic) response: granulation tissue is formed by
capillary proliferation and fibroblastic activity
Granulomatous: granulation tissue plus chronic defense cells
Principal chronic defense cells: lymphocytes, plasma cells, bloodDerived
macrophages, tissue macrophages that develop from histiocytes, and reserve cells
(undifferentiated mesenchymal cells).

64. Cell-derived mediators of inflammation: antibodies from plasma cells,
lymphokines from sensitized T cells (T-type lymphocytes),
histamine and serotonin (5-hydroxytryptarnine)from basophils
Russell bodies: enlarged plasma cells
with numerous antibody inclusions
Eosinophils (later): attracted by mast
Cell, eosinophil chemotactic factor (ECF-A)
and lymphokine. ECF-A modulate inflammation and allergy by destroying
certain vasoactive substances:

65. Platelet activating factor (PAF)
Slow-reacting substance of anaphylaxis (SRS-A)
Foam cells: macrophages after ingesting cells with fatty
degeneration
Favorable environment for osteoclasts
 Occasional cholesterol crystals
Epithelial clusters and strands

66. Zone of stimulation (zone of encapsulation, zone of productive
fibrosis)
At periphery of granulomatous zone toxicity of root canal irritants
diluted and diminished
 Irritants act as a stimulus to fibroblasts
and osteoblasts in this area.
 Wall of collagen fibers is laid down
by fibroblasts in an attempt to encapsulate entire inflammatory
complex, separating granulomatous tissue from bone.

67. Osteoblasts function best in this zone.
Bone apposition and reversal lines evident during recessive and
rest periods.
 Occasional reactive hyperostosis when lesion encroaches on the
cortical plate

69. Kronfeld's mountain pass concept: -
Kronfeld had pointed out that granuloma is not an environment in
which bacteria live but one in which they are destroyed.
 He compared bacteria in root canal (zone I) with an army entrenched
"behind high and inaccessible mountains," foramina serving as mountain passes.
Exudative and granulomatous (proliferative) tissue of granuloma
represents a mobilized army defending plains (periapex) from invaders.

70. If few invaders enter plain through mountain pass, are destroyed by
defenders (leukocytes).
Mass attack of invaders results in battle, analogous to acute
inflammation (acute or exudative forces of zone 11).
 Only complete elimination of the invaders from their mountainous
entrenchment will eliminate need for a defense force in plains.
 Once this is accomplished, defending army of leukocytes withdraws,
local destruction created by battle is repaired (granulation tissue of zone
III), and environment returns to its normal pattern.

71. The objective, therefore, in non surgical root canal therapy of
teeth with periapical pathoses is elimination of irritant from the
canal and keeping it out by a "three-dimensional" filling of the
canal.
Radiographic features:-
appears as radiolucent area of of variable size seemingly attached
to root apex, some cases radiolucency is well- circumscribed
lesion,definitely demarcated from surrounding bone. in these instances
thin radiopaque line or zone of sclerotic bone seen out- lining lesion.

72. Periapical true cyst: -
Definition
An apical inflammatory cyst with a distinct pathological
cavity completely enclosed in an epithelial lining so that no
communication to the root can exists. (AAE definition)
Etiology
Develops from chronic lesions with pre-existing granulomatous tissue.
The process of true cyst formation occurs in three stages.

73. First phase,
Dormant cell rests of Malassez are believed to proliferate,under influence
of growth factors by various cells in lesion.
Second phase,
Epithelium lined cavity forms. Two long-standing hypotheses exist
regarding formation of the cystic cavity.
"nutritional deficiency theory" is based on assumption that central cells
of epithelial strands are removed from their source of nutrition and
consequently undergo necrosis and liquefactive degeneration.
.

74. Accumulating products attract neutrophilic granulocytes into necrotic
area.
Micro cavities containing degenerating epithelial cells, infiltrating
leukocytes, and tissue exudate coalesce to form cystic cavity lined by
stratified squamous epithelium.
"abscess theory" postulates that proliferating
epithelium surrounds an abscess formed by tissue necrosis and
lysis because of inherent nature of epithelial cells to cover
exposed connective tissue surfaces.

75. Third phase
The Cyst grows, the exact mechanism of which has not yet been clarified,
apical pocket cyst which has lumen open to necrotic root canal, can grow
eliminates osmotic pressure as potential factor in development of radicular
cysts.
Although No direct evidence is yet available, tissue dynamics and cellular
components of radicular cysts suggest possible molecular pathways for cystic
expansion.
 Neutrophils perishing in cystic lumen provide a continuous source of
prostaglandins, which can diffuse through porous epithelial wall into
surrounding tissues.

76. Cell population in extra epithelial area includes many T lymphocytes and
macrophages, produces cytokines (IL-l-beta).
Prostaglandins and inflammatory cytokines can activate osteoclasts,
culminating in bone resorption.
Histopathology: -
Apical true cyst has four major components: cyst cavity, epithelial cyst wall,
extra epithelial tissue, and collagenous capsule.
 Cyst cavity, completely enclosed in an epithelial lining, reveals necrotic
tissue, cholesterol clefts and erythrocytes (the presence of erythrocytes is due
to hemorrhage).

77. Thickness of stratified squamous epithelium can vary from a few cell
layers to several.
Inner surface of cyst wall reveals flat epithelial
and globular cells (i.e., the surface of epithelium
and neutrophils protruding through intercellular
spaces).Basal cell side of epithelium is irregular,
forming ridges.
Numerous intraepithelial neutrophils in process of transmigration
across the epithelium into the cyst lumen.

78. Tissue between epithelial lining and fibrous capsule usually
consists of numerous blood vessels and T Lymphocytes, B-
lymphocytes, and plasma cells, neutrophils. Radiographically
periapical cyst is similar to granuloma.

80. Periapical pocket Cyst:
Definition
It is an apical inflammatory cyst containing a sac like, epithelium-lined
cavity that is open and continuous with the root canal. (AAE definition)
Periapical pocket cyst is initiated by accumulation of neutrophils
around apical foramen in response to bacteria in apical root canal.
 Biologically, a pocket cyst constitutes an extension of the infected root
canal space into the peri apex

81. Microluminal space becomes enclosed in stratified squamous epithelium,
grows and forms epithelial collar around root tip.
Epithelial collar forms an "epithelial attachment" to the root surface,
sealing off infected root canal and microcystic lumen from periapical
milieu and rest of the body
Microorganisms at the apical foramen attract neutrophilic granulocytes
into the microlumen by chemotaxis
Pouch like lumen, biologically outside body milieu, acts as a "death
trap" for externalized neutrophils

82. As necrotic tissue and microbial products accumulate, saclike
lumen enlarges to accommodate debris, forming a voluminous
diverticulum of root canal space into periapical area.

83. DIFFERENTIATING CYST AND
GRANULOMA CLINICALLY
 Morse et al devised a test.
 Method :
An endodontic instrument is used to penetrate into the
periapical lesion to induce fluid flow into the canal.
fluid subjected to POLYACRYLAMIDE GEL
ELECTRPHORESIS
Protein migrate in an electric field according to charge
and molecular weight.
Electrophoretic pattern formed by albumin and
globulin proteins of aspirated fluid.
This pattern differs in cysts and granuloma.

85. APICAL ABSCESSES
Definition: -
An abscess is a localized collection of pus in a cavity
formed by disintegration of tissues.
Based on degree of exudate formation and its
discharge, severity of pain, and presence or absence of systemic signs
and symptoms, apical abscesses can be divided into acute or chronic
conditions.

86. Acute periapical abscess:
Definition: -
Acute periapical abscess is an advanced exudative and severely symptomatic
inflammatory response of periapical connective tissues.
Etiology: -
It is caused by contaminants from pulp canal that produces a steadily
increasing amount of inflammatory exudate (edema), leukocyte infiltration, and
suppuration
Lesion can also result from infection and rapid tissue destruction arising from
within chronic apical periodontitis, another example of phoenix
abscess/recrudescent abscess.

87. Clinical features:
Patient may or may not have swelling. When present, swelling may be
localized or diffuse.
On Clinical examination teeth shows varying degrees of sensitivity to
percussion and palpation.
There is no pulp reaction to cold, heat, or electrical stimuli as involved tooth
has a necrotic pulp.
Mobility in acute periapical pathosis is due to exudative pressure exerted
against the root end, which is transmitted laterally to principal fibers of
periodontal ligament

88. Spread of inflammatory response into cancellous bone results in apical
bone resorption.
Since inflammation is not confined to the periodontal ligament but has
spread to the bone, when it spreads to bone it is called acute osteitis.
May have systemic symptoms such as fever and increased white blood
cell count.
Spread of lesion toward a surface, erosion of cortical bone, and
extension of abscess through periosteum and into soft tissues is
accompanied by swelling and some relief. Swelling remains localized,
but it also may become diffuse and spread widely (cellulites).

89. Extent of swelling reflects amount and nature of irritant egressing
from root canal system, virulence and incubation period of involved
bacteria, and host’s resistance.
Radiographic features
Vary from a thickening of periodontal ligament
space to presence of a frank periradicular lesion.

90. Chronic periapical abscess (suppurative apical periodontitis):
Definition: -
Longstanding low-grade inflammatory reaction of periapical
connective tissue to pulpal irritants is characterized by active pus
formation draining through the stoma (mouth) of sinus tract or as fistula
on the skin of face.
Etiology: -
Chronic periapical abscess usually develops from a chronic apical
periodontitis but may also result from an acute periapical abscess that has
found a pathway and subsequent drainage through oral mucosa.

91. Clinical features: -
On clinical examination reveals a range of sensitivity to percussion and
palpation, depending on whether tract is open, draining, or closed.
If mobility present that is due to excessive periradicular bone loss.
Vitality tests are negative on teeth with chronic periapical abscess
because of presence of necrotic pulps.
Sinus tract that leads away from suppurative core to surface may be
partially lined with epithelium or the inner surface composed of inflamed
connective tissue.

92. Exudate can also drain through gingival sulcus of involved tooth,
mimicking a periodontal lesion with a “pocket.”
This is not true periodontal pocket as there is no complete detachment
of connective tissue from the root surface.
If left untreated, it can be covered with an epithelial lining and
becomes a true periodontal pocket.
Mild painful symptoms occur when sinus tract stoma is blocked with
coagulum and or proliferation of mucosal epithelium over stoma. This
symptomatic phase is termed sub acute periapical abscess.

93. Radiographic examination: -
Guttapercha cone can be inserted into stoma of sinus tract of a chronic
periapical abscess to obtain radiographic confirmation of involved tooth
or root.
Chronic periapical abscess may show a diffuse area of bone rarefaction
inflammation and destruction is always greater than radiography shows.

94. Sub acute periapical abscess:
This is painful phase of chronic periapical
abscess cycle.
During nonpainful phase of chronic periapical abscess, pain and
swelling readily regress because of drainage through stoma (mouth) of
the sinus tract.
When sinus tract becomes blocked with coagulum and or proliferation
of mucosal epithelium over stoma, drainage ceases, and periapical
pressure increases, and tooth becomes mildly tender to percussion.

95. Inflammation may now spread to soft tissue
adjacent to sinus tract stoma.
Pressure causes tissue to balloon outward.
parulis (gumboil) develops on mucosa,
and gingiva may develop a circumscribed red swelling.
Exudative changes of acute inflammation are present, as are
proliferative changes characteristic of chronic inflammation.

96. It is impossible to diagnose periapical lesions with any degree accuracy unless a
biopsy is taken and the tissue is examined under microscope, even though the
incidence of cyst is greater for larger lesions.
Term advanced chronic apical periodontitis or pulpoperiapical osteoporosis
may be used until the nature of lesion is confirmed.

97. SPECIAL PATHOLOGIC MANIFESTATIONS: -
Condensing Apical Periodontitis: -
Special radiographic and histologic manifestation of chronic
periradicular inflammation of pulpal origin has been known as condensing
osteitis, or focal sclerosing osteomyelitis.
More prevalent among young and middle-aged groups, and diseased
mandibular first molars are more commonly affected
Lesions appear as well circumscribed radiopacities of periradicular bone of
teeth with necrotic pulps, which may or may not be sensitive to
percussion.

98. Histologically
Reveals a dense mass of bony trabeculae with limited marrow space.
Osseous tissue is lined by osteoblasts, and marrow space may be
infiltrated with lymphocyte.
Conventional root canal treatment usually results in complete
resolution of the condition.
It is differentinl1y diagnosed as cemental dysplasia; which is a benign
tumor of unknown cause that affects healthy teeth with vital pulps.

99. Transient Apical Periodontitis
“Sterile” apical periodontitis of transient nature may develop as a result
of moderate trauma of the periapical tissues.
Periapical radiolucency develops after injury to the apical periodontium
that resolves without intervening treatment
Radiographic lesion appears sometime after injury and is usually
associated with discoloration of tooth and loss of pulpal sensitivity

100. These changes are reversible, and tooth will return to normal.
If radiolucency is principal criteria of diagnosis; radiographic lesion
may be incorrectly diagnosed as apical periodontitis.
Diagnosis should be reached in association with previous history of
trauma and monitoring of tooth for reversibility of tooth discoloration,
pulpal sensitivity, and apical radiolucency.

101. Persistent Apical Periodontitis
Sometimes complete healing of the periapex or reduction in periapical
radiolucency maynot occur in all root canal treated teeth.
Its mainly because the treatment procedures were not satisfactory in
eliminating infection.
Complex morphology of root canal system, inadequate aseptic control,
poor access cavity preparation, missed canals, insufficient
instrumentation, leaking temporary or permanent fillings, compromised
host defence due to systemic diseases like diabetes etc are the main
problems.

102. Cholesterol crystals and Apical periodontitis
Cholesterol is a major structural component of animal plasma
membranes and determinant of membrane properties.
Abundant in myelin and membrane rich tissues and cells, precursor of
bile bile acids, steroid hormones and provitamineD3
Apical periodontitis lesions contain deposits of cholesterol crystals
appears narrow, elongated tissue clefts in histopathological sections.
Crystals dissolve in fat solvents used for tissue processing and leave
behind the spaces they occupied as clefts.

103. Incidence of cholesterol clefts in apical periodontitis 18% to 44%.
Crystals are formed from cholesterol released by
· Disintegrating erythrocytes of stagnant blood vessels with in
the lesion.
· Lymphocytes, plasma cells, and macrophages that die in
greater numbers and disintegrate in chronic periapical lesions.(major
source)
· circulating plasma lipids.
Cholesterol crystals are densely surrounded by macrophages and
multinucleated giant cells forming a well-circumscribed area of tissue
reaction.

104. Accumulation of cholesterol crystals in apical periodontitis can
adversely affect post treatment healing of periapical tissues,
(IEJ 26:225,1993) (IEJ 25:19 1999)

106. Periapical Actinomycosis
 Actinomycosis is a chronic,
granulomatous, infectious disease in
humans and animals caused by the
genera Actinomyces and
Propionibacterium.
 Periapical actinomycosis is a
cervicofacial form of actinomycosis.
 However, the strict growth requirements
of A. israelii make isolation in pure
culture difficult.

108.  Because of the ability of the actinomycotic
organisms to establish extraradicularly, they can
perpetuate the inflammation at the periapex even
after proper root canal treatment.
 The properties that enable these bacteria to
establish in the periapical tissues are not fully
understood, but appear to involve the ability to
build cohesive colonies that enables them to
escape host defense systems

109. Foreign-Body Reaction
Foreign materials trapped in periapical tissue initiates and perpetuate
apical periodontitis lesions, particularly those persisting after root canal
treatment
Endodontic clinical materials and food particles may reach periapex and
cause foreign-body reaction that may appear radiolucent and remain
asymptomatic for many years.
Oral Pulse Granuloma
Lesion denotes foreign body reaction to particles of
vegetable food materials, particularly leguminous seeds (i.e., pulses) get
lodged in the oral tissues

110. Also referred to as the giant cell hyalin angiopathy, vegetable granuloma
and food induced granuloma.
Pulse granulomas are characterized by presence of intensely iodine-
and PAS-positive hyaline rings or bodies, surrounded by giant cells and
inflammatory cells.
Vegetable food materials can get lodged under mucous membrane by
pressure of dentures or can reach periapical tissue via root canals of
teeth exposed to oral cavity by trauma, carious damage, or endodontic
procedures.

111. Cellulose Granuloma
Pathologic-tissue reaction developing against particles of
predominantly cellulose-containing materials that are used in
endodontic practice.
 Endodontic paper points, medicated cotton wool are used for
microbial sampling, drying of root canals etc
Particles can dislodge or get pushed into periapical tissue and induce a
foreign-body reaction at periapex.
Infected paper points can protrude through apical foramen and allow
biofilm to grow around it. This will sustain and intensify apical
periodontitis after RCT, becoming failure.

112. Guttapercha
Root canal sealant used in orthograde obturation of root canals is
guttapercha cone. It is considered to be biocompatible and well tolerated
by human tissues.
Evokes intense, localized tissue response characterized by presence of
macrophages and giant cells.
Accumulation of macrophages in conjunction with fine particles of
guttapercha is clinically observed impairment in healing of apical
periodontitis when teeth are root filled with excess.
Guttapercha cones contaminated with tissue-irritating substances that
can initiate a foreign-body reaction at periapex.

113. Other Foreign Materials
Commonly occur in periapical tissues include amalgam,
endodontic sealants, and calcium salts derived from periapically extruded Ca (OH)2

114. Scar tissue healing
Unresolved periapical radiolucencies may
occasionally be due to healing of lesion by scar tissue that may be
mistaken as radiographic sign of failed endodontic treatment.

115. Radicular cysts and periapical healing
 There are no histological evidence that proves conclusively the
mechanism of inflammatory cyst repair. a number of theories have been
advanced.
Seltzers etal 1969 observed in series of 1yr study, entrapment and
degeneration of epithelium by newly formed collagen fibers during
repair process.
Concluded that pulpoperiapical cysts have potential for healing without
surgical intervention

116. Bhaskar, as a result of his study hypothesized that at least two
mechanisms lead to destruction of epithelial lining:
(1)Transitory acute inflammation attracting PMNs, which liberate lysosomal
enzymes to disrupt or destroy the epithelium
(2)Sub epithelial hemorrhage and subsequent ulceration of epithelium .
Suggested, no matter how careful operator, precystic inflammatory
response or hemorrhage into cystic cavity occurs when canals are
instrumented.
Bhaskar noted when apical lesions become recrudescent, conservative
endodontic therapy is done after drainage has established and acute
symptoms disappears and is successful

117. Bender’s response to Bhasker’s hypothesis gave certain principles with
respect to repair
(1) Drainage is one of basic principles in repair because excess cellular fluid,
pus, and extravasated blood must be eliminated before fibroplasia can occur.
(2) Unless pressure is removed by either drainage or absorption of the fluid, cell
migration will not occur.
(3) Repair process occurs from periphery towards center, as can be evidenced
radiographically. Bender indicated that direct penetration of instruments to center
of cyst to establish drainage and reduce pressure has more merit than does
artificial creation of a mild acute response as suggested by Bhaskar.

119.  Pharmacological modulation of the healing of
apical granuloma can be tried.
 An IL-1 receptor antagonist maybe used in
animals to reduce the bone resorbing activity
(stashenko et al).
 NSAIDs were also used for a similar purpose.
 These two approach were directed at either
blocking the binding of already produced cytokine
to its target cell or interfering with its action on
osteoclasts and osteoblasts that may involve
prostaglandin production.

120.  An alternate strategy maybe to try to locally
“turnoff” the activated macrophages.

121.  APEXUM procedure:
 It allows enucleation of the periapical tissue
through the rootcanal and the apical foramen.
 Apexum protocol is applied just before root canal
obturation.
 Once cleaning, shaping and disinfection of the
rootcanal is completed, the apical foramen is
enlarged by passing a no:35 rotary file to 1-2mm
beyond the apex.

122.  This passage is used to insert a specially designed
Ni-Ti wire into the periapical tissue that rotates and
minces the tissue.
 This is followed by a biodegradable fiber rotated at a
higher speed that turns the tissue into a thin
suspension that is then washed out with salineusing a
30 gauge needle.
 A fresh blood clot forms in the periapical bony crypt
 Ongoing clinical trials indicate a much faster
periapical healing similar to that in apical surgery.

124. CONCLUSION
 Establishment of proper diagnosis is of utmost
importance to carry out the effective clinical
procedure for the benefit of patient .
 Review after the treatment is also to be given
importance .
 Researches done and ongoing research has thrown
light on various aspects untangling the puzzle which
persisted for long. So this knowledge can be used in
the practice to make endodontic treatment a success
when the controversy is going on about to pull out or
salvage the tooth with implant coming strongly on
the field of dentistry.

125.  Huumonen & Ørstavik. Radiological aspects of apical
periodontitis. Endodontic Topics 2002, 1, 3–25
 Murray CA, Saunders WP. Root canal treatment and general
health: a review of the literature. IEJ, 33, 1-18, 2000
 Shimon friedman. Prognosis of initial endodontic therapy.
Endodontic Topics 2002, 2, 59–88.
 PNR Nair. Non-microbial etiology: periapical cysts sustain post-
treatment apical periodontitis. Endodontic Topics 2003, 6, 96–
113.
 PNR Nair. Non-microbial etiology: foreign body reaction
maintaining posttreatment apical periodontitis. Endodontic
Topics 2003, 6, 114–134.
 Lise-lotte KIrkevang & Preben hørsted-bindslev. Technical
aspects of treatment in relation to treatment outcome.
REFERENCES

126.  Idiko J Marton. How does the periapical inflammatory
process compromise general health? Endodontic
Topics 2004, 8, 3–14.
 John I Ingle ,Leif K Bakland. Endodontics,5th edition .
 John I Ingle ,Leif K Bakland,J Craig Baumgartner.
Endodontics,6th edition .
 Franklin S Weine.Endodontic therapy. 4h edition.
 Cohen and Hargreaves. Pathways of pulp,9th edition.
 Leif Tronstad. Clinical endodontics,2nd revised
edition.
 Gunnar Bergenholtz ,Preben Horsted-Bindslev,

127.  Wu M-K, Dummer PMH, Wesselink PR. Consequences of and
strategies to deal with residual post-treatment root canal
infection. IEJ,39, 343–356, 2006.
 Siqueira JF, Jr. Aetiology of root canal treatment failure: why
well-treated teeth can fail (Literature review).IEJ, 34, 1–10,
2001.
 Bergmans L, Moisiadis P, Van Meerbeek B, Quirynen M,
Lambrechts P. Microscopic observation of bacteria: review
highlighting the use of environmental SEM. IEJ, 38, 775–788,
2005.
 Markus Haapasalo, Trude Udnæs, & Unni Endal. Persistent,
recurrent, and acquired infection of the root canal system post-
treatment. Endodontic Topics 2003, 6, 29–56.
 Leif Tronstad & Pia Titterud Sunde. The evolving new
understanding of endodontic infections. Endodontic Topics