Definition of periodontal pocket, classification, Histopathology of periodontal pocket, microflora involved, pathogenesis, periodontal pocket as a healing lesion, microtopography of root surface, treatment of periodontal pocket

1. Periodontal Pocket
Presened By:
Pallavi Prashar
Deptt. of Periodontology and Oral
Implantology

2. Introduction
• The periodontal pocket is defined as a pathologically
deepened gingival sulcus.
• It is one of the most important clinical features of
periodontal disease.
• Progressive pocket deepening leads to destruction of
the supporting periodontal tissues, loosening &
exfoliation of teeth.
• Pocket is derived from French word ; Pochette; a cul-
de-sac or pouch like cavity.

3. Classification

4. • Deepening of the
gingival sulcus may
occur by coronal
movement of the
gingival margin, apical
displacement of the
gingival attachment, or
a combination of the
two processes.

5. Depending upon the type of pocket
• Gingival Pocket (false or pseudo pocket)
• Periodontal Pocket (absolute or true pocket)
– Suprabony Pocket (supracrestal or supraalveolar)
– Intrabony Pocket (infrabony, subcrestal or
inralveolar)

6. Differences between Suprabony and Intrabony
Pockets
Suprabony
Pocket
Intrabony
Pocket
Base of
pocket
Pattern of
bone
destruction

7. Suprabony
Pocket
Intrabony
Pocket
Transseptal
fibers
PDL fibres
(Facial &
Lingual)

8. Infrabony pockets can be further classified as:
1. On the basis of the number of walls remaining-
i) One walled
ii) Two walled
iii) Three walled
2. Depending upon the depth and width of the underlying osseous defect
i) Shallow and narrow
ii) Shallow and wide
iii) Deep and narrow
iv) Deep and wide
3. Depending upon the nature of the soft tissue wall of the pocket;
- Edematous
- Fibrotic
4. Depending upon the disease activity
- Active
- Inactive

9. The pocket can also be classified
according to the involved tooth surfaces
Simple Compound Complex

10. Correlation of Clinical and Histopathologic
Features of the Periodontal Pocket
Clinical Features
• The gingival wall of the
periodontal pocket presents
– various degrees of bluish-red
discoloration;
– flaccidity;
– smooth, shiny surface; and
– pitting on pressure.
Histopathologic Features
• The discoloration is caused by
circulatory stagnation;
• The flaccidity, by destruction
of the gingival fibers and
surrounding tissues;
• The smooth, shiny surface, by
the atrophy of the epithelium
and edema;
• The pitting on pressure, by
edema and degeneration.

11. • Less frequently, the gingival
wall may be pink and firm.
• Bleeding is elicited by gently
probing the soft tissue wall of
the pocket.
• In such cases, fibrotic changes
predominate over exudation
and degeneration, particularly
in relation to the outer surface
of the pocket wall. However,
despite the external
appearance of health, the inner
wall of the pocket invariably
presents some degeneration
and is often ulcerated.
• Ease of bleeding results from
increased vascularity, thinning
and degeneration of the
epithelium, and the proximity
of the engorged vessels to the
inner surface.
Clinical Features Histopathologic Features

12. • When explored with a
probe, the inner aspect of
the periodontal pocket is
generally painful.
• In many cases, pus may
be expressed by applying
digital pressure.
• Pain on tactile stimulation
is due to ulceration of the
inner aspect of the pocket
wall.
• Pus occurs in pockets with
suppurative inflammation
of the inner wall.
Clinical Features • Histopathologic Features

13. Theories of pathogenesis of periodontal
pockets
 Two stage pocket formation (James & Counsell, 1927)
Proliferation of subgingival epithelium
Loss of superficial layers of proliferated epithelium
Space or pocket
• The rate of proliferation of epithelium at the base is such that it
precedes the destruction of the superficial epithelium and the
pocket is therefore always lined with epithelium.

14. Localized pain/
Sensation of
pressure
Foul taste
Tendency to suck
material
Radiating pain
“Deep in the bone”
Gnawing feeling Urge to dig
Foods sticks
between teeth
Sensitivity to heat &
cold
Tooth ache
• Other features:

15. • Pocket formation : Initiated in a defect in sulcus
wall (Becks,1929)
• The formation and maintenance of normal 1mm
deep sulcus results from the co-ordination of
degeneration of the enamel epithelium,
proliferation of the oral epithelium, and atrophy
of gingival papilla.
• Disturbance in this co-ordination leads to
pathologic pocket formation.

16. • Pocket formation occurs between the oral epithelium and
the enamel epithelium rather than by separation of the
enamel epithelium from cuticle.
• If degeneration of oral epithelium takes place rapidly
without being covered by oral epithelium, a defect occurs
in the lateral sulcus wall.
• This defects constitutes a ‘locus minoris resistantial’ which
is a portal of entry for bacteria with inflammation.
• Inflammation is a stimulant to oral epithelium
proliferation, which shuts off nutrition from enamel
epithelium, hastens the degeneration and increase the
pocket depth.

17. • Pathologic destruction of epithelial attachment
due to infection or trauma : Initial histologic
change in pocket formation (Skillen, 1930)
• Epithelial attachment : Area of low resistance
Infection / Trauma
Pathologic dissolution of epithelial attachment
Pocket formation
Accumulation of debris in pocket

18.  Proliferation of the epithelium of lateral wall rather than
epithelium at the base of the sulcus is the initial change in
formation of the periodontal pocket (Wilkinson, 1935)
o Proliferation & down growth of oral epithelium Thickening of
epithelial lining of sulcus Cells along inner aspect of sulcus deprived
of nutrition Degeneration & necrosis Calcification of necrotic
cells Separation of calcified masses from adjacent normal
epithelium Pocket or trough.
o Wilkinson suggested that Vit A deficiency may be an important factor in
pocket initiation.

19. • Initial change in pocket formation occurs in the
cementum. (Gottlieb and Orban,1938).
• Gottlieb stresses the changes in tooth surface rather
than gingiva.
• Down growth of the epithelial attachment as a
physiologic phenomenon that is part of the process
of continuous eruption of teeth throughout life.
• Under physiologic conditions, the continuous
deposition of new cementum acts as a barrier that
prevents accelerated migration of epithelial
attachment.

20. • So long as the continuous cementum deposition
is not disturbed, migration of epithelial
attachment at a pathologic rate can’t occur.
• Harm to cementum and/or gingiva by trauma or
inflammation dissolves the organic connection
between cementum and gingiva and the
epithelium proliferates along the root until it
meets undisturbed connective tissue fibers and
cementum.

21. • Periodontal pocket is initiated by invasion of
bacteria at base of the sulcus or absorption of
bacterial toxins through epithelial lining of
sulcus (Box,1941)
• Acc. to Box, either because of imperfect junction
of the epithelial cells and the cementum or
extreme thinness of the epithelium, the base of
the sulcus offers a poor defense against bacteria.
• Specific bacteria/infective agents possibly related
to Leptothrix falciformis, are capable of
deepening of the periodontal pocket.

22. Initial invasion of bacteria at base of sulcus
Inflammation in underlying CT
Ulceration at base
Sloughing of epithelium
Loss of attachment to cementum
Progressive loss of CT & penetration of pocket into
deeper tissues

23.  Destruction of gingival fibers : Pre-requisite for initiation of
pocket formation (Fish, 1948)
 Proliferation of the epithelial attachment along the root can
take place only if the underlying gingival fibers are destroyed.
 These fibers are considered a barrier to the normal migratory
tendency of the epithelium at the base of the sulcus and it is
believed that their degeneration and necrosis occurs secondary
to inflammation or the action of bacterial enzymes.
 As soon as the topmost fiber is digested and absorbed, the
epithelium proliferates along the root until a healthy fiber is
reached.

24. • Simulation of the epithelial attachment by
inflammation rather than destruction of the
gingival fibers : Prerequisite for initiation of the
periodontal pocket (Aisenberg & Aisenberg, 1948)
• Stimulation by inflammation, the epithelium
migrates along the root without preceeding
destruction of the gingival fibers.
• In such instances that the epithelial cells burrow
between the intact gingival fibers and attach
themselves further apically on the cementum in
bundle free areas.
• This epithelial attachment may move between
healthy connective tissue fibers, forms an epithelial
network, and produce secondary fiber degeneration.

25. • Inflammation is the initial change in the
formation of the periodontal pocket (Nuckolls &
Dienstein, Bell & Rule, 1950)
• 1st change- vascular change in the underlying
connective tissue.
• Inflammation of connective tissue stimulates
epithelial lining of sulcus leading to:
– Inc. mitotic activity in basal epithelial layer
– Inc. production of keratin with desquamation.
• Epithelial cells of basal layer at the bottom the
sulcus and in the area of attachment proliferate
into the underlying connective tissue and breaks
up the gingival fibers.

26. • Dissolution of the connective tissue results in the
formation of an open lesion.
• In pocket formation, epithelium does not
proliferate along the root, but it proliferates from
gingival surface to connective tissue lesion
created by inflammation and thereby forms the
lining of the pocket.

27.  Waerhaug, 1976
Bacteria spreading subgingivally
Pocket formation
 Schroeder and Attstrom (1980)
Microbial invasion of subgingival dentogingival junction
Destroy coronal epithelial attachment
Pathological pockets

28.  Takata & Donath (1988)
Early & established lesion
Degenerative changes in most coronal part of JE
Intraepithelial cleavage
Degeneration of cells lining the cleavage
Deep crevice formation

29. Advanced lesions
Deep pocket epithelium
Toxic bacterial products
Mechanical irritation of calculus
Thin and ulcerated
Typical periodontal pocket

30. Pathogenesis of pocket formation
• The initial lesion in the development
ofperiodontitis is the inflammation of the gingiva
in response to a bacterial challenge.
• Changes involved in the transition from the
normal gingival sulcus to the pathologic
periodontal pocket are associated with different
proportions of bacterial cells in dental plaque.

31. Pocket formation starts as an inflammatory change in
c.t. wall of gingival sulcus
Inflammatory exudate causes degeneration of
surrounding c.t., including the gingival fibers
Just apical to J.E., collagen fibers are destroyed and
area becomes occupied by inflammatory cells and
edema
Two mechanisms assocated with collagen loss:
1. Collagenases and other enzymes (MMPs)
2. Fibroblasts phagocytize collagen fibers

32. Apical cells of J.E. epithelium proliferate along the root
Coronal portion of the J.E. detaches from the root
As a result of inflammation, PMNs invade the coronal
end of J.E. in increasing number
When the relative volume of PMNs reaches
approximately 60% of the J.E.
Tissue losses cohesiveness and detaches from the
tooth surface

33. Thus, the sulcus bottom shifts apically
And the OSE occupies a gradually increasing portion of the sulcular
lining
• Initial deeening of pocket has been described as
occuring between the J.E. and the tooth or the
intraepithelial cleavage within the J.E.
• Extension of the junctional epithelium along the
root requires the presence of healthy epithelial
cells.

34. • Marked degeneration or necrosis of the junctional
epithelium retards rather than accelerates pocket
formation.
• Degenerative changes seen in the junctional
epithelium at the base of periodontal pockets are
usually less severe than those in the epithelium of
the lateral pocket wall.
• Because migration of the junctional epithelium
requires healthy, viable cells, it is reasonable to
assume that the degenerative changes seen in this
area occur after the junctional epithelium reaches its
position on the cementum.

35. • The transformation of a gingival sulcus into a
periodontal pocket creates an area where plaque
removal becomes impossible, and the following
feedback mechanism is established:
• The rationale for pocket reduction is based on the
need to eliminate areas of plaque accumulation.

36. Histopathology
• Soft tissue wall:
– Connective tissue:
Exudative
ProliferativeDegenerative

37. – Junctional epithelium
• Usually much shorter than that of a normal sulcus.
• Usually the coronoapical length of the J.E. is reduced to only 50-
100μm.
– Lateral wall
• Most severe degenerative changes
• Epithelial buds or interlacing cords of epithelial cells
• Dense infiltration
• Cells : Vacuolar degeneration & form vesicles
• Ulceration & suppuration
• The severity of the degenerative changes is not necessarily related
to pocket depth. Ulceration of the lateral wall may occur in
shallow pockets, and deep pockets are occasionally observed in
which the lateral epithelium is relatively intact or shows only
slight degeneration.
• The epithelium at the gingival crest of a periodontal pocket is
generally intact and thickened, with prominent rete pegs.

38. • Bacterial invasion
– Filaments, rods, and coccoid organisms with predominant
gram-negative cell walls have been found in intercellular
spaces of the epithelium.
– Hillmann et al. have reported the presence of Porphyromonas
gingivalis, Prevotella intermedia, Actinobacillus
actinomycetemcomitans in the gingiva of aggressive
periodontitis cases.
– Bacteria may invade the intercellular space under exfoliating
epithelial cells, but they are also found between deeper
epithelial cells and accumulating on the basement lamina.
– Some bacteria traverse the basement lamina and invade the
subepithelial connective tissue.

39. Microtopography of gingival wall
1. Areas of relative quiescence, showing a relatively flat surface with minor depressions and mounds
and occasional shedding of cells.
2. Areas of bacterial accumulation, which appear as depressions on the epithelial surface, with
abundant debris and bacterial clumps penetrating into the enlarged intercellular spaces. These
bacteria are mainly cocci, rods, and filaments, with a few spirochetes.
3. Areas of emergence of leukocytes, where leukocytes appear in the pocket wall through holes
located in the intercellular spaces.
4. Areas of leukocyte-bacteria interaction, where numerous leukocytes are present and covered with
bacteria in an apparent process of phagocytosis. Bacterial plaque associated with the epithelium is
seen either as an organized matrix covered by a fibrin-like material in contact with the surface of
cells or as bacteria penetrating into the intercellular spaces.
5. Areas of intense epithelial desquamation, which consist of semi-attached and folded epithelial
squames, sometimes partially covered with bacteria.
6. Areas of ulceration, with exposed connective tissue
7. Areas of hemorrhage, with numerous erythrocytes.

40. Periodontal pocket as healing lesions
• Periodontal pockets are chronic inflammatory
lesions and as such are constantly undergoing
repair.
• Complete healing does not occur because of the
persistence of the bacterial attack, which
continues to stimulate an inflammatory
response, causing degeneration of the new tissue
elements formed in the continuous effort at
repair.

41. Destructive
tissue
changes
Constructive tissue
changes
Edematous
pocket
Fibrotic
pocket
• The condition of the soft tissue wall of the
periodontal pocket results from the interplay of
the destructive and constructive tissue changes.
• Their balance determines clinical features such as
color, consistency, and surface texture of the
pocket wall.
Destructive
tissue
changes
Constructive tissue
changes
Edematous
pocket
Fibrotic
pocket

42. Pocket contents
• Debris
– Microorganisms & products (enzymes, endotoxins, and other metabolic products),
• Gingival fluid
• Food remnants
• Salivary mucin
• Desquamated epithelial cells
• Leukocytes
• Plaque-covered calculus
• Purulent exudate if present, consists of
– living, degenerated, and necrotic leukocytes;
– living and dead bacteria;
– serum; and
– a scant amount of fibrin

43. o Significance of Pus Formation
 Secondary sign
 Nature of the inflammatory changes
Not an indication of depth of pocket / severity of destruction

44. Root surface wall
Structural Chemical
Cytotoxic
The root surface wall of periodontal pockets often undergoes changes that are
significant because they may perpetuate the periodontal infection, cause pain, and
complicate periodontal treatment. The following changes have been described in
exposed cementum;

45. • Structural changes:
– Pathologic granules:
• Represent areas of collagen degeneration or areas where
collagen fibrils have not been fully mineralized initially.
Pathologic
granules
Areas of increased
mineralization
Areas of
demineralization

46. – Areas of increased mineralization :
• Exchange of minerals & organic components at cementum-
saliva interface. (Selvig 1969)
• Minerals that are increased in diseased root surfaces include
calcium, magnesium, phosphorus and fluoride.
• Microhardness, however, remains unchanged.
• The development of a highly mineralized superficial layer
may increase the tooth resistance to decay and are
associated with increased perfection of the crystal structure.
• These zones are 10 to 20 um thick, with areas as thick as 50
um.

47. – Areas of demineralization:often related to root caries
(Herting 1967)
Exposure to oral fluid & bacteria plaque
Proteolysis of embedded remnants of sharpeys
fibers
Cementum softened
Unergoes fragmentation & cavitation
Root surface caries tend to Progress around the
tooth

48. • Active root caries lesions appear as well-defined
yellowish or light-brown areas, are frequently
covered by plaque, and have a softened or
leathery consistency on probing.
• Inactive lesions are well-defined darker lesions
with a smooth surface and a harder consistency
on probing.
Active root
caries lesions
Inactive root
caries lesions

49. • The dominant microorganism in root surface caries is Actinomyces
viscosus.
• Other bacteria, such as
– Actinomyces naeslundii,
– Streptococcus mutans,
– Streptococcus salivarius,
– Streptococcus sanguis, and
– Bacillus cereus, have been found to produce root caries in animal models.
• Quirynen et al. reported that when plaque levels and pocket depths
decrease after periodontal therapy (both conservative and surgical), a
shift in oral bacteria occurs, leading to a reduction in periodontal
pathogens and an increase in S. mutans and the development of root
caries.
• The tooth may not be painful, but exploration of the root surface reveals
the presence of a defect, and penetration of the involved area with a
probe causes pain.
• Caries of the root may lead to pulpitis, sensitivity to sweets and thermal
changes, or severe pain. Pathologic exposure of the pulp occurs in
severe cases. Root caries may be the cause of toothache in patients with
periodontal disease and no evidence of coronal decay.

50. • Caries of the cementum requires special attention when
the pocket is treated.
– The necrotic cementum must be removed by scaling and root
planing until firm tooth surface is reached, even if this entails
extension into the dentin.
• Areas of cellular resorption of cementum and dentin are
common in roots unexposed by periodontal disease.
– These areas are of no particular significance because they are
symptom free, and as long as the root is covered by the
periodontal ligament, they are likely to undergo repair.
– However, if the root is exposed by progressive pocket formation
before repair occurs, these areas appear as isolated cavitations
that penetrate into the dentin.
– These areas can be differentiated from caries of the cementum
by their clear-cut outline and hard surface.
– They may be sources of considerable pain, requiring placement
of a restoration.

51. • Chemical changes:
– The mineral content of the exposed cementum is
increased.
Exposed cementum may absorb calcium, phosphorous
& fluoride from its environment
development of highly calcified layer that is resistant to
decay.
– The ability to absorb substance may be harmful,
because absorb material may be toxic

52. • Cytotoxic changes:
– Bacterial penetration into the cementum can be found a
deep as the cemento-dentinal junction.
– In addition, bacterial products such as endotoxins have
also been detected in the cementum wall of periodontal
pockets.
– When root fragments from teeth with periodontal
disease are placed in tissue culture, they induce
irreversible morphologic changes in the cells of the
culture. Such changes are not produced by normal roots.
(Hatfield CG, 1971)
– Diseased root fragments also prevent the in vitro
attachment of human gingival fibroblasts, whereas
normal root surfaces allow the cells to attach freely. (Aleo
JJ, 1975)
– When reimplanted in the oral mucosa of the patient,
diseased root fragments induce an inflammatory
response even if they are autoclaved. (Lopez NJ, 1980)

53. Surface morphology of tooth wall with
periodontal pocket

54. Periodontal disease activity
• For many years the loss of attachment produced by
periodontal disease was thought to be a slow but
continuously progressive phenomenon.
• More recently, as a result of studies on the
specificity of plaque bacteria, the concept of
periodontal disease activity has evolved.
• According to this concept, periodontal pockets go
through periods of exacerbation and quiescence,
resulting from episodic bursts of activity followed
by periods of remission.

55. Periods of quiescence Period of exacerbation
Reduced inflammatory
response
Little or no bone & CT
attachment loss
Build-up of unattached
plaque with its gram-negative,
motile, and anaerobic bacteria
Bone & connective tissue
attachment lost
Pocket deepens.

56. • These periods of quiescence and exacerbation are
also known as periods of inactivity and periods of
activity.
• Clinically, active periods show bleeding, either
spontaneously or with probing, and greater amounts
of gingival exudate.
• Histologically, the pocket epithelium appears thin
and ulcerated, and an infiltrate composed predomi-
nantly of plasma cells, polymorphonuclear
leukocytes (PMNs), or both are seen.
• Bacterial samples from the pocket lumen analyzed
with dark-field microscopy show high proportions of
motile organisms and spirochetes.

57. Site specificity
• Periodontal destruction does not occur in all parts of the
mouth at the same time but rather on a few teeth at a time or
even only some aspects of some teeth at any given time.
• This is referred to as the site specificity of periodontal disease.
• Sites of periodontal destruction are often found next to sites
with little or no destruction.
• Therefore the severity of periodontitis increases with the
development of new disease sites and the increased
breakdown of existing sites.

58. Pulp changes associated with
periodontal pockets
• The spread of infection from periodontal pockets may cause pathologic
changes in the pulp.
• Such changes may give rise to painful symptoms or may adversely affect
the response of the pulp to restorative procedures.
• Involvement of the pulp in periodontal disease occurs through either the
apical foramen or the lateral canals in the root after infection spreads
from the pocket through the periodontal ligament.
• Atrophic and inflammatory pulpal changes occur in such cases.

59. Relationship of attachment loss and
bone loss to pocket depth
• Pocket formation causes loss of attachment of the gingiva and
denudation of the root surface.
• The severity of the attachment loss is generally, but not always,
correlated with the depth of the pocket.
• This is because the degree of attachment loss depends on the
location of the base of the pocket on the root surface, whereas
the pocket depth is the distance between the base of the
pocket and the crest of the gingival margin.
• Pockets of the same depth may be associated with different
degrees of attachment loss, and pockets of different depths
may be associated with the same amount of attachment loss.

60. Same pocket depth with different amounts of
recession. A, Gingival pocket with no
recession. B, Periodontal pocket of similar
depth as in A, but with some degree of
recession. C, Pocket depth same as in A and B,
but with still more recession.
Different pocket depths with the same
amount of attachment loss. Arrows point to
bottom of the pocket. The distance between
the arrow and the cementoenamel junctions
remains the same despite different pocket
depths.

61. Area between base of pocket and
alveolar bone
• Normally, the distance between the apical end of the junctional epithelium and
the alveolar bone is relatively constant.
• The distance between the apical extent of calculus and the alveolar crest in
human periodontal pockets is most constant, having a mean length of 1.97 mm
(±33.16%).
• Wade, assessed the relation b/w pocket base, epithelial attachment & alveolar
process &found that the distance from attached plaque to bone is never less
than 0.5 mm and never more than 2.7 mm.
• These findings suggest that the bone resorbing activity induced by the bacteria
is exerted within these distances.
• However, the finding of isolated bacteria or clumps of bacteria in the
connective tissue and on the bone surface may modify these considerations.

62. Relationship of pocket to bone
• In intrabony pockets, the base of the pocket is apical to the crest of the
alveolar bone, and the pocket wall lies between the tooth and the bone.
• Intrabony pockets most often occur interproximally but may be located
on the facial and lingual tooth surfaces.
• Most often the pocket spreads from the surface on which it originated
to one or more contiguous surfaces.
• The base of the suprabony pocket is coronal to the crest of the alveolar
bone.
• The inflammatory, proliferative, and degenerative changes in intrabony
and suprabony pockets are the same, and both types lead to destruction
of the supporting periodontal tissues.

63. Periodontal abscess
• A periodontal abscess is a localized purulent
inflammation in the periodontal tissues.
• It is also known as a lateral or parietal abscess.
• Abscesses localized in the gingiva, caused by injury to
the outer surface of the gingiva, and not involving the
supporting structures are called gingival abscesses.
• They may occur in the presence or absence of a
periodontal pocket.

64. Periodontal abscess formation may occur in the following ways:
1. Extension of infection from a periodontal pocket deeply into the supporting
periodontal tissues and localization of the suppurative inflammatory process
along the lateral aspect of the root.
2. Lateral extension of inflammation from the inner surface of a periodontal
pocket into the connective tissue of the pocket wall. Localization of the
abscess results when drainage into the pocket space is impaired.
3. In a pocket that describes a tortuous course around the root, a periodontal
abscess may form in the cul-de-sac, the deep end of which is shut off from the
surface.
4. Incomplete removal of calculus during treatment of a periodontal pocket. In
this instance, the gingival wall shrinks, occluding the pocket orifice, and a
periodontal abscess occurs in the sealed-off portion of the pocket.
5. A periodontal abscess may occur in the absence of periodontal disease after
trauma to the tooth or perforation of the lateral wall of the root in endodontic
therapy.

65. • Microscopically, an abscess is localized accumulation of
viable and non-viable PMNs within the periodontal pocket
wall.
• The PMNs liberate enzymes that digest the cells and other
tissue structures, forming the liquid product, known as pus,
which constitutes the center of the abscess.
• An acute inflammatory reaction surrounds the purulent
area, and the overlying epithelium exhibits intracellular
and extracellular edema and invasion of leukocytes.
• The localized acute abscess becomes a chronic abscess
when its purulent content drains into a fistula into the
outer gingival surface or into the periodontal pocket and
the infection causing the abscess is not resolved.

66. • Bacterial invasion of tissues has been reported in
abscesses; the invading organisms were identified
as gram negative cocci, diplococci, fusiforms, and
spirochetes.
• Invasive fungi were also found and were
interpreted as being opportunistic invaders.
DeWitt et al 1985.
• Microorganisms that colonize the periodontal
abscess have been reported to be primarily gram-
negative anaerobic rods. Newman 1979.

67. Periodontal cyst
• The periodontal cyst is an uncommon lesion that
produces localized destruction of the periodontal
tissues along a lateral root surface, most often in
the mandibular canine-premolar area .

68. The following possible etiologies have been suggested:
1. Odontogenic cyst caused by proliferation of the
epithelial rests of Malassez; the stimulus initiating
the cellular activity is not known.
2. Lateral dentigerous cyst retained in the jaw after
tooth eruption.
3. Primordial cyst of supernumerary tooth germ.
4. Stimulation of epithelial rests of the periodontal
ligament by infection from a periodontal abscess or
the pulp through an accessory root canal.

69. • A periodontal cyst is usually asymptomatic and without grossly
detectable changes, but it may present as a localized tender
swelling.
• Radiographically, an interproximal periodontal cyst appears on
the side of the root as a radiolucent area bordered by a
radiopaque line.
• Its radiographic appearance cannot be differentiated from that
of a periodontal abscess.
• Microscopically, the cyst lining may be:
1. A loosely arranged, non-keratinized, thickened, proliferating
epithelium;
2. A thin, non-keratinized epithelium; or
3. An odontogenic keratocyst.

70. Conclusion
• Understanding the etiopathogenesis,
histopathology and progression of
periodontal pockets is essential to provide the
patient with the successful treatment
outcomes and monitoring the response to
therapy.

71. Thankyou…