types of periodontal pockets, histopathology

1. Presented by:
Dr. Kishlay Bhartiya
JR-III
Department of Periodontology
F.O.D.S., K.G.M.U., Lucknow

2. The periodontal pocket is defined as a
pathologically deepened gingival sulcus, and
it is one of the most important clinical
features of the periodontal disease.

3. 1. Coronal movement of
gingival margin
2. Apical displacement
of the gingival
attachment
3. A combination the two
process
As Deepening of gingival sulcus may occur by: -

4. Pockets can be classified as follows :
1. Gingival Pocket (Pseudopocket) – formed by gingival
enlargement without destruction of the underlying tissues. The
sulcus is deepened because of the increased bulk of the gingiva.
2. Periodontal Pockets – it occurs with destruction of supporting
periodontal tissues.
Two types of periodontal pockets exist :
I. Suprabony (Supracrestal or Supraalveolar) - In this,
bottom of the pocket is coronal to the underlying alveolar bone.
II. Intrabony (Infrabony, Subcrestal or intraalveolar) - In
this, bottom of the pocket is apical to the level of the adjacent
alveolar bone and the lateral pocket wall lies between the
tooth surface & alveolar bone.

5. A. Gingival Pocket B. Suprabony C. Intrabony Pocket

6. Periodontal pockets can also be classified-
[A] According to involved tooth surface
1. Simple
2. Compound
3. Complex or Spiral – originating on one surface and twisting around
the tooth to involve one or more additional surfaces ( most
commonly found in furcation area)
I II III

7. [B] Depending upon the nature of the soft tissue wall of the
pocket:
(1) Edematous Pocket.
(2) Fibrotic Pocket.
[C] Depending upon disease activity:
(1) Active Pocket.
(2) Inactive Pocket.

8. SIGNS :
1) Bluish red, thickened marginal gingiva.
2) A Bluish red vertical zone from the gingival margin to alveolar
mucosa.
3) Gingival bleeding and suppuration.
4) Tooth mobility.
5) Diastema formation.
6) A rolled edge separating the gingiva Margin from the tooth
surface.
7) A break in the facio-lingual continuity of interdental gingiva.
8) Shiny, puffy gingiva leads to exposed root surface.

9. SYMPTOMS
1) Localized pain or “pain deep in the bone”
2) Usually painless but may give rise to localized / radiating
pain or sensation of pressure after eating which gradually
reduces.
3) A foul taste in localized areas.
4) Sensitivity to hot & cold.
5) Toothache in the absence of caries is also sometimes
present.
6) A tendency to suck material inter proximally.
7) Feeling of itching in the gums.
8) Urge to dig a pointed instrument in the gums.
9) Feeling of loose teeth.

10. CLINICAL FEATURES
1. Bluish red discoloration of gingival
pocket wall
2. Flaccidity
3. Smooth and shiny surface
4. Pitting on pressure
5. Less frequently gingival wall may
be pink and firm
6. Bleeding on gentle probing
7. Inner wall of pocket is painful
8. Pus discharge on applying digital
pressure
HISTOPATHOLOGIC FEATURES
1. Circulatory strangulation
2. Destruction of gingival fibers and
surrounding tissue
3. Atrophy of epithelium
4. Edema and degeneration
5. Fibrotic changes predominate over
exudation and degeneration
6. Increased vascularity, thinning of
epithelium and proximity of
engorged vessels to inner surface.
7. Ulceration of inner aspect of
pocket wall.
8. Suppurative inflammation of inner
wall.

11. The only reliable method of locating periodontal pockets and determining
their extent is careful probing along each tooth surface. There are two
different pocket depths -
Biologic or Histologic depth :- is the distance between the gingival margin
and the base of the pocket (the coronal end of the junctional epithelium.
Clinical or probing depth :- Is the distance from the gingival margin to
which a probe penetrates in to the pocket.
◉ According to several investigators - The probing force of 0.75 N or
25 gm have been found to be well tolerated and accurate.

12.  In normal sulcus, the probe penetrates about one third to one
half the length of junctional epithelium
 In periodontal pocket with a short junctional epithelium the
probe penetrates beyond the apical end of junctional
epithelium.

13. Vertical insertion of the probe (Left) may not detect interdental
craters, oblique positioning of the probe (Right) reaches the
depth of the crater.
Vertical Oblique

14. “Walking” the probe to explore the entire pocket

15.  The initial lesion in the development of Periodontitis in response to
a bacterial challenge is inflammation of the gingiva.
o Changes involved in the transaction from the normal gingival sulcus
to pathologic periodontal pocket are as follows:
Inflammatory change occur in
connective tissue wall of the
gingival sulcus
↓
Cellular & inflammatory exudates
cause degeneration of surrounding
connective tissue & gingival fibers
↓
Collagen fibers are destroyed just
apical to junctional epithelium
↓
Area becomes occupied by
inflammatory cells & edema

16. There are two mechanisms of collagen loss
I II
Collagenases & other enzymes
secreted by various cells such
as fibroblasts, PMNs, leukocyte
& macrophages, becomes
extracellular and destroy
collagen; these enzymes that
degrade collagen and other
matrix macro molecules into
small peptides are called
matrix metalloproteinases.
Fibroblasts phagocytize
collagen fibers by extending
cytoplasmic process to the
ligament-cementum interface
and degrade the inserted
collagen fibrils and the fibrils
of the cementum matrix.

17. After collagen loss, apical cells of
Junctional Epithelium proliferate along
the root, extending finger like
projections two or three cells in
thickness.
↓
Coronal portion of Junctional Epithelium
detaches from the roots as the apical
portion migrates.
↓
As a result of inflammation PMNs invades
the coronal end of Junctional Epithelium
and when relative volume becomes
approx. 60% or more of the Junctional
Epithelium, the tissue looses
cohesiveness & detaches from the tooth
surface.
Area of destroyed collagen at base
of the pocket and thin fingerlike
extension of epithelium covering
the cementum

18. Some Important Points
 Extension of Junctional Epithelium along the root requires the
presence of healthy viable, epithelial cells and so it is reasonable to
assume that the degenerative changes seen in this area occur after
the junctional epithelium reaches its position on cementum.
 The degree of leukocyte inflammation of junctional epithelium is
independent of the volume of inflamed connective tissue.
 The transformation of a gingival sulcus into a periodontal pocket
creates an area where plaque removal becomes impossible and
following feedback mechanism is established:-
Plaque
Accumulation
Gingival
Inflammation
Pocket
Formation
Area difficult
to clean

19. Once the pocket is formed, several microscopic features are present
and discussed in following sections:-
Changes in the soft tissue wall:
 The connective tissue is edematous & densely infiltrated with plasma
cells (approx. 80%), lymphocytes & a scattering of PMNs.
 Blood vessels are increased in number, dilated and engorged
particularly in the subepithelial connective tissue layer.
 Connective tissue exhibit varying degrees of degeneration.
 The connective tissue shows proliferation of endothelial cells with
newly formed capillaries, fibroblasts and collagen fibres.
 The Junction Epithelium at the base of the pocket is usually much
shorter than that of a normal sulcus and usually coronoapical length
of junctional epithelium is reduced to only 50-100 m.

20. Changes along the lateral wall :
Most severe degenerative changes occur along lateral wall.
 The epithelium presents striking proliferative & degenerative changes .
 Epithelial buds or interlacing cords of epithelial cells project from lateral wall
into adjacent inflamed connective tissue & may extend farther apically to
Junctional Epithelium.
 These epithelium projection and remainder of lateral epithelium are densely
infiltrated by Leukocytes and edema from the inflamed connective tissue.
 These cells can undergo vacuolar degeneration and rupture to form vesicles.
 Progressive degeneration & necrosis of epithelium lead to Ulceration of
lateral wall,Exposure of inflamed connective tissue and suppuration.
 The severity of degenerative changes are not necessarily related to pocket
depth.
 Ulceration may occur in shallow pockets and deep pockets with intact lateral
epithelium is rarely observed.
 The Epithelium at the gingival crest of a periodontal pocket is generally
intact & thickened, with prominent rete pegs.

21. Lateral wall showing epithelial
proliferation and atrophic changes
Base of the pocket showing extensive
proliferation of lateral epithelium

22. Bacterial Invasion
 Occurs along the lateral & apical areas of the pocket in cases of
chronic periodontitis.
 Filaments, Rods & coccoid organisms with predominent gram-
negative cell walls have been found in intercellular spaces of
epithelium.
 Hillmann et al reported presence of Porphyromonas gigivalis and
Prevotella intermedia in the gingiva of aggressive Periodontitis cases
 Actinobacillus actinomycetumcomitans (AA) has also been found in
the tissues.
 Bacteria may invade intercellular space under exfoliating epithelial
cells but also found between deeper epithelial cells and accumulating
on the basement lamina.
 Some bacterial traverse the basement lamina and invade the
subepithelial connective tissue.

23. The micro topography of the gingival wall of the
pocket
 SEM reveals several areas in the soft tissue wall of the
pocket where different types of activity take place.
 These areas are irregularly oval or elongated and
adjacent to one another and measure about 50-200
micrometer.
 This suggests that the pocket wall is the constantly
changing as a result of interaction between host and
bacteria. Following areas have been noted-:
(a) Area of relative quiescence: Shows relatively flat
surface with minor depressions & mounds and
occasional shedding of cells.
(b)Area of bacterial accumulation: which appear as
depression on the epithelial surface with abundant
debris and bacterial clumps penetrating into the
enlarged intercellular spaces. These Bacteria are
mailnly Rod, cocci, filamentous & a few spirochetes.
(c) Areas of emergence of leukocyte: leucocyte appear in
the pocket wall through holes located in the
intercellular spaces.
Scanning electron frontal micrograph of the
periodontal pocket wall. Different areas can be
seen in the pocket wall surface. A, Area of
quiescence; B, bacterial accumulation;
C, bacterial-leukocyte interaction; D, intense
cellular desquamation. Arrows point to
emerging leukocytes and holes left by
leukocytes in the pocket wall. (×800.)

24. (d)Areas of Leukocyte-bacteria
interaction:
 Numerous leukocytes are present
& covered with bacteria in an
apparent process of
phagocytosis.
 Bacterial plaque associated with
the epithelium is seen either as
an organised matrix covered by a
fibrin like material in contact with
the surface of cells or as bacteria
penetrating into the intercellular
spaces.
(e)Areas of intense epithelial
desquamation: consist of semi-
attached & folded epithelial
squames, sometimes partially
covered with bacteria.
(f)Areas of ulcerations with exposed
connective tissue.
(g)Areas of haemorrhage with
numerous erythrocytes.
Note the desquamating epithelial cells and
leukocytes (white arrows) emerging onto
the pocket space. Scattered bacteria can
also be seen (black arrow)

25. The transition from one area to another could
result from:
Bacterial accumulation in previously quiescent areas
↓
Triggering the emergence of leukocytes
↓
Leukocyte-bacteria interaction
↓
Lead to intense Epithelial desquamation
↓
Finally to ulceration & haemorrhage

26. PERIODONTAL POCKET AS A HEALING LESIONS
 Periodontal pocket are chronic inflammatory lesion and thus
constantly undergoing repair.
 Complete healing does not occur because of persistence of
the bacterial attack which continues to stimulate an
inflammatory response, causing degeneration of the new
tissues formed in continuous effort at repair.
 There are destructive and constructive tissue changes and
their balance determines the clinical features as color,
consistency & surface texture of the pocket wall.
 If Inflammatory fluid & cellular exudate predominate, the
pocket wall is bluish-red, soft, spongy and friable, with a
smooth, shiny surface, at the clinical level and this is referred
to as an edematous pocket wall.

27.  If there is predominance of newly formed
connective tissue cells & fibers, the pocket
wall is more firms and pink, and known as
fibrotic pocket wall.
 Edematous and fibrotic pockets represent
opposite extremes of the same Pathologic
process, not different disease entities.
 Fibrotic pocket walls may be misleading
because they do not necessarily reflect what
is taking place throughout the pocket wall.
 The most severe degenerative changes in
periodontal tissues occur adjacent to the
tooth surface & subgingival plaque.
 In some cases inflammation and ulceration on
inside of the pocket are walled off by fibrous
tissue on the outer aspects. Externally the
pocket appears pink and fibrotic, despite the
inflammatory changes occurring internally.

28. POCKET CONTENT
Periodontal pocket contains –
 Debris (consisting of microorganism &
their products mainly enzymes,
endotoxins and other metabolic
product)
 Gingival fluid
 Food remnants
 Salivary mucin
 Desquamated epithelial cells &
Leukocytes
Plaque covered calculus projects from
tooth surface.
 If purulent exudate present:consists of–
Living, degenerated and necrotic
leukocytes,
Living and dead bacteria
Serum
A scant amount of fibrin.

29. Significance Of Pus Formation
 Pus is common feature of periodontal diseases, but it is only
a secondary sign.
 The presence of pus or ease with which it can be expressed
from the pocket merely reflects nature of the inflammatory
changes in the pocket wall.
 It is not an indication of the depth of the pocket or the
severity of the destruction of the supporting tissues.
 Extensive pus formation may occur in shallow pockets
whereas deep pockets may exhibit little or no pus.

30. ROOT SURFACE WALL
The root surface wall of periodontal pocket often undergoes changes that
are significant because they may perpetuate the periodontal infection,
causing pain, and complicate periodontal treatment.
As the pocket deepens, collagen fibers embedded in the cementum are
destroyed
↓
Cementum become exposed to the oral environment
↓
Remanents of Sharpey’s fibers in the cementum undergo degeneration
↓
Creating a favorable environment for bacterial penetration
↓
Penetration and growth of bacteria leads to fragmentation and breakdown of
the cementum surface
↓
Result in area of necrotic cementum, separated from the tooth by mass of
bacteria

31. Decalcification And Remineralisation Of Cementum
Areas of increased mineralization:
 Probably a result of an exchange, on exposure to the oral cavity, of
minerals and organic components at the cementum- saliva interface.
 The mineral content of exposed cementum increases.
 The minerals that are increased in diseased root surfaces include Ca,
Mg, P & F.
 Micro hardness, however, remains unchanged.
 The development of highly mineralized superficial layer may increase the
tooth resistance to decay.
Areas of demineralization/Root carries:
 Exposure to oral fluid and bacterial plaque results in proteolysis of the
embedded remnants of the Sharpy's fibres.
 The cementum may be softened & may undergo fragmentation and
cavitations.
 Unlike Enamel caries, root surface caries tend to progress around rather
that into the tooth.

32. Active
 well defined yellowish/ Light
brown areas
 frequently covered by plaque
have softened or leathery
consistency on probing
Inactive
 well defined darken lesion with
a smooth surface
 harder consistency on probing
Root caries lesion
 Caries of the cementum require 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 extended
in dentin

33. Areas of cellular resorption of cementum and dentin
 They are common in roots unexposed by periodontal
diseases.
 They are of no significance because they are symptom free
and as along as the root is covered by the periodontal
ligament, they are likely to undergo repair.

34. Surface Morphology Of Tooth Wall
Of Periodontal Pocket
The following zones can be found in the
bottom of a periodontal pocket:
1. Cementum covered by calculus
2. Attached Plaque – covers calculus and
extends apically from it to a variable
degree (100-500 m)
3. The zone of unattached plaque
Surround attached plaque & extends
apically to it.
4. The zone of attachment of Junctional
Epithelium to the tooth – this zone
reduced to 100 m (in periodontal
pocket) from 500 m found in normal
sulcus.
5. a zone of semi-destroyed connective
tissue fibres – apical to the JE

35. PERIODONTAL DISEASE ACTIVITY
According to the concept of periodontal disease activity, periodontal
pockets go through -
1. PERIODS OF QUIESCENCE OR INACTIVITY
 Characterized by a reduced inflammatory response & little or no loss of
bone and connective tissue attachment.
 A build up of unattached plaque with its gram-negative, motile and
anaerobic bacteria.
2. PERIODS OF EXACERBATION OR ACTIVITY
 Bone and connective tissue attachment are lost and the pocket deepens.
 This period may lasts for days, weeks, months & eventually followed by a
period of remission or quiescence in which G+ve bacteria proliferate and
a more stable condition is established.
 Clinical features: shows bleeding spontaneous or on probing and greater
amount of gingival exudates.
 Histological Features : Pocket Epithelium appears thin and ulcerated,
Infiltrate composed of plasma cells & PMN leukocytes.

36. 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 the periodontal disease.

37. PULP CHANGES ASSOCIATED WITH
PERIODONTAL POCKET
Spread of infection from periodontal pockets
may cause pathologic changes to the pulp. It may
give rise to painful symptoms. Involvement of the
pulp may occure through either the apical foramen
or the lateral canals. Atrophic and inflammatory
pulpal changes may occur in such cases.

38. RELATION OF ATTACHMENT LOSS & BONE LOSS TO
POCKET DEPTH
 Pocket formation leads to loss of attachment of
gingiva & denudation of root surface.
 The severity of attachment and bone loss is generally
correlated with the depth of the pocket.
 The degree of attachment loss depends on the
location of base of pocket on the root surface.
 Whereas pocket depth is the distance between the
base of the pocket & the crest of the gingival margin.
 Excessive attachment & bone loss may be associated
with shallow pocket if the attachment loss is
accompanied by recession of gingival margin, and
slight bone loss can occur with deep pockets.

39. AREA BETWEEN THE BASE OF THE POCKET AND
ALVELOR BONE
 Normally the distance between the apical end of
the Junctional epithelium & alveolar bone is
relatively constant.
 The distance between apical extent of calculus &
alveolar crest in periodontal pocket is most
constant and has 1.97mm (± 33.16%)
 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 bacteria is exerted within these
distances.

40. RELATIONSHIP OF PERIODONTAL POCKET TO BONE:
INTRABONY POCKET
 Base of the pocket is apical to the crest of alveolar bone, and the
pocket wall lies b/w the tooth and the bone.
 Mostly occur interproximally but may be located on facial and
lingual tooth surfaces.
 The bone destructive pattern is vertical/Angular.
 On facial and lingual surface, the periodontal fibres follow
angular pattern of adjacent bone.
SUPRABONY POCKET
 Base of pocket is coronal to the level of alveolar bone.
 Pattern of destruction of underlying bone is horizontal.
 The transseptal fibers are arranged horizontal in space between
base & alveolar bone.
 On the facial and lingual surface, PDL fibers beneath pocket
follow their normal horizontal-oblique pattern.

41. Radiographic and Microscopic features of intrabony pockets

42. “ A periodontal abscess is a localized purulent
inflammation in the periodontal tissue” It is also k/a
lateral abscess or parietal abscess.
“abscess localized in gingiva, caused by injury to the
outer surface of the gingiva, and not involving the
supporting structure are called gingival abscesses”
Periodontal abscess on an upper right central incisor.

43. 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. Formation of the abscess
results when drainage into the pocket space is impaired.
3. Formation in a pocket with 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. The
gingival wall shrinks, occluding the pocket orifice, and a periodontal abscess
occurs in the sealed-off portion of the pocket.
5. After trauma to the tooth or with perforation of the lateral wall of the root in
endodontic therapy. In these situations, a periodontal abscess may occur in
the absence of periodontal disease.

44. Periodontal abscesses are classified according to
location as follows:
1. Abscess in the supporting periodontal tissues along the
lateral aspect of the root. In this condition, a sinus generally
occurs in the bone that extends laterally from the abscess to
the external surface.
2. Abscess in the soft tissue wall of a deep periodontal pocket.

45. The localized acute
abscess becomes a chronic
abscess when its purulent
content drains through a
fistula into the outer
gingival surface or into the
periodontal pocket and the
infection causing the
abscess is not resolved.
Microscopic view of a periodontal abscess showing dense
accumulation of polymorphonuclear leukocytes (PMNs) covered by
squamous epithelium.
Microscopically, an abscess is a localized accumulation of viable and nonviable
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.

46.  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.
 It is considered to be derived from rests of Malassez or other
proliferating odontogenic rests.
 A periodontal cyst is usually asymptomatic, without grossly
detectable changes, but it may present as a localized, tender
swelling.

47. 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 cystic lining may be
1. A loosely arranged, thin, nonkeratinized, epithelium,
sometimes with thicker proliferating areas or
2. An odontogenic keratocyst.