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.

As Deepening of gingival sulcus may occur by:

1. Coronal movement of
gingival margin
2. Apical displacement
of the gingival
attachment
3. A combination the
two process

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.

A. Gingival Pocket

B. Suprabony

C. Intrabony Pocket

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)

II

III

[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.

SIGNS :
1)
2)

3)
4)
5)
6)

7)
8)

Bluish red, thickened marginal gingiva.

A Bluish red vertical zone from the gingival margin to alveolar
mucosa.
Gingival bleeding and suppuration.
Tooth mobility.
Diastema formation.
A rolled edge separating the gingiva Margin from the tooth
surface.
A break in the facio-lingual continuity of interdental gingiva.
Shiny, puffy gingiva leads to exposed root surface.

SYMPTOMS
1)
2)

3)
4)
5)

6)
7)
8)
9)

Localized pain or pain deep in the bone

Usually painless but may give rise to localized / radiating
pain or sensation of pressure after eating which gradually
reduces.
A foul taste in localized areas.
Sensitivity to hot & cold.
Toothache in the absence of caries is also sometimes
present.
A tendency to suck material inter proximally.
Feeling of itching in the gums.
Urge to dig a pointed instrument in the gums.
Feeling of loose teeth.

CLINICAL FEATURES

HISTOPATHOLOGIC FEATURES

1. Bluish red discoloration of

gingival pocket wall
2. Flaccidity

1. Circulatory strangulation

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

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.

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.

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.

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

Walking the probe to explore the entire pocket

The initial lesion in the development of Periodontitis in response to

a bacterial challenge is inflammation of the gingiva.
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

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 ligamentcementum interface and
degrade
the
inserted
collagen fibrils and the
fibrils of the cementum
matrix.

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

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:-

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.

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.

Lateral wall showing epithelial

proliferation and atrophic changes

Base of the pocket showing extensive

proliferation of lateral epithelium

Bacterial Invasion

Occurs along the lateral & apical areas of the pocket in cases of
chronic periodontitis.

Filaments, Rods & coccoid organisms with predominent gramnegative 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.

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.)

(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)

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

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.

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.

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.

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.

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 Sharpeys 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

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.

Root caries lesion

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

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

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.

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

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.

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.

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.

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.

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.

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.

Radiographic and Microscopic features of intrabony pockets

 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.

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.

Periodontal abscesses are classified according to

location as follows:
1. Abscess in thesupporting periodontal tissuesalong 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 thesoft tissue wallof a deep periodontal
pocket.

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 aspus,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 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.

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 caninepremolar 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.

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.