PERIODONTAL POCKET

DEFINITION
A periodontal pocket is defined as pathologically
deepened gingival sulcus.
It is one of the most important clinical features of
periodontal diseases.

CLASSIFICATION
Gingival pocket
Periodontal Pocket
Suprabony(supracrestal/supraalveolar)
Intrabony(infrabony/subcrestal/intraalveolar)

CLINICAL FEATURES

Bluish red,thickend marginal gingiva

Bluish red vertical zone(GM
AM)
Gingival bleeding
Suppuration
Tooth mobility
Diastema formation
Symptoms-localised pain/pain deep in the bone

PATHOGENESIS

Inflammatory changes in CT of GS
Cellular&fluid inflm. exudate causes
degeneration of CT&gingival fibers
Just apical to JE collagen fibers destroyed
Area is occupied by inflammatory cells & edema

PATHOGENESIS Contd..
Two mechanism of collagen loss
Collagenases+Enzymes secreated by
fibroblasts,PMNs&Macrophages- MMPs became extracellular
&destroyes collegen
fibroblast phagocytise collagen fibers by extending cytoplasmic
process to the ligamentum-cementum interface&degrade collagen
fibrils&fibrils of cementum matrix

PATHOGENESIS Contd..
As a result of the loss of collagen the apical cells of JE
proliferate along the root ,extending finger like
projections 2/3cells in thickness.
PMNs invade the coronal end of JE in no.
PMNs not joined to one another/to epithelial cells by
desmosomes

PATHOGENESIS Contd..
Relative volume of PMNs reaches 60%/more of JE
Tissue losses cohesiveness detach from tooth surface
Coronal portion of JE detach from the root as the apical
portion migrate
Resulting in its apical shift &oral SE gradually occupies
increased portion of the sulcus(pocket lining)

PATHOGENESIS Contd
Extension of the JE along the root requires the presence
of healthy epithelial cells.

Marked degeneration/necrosis of JE impairs rather than

accelerates pocket formation(NUG-ulcer and not pocket
formation)

HISTOPATHOLOGY
C.T.
-Edematous&densely infilterated
plasma(80%),lymphocytes,PMNs
-various degree of degeneration
-single/multiple necrotic foci
-proliferation of endothelial cells
-newly formed capillaries,fibroblast,
colagen fibres

HISTOPATHOLOGY Contd
J.E.
-at base of pocket is much shorter than sulcus
-coronoapical length 50-100m
-variation in length,width
&condition of epithelial cells

HISTOPATHOLOGY Contd
Epithelial of lateral wall of pocket shows
proliferative&degenerative changes
Epithelial buds/interlacing cords of
epithelial cells from lateral wall
adjacent
inflamed c.t.
Apically than JE
Epithelial projections+remainder
of lateral epithelium infiltrated
with leucocytes &edema

HISTOPATHOLOGY Contd
Cells under go vascular degeneration
&rupture to form vesicles
Progressive degeneration&necrosis of
epithelium
ulceration of lateral wall
Exposure of underlying CT
&suppuration

BACTERIAL INVASION
Filaments,rods&coccoid organism with gm-ve cell walls
found in intercellular spaces(CP)
P.gingivalis&P.intermedia&AA in Gingiva (AP)
Bacteria invade intercellular spaces
&accumulate on BL
Some cross BL &invade CT
(Bacterial invasion/translocation)

MICROTOPOGRAPHY OF THE
GINGIVAL WALL OF THE POCKET
Several irregular&oval/elongated areas(pocket wall) with
adjacent distance 50-200m(SEM)
Following areas
1-Areas of relative quiescence
2-Areas of bacterial accumulation
3-Areas of emergence of leukocytes
4-Areas of leukocyte-bacteria interaction
5-Areas of intense epithelial desquamation
6-Areas of ulceration
7-Areas of hemorrhage

PERIODONTAL POCKET AS
HEALING LESIONS
PP are ch infl lesion constantly repair
Distructive & constructive changes
Edematous pocket

Fibrotic pocket

POCKET CONTENTS
Debris consisting
microorganism&products(enzymes,endotoxins&metaboli
c products)
Gingival fluid remnants,salivary mucin
Desquamated epithelial cells&leukocytes
Purulent exudate consists of living,degenerated&scant
amount of fibrin

SIGNIFICANCE OF PUS
FORMATION

Pus is common feature of periodontal diseases

Secondary sign
Reflects nature of inflammatory changes in pocket wall
Not indicated severity of the supporting tissue

ROOT SURFACE WALL

In deepen pocket, collagenous fibers embedded in
cementum destroyed&exposed to oral environment
Remanants of sharpeys undergo degeneration &create
environment for penetration of viable bacteria
Pathologic granules represent areas of collagen
degeneration(optical/electron microscopy)

ROOT SURFACE WALL Contd..

Penetration of growth of bacteria leads to
fragmentation&breakdown of the cementum
Results in areas of necrotic cementum,seprated from the
tooth by masses of bacteria
Endotoxin also detected in the cemental wall of
periodontal pocket

DECALCIFICATION&REMINERALI
ZATION OF CEMENTUM

se mineralization an exchange,on exposure to the oral

cavity of minerals&organic components at cementum
saliva interface

se in disease root surface,Ca,Mg,P,&F

Microhardnes remains unchanged

Hypermineralised zone 10-20m thick& up to 50m

AREAS OF DEMINERALIZATION
Commonly related to root caries
Exposure to oral fluid&bacterial plaque results
proteolysis of sharpeys fibers
Cementum may be softened &undergo
fragmentation&cavitation
Active root caries lesions-yellowish/light brown areas
,covered with plaque&soft
Inactive lesions- darker with smooth surface&harder
consistency
Actinomyces viscosus major organism& others
A.naeslundii,S.mutans,S.salivarious,S.sanguis&B.cereus

SURFACE MORPHOLOGY OF
THE TOOTH WALL OF PP
1-cementum covered by calculus
2-attached plaque
3-the zone unattached plaque
4-the zone where JE is attached to the tooth
5-zone of semidestroyed CT fibres
3,4,5-plaque free zones
-it is remember that plaque free zone refers
to attached plaque
-unattached plaque contains gm+ve
cocci,rods,filaments,fusiforms&spirochetes
-most apical zone contains gm-ve rods&cocci

PERIODONTAL DISEASE
ACTIVITY
PP go through periods of excervation&quiescence
Period of quiescence:
*reduced inflammatory response
*little/no bone&CT attachment loss
*unattached plaque with gm-ve
motile&anaerobic bacteria

PERIODONTAL DISEASE
ACTIVITY Contd..
Period of excervation:
*bone & CT attachment loss
*pocket deepens
*this period may lost for days/months&is followed
by period of remission/quiescence

These periods of quiescence& excervation are also

known as period of activity&period of inactivity

SITE SPECIFICITY
Periodontal destruction does not occur in all parts of the
mouth but rather on a few teeth at a time or even only
some aspect of some teeth at any given time

Severity of periodontal diseases increases by the

development of new disease site, the increased
breakdown of existing sites

PULP CHANGES ASSOCIATED

WITH PERIODONTAL POCKETS
Spread of infection from PP may cause pathologic
changes in the pulp
Such changes give rise to painful symptoms
Involvement of pulp in the periodontal diseases through
apical foramen/lateral canals

RELATION OF CAL&BONE LOSS

TO POCKET DEPTH
Severity of attachment loss is generally not correlated
with pocket depth
Degree of attachment loss depends on the location of
the base of the pocket on the root surface
Where as pocket depth is the distance between the base
of the pocket &crest of the gingival margin

AREA BETWEEN THE BASE OF

POCKET&ALVEOLAR BONE
Distance between apical end of JE &alv bone is constant
Distance between apical end of calculus &alv bone is
constant in human PP=1.97mm33.16%

Distance between attached plaque to bone is never less

than0.5mm&never more than2.7mm

PERIODONTAL ABSCESS
It is a localized purulent inflammation in the
periodontal tissues.
Also known as lateral/parietal abscess
Abscess localized in gingiva(gingival abs)

Microscopically:
-localized accumulation of viable&non viable
PMNs
pus(center)
-acute inflammatory reaction surrounds the
purulent area &overlying epithelium
-acute abscess
chronic abcess

PERIODONTAL CYST
Uncommon lesion that produces localized destruction of
periodontal tissue along a lateral root surface ,most often
in mandibular canine premolar area
Microscopically :
The cystic lining may be
-loosely arranged,nonkeratinized,thickend,
proliferating epithelium
-thin nonkertinized epithlium
-an odantogenic keratocyst