A periodontal pocket is defined as a pathologically deepened gingival sulcus, which is a key clinical feature of periodontal disease. It develops through inflammatory changes in the connective tissue that cause degradation of collagen fibers and loss of attachment between the tooth and tissue. This allows epithelial cells and leukocytes to migrate apically, forming a pocket lined by junctional epithelium. The severity of periodontal disease is dependent on loss of attachment, not just pocket depth. Periods of disease activity involve bone and attachment loss, while periods of quiescence have reduced inflammation and minimal tissue destruction.

1. PERIODONTAL POCKET

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

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

4. 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

5. 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

6. 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

7. 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

8. 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)

9. 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)

10. 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

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

12. 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

13. 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

14. 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)

15. MICROTOPOGRAPHY OF THE
GINGIVAL WALL OF THE POCKET
• Several irregular&oval/elongated areas(pocket wall) with
adjacent distance 50-200µm(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

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

17. 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

18. 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

19. ROOT SURFACE WALL
• In deepen pocket, collagenous fibers embedded in
cementum destroyed&exposed to oral environment
• Remanants of sharpey’s undergo degeneration &create
environment for penetration of viable bacteria
• Pathologic granules represent areas of collagen
degeneration(optical/electron microscopy)

20. 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

21. 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 10-20µm thick& up to 50µm

22. AREAS OF DEMINERALIZATION
• Commonly related to root caries
• Exposure to oral fluid&bacterial plaque results
proteolysis of sharpey’s 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

23. 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

24. 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

25. 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

26. 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

27. 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

28. 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

29. 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=1.97mm±33.16%
• Distance between attached plaque to bone is never less
than0.5mm&never more than2.7mm

30. 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

31. 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

32. MCQ-1
• How much probing pocket depth of a
clinically normal gingival sulcus in humans
(a)1-2mm
(b)2-3mm
(c )3-4mm
(d)4-5mm

33. MCQ-2
• The pocket is formed by gingival
enlargement without underlying
periodontal destruction is called
(a)Pseudo pocket
(b)True pocket
(c )subcrestal pocket
(d)Infrabony pocket

34. MCQ-3
• Which type of pocket is most common in
furcation areas
(a)Simple pocket
(b)Compound pocket
(c )spiral pocket
(d)Supracrestal pocket

35. MCQ-4
• A patient has a chief complain of pain in upper
right first molar. On examination a purulent
inflammation with 8mm of pocket depth was
observed on facial aspect of 16.What is the
confirmatory diagnosis of that lesion?
(a)Periodontal cyst
(b)Periodontal abscess
( c)Periapical cyst
( d)Gingival abscess

36. MCQ-5
• One of the following lesions have a reduced
inflammatory response and little or no loss of
connective tissue and bone. A buildup of
unattached plaque, with its gram-negative,
motile and anaerobic bacteria .
(a)period of specificity
(b)period of quiescence
(c)period of exacerbation
(d)period of inactivity

37. MCQ-6
• The severity of periodontal diseases is
depends on
(a)probing pocket depth
(b)loss of attachment
(c)periodntal abscess
(d)gingival abscess

38. MCQ-7
• Which of the following factor is responsible
for flaccidity in the gingival wall of the
periodontal pocket
(a)circulatory stagnation
(b)destruction of gingival fibers
(c)atrophy of the epithelium
(d)edema and degeneration