periodontal pocket classification and pathogenesis

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