Periodontal pockets formation. Pathogenesis of periodontal pockets. Types of pockets.

1. PERIODONTAL POCKETS
&
IT’s PATHOGENESIS
Presented by:
Dr. Maryam Mastoor

2. PERIODONTAL POCKET:
“It is a pathologically deepened gingival sulcus
i.e. more than 3mm” (either due to coronal
movement of gingival margin or apical migration
of Junctional Epithelium or a combination of
both processes).

3. Classification
of
periodontal pockets

4. CLASSIFICATION table
1. Based on
morphology
i)Gingival
ii)Periodontal Pocket
iii)Combined Pocket
2. Based on
Relationship
to crestal bone
i)Suprabony Pocket
ii)Infrabony Pocket
3. Based on number of
surfaces involved
i)Simple Pocket
ii)Compound Pocket
iii)Complex Pocket
4. Based on nature of
soft tissue wall of
the pocket
i)Edematous Pocket
ii)Fibrotic Pocket
5. Based on
disease activity
i)Active Pocket
ii)Inactive Pocket
Edematous
Active
Inactive
Fibrotic

5. (1)
Based upon Morphology of Gingiva
i) Pocket due to coronal
movement of gingival margin
(Gingival/Pseudo Pocket)
ii) Pocket due to apical
detachment of Junctional
Epithelium (Periodontal
Pocket)
iii) Combine Pocket
Normal gingiva
Coronal movement
of gingiva
Apical detachment

6. i) GINGIVAL POCKET:
(pseudopocket)
• Formed by gingival enlargement & coronal movement
of gingival margin without destruction of underlying
periodontal tissues.
• The sulcus is deepened because of the increased
bulk of the gingiva.
Healthy gingiva Gingival Pocket

7. ii) PERIODONTAL POCKET:
• It is pathological deepening of sulcus due to apical
detachment of Junctional Epithelium with destruction
of periodontal tissue .
Progressive
Bone loss
Healthy
side
Apical detachment of
Junctional epithelium
+
Periodontal Pocket
formation
Diseased
side

8. (2)
Based upon relation to Crestal bone
Suprabony
pocket
Infrabony
pocket
Normal Gingiva
i) Suprabony Pocket ii) Infrabony Pocket
• Base of the pocket is
coronal (superior) to
the level of underlying
bone.
• Base of the pocket is
apical (inferior) to the
level of underlying
bone.
• Horizontalboneloss • Vertical bone loss

10. i) SIMPLE POCKET:
Involving one tooth surface.
ii) COMPOUND POCKET:
Involving two or more
tooth surfaces.
iii)COMPLEXPOCKET/SPIRALPOCKET:
Originates from one surface and twists around the tooth to
involve one or more additional surfaces (commonly found in
furcation area).
(3)
Based upon number of tooth
surfaces involved

12. i) EDEMATOUS POCKET:
Clinically it has bluish-red,
spongy,smooth and shiny
surface due to increase in
inflammatory fluid & cellular
exudate.
ii) FIBROTIC POCKET:
Clinically it has a firm pink
surface due to newly
formed connective tissue &
fibers.
(4)
Based upon Nature of Soft Tissue
Wall of the Pocket:
Edematous
Fibrotic

13. i)Active pocket:
Occurs during Period of
Exacerbation or activity of
disease.
Loss of bone and connective
tissue attachment.
Pocket deepens.
Increased inflammation.
ii) Inactive pocket:
Occurs during Period of
Quiescence or inactivity of
disease.
Little or No further bone loss
and connective tissue attachment.
Pocket level remains same.
Reduced inflammation.
(5)
Based upon Disease Activity
Normal
Periodontium
Increased
inflammatory
neutrophils
Bone loss
Pocket deepens
Reduced
inflammation
Everything
remains same

14. PATHOGENESIS
of
periodontal pocket

15. Summary of Periodontal Pocket Formation
STAGE 1
• Accumulation of Supragingival Plaque
STAGE 2
• Extension of Plaque Subgingivally
STAGE 3
• Coronal Detachment & Apical Migration
STAGE 4
• Phagocytic action of Neutophils in Pocket Epithelium
STAGE 5
• Ulceration of Pocket Epithelium
STAGE 6
• Periodontal Pocket established

16. PATHOGENESIS:
 Plaque accumulationon
supragingivaltooth surface
 Chemotacticagentsreleasedby
bacterialplaqueattracting
inflammatorycells
 Marginalgingivabecomesinflammed
andedematized
 Gingivalsulcusdeepens dueto
edematousenlargementofgingiva
GingivalPocketformed

17.  Extension of plaque subgingivally 
change in bacterial environment from
Gram –ve toGram +ve i.e. Dysbiosis
 Bacterial toxicproducts subgingivally 
cause coronal junctional epithelium to
produce inflammatory mediators 
causing dilatation of blood vessels.
 Neutrophils fromconnective tissure
transmigrate into gingival sulcus and
make a layer on subgingival plaque to
prevent itsfurther subgingival
extension.

18. Engorged blood vessels  increases supply of
nutrients into soft tissue  junctional epethelial
cells proliferate making Rete’ Pegs  Bacteria
feed on these nutrients  inflammation
intensifies  Collagen destruction starts just
apical to junctional epithelium by two methods:
METHOD 1
Collagenases & other enzymes produced by
fibroblasts, PMNs and macrophages  degrade
collagen and other matrix macromolecules into 
matrix metalloprotinases (small peptides)
METHOD 2
Fibroblasts extend their cytoplasmicprocesses into the
ligament-cementum interface  phagocytizeinserted
collagen fibrils andthe fibrils of the cementum matrix.
Collagen destruction apically apical infiltration
of inflammatory cells  Coronal Junctional
epithelium detaches  Apical part of J.E.
Migrates along the root surface

19. Coronal portion of J.E. invaded by PMNs
Phagocytic action of neutrophils in pocket
epithelium continues  Lateral wall of
Periodontal pocket degenerates extensively
Increased proliferation of epithelial rete’
pegs into connective tissue for nutrients.
Increasing number of transmigrating
neutrophils in pocket  volume reaches
60% or more of J.E.  disruption of
epithelial barrier i.e ulceration  open
communication b/w pocket and connective
tissue  bacteria invade into C.T.
phagocytic action of macrophages inside C.T.
starts.
Fig E : Phagocytic action of
Neutrophils

20. Breakage of Epithelial barrier 
Periodontal Pocket established
Increased bacteria  increased
immune response  increased blood
flow  increased nutrients for
bacteria
Increased immune response 
activates osteoclasts  alveolar
bone resorbs  decreased support
of tooth  tooth mobility increases
 tooth loss

22. HISTOPATHOLOGY
 Extensive
proliferation of
Lateral Epithelium
 Atrophied pocket
wall
 Marked
inflammatory
neutrophils
Normal gingival sulcus
epithelium
(a) Epithelial Changes:

23. (b) Connective Tissue changes:
 Densely infiltrated with
lymphocytes and PMNs.
 Blood vessels engorged
in subepithelial
connective tissue layer.
 Multiple necrotic foci
 Proliferation of
endothelial cells, with
newly formed capillaries
and collagen fibers.
Fig. Interdental papilla showing
densely inflamed connective tissue
with infiltrate extending between
collagen fibers and
proliferating ulcerated pocket
epithelium.