A periodontal pocket is a pathologically deepened gingival sulcus caused by an inflammatory response to oral infection. It is characterized by the apical migration of junctional epithelium along the root surface. Periodontal pockets can be classified based on their morphology, the surfaces and structures involved, and the nature of the soft tissue wall. The pathogenesis of pocket formation involves the destruction of collagen fibers by collagenases and other enzymes released during the host inflammatory response to bacterial plaque accumulation. This results in the apical migration and proliferation of junctional epithelium along the root, forming a periodontal pocket. Histopathologically, the soft tissue wall shows edema, inflammation and ulceration while the root surface undergoes structural and chemical changes with

1. Periodontal Pocket
1 M.E.AlmaQaleh

2. Done by:
Mohammed Eskander AlmaQaleh
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3. Definition
 Periodontal pocket:
• Apical migration of junctional epithelium down root surface &
transformation of (JE) into pocket epithelium (Glauser 1982)
• Is histopathology change in the soft tissue and possibly the
underlying bony tissues, reflecting an inflammatory response to oral
infection. (Rose 2000)
•
Is pathologically deepened gingival sulcus.
(Carranza 12ed 2016)
• Is pathologically deepened gingival sulcus which is formed due
to increase in original sulcular depth and apical migration of
junctional epithelium.
(Shalu Bathla textbook 2017)
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4. Classification
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5. Depending on morphology
Depending on surfaces involved
Depending on the nature of soft-tissue wall
Depending on lateral wall of pocket
Depending on disease activity
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6. 1-Gingival pocket
2-Periodontal pocket
a-suprabony pocket(supracrestal or supraalveolar)
b- infrabony pocket(infrabony, subcrestal, or intraalveolar)
Depending on morphology
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7. Gingiva pocket Periodontal pocket
Pseudo pocket Absolut or true pocket
Seen in gingivitis Seen in periodontitis
Formed by gingival
enlargement without
destruction of underlying
periodontal tissueof
Occurs with destruction of the
supporting periodontal tissues
cause loosening of the teeth
Depending on morphology
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8. Suprabony pocket Infrabony pocket
I. Base of pocket is coronal to the level of
alveolar bone.
II. Horizontal pattern of bone
destruction.
III. On facial and lingual surfaces , pdl fibers
beneath pocket follow their normal
oblique course.
IV. Transeptal fibers are arranged
horizontally.
I. Base of pocket is apical to crest of
alveolar bone.
II. Vertical (angular) pattern of bone
destruction.
III. They follow angular pattern.
IV. Transeptal fibers are arranged obliquely
Depending on morphology
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9. Depending on surfaces involved
-Simple pocket
-Compound pocket
-Complex/Spiral pocket
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10. Depending on the nature of soft-tissue wall
1-Edematous
2-Fibrotic
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11. Depending on lateral wall of pocket
₋ suprabony pocket
₋ infrabony pocket
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12. Depending on disease activity
₋ Active pocket
₋ Inactive pocket
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13. Clinical Features
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14. Symptoms
a. Localized pain or a sensation of pressure in the gingiva after eating.
b. A foul taste in localized areas.
c. A tendency to suck material from the interproximalspaces.
d. Radiating pain “deep in the bone”.
e. A “gnawing’ feeling or feeling of itching in the gums.
f. Urge to dig with pointed instrument into the gingiva.
g. Food “sticks between the teeth”.
h. Sensitivity to heat and cold.
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15. Signs
Parameters signs cause
Color bluish-red Circulatory stagnation
Surface
Texture
Smooth, Shiny
pits on pressure
Atrophy of epithelume&edema
Edema & degeneration
consistency Flaccid Destruction of gingival
fibers
Bleeding Gently probing bleeding 1-Increased vascularity
2-thining & degeneration of epithelium
3-proximity of engorged vessels
Pain Generally painful Ulceration of inner surface
of pocket
Pus Expressed by gentle pressure Supportive inflammation of
inner wall15 M.E.AlmaQaleh

16. Diagnosis
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17. Using periodontal probe
X-Ray
Microscopy Diagnosis
17
Photoacoustic Imaging
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18. periodontal probe
• Carful examination of gingival margin along each tooth
surface gives exact location and extent of periodontal
pocket.
• G.V BLACK use of very thin flat explorers to
determine the depth of pockets (1924)
• Periodontal probe and its use was first
described by F.V. Simoton of the University
OfCalifornia, San Francisco in
(1925)
• The Latin word probo means “to test.
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19. • Carful examination of gingival margin along each tooth surface gives exact
location and extent of periodontal pocket.
periodontal probe
WALKING
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20. periodontal probe
1- Pocket depth:distance between base of pocket& gingival margin.
2-Level of attachment:distance between base of pocket and fixed point (CEJ)2-3mm
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21. Florida probe
 Clark and Yang trained operators and
performing the ‘double pass’ method, the
measurements taken with Florida probe
system shows more accuracy than those
obtained with conventional probing.
Limitations
Lack of tactile sensitivity.
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22. FP Handpiece tip as it enters the sulcus Handpiece tip with constant force in
use (tip at bottom of sulcus) and sleeve
properly positioned at the top of the
gingival margin allowing the computer
to measure the difference.
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23. 23 M.E.AlmaQaleh

24. Gingival Temperature Kung et al (1990)
diagnostic devices for measuring early inflammatory changes in gingival
tissue.
Subgingival temperature at diseased sites is increased as compared to
normal healthy sites
Possible explanation for ↑ temperature with increasing
Haffajee et al. (1992): found that elevated subgingival
site temperature is related to attachment loss in shallow pockets
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25. X-Ray
• By using gutta-percha & insertion it in the pocket then
use x-ray.
A-Conventional Radiography.
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26. B-Digital radiography
Capturing radiographic image using a sensor
The first direct digital imaging system, RadioVisioGraphy
(RVG), was invented by Dr. Frances Mouyens.
This technique facilitates both quantitative and
qualitative visualization of even minor density changes
in the bone
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27. Microscopy Diagnosis
Tissue remaining
Analysis of GCF:
• collagen breakdown + Pocket
27
Hydroxyproline
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Depending on disease activity September 7, 2017
Source: University of California - San Diego
Combination of squid ink with light and ultrasound, a team led
by engineers has developed a new dental imaging method to
examine a patient's gums that is noninvasive, more
comprehensive and more accurate than the state of the art.
 The squid ink component: melanin nanoparticles
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29. 29
The method:
oral rinse
melanin
nanoparticles get
trapped in the
pockets
squid ink heats up
and quickly swells
detecting by
ultrasound
creating pressure
differences in the
pockets
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30. Pathogenesis
2018-2017

31. Theories of pathogenesis:
1- Hermann Becks theory(1929): defect in sulcus.
2-Skillen theory (1930):pathological destruction of
epithelial by infection or trauma
3- Wilkinson theory (1935): proliferation of the
lateral wall epithelium rather than the base epithelium of
the sulcus
4-Box theory(1941): invasion of bacteria at the base
of the sulcus Or absorption of bacterial toxins
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32. 5- Fish theory ( 1946): destruction of gingival fiber.
6- Gottlieb theory (1948): the initial change in
pocket formation occurs in cementum.
7- Aisenberg theory (1948):stimulation of epithelial
attachment by inflammation rather than destruction
of gingival fibers
8- J Nuckolls (1950): inflammation is the initial
change in formation p.pocket.
Theories of pathogenesis:
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33. Pathogenesis
• The first event in pocket formation is the inflammation of
gingiva in response to bacterial challenge.
• Healthy gingiva associated with (coccoid cells and straight
rods).
• Diseased gingiva associated with (spirochetes & motile
rods).
• The microbiota of diseased sites cannot be used as a
predictor of future attachment or bone loss, because their
presence alone is not sufficient for disease to start or
progress. 33 M.E.AlmaQaleh

34. • Early concepts assumed that, after the initial bacterial
attack, periodontal tissue destruction continued to be
linked to bacterial action. Recently, it was established that
the host's immunoinflammatory response to the initial and
persistent bacterial attack unleashes mechanisms that
lead to collagen and bone destruction.
• The mechanisms of formation of p.pocket are related to
various cytokines which are produced normally by cells in
non-infiamed tissue and others by cells that are involved
in the inflammatory process, such as leukocytes (PMNs),
monocytes, and other cells which lead to collagen & bone
loss.
Pathogenesis
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35. i. Collagenases & matrix metalloproteinase degrade collagen & other matrix
macromolecules to small peptide.
i. Fibroblasts phagocytize collagen fibers by extending cytoplasmic processes
to the ligament-cementum interface and degrading the inserted collagen
fibrils and the fibrils of the cementum matrix
Con..:
Tow mechanisms of losing collagen:
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36. 1-As a consequence of the loss of collagen, the
apical cells of the junctional epithelium proliferate
along the root and extend fingerlike projections
2-The coronal portion of the junctional epithelium
detaches from the root as the apical portion
migrates, thereby resulting in its apical shift and this
as result of:
A-increasing the PMNs in the coronal portion of
the junctional epithelium (60% or more).
B-Physical force exerted by rapidly growing
bacteria .
c-Exudate associated with the advancing
bacteria .
Inflammation changes that form P.Pocket
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37. 3- Bacteria VS immunosystem:
1-In normal conditions neutrophils emigrate from the vessels of the gingival
plexus through the junctional epithelium into the gingival sulcus and oral
cavity (the transmigrating cells leave no trace of their passage and cause no
damage).
Neutrophils are the primary and first line of defense around the teeth &
the epithelial barrier is the second.
2-In presence of bacteria the substance produced by it chemotactically attract
neutrophils also chemotactic agent is produced by intact junctional
epithelium.
 Con..:
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38. 3- Extension of plaque subgingivally causes an
increase in the number of transmigrating
neutrophils due to the increased concentration
of chemotactic factors & other inflammation
induced substances produced by bacteria which
cause vasculitis.
4- Neutrphils pass through the junctional
epithelium form a thick layer that covers the
surface of the subgingival plaque(neutrophils
are viable partly, but not completely functional)
to limit further extension and spread of bacteria
by phagocytosis and killing.
5-Increasing growth rate of bacteria, swamps
the neutrophil system and permits tissue
destruction to occur (First defense line is
broken).
 Con..:
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39. 6-Aggressive growth and action of bacteria cause increasing
number of neutrophils that transmigrate through the
junctional
epithelium and pocket epithelium causes open communication
between the pocket and connective tissue by disrupting the
epithelial barrier(2nd defense line is broken) .
Ulceration of this sort is the second major event in pocket
formation.
7- After the epithelial barrier is breached:
I. The chemotactic agents released by it is stopped & as a
result the neutrophils have no guidance systems to direct
them from the vessels through tissues and into the pocket
they remain in the connective tissue moving randomly.
II. Bacterial substances, and bacteria may enter the connective
tissue
 Con..:
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40. 8-The neutrophils encounter substances within the C.T rather
than outside & neutrophils become completely activated and
undertake phagocytosis, release lysosomal enzymes,
collagenases and other substances (PGE2) that cause
extensive tissue damage.
9-As soon as the bacterial substances have entered the
connective tissue many systems other than the neutrophils
are activated like macrophages lymphocytes and
complement system.
10-When the epithelial barrier is re-established the
chemotactic gradient is formed again and the destructive
process subsides. If this barrier is not re-established, tissue
destruction continues and alveolar bone is resorbed. A
periodontal pocket is now established.
 Con..:
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41. Inflammatory changes in the the C.T of gingival
sulcus
Collagenase &
MMPs
Activate Fibroblasts for
phagocytizing collagen
Gingival Collagen Fiber Destruction
apical cells of the junctional epithelium
proliferate along the root
coronal portion of the junctional
epithelium detaches from the root
Intraepithelial cleft & pocket progression
Summary of
pathogenesis
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42. Histopathology
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43. 1-The connective tissue is edematous and
densely infiltrated with plasma
cells(80%) ,lymphocytes, and PMNs.
2-Blood vessels are increased in number,
dilated and engorged in sub-epithelial
connective tissue layer.
3-Single or multiple necrotic foci are present
in the connective tissue.
Soft-Tissue wall
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44. 4-Proliferation of endothelial cells with newly formed capillaries ,fibroblasts,
and collagen fibers
.
5-The junctional epithelium at the base of the pocket is usually much shorter
than that of a normal sulcus.
 Con..:
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45. 6-Changes occur along lateral wall of the
p.pocket:
I.The epithelium along the lateral wall of the pocket
presents striking proliferative and degenerative
changes.
II.The epithelium is infiltrated with leukocytes and
other inflammatory cells.
III. Degeneration and necrosis of the epithelium
leading toulceration of the epithelium and exposure
of the underlying connective tissue.
IV.Bacterial invasion along the lateral and apical areas
of the pocket. Some bacteria traverse the basement
lamina and invade the subepithelial connective
tissue.
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46. Bacterial Invasion
-Bacterial invasion of the apical and lateral
areas of the pocket wall has been described in
human chronic periodontitis: Filaments, rods,
and coccoid organisms with predominant
gram-negative cell walls have been found in
intercellular spaces of the epithelium.
-Hillmann and colleagues have reported the
presence of Porphyromonas gingivalis and
Prevotella intermedia in the gingiva of
aggressive periodontitis cases. A.ctinobacillus
actinomycetemcomitans has also been found
in the tissues
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47. Changes in the Root Surface Wall
Structural
Changes Chemical
changes
Cytotoxic
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48. 1-Collagenous remnants of Sharpey fibers in the cementum undergo
degeneration thereby creating an environment favorable to the penetration
of bacteria
2-Viable bacteria have been found in the roots of 87% of periodontally
diseased non-carious teeth.
3-Bacterial penetration into the cementum can be found as deep as the
cementodentinal junction & it may also enter the dentinal tubules.
4-Formation of areas of increased mineralization due to exchanging of
minerals and organic components at the cementumsaliva interface after
exposure to the oral cavity.
Structural Changes
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49. 5-Formation of Areas of
demineralization often
related to root caries.
6-Pathologic granules :
Collagen degeneration /
Incompletely mineralized
collagen fibrils
Structural Changes
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50. • Mineral content change
1-Bacterial penetration : Cemento-dentinal Junction
2-Endotoxins
Chemical Changes
Cytotoxic Changes
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51. • 1- debris
• 2-principally containing micro-organisms and their products, (like
enzymes, endotoxins and othermetabolic products)
• 3-dental plaque
• 4-gingival fluid,
• 5-foodremnants,
• 6-salivary mucin,
• 7-desquamated epithelial cells and
Pocket Content
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52.  Surface Morphology of Tooth Wall:
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53. • 1. Cementum covered by calculus,.
• 2. Attached plaque, which covers
calculus and which extends apically from it
to a variable degree (typically 100 to 500
µm).
• 3. The zone of unattached plaque that
surrounds attached plaque and extends
apically to it.
Surface Morphology of Tooth Wall
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54. 4.The zone of attachment of the
junctional epithelium to the tooth. The
extension of this zone, which in normal
sulci is more than 500 µm, is usually
reduced in periodontal pockets to less
than 100 µm.
5.A zone of semi-destroyed connective
tissue fibers may be apical to the
junctional epithelium
Surface Morphology of Tooth Wall
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Thank You
M.E.AlmaQaleh