PERIODONTAL
POCKET
DEFINITION
• “A pathologically deepened gingival sulcus.”
2
Dept. of Periodontics, PDCH
CLASSIFICATION
1. Depending on mechanism of pocket
formation.
2. Depending on the relation of the pocket base
to the alveolar crest.
3. Depending on the number of surfaces
involved.
3
1.DEPENDING ON MECHANISM
GINGIVAL POCKET / PSEUDO POCKET
• Formed by gingival enlargement without
destruction of underlying periodontal tissues.
PERIODONTAL POCKET
• Formed by apical migration of the junctional
epithelium and destruction of supporting
periodontal tissues.
4
2.DEPENDING ON THE RELATION BETWEEN POCKET BASE
AND THE BONE CREST
• SUPRABONY / SUPRACRESTAL / SUPRAALVEOLAR
• Bottom of the pocket is coronal to the
underlying alveolar bone.
• INFRABONY / INTRABONY / SUBCRESTAL /
INTRAALVEOLAR
• Bottom of the
pocket is
apical to the
level of
alveolar bone.
5
3.DEPENDING ON THE NUMBER
OF SURFACES INVOLVED
SIMPLE POCKET
COMPOUND POCKET
COMPLEX/SPIRAL POCKET.
6
CLINICAL FEATURES
SIGNS-
 Enlarged Bluish red thickened
marginal gingiva.
 Bluish red vertical zone from
margin to alveolar mucosa.
 Bleeding.
 Suppuration.
 Tooth mobility.
 Diastema formation.
 Pain- Localized or Deep in the bone.
 Careful periodontal probing is the only way to
locate the pocket and to determine its full extent.
7
SYMPTOMS-
 Localized pain or sensation of pressure
after eating.
 Foul taste
 Tendency to suck materials
 Radiating pain deep in bone
 Gnawing or itching in gingiva
 Food lodgment
 Sensitivity to heat and cold
 Pain
8
PATHOGENESIS
Dept. of Periodontics, PDCH
9
• Healthy gingiva - Few microbes—Coccoid cells and
straight rods.
• Diseased gingiva — increased no. of spirochetes
and motile rods.
• Changes in the microflora accompany the
transition from gingival sulcus to periodontal pocket.
10
Dept. of Periodontics, PDCH
Plaque
accumulation
Inflammatory
Exudate
Cells & fluid
Inflammatory
mediators
destroys
Gingival
fibers
Cells form
MMPs,
Fibroblasts
phagocytose
collagen
Cells of J.E.
Proliferate
apically,
Coronal cells
detach
Gingiva is
bulky,
separates
apically
Pathogene
sis
• Pocket formation starts
as an inflammatory
change in C.T wall of
gingival sulcus
11
 Collagen destruction by 2 mechanisms-
1. Collagenase secreted by fibroblasts, phagocytes and
macrophages become extracellular and destroy
collagen.
2. Fibroblasts phagocytize collagen fibers by extending
cytoplasmic processes.
 Apical cells of JE proliferate along the root and extend
fingerlike projections.
 PMNs invade coronal end of JE.
 PMNs volume reaches 60% or more of JE loses
cohesiveness. Coronal portion of JE detaches from root
and apical portion migrates .
Dept. of Periodontics, PDCH
12
HISTOPATHOLOG
Y
13
SOFT-TISSUE WALL
• Epithelium at the gingival crest is generally
intact and thickened.
• Junctional Epithelium is reduced in height,
only 50-100 microns. Cells may exhibit slight
to moderate degeneration.
• Connective tissue is edematous, densely
infiltrated with plasma cells, lymphocytes &
PMNs.
• Blood vessels are numerous, dilated,
engorged.
• Varying degrees of degenerative and necrotic
changes are seen.
14
Lateral wall of pocket:
 Shows maximum degenerative changes.
 Epithelium proliferates & extends into the
adjacent inflamed connective tissue.
 This epithelium is densely infiltrated by
WBCs & edema.
 The cells undergo degeneration and form
vesicles.
 Progressive necrosis give rise to ulceration
of lateral wall, exposure of the C.T. and
suppuration.
15
 Severity of degenerative changes is not dependent
on depth of pocket. Suppuration and ulceration
may be seen with a shallow pocket and not with a
deep one and vice versa.
 On comparison, it was shown that the aggressive
cases show more degenerative changes than the
chronic ones.
16
Bacterial Invasion
 Periodontitis cases show bacterial invasion of the
lateral and apical areas of pocket wall.
 Intercellular spaces of epithelium show presence
of filaments, rods, coccoid forms with Gram
negative cell wall.
 Bacteria are seen in the exfoliating cells, between
deeper epithelial cells, on basement lamina and
also in the subepithelial connective tissue.
17
MICROTOPOGRAPHY OF
THE GINGIVAL WALL OF THE
POCKET
18
 Scanning electron microscopy of the lateral wall of
the pocket reveals areas that are irregularly oval or
elongated and adjacent to one another.
 Each area measures around 50-200microns.
 Transition from one area to another is a rule and it
indicates interaction between the host and the
bacteria.
19
1. Areas of relative quiescence, showing a relatively
flat surface with minor depressions and mounds
and occasional shedding of cells.
2. Areas of bacterial accumulation, which appear as
depressions on the epithelial surface, with
abundant debris and bacterial clumps
penetrating into the enlarged intercellular spaces.
These bacteria are mainly cocci, rods and
filaments, with a few spirochetes.
3. Areas of emergence of leukocytes, where
leukocytes appear in the pocket wall through
holes located in the intercellular spaces .
20
4. Areas of leukocyte-bacteria interaction, where
numerous leukocytes are present and covered
with bacteria in an apparent process of
phagocytosis. Bacterial plaque associated with
the epithelium is seen either as an organized
matrix covered by a fibrin-like material in contact
with the surface of cells or as bacteria penetrating
into the intercellular spaces.
5. Areas of intense epithelial desquamation, which
consist of semi-attached and folded epithelial
squames, sometimes partially covered with
bacteria .
21
6. Areas of ulceration, with exposed connective
tissue.
7. Areas of hemorrhage, with numerous
erythrocytes.
The transition from one area to another could be
postulated as follows:
 Bacteria accumulate in previously quiescent areas,
triggering the emergence of leukocytes and the
leukocyte-bacteria interaction.
 This would lead to intense epithelial desquamation
and finally to ulceration and hemorrhage.
22
Periodontal
Pockets as
Healing Lesions
Periodontal pockets as
healing lesions
 It is characterized by interplay of destructive and
constructive tissue changes
 The balance between destructive and constructive
changes determines clinical features such as color,
consistency and surface texture of the pocket wall.
24
25
Pocket contents
 Debris-
 Microorganisms and their products.
 Gingival fluid
 Food remnants
 Salivary mucin
 Desquamated epithelial cells
 Leucocytes
 Purulent exudate-
 Living, degenerated and necrotic leucocytes
 Living and dead bacteria
 Serum and scant amount of fibrin
26
Root Surface Wall
Periodontal Pocket
27
Root Surface Wall
 Pathologic granules
 Bacterial penetration causes fragmentation &
breakdown of cementum leading to necrotic
cementum
 Endotoxins
 Detected in cementum
 Diseased root fragments prevent attachment of
gingival fibroblasts
 Decalcification & Remineralization
 Ca, Mg, P& F are increased – resistant to decay
28
 Areas of Demineralization often related to
– Root Caries
 A. viscosus,
 A. naeslundii,
 S. mutans, sanguis,
 S. salivarius & Bacillus cereus.
29
30
Surface Morphology of the Tooth Wall of
Periodontal Pockets
31
Disease Activity
Site Specificity
32
PERIODONTAL DISEASE ACTIVITY
 Periodontal pockets go through periods of
exacerbation and quiescence, resulting
from episodic bursts of activity followed
by periods of remission
 Periods of quiescence and exacerbation
are also known as periods of activity and
inactivity
33
SITE SPECIFICITY
 Periodontal destruction does not occur in
all parts of the mouth at the same time
but rather on a few teeth at a time or
even only some aspects of some teeth at
any given time.
34
Relation
of Attachment Loss
And
Bone Loss To Pocket
Depth
Attachment Loss
Attachment Level
Pocket Depth
₪Attachment Level
₪C E J
₪Base of the Pocket
₪Pocket Depth:
₪Gingival Margin
₪Base of the Pocket
36
Same
Pocket Depth
With Different
Amounts of
Recession (CAL)
A, Gingival pocket with no recession.
B, Periodontal pocket of similar depth as in A, but with some degree
of recession.
C, Pocket depth same in A and B, but with still more recession.
37
Different Pocket
depths with the same
amount of
attachment loss
 Arrows point to bottom of the pocket.
 The distance between the arrow and the cementoenamel junctions
remains the same despite different pocket depths
38
Suprabony
and
Intrabony
Periodontal Pockets
Distinguishing Features of the Suprabony and
Intrabony Pockets
 The base of the pocket
is coronal to the level
of the alveolar bone.
 The pattern of
destruction of the
underlying bone is
horizontal.
 The base of the pocket
is apical to the crest of
the alveolar bone so
that the bone is
adjacent to the soft
tissue wall
 The bone destructive
pattern is vertical
(angular)
Suprabony
Pocket
Infrabony
Pocket
40
 Interproximally, the
transseptal fibers that
are restored during
progressive
periodontal disease
are arranged
horizontally in the
space between the
base of the pocket
and the alveolar bone
 Interproximally, the
transseptal fibers are
oblique rather than
horizontal. They extend
from the cementum
beneath the base of
the pocket along the
bone and over the
crest to the cementum
of the adjacent tooth
Suprabony
Pocket
Infrabony
Pocket
41
 On the facial and
lingual surfaces, the
periodontal ligament
fibers beneath the
pocket follow their
normal horizontal-
oblique course
between the tooth
and the bone
 On the facial and
lingual surfaces, the
periodontal ligament
fibers follow the
angular pattern of the
adjacent bone. They
extend from the
cementum beneath
the base of the pocket
along the bone and
over the crest to join
with the outer
periosteum.
Suprabony
Pocket
Infrabony
Pocket
42
PERIODONTAL
CYST
43
Origin:
Odontogenic cyst caused by
proliferation of the epithelial rests of
Malassez; the stimulus initiating the
cellular activity is not known.
Lateral dentigerous cyst retained in
the jaw after tooth eruption.
44
Primordial cyst of supernumerary
tooth germ.
Stimulation of epithelial rests of the
periodontal ligament by infection
from a periodontal abscess or the
pulp through an accessory root
canal.
45
A periodontal cyst is usually
asymptomatic and without grossly
detectable changes, but it may
present as a localized tender swelling.
46
Radiographic Appearance
47
An interproximal
periodontal cyst
appears on the
side of the root as
a radiolucent area
bordered by a
radiopaque line.
o Its radiographic appearance cannot be differentiated
from that of a periodontal abscess

Periodontal pocket copy.pptx perio mds ppt

  • 1.
  • 2.
    DEFINITION • “A pathologicallydeepened gingival sulcus.” 2 Dept. of Periodontics, PDCH
  • 3.
    CLASSIFICATION 1. Depending onmechanism of pocket formation. 2. Depending on the relation of the pocket base to the alveolar crest. 3. Depending on the number of surfaces involved. 3
  • 4.
    1.DEPENDING ON MECHANISM GINGIVALPOCKET / PSEUDO POCKET • Formed by gingival enlargement without destruction of underlying periodontal tissues. PERIODONTAL POCKET • Formed by apical migration of the junctional epithelium and destruction of supporting periodontal tissues. 4
  • 5.
    2.DEPENDING ON THERELATION BETWEEN POCKET BASE AND THE BONE CREST • SUPRABONY / SUPRACRESTAL / SUPRAALVEOLAR • Bottom of the pocket is coronal to the underlying alveolar bone. • INFRABONY / INTRABONY / SUBCRESTAL / INTRAALVEOLAR • Bottom of the pocket is apical to the level of alveolar bone. 5
  • 6.
    3.DEPENDING ON THENUMBER OF SURFACES INVOLVED SIMPLE POCKET COMPOUND POCKET COMPLEX/SPIRAL POCKET. 6
  • 7.
    CLINICAL FEATURES SIGNS-  EnlargedBluish red thickened marginal gingiva.  Bluish red vertical zone from margin to alveolar mucosa.  Bleeding.  Suppuration.  Tooth mobility.  Diastema formation.  Pain- Localized or Deep in the bone.  Careful periodontal probing is the only way to locate the pocket and to determine its full extent. 7
  • 8.
    SYMPTOMS-  Localized painor sensation of pressure after eating.  Foul taste  Tendency to suck materials  Radiating pain deep in bone  Gnawing or itching in gingiva  Food lodgment  Sensitivity to heat and cold  Pain 8
  • 9.
  • 10.
    • Healthy gingiva- Few microbes—Coccoid cells and straight rods. • Diseased gingiva — increased no. of spirochetes and motile rods. • Changes in the microflora accompany the transition from gingival sulcus to periodontal pocket. 10 Dept. of Periodontics, PDCH
  • 11.
    Plaque accumulation Inflammatory Exudate Cells & fluid Inflammatory mediators destroys Gingival fibers Cellsform MMPs, Fibroblasts phagocytose collagen Cells of J.E. Proliferate apically, Coronal cells detach Gingiva is bulky, separates apically Pathogene sis • Pocket formation starts as an inflammatory change in C.T wall of gingival sulcus 11
  • 12.
     Collagen destructionby 2 mechanisms- 1. Collagenase secreted by fibroblasts, phagocytes and macrophages become extracellular and destroy collagen. 2. Fibroblasts phagocytize collagen fibers by extending cytoplasmic processes.  Apical cells of JE proliferate along the root and extend fingerlike projections.  PMNs invade coronal end of JE.  PMNs volume reaches 60% or more of JE loses cohesiveness. Coronal portion of JE detaches from root and apical portion migrates . Dept. of Periodontics, PDCH 12
  • 13.
  • 14.
    SOFT-TISSUE WALL • Epitheliumat the gingival crest is generally intact and thickened. • Junctional Epithelium is reduced in height, only 50-100 microns. Cells may exhibit slight to moderate degeneration. • Connective tissue is edematous, densely infiltrated with plasma cells, lymphocytes & PMNs. • Blood vessels are numerous, dilated, engorged. • Varying degrees of degenerative and necrotic changes are seen. 14
  • 15.
    Lateral wall ofpocket:  Shows maximum degenerative changes.  Epithelium proliferates & extends into the adjacent inflamed connective tissue.  This epithelium is densely infiltrated by WBCs & edema.  The cells undergo degeneration and form vesicles.  Progressive necrosis give rise to ulceration of lateral wall, exposure of the C.T. and suppuration. 15
  • 16.
     Severity ofdegenerative changes is not dependent on depth of pocket. Suppuration and ulceration may be seen with a shallow pocket and not with a deep one and vice versa.  On comparison, it was shown that the aggressive cases show more degenerative changes than the chronic ones. 16
  • 17.
    Bacterial Invasion  Periodontitiscases show bacterial invasion of the lateral and apical areas of pocket wall.  Intercellular spaces of epithelium show presence of filaments, rods, coccoid forms with Gram negative cell wall.  Bacteria are seen in the exfoliating cells, between deeper epithelial cells, on basement lamina and also in the subepithelial connective tissue. 17
  • 18.
    MICROTOPOGRAPHY OF THE GINGIVALWALL OF THE POCKET 18
  • 19.
     Scanning electronmicroscopy of the lateral wall of the pocket reveals areas that are irregularly oval or elongated and adjacent to one another.  Each area measures around 50-200microns.  Transition from one area to another is a rule and it indicates interaction between the host and the bacteria. 19
  • 20.
    1. Areas ofrelative quiescence, showing a relatively flat surface with minor depressions and mounds and occasional shedding of cells. 2. Areas of bacterial accumulation, which appear as depressions on the epithelial surface, with abundant debris and bacterial clumps penetrating into the enlarged intercellular spaces. These bacteria are mainly cocci, rods and filaments, with a few spirochetes. 3. Areas of emergence of leukocytes, where leukocytes appear in the pocket wall through holes located in the intercellular spaces . 20
  • 21.
    4. Areas ofleukocyte-bacteria interaction, where numerous leukocytes are present and covered with bacteria in an apparent process of phagocytosis. Bacterial plaque associated with the epithelium is seen either as an organized matrix covered by a fibrin-like material in contact with the surface of cells or as bacteria penetrating into the intercellular spaces. 5. Areas of intense epithelial desquamation, which consist of semi-attached and folded epithelial squames, sometimes partially covered with bacteria . 21
  • 22.
    6. Areas ofulceration, with exposed connective tissue. 7. Areas of hemorrhage, with numerous erythrocytes. The transition from one area to another could be postulated as follows:  Bacteria accumulate in previously quiescent areas, triggering the emergence of leukocytes and the leukocyte-bacteria interaction.  This would lead to intense epithelial desquamation and finally to ulceration and hemorrhage. 22
  • 23.
  • 24.
    Periodontal pockets as healinglesions  It is characterized by interplay of destructive and constructive tissue changes  The balance between destructive and constructive changes determines clinical features such as color, consistency and surface texture of the pocket wall. 24
  • 25.
  • 26.
    Pocket contents  Debris- Microorganisms and their products.  Gingival fluid  Food remnants  Salivary mucin  Desquamated epithelial cells  Leucocytes  Purulent exudate-  Living, degenerated and necrotic leucocytes  Living and dead bacteria  Serum and scant amount of fibrin 26
  • 27.
  • 28.
    Root Surface Wall Pathologic granules  Bacterial penetration causes fragmentation & breakdown of cementum leading to necrotic cementum  Endotoxins  Detected in cementum  Diseased root fragments prevent attachment of gingival fibroblasts  Decalcification & Remineralization  Ca, Mg, P& F are increased – resistant to decay 28
  • 29.
     Areas ofDemineralization often related to – Root Caries  A. viscosus,  A. naeslundii,  S. mutans, sanguis,  S. salivarius & Bacillus cereus. 29
  • 30.
    30 Surface Morphology ofthe Tooth Wall of Periodontal Pockets
  • 31.
  • 32.
  • 33.
    PERIODONTAL DISEASE ACTIVITY Periodontal pockets go through periods of exacerbation and quiescence, resulting from episodic bursts of activity followed by periods of remission  Periods of quiescence and exacerbation are also known as periods of activity and inactivity 33
  • 34.
    SITE SPECIFICITY  Periodontaldestruction does not occur in all parts of the mouth at the same time but rather on a few teeth at a time or even only some aspects of some teeth at any given time. 34
  • 35.
    Relation of Attachment Loss And BoneLoss To Pocket Depth Attachment Loss Attachment Level Pocket Depth ₪Attachment Level ₪C E J ₪Base of the Pocket ₪Pocket Depth: ₪Gingival Margin ₪Base of the Pocket
  • 36.
  • 37.
    Same Pocket Depth With Different Amountsof Recession (CAL) A, Gingival pocket with no recession. B, Periodontal pocket of similar depth as in A, but with some degree of recession. C, Pocket depth same in A and B, but with still more recession. 37
  • 38.
    Different Pocket depths withthe same amount of attachment loss  Arrows point to bottom of the pocket.  The distance between the arrow and the cementoenamel junctions remains the same despite different pocket depths 38
  • 39.
  • 40.
    Distinguishing Features ofthe Suprabony and Intrabony Pockets  The base of the pocket is coronal to the level of the alveolar bone.  The pattern of destruction of the underlying bone is horizontal.  The base of the pocket is apical to the crest of the alveolar bone so that the bone is adjacent to the soft tissue wall  The bone destructive pattern is vertical (angular) Suprabony Pocket Infrabony Pocket 40
  • 41.
     Interproximally, the transseptalfibers that are restored during progressive periodontal disease are arranged horizontally in the space between the base of the pocket and the alveolar bone  Interproximally, the transseptal fibers are oblique rather than horizontal. They extend from the cementum beneath the base of the pocket along the bone and over the crest to the cementum of the adjacent tooth Suprabony Pocket Infrabony Pocket 41
  • 42.
     On thefacial and lingual surfaces, the periodontal ligament fibers beneath the pocket follow their normal horizontal- oblique course between the tooth and the bone  On the facial and lingual surfaces, the periodontal ligament fibers follow the angular pattern of the adjacent bone. They extend from the cementum beneath the base of the pocket along the bone and over the crest to join with the outer periosteum. Suprabony Pocket Infrabony Pocket 42
  • 43.
  • 44.
    Origin: Odontogenic cyst causedby proliferation of the epithelial rests of Malassez; the stimulus initiating the cellular activity is not known. Lateral dentigerous cyst retained in the jaw after tooth eruption. 44
  • 45.
    Primordial cyst ofsupernumerary tooth germ. Stimulation of epithelial rests of the periodontal ligament by infection from a periodontal abscess or the pulp through an accessory root canal. 45
  • 46.
    A periodontal cystis usually asymptomatic and without grossly detectable changes, but it may present as a localized tender swelling. 46
  • 47.
    Radiographic Appearance 47 An interproximal periodontalcyst appears on the side of the root as a radiolucent area bordered by a radiopaque line. o Its radiographic appearance cannot be differentiated from that of a periodontal abscess