4. GINGIVAL POCKET [ false ]
Formed by gingival enlargement without
destruction of underlying periodontal tissue
5. PERIODONTAL POCKET [ absolute or true ]
Occurs with destruction of the supporting
periodontal tissues
THESE ARE 2 TYPES :
6. i. SUPRABONY
Bottom of the pocket is coronal to the
underlying Al.bone
ii. INFRABONY
Bottom of the pocket is apical to level of
adjacent Al.bone
7. A B C
A. GINGIVAL POCKET: There is no destruction of the
supporting periodontal tissues
B. SUPRABONY POCKET: The base of the pocket is Coronal
to the level of underlying bone. Boneloss is horizontal
C. INFRABONY POCKET: The base of the pocket is apical
to the level of adjacent bone. Boneloss is vertical
8. II ACCORDING TO NO. OF SURFACES INVOLVED
SIMPLE
COMPOUND COMPLEX
10. b. COMPOUND
Involves 2 or more tooth surfaces
Here the base of the pocket is in direct
communication with the gingival margin along
each of the involved tooth surfaces
b
11. C. COMPLEX
It is a spiral type of pocket that originates on
one tooth surface and twists around the tooth
to involve one or more additional surfaces
The only communication with the gingival margin is
at the surface where the pocket originates
Most common in furcation areas C
13. CLINICAL FEATURES
SIGNS
enlarged, bluish red marginal gingiva with
“rolled” edge separated from tooth surface
a reddish blue vertical zone extending from
gingival margin to attached gingiva
a break in the facio-lingual continuity of the
interdental gingiva
14. shiny, discolored, puffy gingiva associated with
exposed root surfaces
gingival bleeding
purulent exudate of gingival margin
looseness,extrusion and migration of the teeth
15. SYMPTOMS
localized pain or sensation of pressure after eating
foul taste in localized areas
tendency to suck material from interproximal spaces
radiating pain “deep in the bone”
feeling of itchiness in the gums
urge to dig a pointed instrument deep into the gums
with relief obtained from the resultant bleeding
complains that food sticks between the teeth
16. PATHOGENESIS
Periodontal pockets are caused by micro-organisms
and their products, which produce pathologic tissue
changes that lead to deepening of the gingival sulcus
17. Pocket formation starts as inflammatory
change in the CT wall of the gingival sulcus
caused by bacterial plaque
The cellular and fluid inflammatory exudate
causes degeneration of connective tissue, including
the gingival fibers
18. Just apical to the JE, an area of destroyed
collagen fibers develops and becomes occupied
by inflammatory cells and edema. Immediately
apical to this, an area of normal attachment
19. Two hypothesis have been advanced regarding the
mechanism of collagen loss
1] collagenase and other lysozomal enzymes from
PMNLs and macrophages become extracellular
and destroy collagen
2] fibroblasts phagocytose collagen fibers
20. As a consequence of the loss of collagen,
the apical portion of JE proliferates along the root
The coronal portion of the JE detaches
from the root as apical portion migrates. PMNs
invade the coronal end of junctional epithelium
21. When the relative volume of PMNs reaches
60% or more of JE. It detaches from the tooth surface
Thus the sulcus bottom shifts apically, and
the oral sulcular epithelium occupies a gradually
increasing portion of the sulcus
22. HISTOLOGICAL FEATURES
SOFT TISSUE WALL
The connective tissue is edematous and
densely infiltrated with plasma cells [appr 80%]
lymphocytes and a scattering of PMNs cells
The blood vessels are increased in number,
dilated, and engorged
The connective tissue shows proliferation of
endothelial cells, with newly formed capillaries,
fibroblasts, and collagen fibers
23. The most severe degenerative changes in the
periodontal pocket occur along the lateral wall
Epithelial buds or interlacing cords of
epithelial cells project from the lateral wall into
the adjacent inflamed CT and frequently extent
farther apically than the JE
The cells undergo degeneration and rupture
to form vesicles
24. Progressive degeneration and necrosis of
epithelium lead to ulceration of the lateral wall,
exposure of the underlying inflamed connective
tissue and suppuration
The epithelium at the gingival crest of
periodontal pocket is generally intact and
thickened, with prominent rete pegs
25. BACTERIAL INVASION
Filaments, rods, and coccoid organisms with
predominant gram-negative cells have been
found in intercellular spaces of epithelium
Some bacteria travel basement membrane lamina
and invade the sub-epithelial connective tissue
26. MICROSCOPIC FEATURES
THERE ARE SEVERAL AREAS IN THE SOFT TISSUE
WALL OF POCKET WHERE DIFFERENT TYPES OF
ACTIVITY TAKE PLACE:
1. AREAS OF RELATIVE QUIESCENCE: shows a
relatively flat surface with minor depressions and
occasional shedding of cells
27. 2. AREAS OF BACTERIAL ACCUMULATION: shows
abundant debris and bacterial clamps penetrating
into the enlarged intercellular spaces
These bacteria are mainly cocci, rods and filaments
with few spirochetes
28. 3. AREAS OF EMERGENCE OF LEUKOCYTES:
Leukocytes appear in the pocket wall through
holes located in the intercellur spaces
4. AREAS OF LEUKOCYTE-BACTERIAL INTERACTION:
Numerous leukocytes covered with bacteria
29. 5. AREAS OF INTENSE EPITHELIAL DESQUAMATION:
semi-attached and folded epithelial squames
6. AREAS OF ULCERATION: exposed CT
7. AREAS OF HEMORRHAGE: numerous erythrocytes
30. PERIO . POCKETS AS HEALING LESIONS
The condition of soft tissue wall of the
periodontal pocket results from the interplay of
destructive and constructive tissue changes
31. The destructive changes are characterized
by fluid and cellular inflammatory exudate
and by the associated degenerative changes
initiated by plaque bacteria
The constructive changes consists of the
formation of blood vessels in an effort to
repair tissue damage caused by inflammation
32. The balance between destructive and
constructive changes determines clinical features
such as color , consistency, and surface texture
of the pocket wall
33. POCKET CONTENTS
MICROORGANISMS AND THEIR PRODUCTS
[enzymes, endotoxins, and other metabolic Products]
DENTAL PLAQUE, GINGIVAL FLUID, FOOD REMNENTS,
SALIVARY MUCIN, DESQUAMATED EPITHELIAL CELLS,
AND LEUKOCYTES
34. ROOT SURFACE WALL
CHANGES IN CEMENTUM CAN BE STRUCTURAL,
CHEMICAL AND CYTOTOXIC FEATURES
a] STRUCTURAL CHANGES
i] presence of pathological granules :
These represent areas of collagen degeneration
or areas of where collagen fibrils had not been
fully mineralized
35. ii] areas of increased mineralization:
This is the result of exposure of cementum to
minerals & organic components of oral cavity
36. iii] areas of demineralization:
Exposure to oral fluids and bacterial plaque
results in proteolysis of embedded remnants of
sharpeys fibres; the cementum may be softened
and undergo fragmentation and cavitation
Involvement of cementum is followed by
penetration of bacteria into dentinal tubules,
resulting in destruction of dentin
37. In severe cases, large sections of necrotic
cementum become detached from the tooth and
separated from it by masses of bacteria
The dominant microorganisms in
root surface caries is actinomyces viscosus
38. CHEMICAL CHANGES:
The mineral content of exposed cementum is
increased such as calcium
magnesium
phosphorus
fluoride
40. 1.CEMENTUM COVERED BY CALCULUS
2.ATTACHED PLAQUE WHICH IS
COVERED BY CALCULUS
3.ZONE OF UN-ATTACHED PLAQUE
THAT SURROUNDS ATTACHEDPLAQUE
4.ZONE WHERE THE JE IS ATTACHED
TO THE TOOTH
5.APICAL TO JE THERE IS ZONE OF
SEMI-DESTROYED CT FIBRES
AREAS 3, 4, 5, COMPOSE THE
PLAQUE-FREE ZONE SEEN IN THE
EXTRACTED TEETH
PLAQUE – FREE ZONE