PERIODONTAL POCKET

1. PERIODONTAL
POCKET
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2. INTRODUCTION
Periodontitis is defined as “an inflammatory disease of
the supporting tissues of the teeth caused by specific
organisms or groups of specific organisms, resulting in
progressive destruction of the periodontal ligament
and alveolar bone with pocket formation, recession or
both.”
Pocket formation is one of the characteristic feature
of periodontitis.
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3. It is the pathologically deepened gingival
sulcus.
One of the most important clinical feature
of the periodontal diseases.

4. •CLASSIFICATION OF POCKETS
Gingival pocket (pseudo
pocket, False Pocket
,Relative Pocket): This type
of pocket formed by gingival
enlargement without
destruction of the underlying
periodontal tissues. The
sulcus deepened because of
the increased bulk of the
gingiva.
Periodontal pocket (True
Pocket /Absolute Pocket )
: This type of pocket occurs
with destruction of the
supporting periodontal
tissues, Progressive pocket
deepening leads to
destruction of supporting
periodontal tissues and
loosening and exfoliation of
the teeth.
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5. Suprabony (Supracrestal
or supraalveolar) in which
the bottom of the pocket is
coronal to the underlying
alveolar bone.
Intrabony (infrabony,
subcrestal or
intraalveolar) in which the
bottom of the pocket is
apical to the level of the
adjacent alveolar bone. In
this second type, the lateral
pocket wall lies between
the tooth surface and the
alveolar bone
PERIODONTAL POCKET IS CLASSIFIED AS:
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6. •Involves one tooth surface
Simple:.
•Involves 2 or more tooth surfaces. The base of the pocket is in
direct communication with gingival margin along each of the
involved surfaces
Compound:.
•Spiral type of pocket that originates on one tooth surface and
twists around the tooth to involve one or more additional surfaces.
These types of pockets are most common in furcation areas
Complex:.
ACCORDING TO INVOLVED TOOTH SURFACES
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7. •CLINICAL FEATURES
SIGNS
Enlarged, bluish red marginal gingiva with a “rolled” edge separated from the tooth
surface
A reddish blue vertical zone from the gingival margin to the attached gingiva, &
sometimes into the alveolar mucosa
A break In the faciolingual continuity of the interdental gingiva
Shiny, discolored & puffy gingiva associated with exposed root surfaces
Gingival bleeding
Purulent exudates at the gingival margin or its appearance in response to digital pressure
on the lateral aspect of the gingival margin
Looseness, extrusion & migration of teeth
The development of diastema where none had existed
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8. Localized pain or a sensation of pressure after eating which gradually diminishes
Foul taste in localized area
Tendency to suck material from the interproximal spaces
Radiating pain “deep in the bone” which is worse on rainy days
A “gnawing” feeling or feeling of itchiness in the gums sometimes described as feeling like
“worms’
Urge to dig a pointed instrument into the gums with relief from the resultant bleeding
Complaints that food “sticks between the teeth”
The teeth “feel loose” or preference to “eat on the other side”
Sensitivity to heat & cold
Toothache in the absence of caries
SYMPTOMS
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9. 9

10. • Only accurate method – Careful
exploration with periodontal probe.
• CANNOT BE DETECTED ON RADIOGRAPH
• Gutta percha points or calibrated silver
point’s can be used with the radiographs.
DETECTION OF PERIODONTAL POCKETS

11. • Biologic or Histologic Depth – Gingival margin to base of
pocket (Coronal end of JE).
• Clinical or Probing Depth – Distance to which probe
penetrates into the pocket.
• Probing depth depend on
Direction of penetration
Force
Size of probe
Resistance of tissue
Convexity of crown
Pocket Probing

12. • Probe tip penetrates to the most coronal
intact fibers of connective tissue attachment.
• Force 0.75 N.
• Intraexaminer error 2.1 mm (avg 1.5 mm)

13. PROBING TECHNIQUE
The probe should be inserted parallel to the
vertical axis of the tooth and "walked"
circumferentially around each surface of each
tooth to detect the areas of deepest
penetration.
To detect an interdental crater, the probe
should be placed obliquely from both the
facial and lingual surfaces so as to explore the
deepest point of the pocket located beneath
the contact point.
In multirooted teeth the possibility of
furcation involvement should be carefully
explored. The use of specially designed
probes (e.g., Nabers probe)
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14. PROBING AROUND IMPLANTS
• To prevent scratching of the implant surface, plastic
periodontal probes should be used instead of the usual steel
probes used for the natural dentition.
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15. Etiopathogenesis

16. Toxins in plaque destroy the gum and connective tissues
beneath the gumline
The gums pull away from the teeth, forming a pocket (space)
The pocket fills with plaque and calculus
The bone and connective tissue surrounding the tooth may
become severely damaged
Tooth will fall out or need to be extracted.
If not treated
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17. Two mechanisms are considered to be
associated with collagen loss:
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(1) Collagenases and other enzymes secreted by various
cells in healthy and inflamed tissue such as fibroblasts,
polymorphonuclear leukocytes, and macrophages become
extracellular and destroy collagen; these enzymes that
degrade collagen and other matrix macromolecules into
small peptides are called matrix metalloproteinases;
(2) Fibroblasts phagocytize collagen fibers by extending
cytoplasmic processes to the ligament-cementum interface
and degrade the inserted collagen fibrils and the fibrils of
the cementum matrix.

18. Loss of collagen
the apical cells of the junctional epithelium proliferate
along the root, extending fingerlike projections two or
three cells in thickness
The coronal portion of the junctional epithelium
detaches from the root as the apical portion migrates.
polymorphonuclear neutrophils (PMNs) invade the
coronal end of the junctional epithelium in increasing
numbers
the tissue loses cohesiveness and detaches from the
tooth surface.
the sulcus bottom shifts apically, and the oral sulcular epithelium
occupies a gradually increasing portion of the sulcular (pocket)
lining.
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19. • Extension of the junctional epithelium along
the root requires the presence of healthy
epithelial cells.
• Marked degeneration or necrosis of the
junctional epithelium retards rather than
accelerates pocket formation.
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20. • Degenerative changes seen in the junctional
epithelium at the base of periodontal pockets
are usually less severe than those in the
epithelium of the lateral pocket wall.
• Leukocyte infiltration to the JE is
independent of the volume of inflamed CT.
• Gingiva increases in bulk & crest of the
marginal gingiva extends coronally.

21. • JE continues to migrate along the root &
separate from it.
• The epithelium of the lateral wall of the pocket
proliferates to form bulbous, cordlike extension
into the inflamed CT.
• Leukocytes & edema from the inflamed CT
infiltrate the epithelial lining the pocket, resulting
in various degrees of degeneration & necrosis.

22. • The transformation of a gingival sulcus into a periodontal
pocket creates an area where plaque removal becomes
impossible, and the following feedback mechanism is
established:
PLAQUE
GINGIVAL
INFLAMM
ATION
POCKET
FORMATIO
N
The rationale for pocket
reduction is based on the
need to eliminate areas of
plaque accumulation
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23. •HISTOPATHOLOGY
SOFT TISSUE WALL
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24. • Connective tissue- The connective tissue is
edematous and densely infiltrated with plasma cells
(approximately 80%), lymphocytes, and a scattering of
PMNs.
• The connective tissue exhibits varying degrees of
degeneration and shows proliferation of the endothelial
cells, with newly formed capillaries, fibroblasts, and
collagen fibers.
• Blood vessels- The blood vessels are increased in
number, dilated, and engorged, particularly in the
subepithelial connective tissue layer.
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25. • Junctional Epithelium- The junctional epithelium
at the base of the pocket is usually much shorter than that
of a normal sulcus. Although marked variations are found
as to length, width, and condition of the epithelial cells,
usually the coronoapical length of the junctional
epithelium is reduced to only 50 to 100 μm. The cells may
be well formed and in good condition or may exhibit slight
to marked degeneration.
• Lateral wall of pocket- The most severe
degenerative changes.
• The epithelium of the lateral wall of the pocket presents
striking proliferative and degenerative changes.
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26. • Epithelial buds or interlacing cords of epithelial cells
project from the lateral wall into the adjacent inflamed
connective tissue and may extend farther apically than
the junctional epithelium.
• These epithelial projections, as well as the remainder
of the lateral epithelium, are densely infiltrated by
leukocytes and edema from the inflamed connective
tissue.
• The cells undergo vacuolar degeneration and rupture
to form vesicles.
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27. • Progressive degeneration and necrosis of the
epithelium lead to ulceration of the lateral wall,
exposure of the underlying inflamed connective
tissue, and suppuration. In some cases, acute
inflammation is superimposed on the underlying
chronic changes.
• The severity of the degenerative changes is not
necessarily related to pocket depth.
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28. • Chronic Periodontitis –
Filaments, rods & coccoid organisms.
Predominant gram negative.
• P. gingivalis & P. intermedia in gingiva of Aggressive
Periodontitis patients.
AA has also been found in the tissues.
Bacterial Invasion

29. • Bacteria may invade the intercellular space under
exfoliating epithelial cells.
• Also found bet deeper epithelial cells &
accumulating on the basement lamina.
• Some bacteria may invade the subepithelial CT.
• The presence of bacteria in the gingival tissues –
bacterial invasion or passive translocation of plaque
bacteria.

31. GOOD
AERNOON
31
LETS
CONTINUE
WITH
PERIODONTAL
POCKET…

32. • SEM describe several area with different types of
activity.
• These areas are irregularly oval or elongated & adjacent
to one another & measure about 50-200 µm.
• Pocket wall is constantly changing.
Microtophography of the Gingival Wall of the
Pocket

33. 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.
Following areas have been noted:
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34. 4. Areas of leukocyte-bacteria interaction, where numerous leukocytes
are present and covered with bacteria in an apparent process of
Phagocytosis.
5. Areas of intense epithelial desquamation, which consist of semi-
attached and folded epithelial squames, sometimes partially covered
with bacteria.
6. Areas of ulceration, with exposed connective tissue.
7. Areas of hemorrhage, with numerous erythrocytes.
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35. • Pocket constantly undergo repair.
• Complete healing dose not occur.
• The balance between the destructive & constructive
determines the clinical features such as color,
consistency & surface texture of the pocket wall.
Periodontal Pocket as Healing Lesions

36. • When the inflammatory fluid & cellular exudate
predominate – edematous pocket wall.
• If there is relative predominance of newly formed CT
cells & fibers – fibrotic pocket wall.

37. • Most severe degenerative changes in periodontal
tissues occur adjacent to the tooth surface &
subgingival plaque.
• In some cases, inflammation & ulceration are walled
off by fibrous tissue on the outer aspect.
• Externally pink & fibrotic, despite the inflammatory
changes occurring internally.

38. CONTENTS OF THE PERIODONTAL POCKET
• Periodontal pockets contain debris consisting principally
of:
• Microorganisms and their products (enzymes, endo-
toxins, and other metabolic products),
• Food remnants,
• Salivary mucin,
• Gingival fluid,
• Desquamated epithelial cells, and
• Leukocytes
• Purulent exudates, if present, consists of living,
degenerated, and necrotic leukocytes; living and dead
bacteria; serum; and a scant amount of fibrin.
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39. Importance of Pus Formation
• Pus is a common feature of periodontal
disease, but it is only a secondary sign.
• The presence of pus expressed from the pocket is not an
indication of the depth of the pocket or the severity of the
destruction of the supporting tissues. It merely reflects the
nature of the inflammatory changes in the pocket wall.
Extensive pus formation may occur in shallow pockets,
whereas deep pockets may exhibit little or no pus.
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40. • Often undergo changes that are significant because
they may perpetuate the periodontal infection, cause
pain & complicate periodontal treatment.
• As the pocket deepens, collagen fibers embedded in
the cementum are destroyed & cementum become
exposed to oral environment.
• Collagenous remnant of sharpey’s fibers in the
cementum undergo degeneration, creating an
environment favorable to the penetration of the
bacteria.
Root Surface Wall

41. • Bacterial penetration into the cementum can be
found as deep as CEJ & may also enter dentinal
tubules.
• Pathologic granules – Areas of collagen
degeneration & areas where collagen fibrils have
not been fully mineralized initially.

42. • Penetration & growth of bacteria leads to
fragmentation & breakdown of cementum
surface & result in areas of necrotic
cementum.
• Bacterial endotoxins have also been detected
in cemental wall of periodontal pockets.

43. • Softening of cemental surface is usually
asymptomatic but can be painful when a probe or
explorer penetrates the area.
• Removed by root planing until a hard, smooth
surface is reached.

44. • Areas of increased mineralization – Exchange, on
exposure to oral cavity, of minerals & organic
components at cementum-saliva interface.
• Mineral content increases.
• Microhardness remains unchanged.
• Development of highly mineralized superficial layer
may increase the tooth resistance to decay.
•Decalcification & Remineralization of Cementum

45. • Often related to root caries.
• Exposure to oral fluid & bacterial plaque
results in proteolysis of the embedded
remnants of sharpey’s fibers: cementum may be
softened & may undergoes fragmentation &
cavitations.
• Dominant bacteria is Actinomyces viscosus.
• Other – A. naeslundii, S. mutans, S. salivaris, S.
sanguis
•Areas of Demineralization

46. • Tooth may not be painful, but exploration of the
root surface reveals the presence of the defect &
penetration of the involved area with a probe
causes pain.
• Root caries may be the cause of toothache.

47. • If the root is exposed by progressive pocket
formation before repair occur, these areas appear
as isolated cavitations that penetrate into dentin.
• Clear cut outline & hard surface.
• They may be sources of considerable pain, requiring
placement of restorations.
•Areas of Cellular Resorption of Cementum &
Dentin

48. •where all the changes described in the preceding paragraphs can be found.
1. Cementum covered by calculus:
•which covers calculus and extends apically from it to a variable degree, probably 100 to
500µm.
2. Attached plaque:
•that surrounds attached plaque and extends apically to it.
3. The zone of unattached plaque:
•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.
4. The zone where the junctional epithelium is attached to the tooth:
•there may be a zone of semidestroyed connective tissue fibers.
5. Apical to the junctional epithelium:
Surface Morphology of the Tooth Wall of Periodontal Pockets
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49. Diagram of the area at the bottom of a pocket.
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50. Periodontal Disease Activity
Periods of quiescence are characterized by a reduced
inflammatory response and little or no loss of bone
and connective tissue attachment.
Period of exacerbation starts with a buildup of un-
attached plaque, with its gram-negative, motile, and
anaerobic bacteria in which bone and connective
tissue attachment are lost and the pocket deepens.
According to this concept, periodontal pockets go through
periods of exacerbation and quiescence, resulting from
episodic bursts of activity followed by periods of remission.
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51. • The period of exacerbation may last for days,
weeks, or months and is eventually followed by a
period of remission or quiescence in which gram-
positive bacteria proliferate and a more stable
condition is established.
• These periods of quiescence and exacerbation are
also known as periods of inactivity and activity.
•
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52. •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.
This is referred to as the site specificity of periodontal
disease.
• It is very common to find sites of periodontal destruction
next to sites with little or no destruction. Therefore the
severity of periodontitis increases by the development of
new disease sites, the increased breakdown of existing sites,
or both.
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53. • RELATION OF ATTACHMENT LOSS AND BONE
LOSS TO POCKET DEPTH
This is because the degree of
attachment loss depends on the
location of the base of the pocket on
the root surface, whereas the pocket
depth is the distance between the
base of the pocket and the crest of
the gingival margin.
Pocket formation causes loss of attachment of the gingiva
and denudation of the root surface. The severity of the
attachment loss is generally, but not always, correlated with
the depth of the pocket.
Pockets of the same depth may be associated with different
degrees of attachment loss, and pockets of different depths
may be associated with the same amount of attachment loss.
Same Pocket Depth with different
amounts of Recession
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54. Different Pocket Depths with same amount of
attachment loss
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55. AREA BETWEEN THE BASE OF THE POCKET AND THE
ALVEOLAR BONE
• Normally, the distance between the apical end of the
junctional epithelium and the alveolar bone is relatively
constant. The distance between the apical extent of
calculus and the alveolar crest in human periodontal
pockets is most constant, having a mean length of 1.97
mm ± 33.16%.
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56. RELATIONSHIP OF THE PERIODONTAL POCKET TO
BONE
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Suprabony Pockets Infrabony Pockets
Base of pocket is coronal to
alveolar bone
Base of pocket is apical to the crest
of alveolar bone
Bone destructive pattern is horizontal Pattern of bone destruction is vertical
Interproximally, transseptal fibers
restored during progressive
periodontal disease are arranged
horizontally.
Transseptal fibers are oblique
On facial and lingual surfaces, PDL
fibers beneath the pocket follow
normal horizontal-oblique course
between tooth and bone.
PDL fibers follow angular pattern of
adjacent bone

57. • It is a localized purulent inflammation in the
periodontal tissues.
• Also known as lateral or parietal abscess.
Periodontal Abscess

58. 1. Extension of infection from a periodontal pocket deeply into the supporting
periodontal tissues and localization of the suppurative inflammatory process
along the lateral aspect of the root.
2. Lateral extension of inflammation from the inner surface of a periodontal
pocket into the connective tissue of the pocket wall. Localization of the
abscess results when drainage into the pocket space is impaired.
3. In a pocket that describes a tortuous course around the root, a periodontal
abscess may form in the cul-de-sac, the deep end of which is shut off from the
surface.
4. Incomplete removal of calculus during treatment of a periodontal pocket. In
this instance, the gingival wall shrinks, occluding the pocket orifice, and a
periodontal abscess occurs in the sealed-off portion of the pocket.
5. A periodontal abscess may occur in the absence of periodontal disease after
trauma to the tooth or perforation of the lateral wall of the root in endodontic
therapy.
Periodontal abscess formation may occur in the following ways:
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59. • Abscess in the supporting periodontal tissue along
the lateral aspect of the root. Sinus generally occurs
in the bone that extends laterally from the abscess
to the external surface.
• Abscess from the soft tissue wall of the deep
periodontal pocket.
Classification According to the Location

60. • Localized accumulation of viable & nonviable PMNs
within the periodontal pocket wall.
• Pus constitute the centre of the abscess.
• An acute inflammatory reaction surrounds the
purulent area & the overlying epithelium exhibits
intracellular & extracellular edema & invasion of
leukocytes.
• A localized acute abscess become a chronic abscess.
Microscopy