classification, clinical and radiographic features ,histopathology of periodontal pockets

1. PERIODONTAL
POCKET
Dr. D.Navya, MDS

2. INTRODUCTION
 Periodontal pocket is defined as
a pathologically deepened gingival
sulcus [Carranza,10th Edi]
 A pathologic fissure between a tooth and the
crevicular epithelium, and limited at its apex by the
junctional epithelium. [GPT]
 Clinically speaking, the lesion should be termed a
“diseased gingival attachment”
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SAUL SCHLUGER, RALPH YUODELIS, ROY C PAGE, ROBERT H. JOHNSON
Periodontal Diseases 2nd Edition

3. CLASSIFICATION
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4. SUPRABONY
 base of pocket is
coronal to the crest of
the bone.
 Horizontal bone loss
 Interproximally,
transseptal fibers are
arranged horizontally
 Pdl fibers are
arranged in their
normal pattern
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•Apical
•Vertical / Angular bone
loss
•Interproximally,
transseptal fibers are
arranged obliquely
•Angular pattern
INFRABONY

5. CLASSIFICATION
 Simple Compound
Complex/Spiral
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6. ACTIVE & INACTIVE
POCKETS
 Active pocket :-
 underlying bone Is lost
 diagnosed clinically by bleeding
Inactive pocket:
 after phase I therapy the inflammatory changes in
pocket wall subside, rendering the pocket inactive
with decreased depth.
 They may heal by long junctional epithelium
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7. CLINICAL FEATURES
 a bluish – red vertical zone from the gingival
margin to the alveolar mucosa
 gingival bleeding
 suppuration
 tooth mobility
 diastema formation
 localized pain or pain “deep in the bone”
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8. Clinical
Features
 Bluish red
discoloration
 Flaccidity
 Smooth & shiny
surface
 Pitting on pressure
 Gingival wall- pink &
firm
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Histopathological
Features
 Circulatory
stagnation
 Destruction of
gingival fibers
 Atrophy of
epithelium & edema
 Edema &
degeneration
 Predominant Fibrotic
changes

9. Clinical
Features
 Bleeding on probing
 Pain On Probing
 Pus
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Histopathological
Features
 Increased
vasculature
 Degeneration of
epithelium
 Ulceration
 Suppurative
inflammation

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11. HISTOPATHOLOGY
SOFT TISSUE WALL
 Connective tissue – edematous, with plasma
cells(80%),PMNs (scattered)
- shows proliferative and
degenerative changes
 Blood Vessels – dilated, engorged, increase in
no.
 JE – Shorter than normal sulcus
 Severe degeneration occurs at lateral wall
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12. MICROTOPOGRAPHY OF
GINGIVAL WALL
 Pocket wall is constantly changing as a result of
interaction between host & bacteria
 Gingival wall has Following Areas :-
1. Relative quiescence
2. Bacterial accumulation
3. Emergence of leukocytes
4. Leukocyte – bacteria interaction
5. Intense epithelial desquamation
6. Ulceration
7. Areas of hemorrhage
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15. PERIODONTAL POCKETS AS
HEALING LESION
 Constantly undergoes repair
 Complete healing doesn't occur
 Condition of soft tissue depends on changes
(Destructive / Constructive)
 Edematous Pocket Wall
 Fibrous Pocket Wall
 Edematous & Fibrous Pockets represent
opposite extremes of same pathologic
process,not different entities
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16. CONTENTS OF POCKET
 Microorganisms & their products
 Gingival Fluid
 Food remnants
 Salivary mucin
 Desquamated epithelial cells
 Leukocytes
 Plaque covered with calculus
 Purulent exudate (living, degenerated. necrotic
leukocyte, living &dead bacteria, serum, scant
amount of fibrin)
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17. SIGNIFICANCE OF PUS
FORMATION
 The presence of pus or the ease with which it can
be expressed from the pocket merely reflects the
nature of the inflammatory changes in the pocket
wall.
 It is not an indication of the depth of the pocket or
the severity of the destruction of the supporting
tissues.
 Extensive pus formation may occur in shallow
pockets, whereas deep pockets may exhibit little or
no pus.
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18.  Pus is a common feature of periodontal
disease, but it is only a secondary sign.
 Localized accumulation of pus constitutes
an abscess.
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19. ROOT SURFACE WALL
 Pocket deepens
 Collagen fibers in cementum – destroyed
 Exposure of cementum to environment
 Penetration of bacteria into cementum
 Areas of necrotic cementum separated by
masses of bacteria
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20.  Pathologic granules - represent areas of
collagen degeneration or areas where collagen
fibrils have not been fully mineralized initially.
 Clinically – softening of cementum surface which
is usually asymptomatic but painful on probing.
 Treatment should be aimed at removal of
necrotic areas by root planing
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21. MINERALIZATION OF
CEMENTUM
INCREASED MINERALIZATION:-
 They are probably a result of an exchange of
minerals and organic compounds at cementum
at cementum saliva interface
 Mineral content of exposed cementum increases
 Ca,Mg,P,F - in diseased roots
 This increases resistance to decay
 Selvig et. al (1977) – these zones as a layer 10-
20µm thick with areas as thick as 50µm
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22. AREAS OF DEMINERALIZATION:-
 Exposure to oral fluid and bacterial plaque
causes proteolysis of embedded remnants of
sharpey’s fibers
 The cementum undergoes fragmentation and
cavitations leading to root caries
 Dominant microorganism – Actinomyces
viscosus
[ Syed et al(1975)]
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23.  Caries of cementum requires special attention
when pocket is treated
 Necrotic cementum must be treated by scaling &
root planing until firm tooth surface is reached
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24. SURFACE MORPHOLOGY OF
TOOTH WALL
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25. PERIODONTAL DISEASE
ACTIVITY
 Earlier – Loss of attachment is slow but
continuously progressive phenomenon
 Now – Periodontal disease activity (specificity of
plaque bacteria)
 Pockets undergo periods of exacerbation &
Quiescence
 Results in episodic bursts of activity followed by
periods of remission
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26. ACTIVITY Vs INACTIVITY
 Period of
Quiescence
 Inflammatory
response
 Little /no bone & CT
loss
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 Built up of
unattached plaque
with Gm –ve, Motile
anaerobic bacteria
 Bone & CT loss
 Pocket deepens
 Proliferation Of Grm
+ve bacteria

27. SITE SPECIFICTIY
 Periodontal destruction doesn't occur in all parts
of the mouth at same time
 But it occurs on few teeth at a time or even only
some aspects of some teeth at any given time
 This is site specificity
 Severity of periodontitis increases with
development of new disease sites & increased
breakdown of existing sites.
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28. PULPAL CHANGES
 Spread of infection from periodontal pocket to
pulp causes pathological changes in pulp
 Involvement of pulp occurs through either apical
foramen or lateral canals via PDL
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1.Periodontal pocket deepens
into apex and secondarily
involve pulp
2.Periodontal pocket can
infect pulp through lateral wall

29. POCKET DEPTH Vs CAL
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 Pocket depth – distance between base of pocket &
gingival margin
 Clinical Attachment Level [CAL] – distance
between base of pocket & fixed portion on the
crown like CEJ
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32. POCKET DEPTH & BONE
LOSS
 Severity of bone loss is generally but not always
correlated to pocket depth.
 Extensive attachment & bone loss may be
accompanied by recession of gingival margin
where pocket can be less
 Slight bone loss can occur with deep pockets
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33. PERIODONTAL ABSCESS
 Localized purulent inflammation in periodontal
tissues
 Also called lateral abscess/ parietal abscess
 Classification
 Abscess in supporting periodontal tissues along
lateral aspect of root
 Abscess in soft tissue wall of deep pocket
 Mainly Grm –ve anerobic rods
 Others – grm –ve cocci,diplococci,fusiforms &
spirochetes
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34.  Formation
 Infection from pocket deeply into supporting
periodontal tissue
 Lateral extension of inflammation from inner surface
of pocket into connective tissue
 Formation in a pocket with tortuous course around
root
 Incomplete removal of calculus
 With perforation of lateral wall of root in endodontic
therapy
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35. DETECTION OF POCKET
 Inserted parallel to vertical
axis of tooth
 WALKED circumferentially
around each surface of
each tooth
 Graduated periodontal probe with
a standardized tip diameter of
approximately 0.4–0.5 mm
 Probing force should be 25g or 0.75N
[Van der Velden (1979), Chamberlain et
al(1985)]
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36. WHEN TO PROBE ?
INTIAL PROBING
 Usually masked by heavy inflammation &
abundant calculus. So cannot be done
accurately.
 Purpose – determine whether tooth can be
saved or should be extracted.
SECOND PROBING
 Establish accuracy of level of attachment &
degree of involvement of roots & furcation
 Sulcus can be safely probed after periodontal
surgery – 3 months post op
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37. TREATMENT
 According to pocket depth, periodontitis can be
divided into
Purpose of surgical treatment
 To eliminate the pathologic changes in pocket
wall.
 To create a stable, easily maintainable state.
 To promote periodontal regeneration if possible.
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38. THERAPY FOR GINGIVAL
POCKETS
 Factors to be considered
 Character of the pocket wall
Edematous Fibrotic
 SRP SRP followed by gingivectomy
Modified Widman Flap Technique (in
marked enlargements)
 Accessibility of the pocket
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39. THERAPY FOR SLIGHT
PERIODONTITIS
 Pockets are shallow, small degree of bone loss
 A thorough Scaling & root planing is sufficient
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40. THERAPY FOR MODERATE TO SEVERE
PERIODONTITIS IN ANTERIORS
 Scaling & root planing
 Papilla preservation flap- For esthetics in wide
embrasures
 In narrow embrasures – sulcular incision
 Modified widman flap – when esthetics are not
concerned
 When bone contouring is needed – apically
displaced flap with bone contouring is technique
of choice
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41. THERAPY FOR MODERATE TO SEVERE
PERIODONTITIS IN POSTERIORS
 Offers no esthetic problem but difficult
accessibility
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42. TREATMENT
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Pseudopocket
Scaling & Root Planing
Re –evaluation
Persistent pockets
Gingivectomy & Gingivoplasty

43. Periodontal pocket
Scaling & root planing
Re- evaluation
Resective & Regenerative therapy
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44.  A through and sound knowledge of nature of
pocket along with its lining, contents and the
tooth wall surface is necessary for appropriate
planning of its treatment
 However, the benefit to the patient should
always be minded in long run.
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