Periodontal Pocket presentation

1. THE PERIODONTAL POCKET
Sambhav Acharya
4th year

2. OUTLINE
DEFINITION
CLASSIFICATION
CLINICAL FEATURES
PATHOGENESIS
HISTOPATHOLOGY
CONTENTS OF POCKET
DETECTION OF POCKET
MANAGEMENT
REFERENCE

3. • The periodontal pocket is defined as a pathologically
deepened gingival sulcus
• It is one of the most important clinical features of periodontal
disease

4. •Deepening of the gingival sulcus may occur by
coronal movement of the gingival margin , apical
displacement of the gingival attachment or a
combination of the both

5. Pockets can be classified as follows:
a) Gingival pocket (pseudo pocket) : This type of pocket is formed by
the gingival enlargement without destruction of the underlying
periodontal tissues . The sulcus is deepened because of the bulk of the
gingiva
b) Periodontal pocket : This type of pocket occurs with the
destruction of the supporting periodontal tissues.
2 types of periodontal pocket exist, as follows
• Suprabony (supracrestal, supraalveolar), in which the bottom of the
pocket is coronal to the underlying alvelor bone
• Intrabony (infrabony ,subcrestal,intralveolar) , in which the bottom of
the pocket is apical to the level of the adjacent alvelor bone. The lateral
pocket wall lies between the tooth surface and the alveolar bone.

6. Fig : Different types of periodontal pockets

7. It can also be classified as
1. According to the involved tooth surface
a) Simple pocket
• Involves one surface
b) Compound pocket
• Involves more than one
surface
c)Complex pocket (spiral)
• Originating on one tooth surface
and twisting around the tooth to
involve one or more additional
surfaces
• Most common in furcation areas

8. 2.Depending upon the nature of the soft tissue wall
• Edematous pocket
• Fibrotic pocket
3.Depending upon the disease activity
• Active pocket
• Inactive pocket

9. Clinical Features
Enlarged, bluish-red marginal gingiva
“rolled” edge
Reddish blue vertical zone
Extrusion & migration
diastema
shiny & puffy gingiva
gingival bleeding
 purulent exudate

10. (B) SYMPTOMS
•Localized pain or pain “ deep in the bone”
•Usually painless but may give rise to the localized/radiating
pain or sensation of the pressure after eating which
gradually decreases
•Sensitivity to hot and cold fluid
•Tooth may become loose
•Feeling of itching in the gums

11. Correlation of clinical and histopathologic features of
periodontal pocket
Clinical features
Gingival wall of pocket presents various
degrees of bluish red discoloration
 Flaccidity
A smooth shiny surface and pitting on
pressure
Bleeding is elicited on gentle probing soft
tissue wall of pocket
Gingival wall – pink & firm
Histopathologic features
 Discoloration caused by circulatory
stagnation
Destruction of gingival fibers and
surrounding tissues
Atrophy of epithelium and edema & the
pitting on pressure by edema and
degeneration
Results from the increased vascularity,
thinning and degeneration of epithelium
and proximity of engorged vessel to inner
surface
Fibrotic changes predominate over
exudation and degeneration

12. PATHOGENESIS
The initial lesion in the development of periodontitis is the inflammation of gingiva
in response to a bacterial challenge
 Changes involved in transition from the normal gingival sulcus to the pathological
periodontal pocket are associated with different proportions of bacterial cells in
dental plaque
Pocket formation starts as an inflammatory change in the connective
tissue wall of the gingival sulcus
Cellular and fluid inflammatory exudates causes degeneration of the
surrounding connective tissue including gingival fibers
Just apical to the junctional epithelium, collagen fibers are
destroyed
And the areas become occupied by inflammatory cells and
edema

13. PMNLs and
macrophages secreted by
various cells become
extracellular and destroy
collagen fibers in gingival
CT .These enzyme that
degrade collagen into
small peptide are called
matrix
metalloprotinases
Fibroblast phagocytize
fibers by extending
cytoplasmic process to the
ligament cementum
interface and degrade the
collagen fibers of the
cementum matrix
Collagen loss is caused by 2 mechanisms

14. After collagen loss, apical cells of Junctional
epithelium proliferate along the root, extending
finger like projections two or three cells in
thickness
Coronal portion of Junctional Epithelium detaches
from roots as apical portion migrates.
As a result of inflammation PMNs invades coronal
end of Junctional Epithelium in increasing
number and when relative volume of PMNs
becomes approx. 60% or more of Junctional
Epithelium, tissue looses cohesiveness &
detaches from tooth surface.

15. The transformation of a gingival sulcus into a pocket creates
an area where plaque removal becomes impossible and
feedback mechanism is established
Plaque
accumulation
Gingival
inflammation
Pocket
formation
Area difficult
to clean

16. Histopathology
Once the pocket is formed several microscopic features are present:
Soft tissue wall
The connective tissue is edematous and densely infiltrated with the
plasma cells(approx 80%),lymphocytes, and scattering of PMNs
The blood vessels are increased in number, dilated and engorged
The connective tissue exhibits varying degrees of degeneration
Single or multiple necrotic foci are present
The connective tissue also shows the proliferation of the endothelial
cells with the newly formed capillaries, fibroblast, and collagen fibers

17. Junctional epithelium : coronoapical length reduced to
 50 -100ɱm
 Cells : well formed & in good condition
Slight to marked degeneration
Connective tissue:

18. Lateral wall
Most severe degenerative changes
Epithelial buds or interlacing cords of epithelial cells project
from the lateral wall into the adjacent inflamed connective
tissue
Dense infiltration
Cells : vacuolar degeneration & rupture to for vesicles
Ulceration and suppuration

19. Fig 1: Lateral wall showing epithelial
proliferation and atrophic changes
Fig2: Base of the pocket showing extensive
proliferation of lateral epithelium

20. Bacterial invasion
• Filaments , rods and coccoid organism with predominant gram-
negative cell walls have been found in intercellular spaces of
the epithelium
• Bacteria may invade the intercellular space under exfoliating
epithelial cells<but they are also found between deeper
epithelial cells and accumulating on the basement lamina.
Some bacteria transverse the basement lamina and invade the
sub epithelial connective tissue

21. Microtopography of Gingival wall
Scanning electron microscopy has permitted the description of several areas in
the soft tissue wall of periodontal pocket. Seven different type of disease
activity have been noted
1. Area of relative quiescence :
Region with minor depressions
and elevation
2. Areas of bacterial accumulation :
accumulates in depression of
epithelial cells

22. 4.Areas of leukocytes-bacteria interaction:
where numerous leukocytes are present and covered
with bacteria in an apparent process of phagocytosis
5.Areas of intense epithelial desquamation
6.Areas of hemorrhage
7.Areas of ulceration
3.Areas of emergence of leukocytes :
leukocytes emerging through intercellular space

23. Periodontal pocket as a healing lesion
Periodontal pocket are chronic inflammatory lesions and thus are
constantly undergoing repair
Complete healing doesn’t occur because of the persistence of the
bacterial attack which continues to stimulate an inflammatory
response causing degeneration of the new tissue element
FIBROTIC POCKET WALL:
When the reparative
changes predominate , the gingiva
appear fibrotic & pink

24. EDEMATOUS POCKET WALL :
When the inflammatory fluid
and the cellular exudates
predominates, the lateral wall
appears bluish red, soft, spongy
and friable with a smooth shiny
surface referred to as an
edematous pocket wall

25. CONTENTS OF A POCKET
• Debris ( consisting of microorganism & their product mainly enzymes,
toxin and other metabolic products)
• Gingival fluid
• Food remnants
• Salivary mucin
• Desquamated epithelial cells & leukocytes
Plaque covered calculus projects from
the tooth surface
• If purulent exudates present: consist of
living, degenerated and necrotic leukocyte,
living and dead bacteria ,Serum
• Scant amount of fibrin

26. SIGNIFICANCE OF PUS FORMATION
Pus is a common feature of
periodontal disease, but it is only a
SECONDARY SIGN
It is NOT AN INDICATION OF THE
DEPTH OF THE POCKET or the
severity of the destruction of the
supporting tissues

27. ROOT SURFACE WALL
Undergoes following changes:
STRUCTURAL CHEMICAL
CYTOTOXIC

28. RUCTURAL CHANGES
Exposure of cementum to the oral environment
Mineral present in saliva tend to get deposited in cementum surface
Areas of hypermineralization
Root surface is exposed to oral fluids and bacterial plaque
Proteolysis of embedded remnants of sharpeys fiber
Root caries( yellowish or light brown patch)
soft and lethargy on probing
Patient feels severe sensitivity to thermal changes and sweet
pulp exposure may occur in severe forms

29. CHEMICAL CHANGES
• Mineral content increased
• Fluoride, Calcium, Magnesium, Phosphorus
• Exposed cementum : Resistant to decay
CYTOTOXIC CHANGES
• histological studies of the periodontally involved cementum shows
the presence of bacteria in the cementum or the endotoxin in the
cementum

30. SURFACE MORPHOLOGY OF TOOTH WALL
Five zones can be seen on the
base of the pocket
(1) Cementum covered by
calculus
(2) Attached plaque
(3) Zone of unattached
plaque
(4) Zone of attachment of the
junctional epithelium to
the tooth
(5) Zone of semi destroyed
connective tissue fibers

31. PERIODONTAL DISEASE ACTIVITY
• Periodontal pocket go through the periods of exacerbation and
quiescence
PERIODS OF QUIESCENCE
•REDUCED INFLAMMATORY
RESPONSE
• LITTLE OR NO LOSS OF
BONE AND CONNECTIVE
TISSUE ATTACHMENT
PERIODS OF EXACERBATION
•BONE AND CONNECTIVE TISSUE
ATTACHMENT ARE LOST AND THE
POCKET DEEPENS
•BLEEDING EITHER
SPONTANEOUSLY OR WITH
PROBING
•GREATER AMOUNT OF GINGIVAL
EXUDATE

32. Detection of pocket
The only accurate method for detecting and measuring periodontal
pockets is careful exploration with periodontal probe
Disadvantage of a radiograph
• Pocket is a soft tissue change.
• Radiograph indicate areas of bone loss where pockets may be
suspected.
•They don’t show pocket presence or depth, and consequently they
show no difference before and after pocket elimination unless bone loss
has been modified.

33. Pocket probing
Two probing depths present
(A) Biologic or histologic depth : it is the distance between gingival
margin and the base of the pocket ( the coronal end of junctional
epithelium)
(B) Clinical or probing depth :it is the distance from the gingival
margin to which a probe penetrates into the pocket
The probing force of 0.7 N or 25gm have been found to be well
tolerated or accurate

34. Pocket depth versus Attachment loss
• Pocket depth : Distance between base of pocket & the gingival margin
• Level of attachment loss : Distance between the base of the pocket
and the fixed point on a crown such as CEJ

35. ‘WALKING’ the probe to explore
the entire pocket
Probing technique
Vertical insertion of the probe
(left) may not detect interdental
craters ,oblique positioning of
the probe(right) reaches the
depth of the crater

37. Management of pocket
• NON- SURGICAL MANAGEMENT : including
a) phase I therapy
b)local drug delivery
c)systemic antimicrobials
• SURGICAL MANAGEMENT : including
a) Resective surgeries
Gingival curettage
Gingivectomy
 periodontal Flap procedue
b) Regenerative surgeries

38. CONCLUSION
• Periodontal pocket is defined as pathologically deepened gingival sulcus
• Deepening of the gingival sulcus may occur by coronal movement of the gingival
margin , apical displacement of the gingival attachment or a combination of the both
•Periodontal pocket is classified depending upon morphology ,nature of soft tissue
wall, involved tooth surface and disease activity
•The clinical features seen in periodontal pockets are correlated with the
histological features
• Detection and treatment of periodontal pocket is important as it starts as a first
step in the periodontal breakdown

39. REFERENCE
•CARRANZA’S CLINICAL PERIODONTOLOGY
TENTH EDITION