perioDONTAL pocket

1. Presented by: Dr. Fatima Gilani (JR-II)
Moderator : Dr. Shivjot Chhina
Perceptor- Dr. Kumar Saurav
PERIODONTAL POCKET
Seminar-6

2. 1.Definition
2.Classification of pocket
3.Pathogenesis of pocket
4.Soft tissue wall changes
5.Clinical features and their causes
6.Microtopography of gingival wall of pocket
6.Contents of pocket
7.Root surface wall of pocket
8.Diagnosis and detection of pocket
9.Treatment
CONTENTS

3.  A pocket is defined as a ‘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 two processes. 1
SOURCE:- www.arestin.com
DEFINITION

4. I.) Depending upon its morphology
1.) GINGIVAL/PSEUDO/RELATIVE POCKET 2.) PERIODONTAL POCKET
SOURCE: Fermin A. Carranza, Newmann, Takei, Klokkevold ; Clinical Periodontology; 10TH edition.
CLASSIFICATION OF
POCKET

5. B.) Types of periodontal pocket upon its relationship to crestal bone
 1.) SUPRABONY POCKET 2.) INTRABONY
SOURCE: Fermin A. Carranza, Newmann, Takei, Klokkevold ; Clinical Periodontology; 10TH edition.
POCKET

6. DISTINGUISHING FEATURES OF SUPRA AND INFRABONY
POCKETS 1
SUPRABONY POCKET INFRABONY POCKET
Also known as supracrestal or supraalveolar pocket Also known as infrabony, subcrestal and intra-alveolar pocket
The base of the pocket is coronal to the level of the alveolar
bone.
Bottom of pocket is apical to the crest of underlying alveolar
bone
Lateral wall consist of soft tissue alone Lateral wall consist of soft tissue and bone
Pattern of destruction of bone is horizontal Pattern of destruction of bone is vertical
Interproximally transeptal fibers arrange horizontally Interproximally transeptal fibers are oblique rather than
horizontal
On facial and lingual surfaces periodontal ligament fibers
follow horizontal- oblique course between the tooth and
bone
On the facial and lingual surfaces periodontal ligament fibers
follow angular pattern.

7.  Pockets can involve one, two, or more tooth surfaces
 It can be of different depths and types on different surfaces of the same tooth.
TOPOGRAPHY OF HUMAN
PERIODONTAL POCKET2,3

8. C). Depending upon the number of surfaces involved 2,3 :
 A.) Simple pocket- involving one tooth surface
 B.) Compound pocket- involving two or more tooth surfaces
 C.) Complex pocket- where the base of the pocket is not in direct
communication with gingival margin, also known as spiral pocket .
SOURCE: Fermin A. Carranza, Newmann, Takei, Klokkevold ; Clinical Periodontology; 10TH edition.

9. D.) Depending upon the nature of the soft tissue wall of the
pocket
A.) Edematous pocket B.) Fibrotic pocket
SOURCE:-WWW..POCKETDENTISTRY.COM

10. E.) Depending upon the disease activity 4
A.) Active pocket :-
*Underlying bone is lost
* After Phase I therapy the
inflammatory changes in the
pocket wall subside, rendering
the pocket inactive and
reducing its depth
*The extent of this reduction
depends on the depth before
treatment and the degree to
which the depth reduces, is
the result of the edematous
and inflammatory component
of the pocket wall.
B.) Inactive pocket :-
*Inactive pockets can
sometimes heal with a
long junctional
epithelium
*Unstable
condition,chances of
recurrence
SOURCE:- WWW.PERIOBASICS.COM

11. SIGNS:-
Bluish red,
thickend marginal
gingiva
Bluish red
vertical zone
extending from
(GM-AM)
Break in
faciolingual
continuity of the
interdental gingiva
Gingival bleeding
Suppuration
Tooth mobility,
extrusion and
migration of teeth
SOURCE:-
WWW..POCKETDENTISTRY.COM
CLINICAL FEATURES 1

12. Localised pain/pain deep in
the bone.
Foul taste in localised
areas.
A tendency to suck
material from
interproximal spaces
The urge to dig a pointed
instrument into the gums
and relief obtained from
resultant bleeding.
Sensitivity to heat
and cold, toothache
in absence of caries
SYMPTOMS

13. CLINICAL FEATURES HISTOLOGIC FEATURES
1.)Bluish red discoloration of gingival wall of pocket. Due to circulatory stagnation
2.) Flaccidity Due to destruction of gingival fibers
3.) Smooth shiny surface Due to atrophy of epithelium and edema
4.) Pitting on pressure Due to edema and degeneration
5.) Bleeding on probing Due to-
1-Increased vascularity
2-Thinning and degeneration of epithelium
3-Proximity of engorged vessel to inner surface
6. Pain on probing Due to ulceration of inner aspect of pocket wall
CORELATION BETWEEN CLINICALAND HISTOLOGIC FEATURES

14.  It starts with inflammatory changes in Connective tissue of Gingival Sulcus.
Cellular & fluid inflammatory exudate cause:-
 Degeneration of:-
A.) Connective tissue
B.) Gingival fibers &
C.) Collagen fibers
 Just apical to Junctional Epithelium, collagen fibers get destroyed.
ETIOPATHOGENESIS 1

15.  Collagenases + Enzymes secreted by fibroblasts, PMNLs & Macrophages- MMPs
became extracellular & destroyes collagen.
 Fibroblast phagocytise collagen fibers by extending cytoplasmic process to the
ligament - cementum interface & degrade collagen fibrils & fibrils of cementum
matrix.
TWO MECHANISM OF COLLAGEN
LOSS

16.  Connective Tissue changes
-Edematous & densely infilterated plasma (80%), lymphocytes, PMNs
-various degree of degeneration
-single/multiple necrotic foci
-proliferation of endothelial cells
-newly formed capillaries, fibroblast, collagen fibres
HISTOPATHOLOGY 1,5

17.  Cells undergo vascular degeneration & rupture to form vesicles.
 Progressive degeneration & necrosis of epithelium
ulceration of lateral wall and
 Exposure of underlying Connective Tissue & suppuration

18.  Filaments, rods & coccoid organism which are gram -ve found in intercellular
spaces(CP)
 P.gingivalis & P. intermedia & AA in Gingiva (AP)…(Hillmann et al).
 Bacteria invade intercellular spaces & accumulate on basement lamina.
 Some cross Basement Lamina & invade Connective tissue (Bacterial invasion
/translocation)
BACTERIAL INVASION 1,6

19.  Several irregular & oval/elongated
areas (pocket wall) with a width of
50-200 µm (SEM)
 Following areas are seen:-
1 -Areas of relative quiescence
2-Areas of bacterial accumulation
3-Areas of emergence of leukocytes
4-Areas of leukocyte-bacteria interaction
5-Areas of intense epithelial desquamation
6-Areas of ulceration
7-Areas of hemorrhage
MICROTOPOGRAPHY OF THE GINGIVAL WALL
OF THE POCKET

20. 1.Areas of relative quiescence:
Shows flat surface with minor depressions
and mounds; occasional shedding of
cells
2.Areas of bacterial accumulation:
Appears as depressions on the epithelial
surface with abundant debris and Bacterial
clumps. Bacteria are rods ,cocci, filaments,
spirochetes.

21. 3.Areas of emergence of leucocytes
Leucocytes appear in the pocket wall through
holes located in the intercellular spaces
4.Area of leukocyte and bacterial interaction:
Numerous leucocytes are present and are covered
with bacteria in an apparent process of
phagocytosis.

22. 5.Areas of intense epithelial desquamation:
Consists of semi attached and folded epithelial
remnants sometimes covered by bacteria.
6. Areas of ulceration :
with exposed connective tissues
7. Areas of hemorrhage:-
with numerous erythrocytes

23.  Periodontal Pockets are chronic inflammatory lesion and undergo constant
repair
 Changes can be:-
Destructive changes & Constructive
Edematous pocket Fibrotic pocket
PERIODONTAL POCKET AS
HEALING LESIONS

24.  Debris consisting microorganism & products (enzymes, endotoxins & metabolic
products)
 Gingival fluid remnants, salivary mucin
 Desquamated epithelial cells & leukocyte
 Purulent exudate consists of living, degenerated & scant amount of fibrin
POCKET CONTENTS

25. Various zones seen at bottom of the
pocket:
1.Cementum covered by calculus.
2.Covered by attached plaque-extends apically to a
variable degree upto 100-500m
3.Zone of unattached plaque-surrounds the attached
plaque and extends apically to it.
4.Zone where the junctional epithelium is attached
to the tooth .The extension of this zone (in normal
sulcus-500μm) is usually reduced in periodontal
pockets less than 100m.
5.Apical to junctional epithelium.
Total width of plaque free zone varies according to
type of tooth-wider in molars than in incisors.

26. Various zones seen at bottom of the pocket:
1.Cementum covered by calculus.
2.Covered by attached plaque-covers the calculus and extends apically to a
variable degree upto 100-500m
3.Zone of unattached plaque-surrounds the attached plaque and extends
apically to it.1

27.  Periodontal Pocket go through periods of exacerbation & quiescence
Period of quiescence:
Reduced inflammatory response
little/no bone & CT attachment loss
unattached plaque with gram-ve motile & anaerobic bacteria
PERIODONTAL DISEASE
ACTIVITY

28. METHODS OF DETECTING PERIODONTAL
POCKET 7

29. Position of Probe in a Healthy Sulcus. In
health,
the probe tip touches the junctional
Epithelium located above the cemento-
enamel junction.
Position of Probe in a Periodontal Pocket.
In a periodontal pocket, the probe tip touches
the(JE) located on the root
below the cemento-enamel junction..

30. SOURCE:- FUNDAMENTALS OF PERIODONTAL INSTRUMENTATION & ADVANCED ROOT INSTRUMENTATION BY JILL S. NIELD-GEHRIG
PROBING IS DONE WITH SHORT WALKING
STROKES WITH PROBING FORCE OFAROUND
0.75N

31.  Probing is the act of walking the tip of a probe along the junctional epithelium within the sulcus.
 THE WALKING STROKE
 The walking stroke is the movement of a calibrated probe around the perimeter of the base of a
sulcus or pocket.
TECHNIQUE

32. PRODUCTION OF THE WALKING STROKE
Walking strokes are a series
of bobbing strokes that are
made within the sulcus or
pocket. The stroke begins when
the probe is inserted into the
sulcus while keeping the probe
tip against the tooth surface.
The probe is inserted until the
tip encounters the resistance
of the junctional epithelium
that forms the base of the
sulcus.
Create the walking stroke by
moving the probe up and
down in short bobbing strokes
and forward in 1-mm
increments .With each down
stroke, the probe returns to
touch the junctional epithelium.
The probe is not removed
from the sulcus with each
upward stroke.
The pressure exerted with the
probe tip against the
junctional epithelium should
be between 10 and 20 grams.

33. Severity of attachment loss is generally not correlated
with pocket depth.
Degree of attachment loss depends on the location of the
base of the pocket on the root surface
The attachment level (X; mm) was determined by probing,
with the value defined as the distance from the cemento-
enamel junction to the location of the inserted probe tip.
RELATION OF CAL & BONE LOSS
TO POCKET DEPTH 7,8

34. Distance between apical end of JE & alveolar bone is constant
Distance between apical end of calculus & alveolar bone is constant in human
PP=1.97mm±33.16%
Distance between attached plaque to bone is never less than 0.5mm & never more than
2.7mm
AREA BETWEEN THE BASE OF POCKET & ALVEOLAR
BONE 1

35. TREATMENT OPTIONS FOR TREATING POCKETS`-
Methods are:-
 Non surgical therapy
 Surgical therapy
NON SURGICAL therapy:
1.Scaling and root planing.
2. Curettage.
3. Local drug delivery
(tetracycline, metronidazole, doxycycline, minocycline). SOURCE:-WWW.HILLSDENTISTRY.COM

36. SURGICAL THERAPY
 Periodontal flaps based on evaluation of bone loss8
 Gingival pockets —Gingivectomy .
 Suprabony pockets – Scaling and root planning.
Curettage.
Local drug delivery.
Periodontal flap surgery.
 Infrabony pocket - Scaling and root planing.
Resective or regenerative flap surgeries

37. REFERENCES
1 . ) F e r m i n A . C a r r a n z a , N e w m a n n , Ta k e i , K l o k k e v o l d ; C l i n i c a l P e r i o d o n t o l o g y ; 11 T H
e d i t i o n .
2 . ) G l i c k m a n I , S m u l o w J B : P e r i o d o n t a l D i s e a s e : c l i n i c a l , r a d i o g r a p h i c , a n d
h i s t o p a t h o l o g i c f e a t u r e s , P h i l a d e l p h i a , 1 9 7 4 , S a u n d e r s .
3 . ) K r a y e r J W, R e e s T D : H i s t o l o g i c o b s e r v a t i o n o n t h e t o p o g r a p h y o f a h u m a n
p e r i o d o n t a l p o c k e t v i e w e d i n t r a n s v e r s e s t e p - s e r i a l s e c t i o n s , J P e r i o d o n t o l 6 4 : 5 8 5 , 1 9 9 3
4 . ) D a v e n p o r t R H J r, S i m p s o n D M , H a s s e l T M : H i s t o m e t r i c c o m p a r i s o n o f a c t i v e a n d
i n a c t i v e l e s i o n s o f a d v a n c e d p e r i o d o n t i t i s , J P e r i o d o n t o l 5 3 : 2 8 5 , 1 9 8 2
5 . ) C a r r a n z a FA J r, G l i c k m a n I : S o m e o b s e r v a t i o n s o n t h e m i c r o s c o p i c f e a t u r e s o f t h e
i n f r a b o n y p o c k e t s , J P e r i o d o n t o l 2 8 : 3 3 , 1 9 5 7
6 . ) C h r i s t e r s s o n L A , A l b i n i B , Z a m b o n J J , e t a l : Ti s s u e l o c a l i s a t i o n o f A c t i n o b a c i l l u s
a c t i n o m y c e t e m c o m i t a n s i n h u m a n p e r i o d o n t i t i s . I . L i g h t , i m m u n o f l u o r e s c e n c e a n d
e l e c t r o n m i c r o s c o p i c s t u d i e s , J P e r i o d o n t o l 5 8 : 5 2 9 , 1 9 8 7
7 . ) F u n d a m e n t a l s o f P e r i o d o n t a l I n s t r u m e n t a t i o n & A d v a n c e d R o o t I n s t r u m e n t a t i o n J i l l S .
N i e l d - G e h r i g
8 . ) A b e Y , N o g a m i K , M i z u m a c h i W , Ts u k a H a n d H i a s a K . P r o p o s e d s c o r e f o r
o c c l u s a l - s u p p o r t i n g a b i l i t y. O p e n J o u r n a l o f S t o m a t o l o g y , 2 0 1 3 ( 3 ) ; 2 3 0 - 2 3 4 .