Periodontal pocket/histopathology/pathogenesis/clinical features

2.  CONTENTS
• Definition
• Classification
• Clinical features
• Pathogenesis
• Histopathology
• Periodontal disease activity
• Site specificity
• Pulp changes associated with periodontal pockets
• Relationship of attachment loss and bone loss to pocket depth
• Area between base of pocket and alveolar bone relationship of pocket to bone
• Periodontal abscess
• Periodontal cyst
• Conclusion
• Reference

3.  INTRODUCTION
• Gingival sulcus is the space between the neck of the tooth and the
circumferential gingival tissue.
• Sulcus , when it deepens { as in periodontal disease } due to the
apical migration of junctional epithelium, accompanied by attachment
loss, it is referred to as periodontal pocket.
• Probing depth of clinically normal gingival sulcus = 2-3mm

4.  DEFINITION
• The Periodontal pocket is defined as a
pathologically deepened gingival sulcus
.
- CARRANZA 1OTH edition
• It is one of the most important clinical
features of periodontal disease.

6.  CLASSIFICATION
Deepening of the gingival
sulcus may occur by
Coronal movement of
the gingival margin
(gingival enlargement)
Apical displacement
of the gingival
attachment
A combination of the
two processes

7. Acc. To MORPHOLOGY
Acc. To NATURE OF SOFT
TISSUE WALL
Acc. To NUMBER OF SURFACES
involved
Acc. To DISEASE ACTIVITY
CLASSIFICATION

8. Acc. To
NATURE OF
SOFT TISSUE
WALL
Edematous
pocket
Fibrotic
pocket
Acc. To
DISEASE
ACTIVITY
Active
pocket
Inactive
pocket
Acc. To
MORPHOLOGY
Gingival
Pocket
Periodontal
pocket
Acc. To
NUMBER OF
SURFACES
involved
Simple
Compound
Complex

9. 1.ACCORDING TO MORPHOLOGY
A. Gingival pocket (pseudo pocket)- This type of pocket is formed by
gingival enlargement without destruction of the underlying
periodontal tissues. The sulcus is deepened because of the
increased bulk of the gingiva.
B. Periodontal pocket - This type of pocket occurs with destruction of
the supporting periodontal tissues. Progressive pocket deepening
leads to the destruction of the supporting periodontal tissues and
loosening and exfoliation of the teeth.
Periodontal
pocket
Suprabony
pocket
Intrabony
pocket

10. Gingival Suprabony Intrabony
pocket pocket pocket

11.  DIFFERENCES BETWEEN SUPRABONY
& INTRABONY POCKETS
• SUPRABONY POCKET
 Supracrestal or supra alveolar.
 Base of the pocket is coronal to
the level of alveolar bone.
 Lateral wall consist of the soft
tissue alone.
• INTRABONY POCKET
 Infrabony, subcrestal, intraalveolar.
 Base of the pocket is apical to crest
of alveolar bone.
 Lateral wall consist of the soft tissue
and bone.

12. Suprabony pocket
ØHorizontal pattern of bone
destruction.
ØTranspetal fibers are arranged
horizontally.
ØPDL fibers [facial & lingual]
follow normal horizontal-oblique
course
Intrabony pocket
ØVertical (angular) pattern of bone loss.
ØTranseptal fibers are arranged
obliquely.
PDL fibers follow angular patern of
adjacent bone

13. ACCORDING TO THE NUMBER OF
SURFACES INVOLVED
SIMPLE POCKET- It involves only
one tooth surface.
COMPOUND POCKET- It involves
two or more tooth surface.
COMPLEX POCKET- Where the
base of the pocket is not in
direct communication with the
gingival margin. It is also known
as a spiral pocket.
Simple Compound Complex
SIMPLE POCKET- It involves only
one tooth surface.
COMPOUND POCKET- It involves
two or more tooth surface.
COMPLEX POCKET- Where the
base of the pocket is not in
direct communication with the
gingival margin. It is also known
as a spiral pocket.

14. CLINICAL FEATURES
SIGNS--
• Enlarged, bluish – red thickened marginal
gingiva with a 'rolled' edge.
• A bluish red vertical zone from the gingival
margin to alveolar mucosa.
• Gingival bleeding and suppuration.
• Tooth mobility.
• Loss of stippling.
• Diastema formation.
Gingival bleeding
Gingival suppuration

15. SYMPTOMS
• Localized pain or "pain deep in the bone".
• Usually painless but may give rise to
localized /radiating pain or sensation of
pressure after eating which gradually reduces.
• A foul taste in localized areas.
• Sensitivity to hot and cold.
• Toothache in the absence of caries is also
sometimes present.
• A tendency to stuck material inter proximally.
• Urge to dig a pointed instrument in the gums.
• Feeling of loose teeth.

16.  CORRELATION OF CLINICAL AND HISTOPATHOLOGIC FEATURES
OF THE PERIODONTAL POCKET
CLINICAL FEATURES HISTOPATHOLOGICAL FEATURES
1. Gingival wall of pocket presents-
i. Bluish red discoloration
ii. Flaccidity
iii. A smooth, shiny surface
iv. Pitting on pressure
i. Circulatory stagnation.
ii. Destruction of gingival fibers &
surrounding tissues.
iii. Atrophy of epithelium.
iv. Edema and degeneration.
2. Gingival wall may be pink and firm 2. Fibrotic changes
3. Bleeding is elicited by gently probing soft
tissue wall of pocket
3. Increased vascularity, thinning and
degeneration of epithelium, & proximity of
engorged vessels to inner surface.
4. On probing, inner aspect of pocket is
generally painful
5. Pus may be expressed by applying digital
pressure.
4. Pain on tactile stimulation is caused by
ulceration of inner aspect of pocket wall.
5. Pus occurs in pockets with suppurative
inflammation of inner wall.

17. PATHOGENESIS
Inflammatory changes in the C.T. OF
gingival sulcus
Collagenases and
MMPs
Activate fibroblasts
for phagocytizing
collagen
Gingival collagen fiber destruction
Proliferation of apical cells of J.E. along the
root

18. PMNs volume reach 60% or
more
Detachment of the coronal
portion of J.E. from the root
Pocket formation

19. • Two mechanisms of collagen loss
Collagenases & other
enzymes secreted by various
cells such as fibroblasts,
PMNs leukocytes &
macrophages, becomes
extracellular & destroy
collagen; these enzymes that
degrade collagen and other
macromolecules into small
peptides are called
MATRIX
METALLOPROTEINASES
Fibroblast phagocytize
collagen fibers by extending
cytoplasmic process to the
ligament- cementum interface
& degrade the inserted
collagen fibrils & the fibrils of
the cementum matrix.

20. • The transformation of a gingival sulcus into periodontal pocket
creates an area where plaque removal becomes impossible , &
the following mechanism, is followed
Plaque
accmulation
Gingival
inflammation
Pocket
formation
Area
difficult to
clean

25.  HISTOPATHOLOGY
1. SOFT TISSUE WALL
I. Connective tissue
 Edematous and densely infiltrated with plasma cells (approx. 80%),
lymphocytes and a scattering of PMNs.
 Blood vessels - increased in number, dilated and engorged.
 Exhibits varying degrees of degeneration.
 Shows proliferation of endothelial cells with newly formed capillaries,
fibroblast and collagen fibers.
ii. Junctional epithelium:
 At the base of the pocket is usually much shorter
 Coronoapical length is reduced to only 50-100 μm.

26. iii. Lateral wall:
 Most severe degenerative changes.
 Epithelial buds or interlacing cords of epithelial cells project from the
lateral wall into the adjacent inflamed C.T. & apically than the J.E.
 Densely infiltrated by leukocytes & edema from the inflamed C.T.
 Cells : vacuolar degeneration and form vesicles.
 Ulceration and suppuration.

28. 2. BACTERIAL INVASION
 Studies have shown that bacterial invasion occurs in the apical &
lateral areas of the pocket wall.
 Intercellular spaces of the epithelium - Filaments, rods and
coccoid organism with predominant gram-negative cells
• Porphyromonas gingivalis
• Prevotella intermedia ,
• Aggregatibacter actinomycetemcomitans

29. 3. MICROTOPGRAPHY OF GINGIVAL WALL
1. AREAS OF RELATIVE QUIESCENCE-
showing flatten surface with minor
depression and mounds and occasional
shedding of cells.
2. AREAS OF BACTERIAL
ACCUMULATION-presenting
as epithelial surface depressions, with
abundant debris and bacteria clumps
penetrating into the enlarged
intercellular spaces. These bacteria are
usually cocci, rods, and filament with few
spirochetes.

30. 3. AREAS OF
EMERGENCE OF LEUKOCYTES-
where leukocytes appear in the pocket
wall through holes located in the
intercellular spaces.
4. AREAS OF LEUKOCYTE-
BACTERIA INTERACTION- where
numerous leukocytes are present &
covered with bacteria in an apparent
process of phagocytosis. Bacterial
plaque associated with epithelium
is seen either as an organised matrix
covered by a fibrin-like material in
contact with the surface of cells or as
bacteria penetrating into
the intercellular spaces

31. 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.
Areas of
haemorrhage
Areas of
ulceration

32. 4. PERIODONTAL POCKET AS HEALING LESIONS
• Periodontal pockets are chronic inflammatory lesions which undergo
repair.
• The condition of the soft tissue wall of the periodontal pocket result from
the interplay of the destructive and constructive tissue changes.
• Their balance determine clinical features of the pocket wall.
Constructive tissue
changes
Formation of C.T.
cells, collagen fibers,
appear more firm &
pink
Destructive tissue
changes
Fluid & cellular
inflammatory exudate,
pocket wall is bluish red
,soft, spongy & friable
with smooth, shiny
surface
FIBROTIC POCKET
EDEMATOUS
POCKET

33. 5. POCKET CONTENTS
Debris – microorganism and products ( enzymes,
endotoxins, and other metabolic products)
Gingival fluid
Food remnants
Salivary mucin
Desquamated epithelial cells
Leukocytes
Plaque-covered calculus

34. 6. SIGNIFICANCE OF PUS FORMATION
Secondary sign.
Nature of the inflammatory changes.
Not an indication of depth of pocket/ severity of destruction.

35. 7. ROOT SURFACE WALL
• Cause pain
•Recurrence of infection
•Complicate periodontal treatment.
CHANGES IN ROOT
STRUCTURAL CHEMICAL CYTOTOXIC

36. A. STRUCTURAL CHANGES
PATHOGENIC
GRANULES
AREAS OF
INCREASED
MINERALIZATION
AREAS OF
DEMINERALIZATION

37. I. PATHOGENIC GRANULES
• Represents areas of collagen degeneration or areas where collagen fibrils
have not been fully mineralized initially.
II. AREAS OF INCREASED MINERALIZATION
• highly mineralized superficial layer increase the tooth resistance to decay
• associated with increased perfection of the crystal structure.
III. AREAS OF DEMINERALISATION-
• Commonly related to root caries , dominant organism is A. viscosus

38. B. CHEMICAL CHANGES
• The mineral content of the exposed cementum is increased.
Exposed cementum may absorb calcium, phosphorous & fluoride from its
environment.
Development of highly calcified layer that is resistant to decay.
• The ability to absorb substance may be harmful, because absorb material
may be toxic.

39. C. CYTOTOXIC CHANGES
• Endotoxins found in the cementum of periodontally involved teeth.
• Endotoxins limits the proliferation and attachment of fibroblasts to the
diseased root surfaces.

40.  Surface morphology of tooth wall with
periodontal pocket

41.  PERIODONTAL DISEASE ACTIVITY
• Periodontal pockets go through periods of exacerbation and quiescence
resulting from episodic bursts of activity followed by periods of remission.
PERIODS OF REMISSION
OR
QUIESCENCE/INACTIVITY
PERIODS OF
EXACERBATION/ACTIVITY
• Gram positive bacteria
proliferates
• Reduced inflammatory
response
• Little or no born and
connective tissue
attachment loss.
• Build up of unattached
log with its gram
negative, motile, and
anaerobic bacteria
• Bone and connective
tissue attachment loss
• pocket deepens.

42.  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.

43.  Pulp changes associated with
periodontal pocket
 Spread of infection from periodontal
pockets causes pathological changes in
the pulp leading to painfull symptoms
Involvement of the pulp occurs through
either the apical foramen or the lateral
canals in the root.

44.  RELATIONSHIP OF ATTACHMENT LOSS
& BONE LOSS TO POCKET DEPTH
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.
This is because the degree of attachment lost 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.

46.  AREA BETWEEN BASE OF POCKET AND
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 extend of the calculus and the
alveolar Crest in human periodontal pockets is most constant, having a
mean length of 1.97 mm.
Wade, assessed the relation between pocket base, epithelial attachment
and alveolar process and found that the distance from attached plaque is
never less than 0.5 mm and never more than 2.7 mm.

47.  Periodontal abscess
 A localised purulent inflammation in
the periodontal tissues.
 Also known as - lateral or
parietal abscess.
 Abcesses localised in the gingiva, due
to injury to the outer surface of the
gingiva, and not involving the
supporting structures are called
Gingival Abscesses.

48. MICROSCOPICALLY
• localised accumulation of viable and non viable PMNs within the
periodontal pocket wall.
• PMNs liberate enzymes digest tissue & cells pus
(present in center of the Abscess)
• overlying epithelium exhibits intracellular and extracellular
edema
• invasion of leukocytes.
• Chronic abscess when its purulent content drains into a fistula
into the outer gingival surface

49. -PERIODONTAL ABSCESS FORMATION MAY OCCUR IN THE
FOLLOWING WAYS-
Extension of
infection from a
periodontal pocket
Lateral extension of
inflammation from the
inner surface of
periodontal pocket
In a pocket that
describes a tortuous
course around the
root, a periodontal
Incomplete removal of
calculus during
treatment of a
periodontal pocket
After trauma to the tooth
or perforation of the
lateral wall of the root in
endodontic therapy.

50.  PERIODONTAL CYST
• Uncommon
• Lesion that produces
localised destruction of the
periodontal tissues along a
lateral root surface
• Most often in the mandibular
canine-premolar area.

51. • The following possible etiologies have been suggested:
1. Odontogenic cyst
2. Lateral dentigerous cyst
3. Primordial cyst of supernumerary tooth germ.
4. Stimulation of epithelial rests of the periodontal ligament by infection from a
periodontal Abscess or the pulp through an accessory root canal.

52. Asymptomatic
Present as a localised tender swelling.
Radiographically, radiolucent area
bordered by a radiopaque line.
Radiographic appearance cannot be
differentiated from that of a periodontal
Abscess.

53. Microscopically, the
cyst lining maybe;
A loosely arranged,
non-keratinized,
thickened, proliferating
epithelium;
A thin, non keratinized
epithelium; or
An odontogenic
keratocyst.

54.  CONCLUSION
Understanding the etiopathogenesis,
histopathology and progression of periodontal
pockets is essential to provide the patient with
the successful treatment outcomes and
monitoring the response to therapy.

55. REFERENCE
• CARRANZA 10th AND 13th EDITION
• SHALU BATHLA textbook of PERIODONTICS