Etiopathogensis of periodontal pocket

Clinical Periodontology and Implant Dentistry; Jan Lindhe 4th edition2

Definition:
Carranza's Clinical Periodontology 10th edition
Glossary of periodontal terms, 2001 4th edition
4
 The periodontal pocket, defined as a pathologically
deepened gingival sulcus, is one of the most important
clinical features of periodontal disease.
 A pathologic fissure between a tooth and the crevicular
epithelium, and limited at its apex by the junctional
epithelium. It is an abnormal apical extension of the
gingival crevice caused by migration of the junctional
epithelium along the root as the periodontal ligament is
detached by a disease process. (GPT 2001)

Classification
5
Pocket
Periodontal
Supra bony Infra bony
Gingival

6

Suprabony pocket
Two types of
Periodontal Pocket
Infrabony pocket
Gingival Pocket
7

8
According to involved tooth surfaces:

Periodontitis
www.intechopen.com 2012
9
 Periodontal pocket is one of the most important clinical
feature of periodontal disease.
 Periodontitis is a chronic infection that results from the
interaction of perio-donto-pathogenic bacteria and host
inflammatory and immune responses.

Periodontology 2004 Vol. 14, 1997, 9-11
10

Microbial challenge
www.intechopen.com 2012
11
 Bacterial plaque are regarded to be the primary
aetiological factor in the initiation of gingival
inflammation and subsequent destruction of periodontal
tissues (Offenbacher 1996).
 Process of plaque formation:
1. The formation of the pellicle on the tooth surface
2. Initial adhesion and attachment of bacteria
3. Colonization and plaque maturation
 Changes involved in the transition from the normal
gingival sulcus to the pathologic periodontal pocket are
associated with different proportions of bacterial cells in
dental plaque.

12 Carranza's Clinical Periodontology 10th edition
Subgingiv
al plaque

13
 Socransky SS and co workers in 1938

14
 Bacteria associated with healthy periodontium:
 Gram positive facultative species
 Streptococcus
 Actinomyces
 Gram negative species
 P intermedia
 F nucleatum
 Capnocytophaga
Anaerobic organisms
Facultative organisms

Fundamentals of Periodontics. Wilson and Kornman 2nd ed.
15
 Microbial shift during
the disease:
 From gram positive to
gram negative
 From cocci to rods (and
at a later stage to
spirochetes)
 From nonmotile to motile
organisms
 From facultative
anaerobes to obligate
anaerobes
 From fermenting to
proteolytic species

16
 Bacteria associated with gingivitis:
 Gram positive facultative species
 Streptococcus
 Actinomyces
 P micros
 Gram negative species
 P intermedia
 F nucleatum
 Capnocytophaga
 Campylobacter
Anaerobic organisms
Facultative organisms

Host Immuno-Inflammatory
response17
 Pocket formation starts as an inflammatory change in
the connective tissue wall of the gingival sulcus.
 Pathological changes in gingivitis are associated with
the presence of oral microorganisms attached to the
tooth and perhaps in or near the gingival sulcus.
 The interaction of the microorganism with the host
determines the course and extend of the resulting
disease.

Key processes of
the host bacterial
interaction in
periodontal
diseases

19
 Stages of Gingivitis: (Page BC & Schroder HE – 1976-
1982)
1. Initial lesion
2. Early lesion
3. Established lesion
4. Advanced lesion

20

After 4 days of
plaque
accumulation
Neutrophilis
migration
Healthy
junctional
epithelium and
connective tissue
Inflammatory
cell infiltration

Mononuclear cell infiltration Small and medium
sized lymphocytes

Leukocyte traversing the
vessel wall to enter into
the gingival connective
tissue
Extravascular and
intravascular
lymphocytes

Pathways of inflammation from the
gingiva into the supporting tissues
in periodontitis

25

26
 The cellular and fluid inflammatory exudate causes
degeneration of the surrounding connective tissue,
including the gingival fibers.
 Just apical to the junctional epithelium, collagen fibers
are destroyed, and the area become occupied by
inflammatory cells and edema.

Connective tissue metabolism
27
 Two mechanism associated with collagen loss:
1. Matrix metalloproteinases
2. Fibroblasts phagocytosis.

28
Extracellular pathway of
collagen degradation
Intracellular pathway of
collagen degradation
Periodontics: B M Eley and J D Manson. 5th ed.

Periodontics: B M Eley and J D Manson. 5th ed.29

31
Periodontology 2000, Vol. 3, 1993, 9-38
Fibroblasts
phagocytos
is of
collagen

32
 As a consequence of the
loss of the collagen, the
apical cells of the
junctional epithelium
proliferate along the root,
extending fingerlike
projections two or three
cells in thickness.

33
 The coronal portion of the junctional epithelium detaches
from the root as the apical portion migrates.
 Thus the sulcus bottom shifts apically, and the oral
sulcular epithelium occupies a gradually increasing
portion of the sulcular lining. (Schroeder HE, Attstrom R-
1980)
 Extension of the junctional epithelium along the root
requires the presence of healthy epithelial cells.
 Marked degeneration or necrosis of the junctional
epithelium impairs rather than accelerates pocket
formation.

Soft tissue wall
34
Interdental papilla with
suprabony pocket
Lateral epithelial wall

Bacterial invasion
36
 Hillmann et al. have reported the presence in
gingiva:
 Porphyromonas gingivalis
 Prevotella intermedia
 Actionobacillus actinomycetemcomitans

Bacterial penetration into
epithelium and connective
tissue
Bacteria in intercellular space

Theories of pocket formation
Periodontics revisited: Shalu Bathia
History of Periodontology: Fermin Carranza-2003
38
1. E. Wilfred Fish (1948): destruction of gingival fibers is
a prerequisite for the initiation of pocket formation.
2. Bernhard Gottlieb (1946): the initial change in pocket
formation occurs in cementum
3. Aisenberg (1948): stimulation of the epithelial
attachment by inflammation rather than destruction of
gingival fibers is prerequisite for the initiation of
periodontal pocket.

39
4. William Skillen(1930): pathological destruction of the
epithelial attachment due to infection or trauma is the
initial histologic change in pocket formation.
5. Harold Keith Box(1941): the periodontal pocket is
initiated by invasion of bacteria at the base of the
sulcus or the absorption of bacterial toxins through the
epithelial lining of the sulcus.
6. Hermann Becks(1929): pocket formation is initiated
as a defect in suclus
Periodontics revisited: Shalu Bathia

40
7. Wilkinson(1935): proliferation of the epithelium of the
lateral wall, rather than epithelium at the base of the
sulcus, is the initial change in the formation of
periodontal pocket.
8. W. W. James and A. Counsell(1927): two stage
pocket formation
1) Proliferation of the epithelial attachment (subgingival
epithelium)
2) Loss of superficial layer of proliferated epithelium,
which produces space or pocket
9. J Nuckolls: inflammation is the initial change in the
formation of periodontal pocket Periodontics revisited: Shalu Bathia

45
Microtopography of gingival wall
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

Different areas of pocket wall surface

Area of ulceration in the lateral wall of periodontal pocket

48
 Edematous pocket wall
 Fibrotic pocket wall
Periodontal pockets as a Healing
lesion

Root surface wall
49
Deepening of
pocket
Destruction of
collagen fibers
embedded in
cementum
Degeneration of
sharpey’s fiber.
Which allows
Penetration & growth of
bacteria in CDJ &
dentinal tubules
It leads to Fragmentation &
breakdown of cementum resulting in
necrotic cementum, separated from
tooth by masses of bacteria

Caries on root surfaces exposed by periodontal disease

Cementum necrosis

Chemical changes in cementum
52
Area of increased mineralization are probably a result of
exchange, on exposure to the oral cavity of minerals &
organic components at the cementum saliva interface.
-Increased mineral content of exposed cementum is
seen.
-Minerals that are increased on diseased root surface
include calcium, magnesium, phosphorus & fluoride.
Microhardness remains unchanged.
- Development of highly mineralized superficial layer may
increase tooth resistance to decay.

53
Areas of Demineralization-
- Area of demineralization are often related to root
caries.
-Exposure of oral fluid & bacterial plaque results in
proteolysis of embedded remnants of sharpey’s fiber.
-The cementum may be softened & my undergo
fragmentation & cavitation.
-Unlike enamel caries , root surface caries tend to
progress around rather into the tooth.

54
 Active root caries lesion appear as well defined yellowish or light
brown areas, are frequently covered by plaque & have a softened or
leathery consistency on probing.
 Inactive carious lesions are well defined darker lesions with a
smooth surfaces and harder consistency on probing.
 The dominant microorganism in root surface caries is A. Viscosus.
 Other microorganisms such as A Naelundii, S Mutans, S Sanguis,
S. Salivarius, Bacillus Cereus have been found to produce root
caries in animal models.

55
Areas of cellular resorption of cementum & dentin
-are common in roots unexposed to periodontal disease.
-These areas are of no particular significance because they
are symptom free and as long as root is covered by PDL,
they are likely to undergo repair.
-However, if roots exposed to progressive pocket formation
before repair occurs, these areas appears as isolated
cavitations that penetrate into dentin.
-these area can be differentiated from cementum caries by
their clear cut outline and hard surface.
-They may be source of considerable pain, requiring the
placement of a restoration.

Surface morphology of tooth wall

Periodontal disease activity
57
 Periods of inactivity
 Periods of activity
 McHenry et al. in 1981 conducted study based
on radioiodine 125I absorptionmetry, confirmed
that bone loss in untreated periodontal disease
occurs in an episodic manner.

Relationship of attachment loss
and boss loss to pocket depth58
Same pocket depth with different amounts of recession

59
Different pocket depth with same amount of attachment loss

60
Suprabony Pocket Infrabony Pocket
Base of pocket coronal to level of
alveolar bone.
Base of pocket is apical to crest of
alveolar bone.
Pattern of bone destruction is
horizontal.
Pattern of bone destruction is vertical.
Interproximally transseptal fibers are
arranged horizontally in the space
between the base of the pocket and
the alveolar bone.
Interproximally transseptal fibers are
oblique rather than horizontal.
On the facial and lingual surface, the
PDL fibers beneath the pocket follow
their normal horizontal oblique course
between the healthy cementum of the
tooth and the alveolar bone.
On the facial and lingual surface, the
PDL fibers follow the angular bone
pattern of the adjacent bone. They
extend from the healthy cementum
between the base of the pocket along
the base and over the crest to join with
the outer periosteum (over the bone).

61
Clinical features Histopathological Features
Bluish red discoloration of gingival
wall of periodontal pocket,
Caused by Circulatory stagnation
Flaccidity Destruction of gingival fibers &
surrounding tissue
Smooth shining surface Atrophy of epithelium & edema
Pitting on pressure Edema & degeneration
Pink & firm gingival wall Predomination of fibrotic changes over
exudation & degeneration in outer
surface of pocket wall
Bleeding by gentle probing Vascularity, thinning & degeneration of
epithelium & proximity of engorged vessel
to inner surfaces
Pain in periodontal pocket on
exploration with probe
Pain due to ulceration of inner aspect of
pocket wall
Pus expression by application of
digital pressure
Pus occurs with suppurative inflammation
of inner wall

Etiopathogensis of periodontal pocket

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