10. Clinical Features
Localized pain/
Sensation of
pressure
Foul taste
Tendency to suck
material
Radiating pain
“Deep in the bone”
Gnawing feeling Urge to dig
Foods sticks
between teeth
Sensitivity to heat &
cold
Tooth ache
11. Theories of Pathogenesis
Two stage pocket formation (James & Counsell, 1927)
Proliferation of subgingival epithelium
Loss of superficial layers of proliferated epithelium
Space or pocket
12. Theories of Pathogenesis
Pocket formation : Initiated in a defect in sulcus wall
(Becks,1929)
Between oral & enamel epithelium
13. Theories of Pathogenesis
Pathologic destruction of epithelial attachment due to infection
or trauma : Initial histologic change in pocket formation
(Skillen, 1930)
o Epithelial attachment : Area of low resistance
Infection / Trauma
Pathologic dissolution of epithelial attachment
Pocket formation
Accumulation of debris in pocket
14. Theories of Pathogenesis
Proliferation of the epithelium of lateral wall is the initial
change in formation of the periodontal pocket (Wilkinson, 1935)
o Proliferation & down growth of oral epithelium Thickening of
epithelial lining of sulcus Cells along inner aspect of sulcus
deprived of nutrition Degeneration & necrosis
Calcification of necrotic cells Separation of calcified masses
from adjacent normal epithelium Pocket or trough
15. Theories of Pathogenesis
Periodontal pocket is initiated by invasion of bacteria at base of
the sulcus or absorption of bacterial toxins through epithelial
lining of sulcus (Box,1941)
o Initial invasion of bacteria at base of sulcus Inflammation in
underlying CT Ulceration at base Sloughing of
epithelium Loss of attachment to cementum Progressive
loss of CT & penetration of pocket into deeper tissues
17. Theories of Pathogenesis
The initial change in pocket formation occurs in the cementum.
(Gottlieb 1926, 1946)
o Continuous eruption of teeth : Down growth of epithelial
attachment
o Continues deposition of new cementum : Prevents accelerated
migration of epithelial attachment
o Normal deposition of cementum impaired : Dissolution of
organic connection between cementum & gingiva
18. Theories of Pathogenesis
Destruction of gingival fibers : Pre-requisite for initiation of
pocket formation (Fish, 1948)
Top most fibers digested & absorbed
Epithelium proliferates until healthy fiber is reached
19. Theories of Pathogenesis
Simulation of the epithelial attachment by inflammation :
Prerequisite for initiation of the periodontal pocket (Aisenberg
& Aisenberg, 1948)
o Inflammation Epithelium migrates along root Epithelial
cells burrow between intact gingival fibers Enmesh
connective tissue fibers in epithelial network Secondary fiber
degeneration
20. Theories of Pathogenesis
Inflammation is the initial change in the formation of the
periodontal pocket (Nuckolls & Dienstein, Bell & Rule, 1950)
o Inflammation in connective tissue
↑ Mitotic activity
↑ Keratin
Cellular desquamation
21. Theories of Pathogenesis
o Basal epithelial cells at bottom of sulcus : Proliferate into
connective tissue
o Open lesion
o Repair of lesion : Periodontal pocket
23. Theories of Pathogenesis
Schroeder and Attstrom (1980)
Microbial invasion of subgingival dentogingival junction
Destroy coronal epithelial attachment
Pathological pockets
24. Theories of Pathogenesis
Takata & Donath (1988)
o Early & established lesion
Degenerative changes in most coronal part of JE
Intraepithelial cleavage
Degeneration of cells lining the cleavage
Deep crevice formation
25. Theories of Pathogenesis
o Advanced lesions
Deep pocket epithelium
Toxic bacterial products
Mechanical irritation of calculus
Thin and ulcerated
Typical periodontal pocket
26. Pathogenesis
Initial lesion : Inflammation of gingiva
Not a predictor of future attachment & bone loss
Hillman 1998
27. Pathogenesis
Cellular & inflammatory exudate : Degeneration of CT & fibers
Apical Cells of JE : Fingerlike projections
Coronal portion : Detaches from the root
60% PMNs : Loss of tissue cohesiveness
Sulcus shifts apically
Matrix Metalloproteinases
Taichman 1968, Takada 1988
Phagocytosis
Deporter 1980
28. Pathogenesis
Gingival sulcus Periodontal pocket Plaque removal impossible
Rationale for pocket reduction : Eliminate areas of plaque
accumulation
Plaque
Gingival
Inflammation
Pocket
formation
More plaque
formation
35. Histopathology
Periodontal pocket as a healing lesion
Chronic inflammatory lesions
Persistence
bacterial attack
Repair
Degeneration of
new tissue
elements
37. Histopathology
Pocket contents
o Debris
o Microorganisms & products
o Gingival fluid
o Food remnants
o Salivary mucin
o Desquamated epithelial cells
o Leukocytes
o Plaque-covered calculus
o Purulent exudate
38. Histopathology
o Significance of Pus Formation
Secondary sign
Nature of the inflammatory changes
Not an indication of depth of pocket / severity of destruction
41. Histopathology
o Pathologic granules : Collagen degeneration / Incompletely
mineralized collagen fibrils
Bass 1951
o Areas of increased mineralization : Exchange of minerals &
organic components at cementum-saliva interface
Selvig 1969
Perfection of crystal
Subsurface cuticle
10-20µm thick
42. Histopathology
o Areas of demineralization: Root carries
Herting 1967
Oral fluid & bacteria plaque
Proteolysis of embedded remnants
of sharpeys fibers
Cementum softened
Fragmentation & cavitation
Progress around the tooth
44. Histopathology
Severe Cases
Actinomyces viscosus
Caries Pulpitis
Involvement
of
cementum
Bacterial
penetration
of dentinal
tubules
Destruction
of
dentin
45. Histopathology
Necrotic cementum : Removed by scaling & root planing
Areas of cellular resorption of cementum & dentin : Roots
unexposed by periodontal disease
46. Histopathology
Chemical Changes
o Mineral content increased
o Calcium, Magnesium, Phosphorus, Fluoride
o Microhardness : Unchanged
o Exposed cementum : Resistant to decay
Selvig 1966
47. Histopathology
Cytotoxic Changes
o Bacterial penetration : Cemento-dentinal Junction
o Endotoxins
o Diseased root fragments : Prevents in-vitro attachment of
human gingival fibroblasts
49. Periodontal Disease Activity
Models of Disease Progression
o Continuous
o Random / Episodic burst
o Asynchronous multiple burst
o Synchronous burst
o Epidemiologic
o Brownian motion / Stochastic
o Fractural
50. Periodontal Disease Activity
• Exacerbation
Episodic bursts
of activity
• Quiescence
Periods of
remission
Bone loss in untreated periodontal disease occurs in episodic
manner
McHenry 1981
51. Periodontal Disease Activity
Periods of quiescence Period of exacerbation
Reduced inflammatory
response
Little or no bone & CT
attachment loss
Build-up of unattached
plaque
Bone & connective tissue
attachment lost
Pocket deepens
Bleeding & Gingival exudate
Epithelium thin & ulcerated
Inflammatory infiltrate
Motile organisms & spirochetes
52. Site Specificity
Some aspects of some teeth at any given time
New site : Increased severity
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.