PERIODONTAL POCKET
Content Introduction Classification Clinical features Theories of pathogenesis Pathogenesis Histopathology Periodontal Disease Activity Site Specificity Relation of Attachment Loss to Pocket Depth Conclusion References
Introduction
Pathologically deepened gingival sulcus
Classification
Gingival pocket (pseudo pocket)
Periodontal pocket
Classification
Suprabony / Supracrestal / Supraalveolar
Intrabony/ Infrabony / Subcrestal / Intraalveolar
Classification
Suprabony Pocket Intrabony Pocket
Base of
Pattern of
destruction
Classification
Suprabony Pocket Intrabony Pocket
Transseptal
fibers
PDL fibres
(Facial &
Lingual)
Classification
Simple Compound Complex
Clinical Features
Extrusion & migrationDiastema
Enlarged, bluish-red marginal gingiva“Rolled” edge
Reddish-blue vertical zone
Shiny & puffy gingivaGingival bleeding
Purulent exudate
Clinical Features
Localized pain/ Sensation of
pressureFoul 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
Theories of Pathogenesis
Two stage pocket formation (James & Counsell, 1927)
Proliferation of subgingival epithelium
Loss of superficial layers of proliferated epithelium
Space or pocket
Theories of Pathogenesis
Pocket formation : Initiated in a defect in sulcus wall
(Becks,1929)
Between oral & enamel epithelium
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
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
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
Theories of Pathogenesis
Orban & Weinmann,1942
o Subgingival bacterial growth : Secondary to pocket
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
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
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
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
Theories of Pathogenesis
o Basal epithelial cells at bottom of sulcus : Proliferate into
connective tissue
o Open lesion
o Repair of lesion : Periodontal pocket
Theories of Pathogenesis
Waerhaug, 1976
o Bacteria spreading subgingivally Pocket formation
Theories of Pathogenesis
Schroeder and Attstrom (1980)
Microbial invasion of subgingival dentogingival junction
Destroy coronal epithelial attachment
Pathological pockets
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
Theories of Pathogenesis
o Advanced lesions
Deep pocket epithelium
Toxic bacterial products
Mechanical irritation of calculus
Thin and ulcerated
Typical periodontal pocket
Pathogenesis
Initial lesion : Inflammation of gingiva
Not a predictor of future attachment & bone loss Hillman 1998
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
PhagocytosisDeporter 1980
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
Histopathology
Soft tissue wall
o Connective tissue
Exudative
ProliferativeDegenerative
Histopathology
o Junctional epithelium
50-100 µm
Cells : Well formed & in good condition
Slight to marked degeneration
Histopathology
o Lateral wall
Most severe degenerative changes
Epithelial buds or interlacing cords of epithelial cells
Dense infiltration
Cells : Vacuolar degeneration & form vesicles
Ulceration & suppuration
Histopathology
Severity of degenerative changes : Not related to pocket depth
Epithelium of gingival crest : Intact with prominent retepegs
Predominant gram-negative filaments, rods & cocci
? Bacterial invasion
? Passive translocation of plaque bacteria
Histopathology
Microtopograghy
o Irregular oval/elongated areas : 50 - 200 microns
Saglie et al 1975
Relative quiescence
Bacterial accumulation
Emergence of leucocytes
Leucocytes bacterial interaction
Intense epithelial desquamation
Ulceration
Haemorrhage
Histopathology
Histopathology
Periodontal pocket as a healing lesion
Chronic inflammatory lesions
Persistence bacterial attack
RepairDegeneration of new tissue elements
Histopathology
Destructive tissue
changes
Constructive tissue changes
Edematouspocket
Fibrotic pocket
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
Histopathology
o Significance of Pus Formation
Secondary sign
Nature of the inflammatory changes
Not an indication of depth of pocket / severity of destruction
Histopathology
Root surface wall
Structural Chemical
Cytotoxic
Histopathology
Structural Changes
Pathologic granules
Areas of increased mineralization
Areas of demineralization
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
Histopathology
o Areas of demineralization: Root carries
Herting 1967Oral fluid & bacteria plaque
Proteolysis of embedded remnants of sharpeys fibers
Cementum softened
Fragmentation & cavitation
Progress around the tooth
Histopathology
Active root caries lesions
Inactive root caries lesions
Histopathology
Severe Cases
Actinomyces viscosus
Caries Pulpitis
Involvement of cementum
Bacterial penetration of dentinal tubules
Destruction of dentin
Histopathology
Necrotic cementum : Removed by scaling & root planing
Areas of cellular resorption of cementum & dentin : Roots
unexposed by periodontal disease
Histopathology
Chemical Changes
o Mineral content increased
o Calcium, Magnesium, Phosphorus, Fluoride
o Microhardness : Unchanged
o Exposed cementum : Resistant to decay
Selvig 1966
Histopathology
Cytotoxic Changes
o Bacterial penetration : Cemento-dentinal Junction
o Endotoxins
o Diseased root fragments : Prevents in-vitro attachment of
human gingival fibroblasts
Histopathology
Surface Morphology of Tooth Wall
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
Periodontal Disease Activity
• Exacerbation
Episodic bursts of activity
• Quiescence
Periods of remission
Bone loss in untreated periodontal disease occurs in episodic manner
McHenry 1981
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
Site Specificity
Some aspects of some teeth at any given time
New site : Increased severity
Relation of Attachment loss to Pocket Depth
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.
References Newman MG, Takei HH, Klokevold PR, Carranza FA. Carranza’s
Clinical Periodontology. Saunders Elsevier;10th Edition.
Glickman I. Clinical Periodontology. WB Saunders Co; 4th Edition.
Greenstein, Lamster. Changing Periodontal Paradigms: Therapeutic Implications. Int J Periodontics Restorative Dent 2000;20:337-357.
Takada, Donath. Mechanism of pocket formation. J Periodontol 1988; 59; 215-221.
Grant, Stern, Listgarten. Periodontics. CV Mosby Co; 6th ed.
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