Periodontal pockets

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

pocket

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


Pocket formation : Initiated in a defect in sulcus wall

(Becks,1929)

Between oral & enamel epithelium


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


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


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


Orban & Weinmann,1942

o Subgingival bacterial growth : Secondary to pocket


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


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


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


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


o Basal epithelial cells at bottom of sulcus : Proliferate into

connective tissue

o Open lesion

o Repair of lesion : Periodontal pocket


Waerhaug, 1976

o Bacteria spreading subgingivally Pocket formation


Schroeder and Attstrom (1980)

Microbial invasion of subgingival dentogingival junction

Destroy coronal epithelial attachment

Pathological pockets


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


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


• Exacerbation

Episodic bursts of activity

• Quiescence

Periods of remission

Bone loss in untreated periodontal disease occurs in episodic manner

McHenry 1981


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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Periodontal pockets

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