PERIODONTAL POCKET

DEFINITION

Pathologically deepened gingival sulcus

MECHANISMS
Deepening of the sulcus may occur by:

Coronal movement of the gingival margin. Apical displacement of the gingival attachment. Combination.

CLASSIFICATION

Gingival pocket- (Relative/false): Formed by gingival enlargement without destruction of the underlying periodontal tissue.
Periodontal Pocket- (Absolute/true): Caused by actual loss of connective tissue attachment to the root surface.

INFRABONY:- (Intrabony, sub-crestal/intra alveolar) bottom of the pocket is apical to the level of ;the adjacent alveolar bone. Lateral pocket wall lies between the tooth and the alveolar bone SUPRABONY:- (Supra crestal/Suproalveolar) bottom of the pocket is coronal to the underlying alveolar bone

TYPES OF POCKETS

Pockets can involve one two or more tooth surfaces and can be of different depth and types on different surfaces of the same tooth.

SIMPLE / COMPOUND / COMPLEX POCKETS

CLINICAL FEATURES

Signs:Bluish red thickened marginal gingiva. Bluish red vertical zone from the gingival margin to the alveolar mucosa. Gingival bleeding and /or suppuration. Tooth mobility. Diastema formation.
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SYMPTOMS

Localized pain or pain deep in the bone Method of location & determining the extent:-

Probing of the gingival margin along each tooth surface.

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PATHOGENESIS

Caused by micro organisms and their products which produce pathologic tissue changes that lead to deepening of the gingival sulcus. Changes involved in the transition from normal gingival sulcus to pathologic periodontal pocket are associated with different proportions of bacterial cells in dental plaque. Healthy gingiva - (coccoid cell straight rods) Diseased gingiva - (spirochetes/motile rods)
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FORMATION

Inflammatory change in the connective tissue wall of the gingival sulcus caused by bacterial plaque. Cellular and fluid inflammatory exudates cause degeneration of surrounding connective tissue including the gingival fibers. Just apical to JE the area of destroyed collagen fibers develops & becomes occupied inflammatory cells/ edema. Apical to this is zone of partial destruction area of normal attachment.
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INFLAMED / NORMAL TISSUE

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2 hypothesis regarding mechanism of loss of collagen:

Collagenase & other lysosomal enzymes from PMN & macrophage become extra cellular & destroy collagen.
Fibroblasts phagocytoze collagen fibers.
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CHANGES IN JUNCTIONAL EPITHELIUM

As a consequence of the loss of collagen the apical portion of JE proliferates along the root extending finger like projections two or three cells in thickness. As a result of inflammation PMNs invade the coronal end of JE in increasing numbers. When number. reaches approx 60% or more, JE looses cohesiveness. The coronal portion of JE detaches from the root as the apical portion migrates.
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IMPORTANCE OF CELL VIABILITY

Extension of JE along the root requires the presence of healthy epithelial cells. Marked degeneration or necrosis of JE retards, rather than accelerate pocket formation. Degenerative changes are more severe in epithelium of lateral pocket wall rather than at the base of periodontal pocket.
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With continuous inflammation, the gingiva increases in bulk and the crest of the gingival margin extends towards the crown. JE continues to migrate along the root & separates from it. The epithelium of lateral wall proliferates to form bulbous cord like extensions into the inflamed connective tissue. Leukocytes & edema from CT infiltrate the epithelium lining the pocket resulting in various degree of degeneration and necrosis
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FEEDBACK MECHANISMS

Plaque Gingival inflammation Pocket formation more plaque. Rationale for pocket reduction is based on the need to eliminate areas of plaque accumulation.

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HISTOPATHOLOGY

Changes occurring in the initial states of gingival inflammation Microorganisms cause damage to epithelium & CT cells & to intercellular constituents such as collagen, ground substance and glycocalyx. The resultant widening of the spaces between the JE cells during early gingivitis may permit injurious agents derived from bacteria or bacteria themselves to gain access to the CT. Once pocket is formed several microscopic features are present
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SOFT TISSUE WALL

Connective Tissue: edematous/plasma cell approximately 80% /lymphocytes/PMNs Blood vessels increased, dilated and engorged. Shows varying degree of degeneration and proliferation of endothelial cells with new capillary, fibroblast and collagen formation. Single/ multiple necrotic foci occasionally present.
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JUNTIONAL EPITHELIUM & LATERAL WALL

JE at base is much shorter than that of a normal sulcus. Reduced to 50-100 m (corono-apical length). Normally more than 500 m. Epithelium of lateral wall shows striking proliferative & degenerative changes. Epithelial buds or interlacing cords of epithelial cells project from lateral wall farther apically than the JE.
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Epithelial projections as well as the remainder of the lateral epithelium are densely infiltrated by leukocytes and edema from the inflamed CT. Cells undergo vacuolar degeneration rupture vesicles degeneration necrosis ulceration of lateral pocket wall exposure of underlying CT Suppuration. Severity of degenerative changes are not associated with depth.
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MICROTOPOGRAPHY OF GINGIVAL WALL OF POCKET

Soft tissue wall has several areas where different types of activity take place. electron microscopy shows These findings suggest pocket wall is constantly changing as a result of interaction between the host and the bacteria.

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Areas of relative quiescence- relatively flat surface with minor depressions & mounds & occasional shedding of cells. Areas of Bacterial Accumulation- appear as depressions on the epithelial surface with abundant debris & bacterial clumps penetrating into the enlarged intercellular space. Areas of emergence of leukocytes- Through holes between cells. Areas of leukocyte-bacterial interaction
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Areas of intense epithelial desquamationSemi attached and folded epithelial squames, sometimes partially covered with bacteria. Areas of ulcerationAreas of hemorrhage- with numerous erythrocytes Bacteria accumulate- triggering emergence of leukocytes leukocyte-bacterial interaction intense epithelial desquamation ulceration/ hemorrhage
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PERIODONTAL POCKET AS HEALING LESIONS

They are chronic inflammatory lesions & are constantly undergoing repair.

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Destructive changes- Characterized by the fluid & cellular inflammatory exudates /associated degenerative changes initiated by plaque bacteria. Constructive changes- Formation of blood vessels in an effort to repair the tissue damage caused by inflammation

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Complete healing does not occur because of persistence of local irritants. Balance between destructive & constructive changes determines clinical features such as color, consistency/surface texture of the pocket wall. If destructive phase predominates- The pocket wall is bluish red, soft, spongy, friable, smooth & shiny (EDEMATOUS POCKET WALL). If constructive phase predominates pocket wall is more firm & pink (FIBROTIC POCKET WALL)
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POCKET CONTENTS

Debris consisting principally of micro-organisms & their products (enzymes, endotoxins & metabolic products). Gingival fluid. Food remnants. Salivary mucin. Desquamated epithelial cells: leukocytes Plaque covered calculus projecting from tooth surface.
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PURULENT DISCHARGE - PUS

Purulent exudates if present consist of living, degenerated and necrotic leukocytes, living bacteria, serum and fibrin. Pus - common but secondary feature. It reflects the nature of inflammatory changes but not the depth of pocket/severity of destruction. Extensive pus may be seen in shallow pocketsDeep pockets may have little pus.
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CHECKING FOR PUS DISCHARGE

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ROOT SURFACE WALL

Important becausemay perpetuate periodontal Infection Cause pain Root Cementum suffers

Structural Chemical Cytotoxic changes

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STRUCTURAL CHANGES

Presence of pathologic granules- Areas of collagen degeneration or where collagen fibrils are not fully mineralized. Areas of increased mineralization It is a result of exchange, on exposure to oral cavity of minerals and organic component at cementum saliva interface. Areas of demineralization - Related to root caries. Proteolysis of Sharpeys fibers due to exposure to oral fluids. Cementum may softened fragmentation cavitation. organism A viscous Tooth may not be painful but exploration reveals the defect
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CHEMICAL CHANGES

Mineral content of exposed cementum increases by absorption from its local environment Ca, Mg, P & F increases in diseased root surface. Microhardness remains unchanged.

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CYTOTOXIC CHANGES
Bacterial penetration can be found as deep as the CDJ. Zones at the bottom of pocket: 1. Cementum covered by calculus 2. Attached Plaque : 100-500m 3. Zone of unattached Plaque : apical to it 4. Zone where the junctional epithelium is attached to the tooth 5. Zone of semi destroyed connective tissue fiber.

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POCKET BOTTOM

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BIOLOGIC / HISTOLOGIC POCKET DEPTH: Distance from the base of the pocket to the gingival margin

CLINICAL / PROBING POCKET DEPTH:

The distance to which an instrument penetrates inside the pocket

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POCKET BOTTOM

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PERIODONTAL DISEASE ACTIVITY

Periodontal pocket goes through periods of quiescence and exacerbation Quiescence- decreased inflammatory response Little/no loss of bone & connective tissue attachment ( Period of inactivity)

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EXACERBATION
1.Build up of unattached plaque Gm -ve motile anaerobic bacteria 2. Bone/connective tissue loss (pocket deepens)

Bone loss in untreated periodontitis occurs in an episodic manner.

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SITE SPECIFICITY

Periodontal destruction does not occur in all parts of the mouth at the same time, rather few teeth/few aspects Therefore severity of Periodontal destruction increases by: Development of new disease sites Increased breakdown of existing sites
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PULP CHANGES ASSOCIATED WITH PERIODONTAL POCKET

Inflammation may reach pulp & cause pain Involvement may occur through apical foramen or lateral canal. Atrophic/inflammatory changes occur in pulp
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RELATION OF LOSS OF ATTACHMENT AND BONE LOSS TO POCKET

The severity of attachment loss is generally but not always correlated with pocket depth Degree of attachment loss depends on the location of the base of the pocket on the root surface where as the pocket depth is the distance between the base of the pocket and the crest of gingiva. Severity of bone loss is generally but not always correlated with pocket depth.
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POCKET DEPTH / CLINICAL ATTACHMENT LEVEL

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SUPRA / INFRABONY POCKET

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SUPRABONY POCKET 1.Base of pocket coronal to level of alveolar bone.

INFRABONY POCKET 1.Apical to the crest.

2.Pattern of bone destruction is 2.Vertical (angular) horizontal. 3.Interproximal transseptal fibers that are restored during progressive Periodontal disease are arranged horizontal in the space between the base of the pocket and alveolar bone. 3.Transseptal fibers are arranged Obliquely :-Extend from the cementum beneath the base of pocket along the bone & over the crest to the cementum of adjacent tooth.

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THANKS

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PERIODONTAL ABSCESS
Lateral or Parietal abscess. A localized purulent inflammation in the periodontal tissue. May occur: Extension of infection from Periodontal pocket. Lateral extension of inflammation from inner surface of Periodontial pocket into Connective tissue of the pocket wall. In a pocket that describes a tortuous course Periodontal abscess may form in cul-de-sac.

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TYPES OF POCKETS

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Incomplete removal of calculus > Calculus remaining behind > Gingival wall shrinks occluding the Periodontal pocket & abscess occurs in the sealed off portion of the pocket. Occurs in absence of Periodontal disease when trauma to tooth or perforation of lateral wall of tooth during endodontic treatment.

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PERIODONTAL CYST

Uncommon lesion Localized destruction of Periodontal tissue along lateral root surface, most often in the mandibular canine-Premolar area.

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ETIOLOGIES

Odontogenic Cyst Lateral dentigerous Cyst Primordial Cyst Stimulation of epithelial rests of the periodontal ligament by infection from a periodontal abscess or from the pulp through an accessory route canal.

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CLINICAL FEATURES / DIAGNOSIS

Periodontal cyst is usually asymptomatic & without grossly detectable changes. May present as a localized tender swelling. Radiographically appears on the side of the root as radiolucent area bordered by radioopaque line. Radiographically: cannot be differentiated from Periodontal abscess.
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