Pdl Pocket

GOOD MORNING !

Prepared Under the Guidance Of :DR.SURESH D KDR.KAUSHAL LUTHRADR.RAJVIR MALIKDR.SHALU CHANDNA

Presented By :

DR.SAMIR ANAND

CONTENTS

• INTRODUCTION• DEFINITIONS• CLASSIFICATION• SIGNS & SYMPTOMS• PATHOGENESIS• HISTOPATHOLOGY OF POCKET WALL

– SOFT TISSUE WALL– MICROTOPOGRAPHY OF GINGIVAL WALL– PERIODONTAL POCKETS AS HEALING LESIONS– POCKET CONTENTS– ROOT SURFACE WALL

CONTENTS

• CO-RELATION OF CLINICAL & HISTOPATHOLOGICAL FEATURES

• TREATMENT STRATEGIES• CLINICAL SIGNIFICANCE

– PERIODONTAL DISEASE ACTIVITY– SITE SPECIFICITY– RELATIONSHIP BETWEEN LOSS OF

ATTACHMENT & BONE LOSS WITH POCKET DEPTH

– EFFECT OF TFO ON INFRABONY PCKET FORMATION

– PULP CHANGES ASSOCIATED WITH PERIODONTAL POCKET

– FATE OF POCKET EPITHELIUM IN PERIODONTAL TREATMENT

• CONCLUSION

INTRODUCTION

DEFINITION

• defined as a pathologically deepened gingival sulcus

• is one of the most important clinical features of periodontal disease.

• Deepening of gingival sulcus may occur by – coronal movement of the gingival margin– apical displacement of the gingival

attachment – or a combination of the two .

DEFINITIONS

• Glickman (1953) : “ A periodontal pocket is a pathologically deepened gingival sulcus .”

• Goldman (1964) : “ A pocket may be defined as a diseased gingival attachment”

• Shafer (1983) : defines it “as a pathologically altered gingival sulcus, lined to a variable extent with pocket epithelium & classified as either a gingival pocket or a periodontal pocket”

• Glossary of Periodontic terms (1992) : defines it “as a pathologic fissure bordered on one side by the tooth and on the opposite side by crevicular epithelium & 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.

CLASSIFICATION• A general classification of periodontal pockets

may be :– Depending upon its morphology

• Gingival/false/relative pocket.• Periodontal/ absolute/true pocket.• Combined pocket.

– Depending upon its relationship to crestal bone• Suprabony/ supracrestal/ supra-alveolar pocket.• Infrabony/intrabony /subcrestal/intra-alveolar pocket.

– Depending upon the number of surfaces involved:

• Simple pocket -involving one tooth surface.• Compound pocket - involving two or more tooth surfaces.• Complex pocket - where the base of the pocket is not in

direct communication with the gingival margin. It is also known as spiral pocket.

CLASSIFICATION

– Depending upon the nature of the soft tissue wall of the pocket.

• Edematous pocket.• Fibrotic pocket.

– Depending upon the disease activity• Active pocket.• Inactive pocket.

– Pockets adjacent to edentulous areas • Class I /Central lesions• Class II lesions• Class III/ Unilateral central lesions• Class IV / Bilateral central lesions

according to morphology & relationship to

adjacent structures Gingival pocket :

– formed by gingival enlargement without destruction of the underlying periodontal tissues.

– sulcus is deepened because of the increased bulk of the gingiva.

Periodontal pocket : – occurs with the destruction of

the supporting periodontal tissues.

– Progressive pocket deepening leads to destruction of the supporting periodontal tissues and loosening and exfoliation of the teeth.

Gingival pockets

Periodontal pocket2 types :

• Suprabony (Supracrestal or supraalveolar):– the bottom of the pocket is coronal

to the underlying alveolar bone.

• Infrabony (intrabony or subcrestal or intraalveolar): – the bottom of the pocket is apical

to the level of the adjacent alveolar bone.

– the lateral pocket wall lies between the tooth surface and alveolar bone.

Periodontal Pockets

According to

Gottlieb

“an infrabony pocket is not an intra – alveolar pocket”.

because…..• alveolar housing of the affected tooth is

always destroyed in the area of pocket formation.

• thus an infrabony pocket is impossible on the labial side of an upper anterior tooth

• as once the alveolar bone is destroyed here, there is no bone left.

• However, on the palatal side of the same tooth, bone of the hard palate backs the alveolar bone proper.

• Hence, if the alveolar bone disappears from such an area, the palatal bone remains causing the infrabony pocket.

Distinguishing features of suprabony & infrabony pockets

Suprabony pocket Infrabony pocket

The base of the pocket is coronal to the level of the alveolar bone.

The base of the pocket is apical to the crest of the alveolar bone so that the lateral pocket wall lies between tooth surface & bone

The pattern of bone destruction is horizontal.

The pattern of bone destruction is vertical (angular).

Suprabony pocket

Infrabony pocket

Interproximally, the transseptal fibres that are restored during progressive periodontal disease are arranged horizontally in the space between the base of the pocket and the alveolar bone.

Interproximally, the transseptal fibres are oblique rather than horizontal. They extend from the cementum beneath the base of the pocket along the bone and over the crest of the cementum of the adjacent tooth.

On the facial and lingual surfaces, the PDL fibres beneath the pocket follow their normal horizontal-oblique course between the tooth and the bone.

On the facial and lingual surfaces, the PDL fibres beneath the pocket follow the angular pattern of the adjacent bone. They extend from the cementum beneath the base of the pocket along the bone and over the crest to join with the outer periosteum.

Classification of pockets according to involved tooth surfaces

Simple pocket Compound pocket Complex pocket

Simple,compound & complex pockets

• Pockets can involve one, two or more tooth surfaces and can be of different depths and types on different surfaces of the same tooth and on approximating surfaces of the same interdental space.

• Pockets can often be spiral (that is originating on one tooth surface and twisting around the tooth to involve one or more additional surfaces). – These types of pockets are most

common in furcation areas.

• Class I / Central Lesions :– Are lesions where the pocket is confined to the

center of the two proximal margins

• Class II lesions :– Are lesions where the pocket is located at a corner

but does not include the central portion.

• Class III lesions / Unilateral central lesions:– Are where the pocket encompasses one corner &

the central area of the defect.

• Class IV / Bilateral central lesions :– Are where it encompasses both the proximal areas

& the central surface as well.

Pockets adjacent to edentulous areas

Klinsberg 1971

Clinical signs • Enlarged bluish red marginal gingiva with a

‘rolled’ edge separated from the tooth surface.• reddish blue vertical zone extending from the

marginal gingiva to the attached gingiva and sometimes into the alveolar mucosa.

• break in the facio – lingual continuity of the interdental gingiva / papilla.

• Shiny, discolored and puffy gingiva associated with exposed root surfaces.

• Gingival bleeding.• Purulent discharges from the gingival margin• Loosening, extrusion and migration of teeth.• development of diastema

– the only reliable method of locating periodontal pockets and determining their extent is careful probing of the gingival margin along each tooth surface.

SYMPTOMS• Localized pain or a sensation of pressure after

eating gradually diminishes.• foul taste in localized areas.• tendency to suck material from the interproximal

spaces.• Radiating pain deep in the jaws.• gnawing feeling / feeling of itchiness in the gums.• urge to dig a pointed instrument into the gums with

relief obtained form the resultant bleeding.• Complaints that food sticks between the teeth or• teeth feel loose or • a preference to eat on the other side.• Sensitivity to heat and cold, toothache in the

absence of caries.

CLINICAL FEATURES• reliable method of locating &

determining their extent – careful probing of the gingival

margin along each tooth surface.

• On the basis of depth alone– difficult to differentiate between a

deep normal sulcus & a shallow periodontal pocket .

– In such borderline cases, pathologic changes in the gingiva distinguish the two conditions.

PATHOGENESIS• unfolding of a disease process or the sequence

of events in the development of a disease from its beginning

• comparison of periodontitis in humans & animals has provided rare insights on how the pocket deepens.

• SCHROEDER & ATTSTROM 1980 – pockets do not form in absence of bacteria; although other factors like TFO,nutritional deficiencies,hormonal abnormalities etc may influence bacteria to aid pocket formn.

• GLICKMAN 1964 summarized 10 theories :-

PATHOGENESIS• initial lesion in the development of

periodontitis is ■ inflammation of gingiva in response to a

bacterial challenge.,which produce pathologic tissue changes that lead to deepening of the gingival sulcus.

■ The deepening may occur by:– Movement of the gingival margin in the

direction of the crown [produces a gingival pocket].

– Migration of the junctional epithelium apically & its separation from the tooth surface.

– A combination of both processes.• Healthy gingiva

■ few microorganisms■ mostly coccoid cells and straight rods.

• diseased gingiva ■ increase in the number of spirochetes &

motile rods.

THEORIES REGARDING THE MICROSCOPIC TISSUE CHANGES IN THE INITIATION OF POCKET

FORMATIONI. Destruction of the gingival

fibres is a prerequisite for the initiation of pocket formation:

- concept focuses attention upon migration of the epithelial attachment along the root.

- Proliferation of epithelial attachment along the root can take place only if the attachments of the underlying gingival fibres into the cementum are destroyed.

•fibres are a barrier to the normal migratory tendency of the epithelium at the base of the sulcus. •Degeneration and necrosis of these fibers occur secondary to gingival inflammation or the action of the bacterial enzymes such as hyaluronidase. •As soon as the top most fiber is digested and absorbed the epithelium proliferates along the root until a healthy fiber is reached. •Gottlieb and Orban questioned whether proliferation of the epithelial attachment is actually dependant upon the loss of underlying gingival fibres.

•They pointed to areas of repaired idiopathic tooth resorption immediately subjacent to the epithelial attachment, and since the resorption of the tooth entailed detachment of the PDL fibers, repair would not have been possible, had the epithelium proliferated simply because the fibers had been destroyed.

•They also referred to the condition in which the epithelial attachment is attached to the enamel and is separated from the cementum by the unattached connective tissue rather than the fibers embedded in the tooth. •In such instances pathologic migration of the epithelial attachment does not occur.

II.The initial change in pocket formation occurs in the cementum•Gottlieb stressed the changes in

tooth surface rather than the gingiva for pocket formation, •he envisioned down growth of the epithelial attachment as a physiologic phenomenon, which is part of the process of continuous eruption of the teeth, which occurs throughout life. •Under physiologic conditions, the continuous deposition of new cementum acts as a barrier which prevents an acceleration in the rate of migration of the epithelial attachment.

•Nothing can induce the epithelial attachment to move apically in the presence of a highly developed cementum barrier. •If the tooth surface is of low resistance, or if there is some inhibition in the normal deposition of cementum, then inflammation or trauma can do additional harm by destroying either the cementum, or the connective tissue fibres, or both.

•This will dissolve the organic connection between the two, and the epithelium will proliferate along the root, according to its natural tendencies, •until it meets undisturbed connective tissue fibres and cementum, after its organic connection with the periodontal membrane fibres is destroyed.

•Destruction of the underlying gingival fibres is not a prerequisite for epithelial migration. •Stimulated by inflammation, the epithelium will migrate along the root without preceding destruction of the gingival fibers. •In such instances, although the underlying fibres may remain intact, the epithelial cells will burrow between the fibres and attach themselves further apically along the cementum.

III. Stimulation of the epithelial attachment due to infection or trauma is the initial histological change in pocket formation:

•In support of this hypothesis are the findings of epithelial cells attached to the cementum between individual fiber bundles.

•In certain areas, the cementum is bundle-free.

•The epithelial attachment may move between these bundles, enmeshing them in an epithelial network, producing secondary degeneration of the connective tissue fibres.

•According to Skillen, the epithelial attachment has few protective qualities for safeguarding the underlying connective tissue against spread of infection. •It is the normal down growth of the oral epithelium behind the epithelial attachment, which protects the underlying connective tissue.

IV. Pathologic destruction of the epithelial attachment due to infection or trauma is the initial histological change in pocket formation:

•The epithelial attachment is an area of low resistance, which is subject to infection. •In experimental animals, pocket formation occurs because of pathologic destruction of the epithelial attachment due to infection or trauma or both. •The question is raised as to whether accumulation of debris may not be secondary after the pocket is formed as a result of dissolution of the epithelial attachment.

V. The periodontal pocket is initiated by the invasion of bacteria at the

base of the sulcus or the absorption of bacterial toxins through the epithelial lining of the sulcus:

•According to Box, either because of imperfect junction of the epithelial cells and the cementum or extreme thinness of the epithelium, the base of the sulcus offers a poor defense against bacteria.

V. The periodontal pocket is initiated by the invasion of

bacteria at the base of the sulcus or the absorption of bacterial toxins through the epithelial

lining of the sulcus:

•In the evolution of a “ pus-pocket” the following stages follow an initial invasion of bacteria at the base of the sulcus: inflammation in the underlying connective tissue, ulceration at the base of the crevice, sloughing of the epithelium, and loss of attachment to the cementum, progressive loss of connective tissue, and penetration of the pocket into the deeper tissues. •Box also suggested that the specific infective agents possibly related to the Leptothrix falciformis are capable of deepening the pocket.

•According to Becks, the formation and maintenance of the normal sulcus results from the coordination of the degeneration of the enamel epithelium, proliferation of the oral epithelium, and atrophy of the gingival papilla. •Disturbance of this correlation, whether by inflammation or injury, induces pathologic pocket formation.•Pocket formation occurs between the oral epithelium, rather than by separation of enamel epithelium from the cuticle.

VI. Pocket formation is initiated in a defect in the

sulcus wall:

•If degeneration of the enamel epithelium from the cuticle takes place rapidly without being covered by the oral epithelium, a defect occurs in the lateral sulcus wall. •This defect constitutes a “ locus minoris resistentiae” which is a portal of entry for bacteria with resultant inflammation.

•This results in a proliferation of both the basal cells of the enamel epithelium, as well as the oral epithelium, a protective mechanism for the connective tissue. •Inflammation is a stimulant to oral epithelium proliferation. •Proliferation of oral epithelium shuts off nutrition from enamel epithelium hastening its degeneration, and increasing the pocket depth.

VII.Proliferation of the epithelium of the lateral wall, rather than

the epithelium at the base of the sulcus, is the initial change in the

formation of the periodontal pocket:

• Wilkinson regards epithelial proliferation as the primary change in the pocket formation. He describes the following sequence of changes:• Proliferation and downgrowth of the oral epithelium or proliferation of the epithelial attachment results in thickening of the epithelial lining of the sulcus. •

•The cause of this proliferation is not known, because of the increased thickness, the cells along the inner aspect of the sulcus, in relation to the tooth are deprived of their nutrition and undergo degeneration and necrosis.

•The degenerated and necrotic epithelial cells become calcified (serumal calculus). •Seperation of the calcified masses from the adjacent normal epithelium produces a pocket or trough. •These changes are followed by proliferation of the epithelium along the cementum, and detachment of its coronal portion from the root surface.

Destruction of the underlying periodontal membrane fibres and alveolar bone is subsequent to and dependent upon the primary epithelial changes. The epithelial changes, which initiate pocket formation, are not caused by infection. Inflammatory changes in the pocket formation are secondary to the epithelial changes. Wilkinson suggested that vitamin A deficiency may be an important factor in initiating pocket formation.

James and Counsell disagreed with the concept that proliferation of epithelial attachment followed by seperation from cementum forms a pocket. Instead they felt pocket formation occurs in two stages:The first stage is proliferation of the subgingival epithelium.The second stage is loss of the superficial layers of the proliferated epithelium at the base is such that it precedes the destruction of the superficial epithelium, and the pocket is therefore always lined with epithelium.

VIII. Two stage pocket formation:

•“Periodontal lesions of purely local origin have their beginnings in inflammation”.• According to Nukolls the first reaction is an imperceptible one, and consists of a nerve reflex in the epithelium, which stimulates a vascular change in the underlying connective tissue. •Inflammation in the connective tissue stimulates the following changes in the epithelial lining of the sulcus-

IX. Inflammation is the initial change in the formation of the

periodontal pocket:

# Increased mitotic activity in the basal epithelial layer, and sometimes in the prickle cell layer# Increased production of keratin with desquamation. It is the cellular desquamation adjacent to the tooth surface, which tends to deepen the pocket. The epithelial cells of the basal layer at the bottom of the sulcus and in the area of attachment proliferate downward, invade the underlying connective tissue, and break up of gingival fibres. The dissolution of connective tissue, and breakup the gingival fibres.

•The dissolution of connective tissue results in the formation of “open lesion”. •It is the repair of the lesion, in the absence of treatment, which establishes the periodontal pocket. •Granulation tissue fills in the defect created by the open lesion, and the epithelium proliferates inward. •This forms a lining of the repaired open lesion to a point where the connective tissue is attached to the root; instead it proliferates from the gingival surface to cover the connective tissue lesion created by inflammation, and thereby forms the lining of the pocket.

X. Pathologic epithelial proliferation occurs secondary to noninflammatory degenerative changes in the periodontal membrane:Noninflammatory degenerative changes in the periodontal membrane has been described as “periodontosis” – under such conditions the normal barrier afforded by the gingival fibres is diminished, this facilitates the migration of the epithelial attachment along the root and pocket formation, in the presence of local irritation.

There are many hypotheses on pocket formation. Some imply that the subgingival bacterial growth is secondary to the opening of the pocket. Contrary to this, others suggest that the pocket formation is a result of bacteria spreading subgingivally. Recently, Schroeder and Attström proposed a new hypothesis of the development of the gingival pocket using experimentally produced neutropenic dogs. They suggested that pathological pockets are formed by microbial invasion of the subgingival dentogingival junction, thus destroying the coronal epithelial attachment.

•Schroeder and Attström pointed out that almost none of the earlier studies related pocket formation to the presence of bacterial deposits. •They hypothesized that pocket formation is the result of a split in the junctional epithelium from its attachment to the tooth surface through the action of cocci.

EXPERIMENTAL STUDIES

• Animal experimentation – promising investigative approach to the

‘modus operandi’ – divided into following sections

• I. Evaluation Of The Role Of Local Irritation In Pocket Formation

• II. The Role Of Inherent Tendency Toward epithelial proliferation in pocket formation

• III. Evaluation Of The Role Of Gingival Fiber degeneration In Pocket Formation:

The series of experiments led to the following impressions

– Since degeneration of the gingival fibers and proliferation of the epithelial attachment both accompany inflammation in the course of pocket formation, it is extremely hazardous to assume a cause and effect relationship between the two types of tissue changes.

– When the gingival fibers are destroyed by a systemic disturbance, the epithelial attachment does not automatically proliferate along the root.

– A local stimulus is necessary for proliferation of the epithelium along the root at a rate, which is more rapid than normal.


– Degeneration of the gingival fibers makes it easier for stimulated epithelium to proliferate along the root. Such degeneration may result from locally induced inflammation or systemic disturbances.

– Proliferation of the epithelium is the primary change in pocket formation. When stimulated to proliferate the epithelial attachment may extend between intact gingival fiber bundles.


– Local irritation is required for the continued progress of periodontal pocket, but pocket depth is also regulated by systemic factors, which modify the condition of the periodontal tissues and affect their response to local irritation.

• There is no basis for assuming that there is only one pattern of cellular change in the transition from gingival sulcus to a periodontal pocket or one cause of pocket formation. Consideration of the evidence offered in support of the different theories regarding the initiation of pocket formation suggests that it may occur in several ways.

• It is more logical to assume that periodontal pocket generally results from a combination of factors. Variations in the combination could account for difference in the manner in which pocket formation is initiated.

• Despite conceptual limitations and a large body of evidence to the contrary,

“the idea that epithelial proliferation and apical migration with pocket

formation are cardinal events in the pathogenesis of periodontal disease is

the currently accepted concept”.

PATHOGENESIS; sequence of events

• gingivitis progresses with time to destructive periodontitis although this progression does not occur in all cases.

• sequence of events culminating in gingivitis has been separated into the initial, early and established stages and periodontitis has been designated as the ‘advanced lesion’.

The Features Seen In Advanced Lesions Include:

– Persistence of features of the previous stages.

– Extension of the lesion into alveolar bone and periodontal ligament with significant bone loss.

– Continued loss of collagen subjacent to the pocket epithelium with fibrosis at more distant sites.

– Presence of cytopathologically altered plasma cells in the absence of altered fibroblasts.

The Features Seen In Advanced Lesions Include:

– Formation of periodontal pockets.– Periods of quiescence and exacerbations.– Conversions of the bone marrow, distant

form the lesion into fibrous connective tissue.

– Widespread manifestations of inflammatory and immuno pathologic tissue reactions.• Many of these features resemble closely those

of other long-term chronic inflammatory disease of connective tissue of unknown cause, such as rheumatoid arthritis.

MECHANISM OF POCKET FORMATION:

• reflects the sum total of the responses of the host defense mechanisms to the presence and activities of bacteria

• 2 major steps:– Proliferation and apical migration of cells

of the JE, and – their subsequent degeneration and

detachment from the tooth surface.

HYPOTHESES

• Some imply that the sub gingival bacterial growth is secondary to the opening of the pocket. Contrary to this, others suggest that the pocket formation is a result of bacteria spreading sub gingivally.

• Schroeder and Attstrom (1980) proposed that many factors other than bacteria participate in determining pocket morphology. These factors include characteristic of invading flora, animal size and tissue morphology diet and host defense mechanisms.

• A great deal of evidence now supports the view that peripheral blood neutrophils play an important role in preventing the formation of periodontal pockets, as well as participating in the tissue destruction accompanying pocket formation.

• Under normal conditions, a constant stream of neutrophils emigrates form the vessels of the gingival plexus, through the JE, to the gingival margin and into the gingival sulcus and oral cavity.

• This is brought about by chemo tactic factors produced by the bacteria and those that are present in the saliva. These neutrophils are the primary/1st line of defense around the teeth; the epithelial barrier is the second.

• The deepening of the sulcus has been considered to be initiated at the interface between,– The JE and tooth and– At the line of fusion between the JE and the REE with in the JE

The 1st event in pocket formation is the laying down of bacteria (mainly gram +ve) on the tooth surface and its extension into the gingival sulcus.

• Therefore bacteria insinuate themselves into the interface between the JE and the tooth surface, thereby causing detachment of the JE from the tooth surface and the formation of a gingival pocket lined with pocket epithelium.

• Enzymes, physical force exerted by the bacteria or both may be responsible for the detachment. In association with the inflammation, the JE is seen to proliferate along the root in the form of finger like projections 2 – 3 cells in thickness. The coronal portion of the JE is subjected to massive invasion by PMN’s and when their proportion reaches 60% or more of the JE, this tissue detaches from the tooth surface.

• Thus the sulcus bottom shifts apically and the oral sulcular epithelium. occupies a gradually increasing

• portion of the sulcular lining. The degree of leukocytic infiltration of the JE is independent of the volume of inflamed CT, so that this process may occur in gingiva with only slight signs of clinical inflammation.

• With continued inflammation the gingival increases in bulk and the crest of the gingival margin extends towards the crown.

• The JE continues to migrate along the root and separate from it. The epithelium of the lateral wall of the pocket proliferates to form bulbous and cord like extensions into the inflamed CT.

• Leukocytes and edema from the inflamed CT infiltrate the epithelium lining the pocket resulting in varying degrees of degeneration and necrosis.

CONVERSION OF JUNCTIONAL EPITHELIUM INTO POCKET

EPITHELIUM:• increased amount of extra cellular space

(reflecting increased permeability), loss of intercellular junctions, beginning proliferation of basal cells with rete ridge formation and a loss of attachment between epithelium and the tooth surface, via the attachment lamina.

• The pattern of cell may undergo keratinization a process that is completely abnormal for this tissue.

• Adjacent patches may die and slough resulting in ulceration. In this manner the JE is converted to pocket epithelium.

possible mechanisms that may lead to alteration of JE include

– Rapidly growing bacteria require space. This fact may relate to the peeling off of JE cells from the tooth surface in an apical direction.

• This is achieved either by enzymes released from the extending bacteria or thorough the induced inflammatory response.

• ii. Species of bacteria present in plaque and pockets produce hydrolytic enzymes that can damage epithelial cells, lyse intercellular junctions and destroy the extra cellular materials.

• On the other hand a large population of non-epithelial cells including emigrating neutrophils resides in JE. As the disease progress the stream of neutrophils may be great as to disrupt the structure and create ulcers in the pocket wall. These cells may encounter activating microbial substances that include release of determental enzymes and cytotoxic substances.

• About half of the cells that appear in the JE are mononuclear cells and these undergo transformation releasing lymph toxin, which may participate in killing of epithelial cells.

• Barnett (1973) suggested that ‘mast cells’ which comprise a portion of the non-epithelial cells population might play a destructive role by releasing potent trypsin like neutral proteases.

• Enzymes of this type dissociate epithelial cells from one another by digesting the extra cellular substances and lysing intercellular junctions.

• This leads to an influx of serum proteins and leukocytes, which could be beneficial in defense against bacterial substances in the gingival sulcus or pocket.

• The reverse passage of bacterial substances into the CT also occurs thus leading to perpetration of the lesion.

Extension of plaque subgingivally causes a large increase in the number of transmigrating neutrophils.

• This is due to the greatly increased concentration of chemo tactic factors and other inflammation including substances derived from the bacteria.

• Neutrophils adhere to the endothelial lining migrate into the CT and rapidly pass through the junctional or pocket epithelium to form a variable thick layer over the surface of the sub gingival plaque.

• Their role is to limit further extension and spread of the bacteria by the process of phago cytosis and killing of the bacteria.

• They are inhibited by gummy polysaccharide coating of the plaque surface and by leukotoxins released by the plaque bacteria.

• Assuming that pocket formation proceeds either because of aggressive bacterial growth and action, or because of failure of the neutrophil barrier, ever-increasing numbers of neutrophils transmigrate in constant streams through the junctional and pocket epithelium in response to the plaque bacteria.

• These streams may become sufficiently large to disrupt the epithelial barrier and to create open communication between the pocket and underlying CT ‘ulceration’ of this sort is the 2nd major event in pocket formation.

• Once the epithelial barrier has been ruptured the chemo tactic gradient created by bacteria may be disrupted.

• Thus neutrophils no longer have a guidance system to guide them through the tissues and into the pocket. They remain in the CT moving randomly.

• Also, the bacteria enter the CT and neutrophils encounter and react with the bacteria in the CT itself.

• The neutrophils become activated and undergo phagocytosis with release of lysosomal enzymes, collagenase, products of arachidonie acid metabolism etc that perpetuate inflammation and cause extensive tissue damage.

• Bacterial substances also activate the other systems like the alternate complement pathway thereby releasing peptides that enhance and perpetuate the inflammatory response, the macrophages to synthesize hydrolytic enzymes and prostaglandin’s and interact with lymphocytes to cause blast genesis, lumphokine production and antibody synthesis.

• When the epithelial barrier is reestablished the chemo tactic gradient is formed again and the destructive process subsides.

• Tissue destruction continues and the alveolar bone is reabsorbed if barrier is not re-established.

Experiments in dogs and non-human primates have shown that ulceration of the epithelial barrier and the accompanying acute inflammation are important events.

• As soon as ulceration occurs, the CT becomes infiltrated with neutrophils and tissue destruction and bone resorption begins.

• This process happens even when no typical pocket forms and the JE does not extend apically.

• Thus resorption of the alveolar bone does not cause pocket formation.

• On the contrary bacteria are the driving force behind pocket formation resulting in loss of attachment and bone resorption.

• Neutrophils are seen to be actively associated with tissue destruction.

• The lymphoid cells and macrophages are seen to be associated with the dampening of the destructive aspects of the lesion, rather than with tissue destruction.

• This has been demonstrated in squirrel monkeys, where a decrease in alveolar bone resorption is seen to be accompanied by an increase in the number of macrophages and lymphoid cells.

• The experimental ligature induced lesions in dogs also behave in a similar manner, however an infiltrate of lymphoid cells, rather than macrophages is seen to predominate during the damping phase.

• Takata and Donath (1987) proposed a mechanism of pocket formation through the systematic observation of human undecalcified specimens.

• In the early lesion, the degenerative changes occur first in the second or third cell layer from the innermost cell layer of the most coronal part of the JE, which faces the microbial plaque.

• Consequently, an intra epithelial cleavage is formed followed by the degeneration of the cells lining the cleavage resulting in deep crevice formation.

• In the established lesion, as bacterial plaque spreads apically into the deepened crevice, the preceding cellular degeneration of the JE, the intraepithelial cleavage formation, and the subsequent cell desquamation in the gingival pocket occur at the bottom of the deepened crevice in the same manner as described in the early lesion.

• In the advanced lesion in addition to the deepening of the pocket, a conspicuous change occurs in the pocket epithelium.

• The pocket becomes so deep with the pocket epithelium being exposed for such a long distance to the subcrevicular plaque and calculus that the epithelium is easily and directly affected by toxic bacterial products and mechanical irritation by the calculus.

• While the pocket epithelium proliferates reactively in some areas, it also becomes very thin and often ulcerates.

• Concomitant destruction of the periodontium and alveolar bone provide access for the apical migration of the JE.

DESTRUCTION OF THE CONNECTIVE TISSUE

• Several zones have been described in the process of destruction of the CT attachment.

• Apical to the JE, as area of destroyed collagen fibers develop and become occupied by inflammatory cells and edema.

• Immediately apical to this is a zone of partial destruction and then an area of normal attachment.

• Two hypothesis have been advanced regarding the mechanism of collagen loss:

• i. Collagenases and other lysomal enzymes from PMNL and macrophages become extra cellular and destroy collagen.


• ii. Fibroblasts phagocytize collagen fibers by extending cytoplasmic process to the ligament cementum interface and by resorbing the inserted collagen fibrils and the fibrils of the cementum matrix. (Devenport 1982 and Deporter 1980)

• As a consequence of the loss of collagen, the apical portion of the JE proliferates along the root, extending finger like projections 2 – 3 cells in thickness.

• Extension of JE along the root requires the presence of healthy epithelial cells.

• Marked degeneration or necrosis of the JE retards rather than accelerates pocket formation. Degenerative changes seen in the JE at the base of the periodontal pockets are usually less severe than those in the epithelium of the lateral pocket wall.


• The transformation of a gingival sulcus into a periodontal pocket creates an area where plaque removal becomes impossible, and the following feed back mechanism is established;

• Plaque gingival inflammation pocket formation more plaque formation.

• The rationale for pocket reduction is based on the need to eliminate areas of plaque accumulation.

(a) SOFT TISSUE WALL • The CT is edematous and densely infiltrated with plasma

cells (approx 80%) and lymphocytes and a scattering of PMN’s.

• Blood vessels are increased in number, dilated and engorged.

• Single or multiple necrotic foci are occasionally present.• CT also shows proliferation of the endothelial cells with

newly formed capillaries, fibroblasts and collagen fibers.• The JE at the base of the pocket is usually much shorter

than that of a normal sulcus.• The corono-apical length of the JE is reduced to only 50 –

100m.• The cells may be well formed and in good condition or may

exhibit slight to marked degeneration.• The most severe degenerative changes in the periodontal

pocket occur along the lateral wall.

(a) SOFT TISSUE WALL

• The epithelium of the lateral wall of the pocket presents striking proliferative and degenerative changes.

• Epithelial buds or interlacing cords of epithelial cells project form the lateral wall into the adjacent inflamed CT and frequently extend farther apically than the junctional epithelium.

• Dense in infiltration by leukocytes and edema form the inflamed CT occurs.

• The cells undergo vacuolar degeneration and rupture to form vesicles.

(a) SOFT TISSUE WALL

• Progressive degeneration and necrosis of the epithelium lead to ulceration of the lateral wall, exposure of the underlying markedly inflamed CT and suppuration.

• The severity of the degenerative changes is not necessarily related to pocket depth.

• Ulceration of the lateral wall may occur in shallow pockets, and deep pockets are occasionally observed in which the lateral epithelium is relatively intact and shows only slight degeneration.

• The epithelium at the gingival crest of a periodontal pocket is generally intact and thickened, with prominent rete pegs.

BACTERIAL INVASION

• Filaments, rods and coccoid organisms with predominant gram –ve cell walls have been found in intercellular space initially under exfoliating epithelial cells, but they are also found between deeper epithelial cells and accumulating on the basement lamina.

• Some bacteria transverse the basement lamina and invade the subepithelial CT.

(b) Microtopography Of The Gingival Wall Of The Pocket

• Saglie et al (1982) conducted a scanning electron microscopy (S.E.M) study to analyze the salient features of the soft tissue wall in deep periodontal pockets in humans.

• The description of the cell types of tissue structures was made on the basis of cell shapes and sizes, types of cell surface and topographical distribution and relationship with other cells.

• At low magnification the surface morphology of the pocket wall presented different areas that either blended with each other or where distinctly separate.

• These areas are irregularly oval or elongated and adjacent to one another and measure about 50-200 m.

• Findings suggest that the pocket wall is constantly changing as a result of the interaction between the host and the bacteria.

• The following areas have been noted:• 1) Areas Of Relative Quiescence:• Showing a relatively flat surface with minor

depressions and mounds and occasional shedding of cells.• 2) Areas Of Bacterial Accumulation:• Appear as depressions on the epithelial surface,

with abundant debris and bacterial clumps penetrating into the enlarged intercellular spaces. These bacteria are mainly cocci, rods and filaments, with a few spirochetes, and appeared covered by a loose inter-cellular ‘fibrillar like’ substance.

• 3) Areas Of Emergence Of Leukocytes:• Leukocytes appear in the pocket wall through holes

located in the intercellular spaces.


• 4) Areas Of Leukocyte-Bacteria Interaction:• Numerous leukocytes are present and covered with

bacteria in an apparent process of phagocytosis. • Bacterial plaque associated with the epithelium is seen either as

an organized matrix covered by a fibrin-like material in contact with the surface of cells or as bacteria penetrating into the intercellular spaces.

• The epithelium-associated plaque consists of rods, cocci, filaments and spirochetes.

• At high magnifications the surface morphology of epithelial cells appeared distinct from one another.

• Some cells showed a surface covered by numerous micro ridges, often in direct contact with plaque.

• Other cells showed a thin and widely spaced distribution of micro ridges and microvilli.

• The areas adjacent to bacterial plaque aggregation wide spaces between epithelial cells were seen.


• The presence of ‘holes’ on the surface of pocket epithelium was noted with relative frequency and they were found associated with bacteria and/or leukocytes. Their sizes corresponded roughly to that of leukocytes.

• 5) Areas Of Intense Epithelial Desquamation:• Shows semi attached and folded epithelial squares

with one end usually attached to the pocket wall surface and the other end free towards the pocket space.

• Sometimes these cells show bacteria on them consisting of spirochetes, filaments and rods.

• When this occurs, the cells displayed mild to gross alterations and distortions, and in some cases, disruption of cellular integrity.

• 6) Areas Of Ulceration:• Occasionally seen, surrounded by areas of

haemorrhage. The bottom of the ulcer shows exposed collagen fibers and various connective tissues cells.


• 7) Areas Of Haemorrhage:• Numerous erythrocytes are present.• The micro topography of the gingival

sulcus wall, by comparison showed a very smooth surface with barely visible intercellular boundaries, scattered semi-folded desquamating cells and few isolated bacteria. At high magnification thin and spaced microvilli could be seen.

• The transition from one area to another could be postulated as follows:


• Bacteria accumulate in previously quiescent areas, triggering the emergence of leukocytes and the leukocyte-bacteria interaction. This would lead to intense epithelial desquamation, and finally to ulceration and hemorrhage.

– The presence of different areas may also suggest the theory that; periods of guiescence or exacerbation within a pocket may be the result of the summation of all activities within the pocket wall.

• If areas of epithelial inactivity or areas of intense desquamation are pre ponderant, then clinically a period of quiescence is seen.

• If on the other hand, the areas of epithelial bacterial interaction or areas of bleeding and ulceration occupy most of the pocket wall, the pocket would be in a state of exacerbation. These changes may result form or influence the local micro biota.

• The areas described as holes appear to correspond to tunnels in the inter cellular spaces opening into the surface and seen to be produced by PMNL migrating outwards through the epithelium. These ‘holes’ appear to remain open and may be filled by bacteria, which penetrate into the tissue.


PERIODONTAL POCKETS AS HEALING LESIONS

• The condition of the soft tissue wall of the periodontal pocket results from the interplay of destructive and constructive tissue changes.

• The destructive changes are characterized by the associated generative changes initiated by plaque bacteria.

• The constructive changes consist if the formation of blood vessels in a effort to repair the tissue damage caused by inflammation.

• Complete healing does not occur because of the persistence of local irritants, which continue to stimulate fluid and cellular exudates, which in term causes degeneration of the new tissue elements formed in the continuous effort at repair.

• The balance between destructive and constructive changes determines clinical features such as color, consistency and surface texture of the pocket wall.

PERIODONTAL POCKETS AS HEALING LESIONS

• If the inflammatory fluid and cellular exudates predominate, the pocket wall is bluish red, soft, spongy and friable, with a smooth, shiny surface. (Referred to as edematous pocket wall)

• The pocket wall is more firm and pink if there is relative predominance of newly formed CT cells and fibers. (Referred to as fibrotic pocket wall)

• Fibrotic pocket walls may be misleading, because they do not necessarily reflect what is taking place throughout the pocket wall.

• In some cases inflammation and ulceration on the inside of the pocket are walled off by fibrous tissue on the outer aspect.

• Outwardly the pocket appears pink and fibrotic, despite the inflammatory changes occurring within.

POCKET CONTENTS

• Periodontal pockets contain debris consisting principally of microorganisms and their products (enzymes, endotoxins and other metabolic products). Gingival fluid, food remnants, salivary mucin, desquamated epithelial cells, and leukocytes.

• Purulent exudates, if present, consists of living, degenerated, and necrotic leukocytes; living and dead bacteria; serum; and a scant amount of fibrin.

Significance of Pus Formation• There is a tendency to overemphasize the

importance of the purulent exudate and to equate it with severity of periodontal disease.

• Because it is a dramatic clinical finding, early observers assumed that it was responsible for the loosening and exfoliation of the teeth.

• Pus is a common feature of periodontal disease, but it is only a secondary sign.

Significance of Pus Formation

• The presence of pus or the ease with which it can be expressed from the pocket merely reflects the nature of the inflammatory changes in the pocket wall.

• It is not an indication of the depth of the pocket or the severity of the destruction of the supporting tissues.

• Extensive pus formation may occur in shallow pockets, whereas deep pockets may exhibit little or no pus.

• Localized accumulation of pus constitutes an abscess.

(c) ROOT SURFACE WALL

• The root surface wall of periodontal pockets often undergo changes that are significant because they may perpetuate the periodontal infection, cause pain and complicate periodontal treatment.

• Structural, chemical and cytotoxic changes occur in the root cementum.

STRUCTURAL CHANGES:

• (a) Presence of pathologic granules: • Represent areas of collagen degeneration or areas where

collagen fibrils have not been fully mineralized initially.

• (b) Areas of increased mineralization:• Is a result of an exchange, on exposure to the

oral cavity, of minerals and organic components at the cementum – saliva interface.

• The hyper mineralized zones are associated with increased perfection of the crystal structure and organic changes suggestive of a subsurface cuticle.

• These zones have also been seen in micro radiographic studies as a layer 10 – 20 m thick, with areas as thick as 50m.

• No disease in mineralization was found in deeper areas, thereby indicating that increased mineralization does not come from adjacent areas.

• A loss of or reduction in the cross – banding of collagen near the cementum surface and a subsurface condensation of organic material of exogenous origin have also been reported.

• (c) Areas of demineralization:• Commonly related to root caries.• Exposure oral fluid and bacterial plaque results in

proteolysis of the embedded remnants of Sharpey’s fibers; the cementum may be softened and may undergo fragmentation and cavitation.

• Active root caries lesions appear as well defined yellowish or light brown areas, are frequently covered by plaque, and have a softened or leathery consistency on probing.

• Inactive lesions are well – defined darker lesions with a smooth surface and a harder consistency on probing.

• Involvement of the cementum is followed by bacterial penetration of the dentinal tubules, resulting in destruction of the dentin.

• In severe cases large sections of necrotic cementum become detached form the tooth and separated from it by masses of bacteria.

• (ii) CHEMICAL CHANGES• The mineral content of the exposed cementum is increased e.g. calcium,

magnesium, phosphorous and fluoride.• Micro hardness however, remains unchanged.• Exposed cementum may absorb calcium, phosphorus, and fluoride the

development of a highly calcified layer that is resistant to decay.• (iii) CYTOTOXIC CHANGES• Endotoxins have been demonstrated in the cementum of

untreated periodontally involved teeth.• This depresses cell proliferation and viability.• Root surface imperfections can harbour endotoxin and severe as a

substrate for inflammatory exudates.• Components of this exudates include substances like histamine, bradykinin,

IgG, IgA, IgM and complement ‘C’.• Enzymes characteristic of the inflammatory reaction like hyaluronidase and

collagenases are also seen.• Thus cementum may act to perpetuate the destructive effects of periodontal

disease, by acting as a reservoir for potentially destructive materials.

MORPHOLOGY OF THE TOOTH WALL:

• The following zones can be found in the bottom of a periodontal pocket:

• (i) Cementum covered by calculus:• Shows all mentioned root surface changes.• (ii) Attached plaque:• Covers calculus and extends apically from

it to a variable degree, probably 100 – 500 cm.

• (iii) Zone of unattached plaque:• Surrounds attached plaque and extends

apically to it.


• (iv) Zone of attachment of JE to the tooth:• In normal Sulci its extension is more than 500m but is

usually reduced in periodontal pockets to less than 100m.• (v) Zone of semi destroyed CT fibers apical to the JE:• The last three zones compose the so – called plaque free

zone seen in extracted teeth.• The total width of this zone varies according to the type of

tooth (it is wider in molars than in incisors) and the depth of the pocket (narrow in deeper pockets)

• According to several other investigations, the plaque free zone comprises only of zone 3 i.e. the zone of unattached plaque.

• Bass (1946) first described this zone as a non-staining zone on the surface of both healthy and diseased teeth.

• On the enamel of the healthy teeth, this zone is limited coronally by the gingival margin plaque and apically by the JE. It corresponds corono-apically to the healthy crevice.


• Brady (1973) used S.E.M to examine this zone on healthy and periodontitis affected teeth. He too described it as an area virtually free from microorganisms, between the apical plaque border and the attachment epithelium and called it as plaque free zone.

• Several views differ form Brady’s description of its apical limit. On periodontitis affected teeth, the plaque free zone, apical limit, has been described by several investigators.

• Hoffman et al (1971), Powell et al (1978) etc. described the limit as the coronal border of the residual PDL fibers.


• Cobb et al (1990) suggested that in vivo, the zone is apically limited by epithelial cells. Although this zone is now always referred to as plaque free zone and the term is currently accepted, its apical limit on the root surface of diseased teeth is not yet clear and the designation of plaque free requires investigations.

• Friedman et al did a study to identify the components of this specific zone of the root surface of chronic adult periodontics affected teeth and in healthy controls.

• In healthy specimens, the apical plaque border consisted mainly of cocci, and short rods, while on the periodontics-affected specimens spirochetes predominated.

• Isolated or small groups of microorganisms were always present in the ‘plaque free’ zone and its apical limit close to or in contact with JE cells.


• This zone is therefore not completely free of plaque as suggested.• Waerhaug (1970) observed the plaque free zone as a clear gap between

the apical border plaque and the most coronal residual ligament fibers.• Newman (1976) also observed a middle non-staining zone at the same

location and stated that it persisted on the root surface, throughout the disease process.

• Saglic et al (1975) asserted that the width of the plaque free zone decreased as pocket depth and loss of attachment increased.

• Newman (1976) however concluded that the zone width was independent of its distance form the root apex.

• Brady (1973) described the average distance form plaque to epithelium as 80m on healthy specimens and 140 – 440m on periodontics affected teeth.

• The wide range is because both the narrowest and widest regions of the zone were considered.

• The concept that plaque free zone includes the zone of unattached plaque, JE and partially lysed CT fibers, was probably due to the fact that, at low magnifications it is difficult to detect the presence of epithelial cells, and thus the term plaque free zone has persisted in relation to the whole relatively non-staining zone.

Correlation of clinical & histopathologic features of pocket

Clinical features Histopathologic features

gingival wall presents• various degrees of

bluish-red discoloration;

• flaccidity; • smooth, shiny

surface;• & pitting on

pressure.

■ discoloration - circulatory

stagnation;■flaccidity - destruction of

gingival fibres & surrounding tissues;

■ smooth, shiny surface,

- by atrophy of the epithelium and edema

■ pitting on pressure - by edema &

degeneration.


• Less frequently the gingival wall may be pink and firm.

■ fibrotic changes predominate over exudation and degeneration, particularly in relation to the outer surface of the pocket wall.

■ despite the external appearance of health, the inner wall of the pocket invariably presents some degeneration and is often ulcerated.

Bleeding is elicited by gently probing the soft tissue wall of the pocket.

Ease of bleeding results from■ increased vascularity■ thinning and degeneration of the epithelium■ proximity of the engorged vessels to the inner surface.

When explored with a probe, the inner aspect of the probe is generally painful

■ due to ulceration of the inner aspect of the pocket wall.


In many cases, pus may be expressed by applying digital pressure.

■ in pockets with suppurative inflammation of the inner wall.

PERIODONTAL DISEASE ACTIVITY

• Socranskey et al described 3 concepts to explain observed patterns of periodontal destruction.

• A ) Continuous periodontal degeneration: – periodontal afflictions causes damage

slowly, constantly and progressively – and is supported by cross sectional and

longitudinal studies

PERIODONTAL DISEASE ACTIVITY• b) Random Burst Theory:

– periodontal pockets go through periods of ‘quiescence’ and exacerbation

– occur randomly with respect to tissue and at random sites within an individual.

– Periods of quiescence are characterized by an reduced inflammatory response and little or no loss of bone and CT attachment.

– A build up of unattached plaque with its gram –ve motile anaerobic bacteria starts a period of exacerbation in which bone and CT are lost and pocket deepens.

– This period may last for days, weeks or months and is eventually followed by a period of quiescence in which gram +ve bacteria proliferate and a more stable condition is established.

– These periods of quiescence and exacerbation are also known as periods of activity and inactivity.

PERIODONTAL DISEASE ACTIVITY

• (c) Asynchronous Multiple Burst Hypothesis:

• It is stated that disease occurred during a definite period of life and then went into remission.

• In this model many sites would show bursts of activity. Over a period of time followed by an indefinite period of inactivity. The major periodontal destruction occurs over a few years. E.g. post JP.

PULPAL CHANGES ASSOCIATED WITH PERIODONTAL POCKET:

• The spread of infection from periodontal pocket may cause pathologic changes in the pulp. Such changes may give rise to painful symptoms or adversely affect the response of the pulp to restorative procedure.

• Involvement of the pulp in periodontal disease occurs through either the apical foramen or the lateral canals in the root after injection spreads form the pocket through the PDL.

• Atrophic and inflammatory pulpal changes occur in such cases.

• Pain in periodontal pockets might be due to root carried, sensitivity or retrograde pulp involvement

RELATION OF LOSS OF ATTACHMENT & BONE LOSS TO POCKET DEPTH:• Pocket formation causes

– loss of attachment & – denudation of the root surface.severity of attachment loss is generally not always is

correlated with pocket depth.• because the degree of attachment loss depends on the

location of the base of the pocket on the root surface• where as depth is the distance between the base of the

pocket and crest of the gingival margin

• Severity of bone loss is generally correlated with pocket depth but not always.

• Extensive bone loss may be associated with shallow pocket and slight bone loss can occur in deep pockets.

Relationship of attachment loss to pocket depth

• Pockets of same depth may be associated with different degrees of attachment loss and pockets of different depths may be associated with same amount of attachment loss.

EFFECT OF TFO ON INFRA BONY POCKET FORMATION:

• When occlusal forces exceed the adaptive capacity of the tissues, tissue injury results. The Injury is called “Trauma form occlusion”. Studies were conducted on the effect of trauma from occlusion on teeth subjected simultaneously jiggling trauma and plaque induced gingival inflammation. It was seen that the local irritants that initiate gingivitis and periodontal pockets affect the marginal gingival, but trauma from occlusion occurs in the supporting tissues and does not affect the gingiva. Thus it is seen that “Trauma from occlusion does not cause periodontal pockets or gingivitis, nor does it have any influence on the bacterial repopulation of periodontal pockets, after scaling and root planning”.

• Thus in the absence of inflammation the response to trauma from occlusion is limited to adaptation to the increased forces. However in the presence of inflammation the changes seen in the stage of the alveolar crest may be conductive to angular bone loss and existing pockets may become infra bony.

• Considerable controversy has existed about the possible changes in the pathway of gingival inflammation caused by trauma from occlusion.

• Glickman and Smulow (1962) stated that instead of following its usual course into the inter dental bone, the inflammatory exudate is chanelled b/w the transseptal fibers, directly onto the periodontal ligament, incases of trauma from occlusion. This change in the pathway of inflammation, induce the influence of trauma from occlusion, leads to vertical bone loss and infra bony pocket formation.

• Glickman and Smulow concluded that gingival inflammation and trauma from occlusion are different types of pathologic processes, which participate, in a single disease, periodontitis. Together they exert a combined co – destructive affect which produces angular bone defects and infra bony pockets.

POCKET ELIMINATION Vs POCKET MAINTAINANCE :

• after surgical therapy pockets of 4 and even 5mm can be maintained in a healthy state and without radiographic evidence of advancing bone loss

• accomplished by maintenance visits consisting of scaling and root planing, with oral hygiene reinforcement performed at regular intervals of not more than 3 months.


• the residual defect can be penetrated with a thin periodontal probe, but no pain, exudate or bleeding results; this appears to indicate that not plaque has formed on the subgingival root surfaces.

• emphasize the importance of the maintenance phase and of the close monitoring of both level of attachment and pocket depth, together with the other clinical variables (i.e. bleeding, exudation and tooth mobility)

• Probing depths established after active therapy and healing (approximately 6 months after treatment) can be maintained unchanged or reduced even further during a maintenance care program involving careful prophylaxis once every 3 months.

• Ramfjord and associates and Resling et al showed that regardless of the surgical technique used for pocket therapy, a certain pocket depth recurs. Therefore, maintenance of this depth without any further loss of attachment becomes the goal.


CRITERIA FOR METHOD SELECTION :

• The selection of a technique for treatment of a particular periodontal lesion is based on a number of considerations.– Characteristics of the pocket: depth, relation of bone, and

configuration.– Accessibility to instrumentation, including presence of furcation

involvements.– Existence of mucogingival problems.– Response to phase I therapy– patient cooperation and ability to perform effective oral hygiene– Age and general health of the patient– Overall diagnosis of the case: various types of gingival

enlargement and types of periodontitis (slowly or rapidly progressing periodontitis JP, and so forth)

– Aesthetic considerations– Previous periodontal treatments

CRITERIA FOR METHOD SELECTION :

• Of the many techniques available, the one that will most successfully solve the problems with the fewest undesirable effects should be chosen.

POCKET ELIMINATIONMethods are

– Non surgical – Surgical

classified as follows:

• New attachment techniques – – offer the ideal result– eliminate pocket depth by reuniting the

gingiva to the tooth at a position coronal to the bottom of the preexisting pocket.

– usually associated with filling in of bone & regeneration of periodontal ligament and cementum.

• Removal of the tooth side of the pocket, which is accomplished by tooth extraction or by partial tooth extraction hemisection or root resection.

• Removal of the pocket wall– most common method– can be removed by

• Retraction or shrinkage, in which scaling and root planing procedures resolve the inflammatory process and the gingiva shrinks, thereby reducing the pocket depth.

• Surgical removal performed by the gingivectomy technique or by means of an undisplaced flap (internal gingivectomy) and

• Apical displacement with an apically displaced flap

FATE OF POCKET EPITHELIUM IN PERIODONTAL TREATMENT :

• After initial preparation of a site with scaling & root planing,the inflammation may be resolved but the deep fimbriae / rete pegs persist(Schroeder 1977,Carranza 1977)

• Often undesirable characteristics which persist include :

– hyperplastic nature & tendency for ulceration

– presence of deep microorganisms– presence of chronic inflammatory cells

• Fisher et al 1982 stated that complete removal of deep rete pegs may not be possible even after internal bevel incision.

FATE OF POCKET EPITHELIUM IN PERIODONTAL TREATMENT :

• Pippin 1990 did a study where he studied the fate of pocket epithelium when pocket epithelium when apically positioned flap is done by 2 methods :

• sulcular incision• internal bevel incision

– Assessment of sulcular incision specimen revealed that epithelial degeneration & dissolution occurred in 7 days & resulted in collagen to collagen attachment of the periodontal flap to the alveolar bone.

– Internal bevel incision was consistently effective in removing the pocket epithelium & resulted in healing by a connective tissue union of flap to alveolar bone. By 21 days of healing, the 2 surgical methods were indistinguishable histologically.

CONCLUSION :

• Bacterial plaque has an important role to play in the initiation & progression of pocket formation as the accumulation of plaque results in inflammation which in turn favours pocket formation & more plaque accumulation. A vicious cycle thus begins & various stages of disease progression are seen.

• Although pocket formation & loss of attachment remain the hallmark of periodontal disease , identifying the stage of the disease at any period of time or identifying the risk of the patient entering an active phase would have important therapeutic implications .

Pdl Pocket

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