PERIODONTAL POCKET

DEFINITION

• A periodontal pocket is defined as pathologically deepened gingival sulcus.

• It is one of the most important clinical features of periodontal diseases.

CLASSIFICATION

• Gingival pocket• Periodontal Pocket

Suprabony(supracrestal/supraalveolar)

Intrabony(infrabony/subcrestal/intraalveolar)

CLINICAL FEATURES

• Bluish red,thickend marginal gingiva• Bluish red vertical zone(GM AM)• Gingival bleeding• Suppuration• Tooth mobility• Diastema formation• Symptoms-localised pain/pain deep in the bone

PATHOGENESIS

• Inflammatory changes in CT of GS• Cellular&fluid inflm. exudate causes• degeneration of CT&gingival fibers• Just apical to JE collagen fibers destroyed• Area is occupied by inflammatory cells & edema

PATHOGENESIS Contd..

• Two mechanism of collagen loss

Collagenases+Enzymes secreated by fibroblasts,PMNs&Macrophages- MMPs became extracellular &destroyes collegen

fibroblast phagocytise collagen fibers by extending cytoplasmic process to the ligamentum-cementum interface&degrade collagen fibrils&fibrils of cementum matrix

PATHOGENESIS Contd..

• As a result of the loss of collagen the apical cells of JE proliferate along the root ,extending finger like projections 2/3cells in thickness.

• PMNs invade the coronal end of JE in no.• PMNs not joined to one another/to epithelial cells by

desmosomes

PATHOGENESIS Contd..

Relative volume of PMNs reaches 60%/more of JE

Tissue losses cohesiveness detach from tooth surface

Coronal portion of JE detach from the root as the apical portion migrate

Resulting in its apical shift &oral SE gradually occupies increased portion of the sulcus(pocket lining)

PATHOGENESIS Contd…

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

• Marked degeneration/necrosis of JE impairs rather than accelerates pocket formation(NUG-ulcer and not pocket formation)

HISTOPATHOLOGY

C.T.-Edematous&densely infilterated

plasma(80%),lymphocytes,PMNs

-various degree of degeneration

-single/multiple necrotic foci

-proliferation of endothelial cells

-newly formed capillaries,fibroblast,

colagen fibres

HISTOPATHOLOGY Contd

J.E.-at base of pocket is much shorter than sulcus

-coronoapical length 50-100µm

-variation in length,width

&condition of epithelial cells

HISTOPATHOLOGY Contd

• Epithelial of lateral wall of pocket shows proliferative&degenerative changes

• Epithelial buds/interlacing cords of

epithelial cells from lateral wall adjacent

inflamed c.t. Apically than JE• Epithelial projections+remainder

of lateral epithelium infiltrated

with leucocytes &edema

HISTOPATHOLOGY Contd

• Cells under go vascular degeneration

&rupture to form vesicles• Progressive degeneration&necrosis of

epithelium ulceration of lateral wall• Exposure of underlying CT

&suppuration

BACTERIAL INVASION

• Filaments,rods&coccoid organism with gm-ve cell walls found in intercellular spaces(CP)

• P.gingivalis&P.intermedia&AA in Gingiva (AP)• Bacteria invade intercellular spaces &accumulate on BL• Some cross BL &invade CT (Bacterial invasion/translocation)

MICROTOPOGRAPHY OF THE GINGIVAL WALL OF THE POCKET

• Several irregular&oval/elongated areas(pocket wall) with adjacent distance 50-200µm(SEM)

• Following areas 1-Areas of relative quiescence 2-Areas of bacterial accumulation 3-Areas of emergence of leukocytes 4-Areas of leukocyte-bacteria interaction 5-Areas of intense epithelial desquamation 6-Areas of ulceration 7-Areas of hemorrhage

PERIODONTAL POCKET AS HEALING LESIONS

• PP are ch infl lesion constantly repair• Distructive & constructive changes

Edematous pocket Fibrotic pocket

POCKET CONTENTS

• Debris consisting microorganism&products(enzymes,endotoxins&metabolic products)

• Gingival fluid remnants,salivary mucin• Desquamated epithelial cells&leukocytes• Purulent exudate consists of living,degenerated&scant

amount of fibrin

SIGNIFICANCE OF PUS FORMATION

• Pus is common feature of periodontal diseases• Secondary sign• Reflects nature of inflammatory changes in pocket wall• Not indicated severity of the supporting tissue

ROOT SURFACE WALL

• In deepen pocket, collagenous fibers embedded in cementum destroyed&exposed to oral environment

• Remanants of sharpey’s undergo degeneration &create environment for penetration of viable bacteria

• Pathologic granules represent areas of collagen degeneration(optical/electron microscopy)

ROOT SURFACE WALL Contd..

• Penetration of growth of bacteria leads to fragmentation&breakdown of the cementum

• Results in areas of necrotic cementum,seprated from the tooth by masses of bacteria

• Endotoxin also detected in the cemental wall of periodontal pocket

DECALCIFICATION&REMINERALIZATION OF CEMENTUM

• se mineralization an exchange,on exposure to the oral cavity of minerals&organic components at cementum saliva interface

• se in disease root surface,Ca,Mg,P,&F

• Microhardnes remains unchanged

• Hypermineralised zone 10-20µm thick& up to 50µm

AREAS OF DEMINERALIZATION

• Commonly related to root caries• Exposure to oral fluid&bacterial plaque results

proteolysis of sharpey’s fibers• Cementum may be softened &undergo

fragmentation&cavitation• Active root caries lesions-yellowish/light brown

areas ,covered with plaque&soft• Inactive lesions- darker with smooth surface&harder

consistency• Actinomyces viscosus major organism& others

A.naeslundii,S.mutans,S.salivarious,S.sanguis&B.cereus

SURFACE MORPHOLOGY OF THE TOOTH WALL OF PP

1-cementum covered by calculus2-attached plaque3-the zone unattached plaque4-the zone where JE is attached to the tooth5-zone of semidestroyed CT fibres3,4,5-plaque free zones-it is remember that plaque free zone refers to attached plaque -unattached plaque contains gm+ve

cocci,rods,filaments,fusiforms&spirochetes-most apical zone contains gm-ve rods&cocci

PERIODONTAL DISEASE ACTIVITY

• PP go through periods of excervation&quiescence

• Period of quiescence:

*reduced inflammatory response

*little/no bone&CT attachment loss

*unattached plaque with gm-ve motile&anaerobic bacteria

PERIODONTAL DISEASE ACTIVITY Contd..

• Period of excervation: *bone & CT attachment loss *pocket deepens *this period may lost for days/months&is followed

by period of remission/quiescence

• These periods of quiescence& excervation are also known as period of activity&period of inactivity

SITE SPECIFICITY

• Periodontal destruction does not occur in all parts of the mouth but rather on a few teeth at a time or even only some aspect of some teeth at any given time

• Severity of periodontal diseases increases by the development of new disease site, the increased breakdown of existing sites

PULP CHANGES ASSOCIATED WITH PERIODONTAL POCKETS

• Spread of infection from PP may cause pathologic changes in the pulp

• Such changes give rise to painful symptoms

• Involvement of pulp in the periodontal diseases through apical foramen/lateral canals

RELATION OF CAL&BONE LOSS TO POCKET DEPTH

• Severity of attachment loss is generally not correlated with pocket depth

• Degree of attachment loss depends on the location of the base of the pocket on the root surface

• Where as pocket depth is the distance between the base of the pocket &crest of the gingival margin

AREA BETWEEN THE BASE OF POCKET&ALVEOLAR BONE

• Distance between apical end of JE &alv bone is constant

• Distance between apical end of calculus &alv bone is constant in human PP=1.97mm±33.16%

• Distance between attached plaque to bone is never less than0.5mm&never more than2.7mm

PERIODONTAL ABSCESS

• It is a localized purulent inflammation in the periodontal tissues.

• Also known as lateral/parietal abscess• Abscess localized in gingiva(gingival abs)

• Microscopically: -localized accumulation of viable&non viable

PMNs pus(center) -acute inflammatory reaction surrounds the

purulent area &overlying epithelium -acute abscess chronic abcess

PERIODONTAL CYST

• Uncommon lesion that produces localized destruction of periodontal tissue along a lateral root surface ,most often in mandibular canine premolar area

• Microscopically :The cystic lining may be-loosely arranged,nonkeratinized,thickend,proliferating epithelium-thin nonkertinized epithlium-an odantogenic keratocyst

MCQ-1

• How much probing pocket depth of a clinically normal gingival sulcus in humans

(a)1-2mm

(b)2-3mm

(c )3-4mm

(d)4-5mm

MCQ-2

• The pocket is formed by gingival enlargement without underlying periodontal destruction is called

(a)Pseudo pocket

(b)True pocket

(c )subcrestal pocket

(d)Infrabony pocket

MCQ-3

• Which type of pocket is most common in furcation areas

(a)Simple pocket

(b)Compound pocket

(c )spiral pocket

(d)Supracrestal pocket

MCQ-4

• A patient has a chief complain of pain in upper right first molar. On examination a purulent inflammation with 8mm of pocket depth was observed on facial aspect of 16.What is the confirmatory diagnosis of that lesion?

(a)Periodontal cyst

(b)Periodontal abscess

( c)Periapical cyst

( d)Gingival abscess

MCQ-5

• One of the following lesions have a reduced inflammatory response and little or no loss of connective tissue and bone. A buildup of unattached plaque, with its gram-negative, motile and anaerobic bacteria .

(a)period of specificity (b)period of quiescence (c)period of exacerbation (d)period of inactivity

MCQ-6

• The severity of periodontal diseases is depends on

(a)probing pocket depth

(b)loss of attachment

(c)periodntal abscess

(d)gingival abscess

MCQ-7

• Which of the following factor is responsible for flaccidity in the gingival wall of the periodontal pocket

(a)circulatory stagnation

(b)destruction of gingival fibers

(c)atrophy of the epithelium

(d)edema and degeneration