PERIODONTAL POCKETS & IT’s PATHOGENESIS Presented by: Dr. Maryam Mastoor

PERIODONTAL POCKET: “It is a pathologically deepened gingival sulcus i.e. more than 3mm” (either due to coronal movement of gingival margin or apical migration of Junctional Epithelium or a combination of both processes).

Classification of periodontal pockets

CLASSIFICATION table 1.1. Based on morphology i)Gingival ii)Periodontal Pocket iii)Combined Pocket 2. Based on Relationship to crestal bone i)Suprabony Pocket ii)Infrabony Pocket 3. Based on number of surfaces involved i)Simple Pocket ii)Compound Pocket iii)Complex Pocket 4. Based on nature of soft tissue wall of the pocket i)Edematous Pocket ii)Fibrotic Pocket 5. Based on disease activity i)Active Pocket ii)Inactive Pocket Edematous Active Inactive Fibrotic

(1) Based upon Morphology of Gingiva i)Pocket due to coronal movement of gingival margin (Gingival/Pseudo Pocket) ii)Pocket due to apical detachment of Junctional Epithelium (Periodontal Pocket) iii) Combine Pocket Normal gingiva Coronal movement of gingiva Apical detachment

i) GINGIVAL POCKET: ( pseudopocket) Formed by gingival enlargement & coronal movement of gingival margin without destruction of underlying periodontal tissues. The sulcus is deepened because of the increased bulk of the gingiva. Healthy gingiva Gingival Pocket

ii) PERIODONTAL POCKET: It is pathological deepening of sulcus due to apical detachment of Junctional Epithelium with destruction of periodontal tissue. Progressive Bone loss Healthy side Apical detachment of Junctional epithelium + Periodontal Pocket formation Diseased side

(2) Based upon relation to Crestal bone Suprabony pocket Infrabony pocket Normal Gingiva i) Suprabony Pocketii) Infrabony Pocket Base of the pocket is coronal (superior) to the level of underlying bone. Base of the pocket is apical (inferior) to the level of underlying bone. Horizontal bone loss Vertical bone loss

i) SIMPLE POCKET: Involving one tooth surface. ii) COMPOUND POCKET: Involving two or more tooth surfaces. iii) COMPLEX POCKET/ SPIRAL POCKET: Originates from one surface and twists around the tooth to involve one or more additional surfaces (commonly found in furcation area). (3) Based upon number of tooth surfaces involved

i ) EDEMATOUS POCKET: Clinically it has bluish-red, spongy,smooth and shiny surface due to increase in inflammatory fluid & cellular exudate. ii) FIBROTIC POCKET: Clinically it has a firm pink surface due to newly formed connective tissue & fibers. (4) Based upon Nature of Soft Tissue Wall of the Pocket: Edematous Fibrotic

i)Active pocket:  Occurs during Period of Exacerbation or activity of disease.  Loss of bone and connective tissue attachment.  Pocket deepens.  Increased inflammation. ii) Inactive pocket:  Occurs during Period of Quiescence or inactivity of disease.  Little or No further bone loss and connective tissue attachment.  Pocket level remains same.  Reduced inflammation. (5) Based upon Disease Activity Normal Periodontium Increased inflammatory neutrophils Bone loss Pocket deepens Reduced inflammation Everything remains same

PATHOGENESIS of periodontal pocket

Summary of Periodontal Pocket Formation STAGE 1 Accumulation of Supragingival Plaque STAGE 2 Extension of Plaque Subgingivally STAGE 3 Coronal Detachment & Apical Migration STAGE 4 Phagocytic action of Neutophils in Pocket Epithelium STAGE 5 Ulceration of Pocket Epithelium STAGE 6 Periodontal Pocket established

PATHOGENESIS:  Plaque accumulation on supragingival tooth surface  Chemotactic agents released by bacterial plaque  attracting inflammatory cells  Marginal gingiva becomes inflammed and edematized  Gingival sulcus deepens due to edematous enlargement of gingiva  Gingival Pocket formed

 Extension of plaque subgingivally  change in bacterial environment from Gram –ve to Gram +ve i.e. Dysbiosis  Bacterial toxic products subgingivally  cause coronal junctional epithelium to produce inflammatory mediators  causing dilatation of blood vessels.  Neutrophils from connective tissure transmigrate into gingival sulcus and make a layer on subgingival plaque to prevent its further subgingival extension.

 Engorged blood vessels  increases supply of nutrients into soft tissue  junctional epethelial cells proliferate making Rete’ Pegs  Bacteria feed on these nutrients  inflammation intensifies  Collagen destruction starts just apical to junctional epithelium by two methods:  METHOD 1 Collagenases & other enzymes produced by fibroblasts, PMNs and macrophages  degrade collagen and other matrix macromolecules into  matrix metalloprotinases (small peptides)  METHOD 2 Fibroblasts extend their cytoplasmic processes into the ligament-cementum interface  phagocytize inserted collagen fibrils and the fibrils of the cementum matrix.  Collagen destruction apically  apical infiltration of inflammatory cells  Coronal Junctional epithelium detaches  Apical part of J.E. Migrates along the root surface

 Coronal portion of J.E. invaded by PMNs  Phagocytic action of neutrophils in pocket epithelium continues  Lateral wall of Periodontal pocket degenerates extensively  Increased proliferation of epithelial rete’ pegs into connective tissue for nutrients.  Increasing number of transmigrating neutrophils in pocket  volume reaches 60% or more of J.E.  disruption of epithelial barrier i.e ulceration  open communication b/w pocket and connective tissue  bacteria invade into C.T.  phagocytic action of macrophages inside C.T. starts. Fig E : Phagocytic action of Neutrophils

 Breakage of Epithelial barrier  Periodontal Pocket established  Increased bacteria  increased immune response  increased blood flow  increased nutrients for bacteria  Increased immune response  activates osteoclasts  alveolar bone resorbs  decreased support of tooth  tooth mobility increases  tooth loss

HISTOPATHOLOGY  Extensive proliferation of Lateral Epithelium  Atrophied pocket wall  Marked inflammatory neutrophils Normal gingival sulcus epithelium (a) Epithelial Changes:

(b) Connective Tissue changes:  Densely infiltrated with lymphocytes and PMNs.  Blood vessels engorged in subepithelial connective tissue layer.  Multiple necrotic foci  Proliferation of endothelial cells, with newly formed capillaries and collagen fibers. Fig. Interdental papilla showing densely inflamed connective tissue with infiltrate extending between collagen fibers and proliferating ulcerated pocket epithelium.