Department of Periodontology.

.

PERIODONTAL POCKETS.

Presented by:

SAVAN UNNI IV th Year BDS C.D.C.R.I

Guided by: Dr.Saravana Kumar

TOPIC

• Define and classify pockets.Write in detail about the pathogenesis and histo-pathological changes that occur during pocket formation?

April 2001 Essay. October 1996 Essay.

DEFINITION

• The periodontal pocket is defined as a pathologically deepened gingival sulcus.

• A sulcus depth of 2-3mm is considered normal.

CLASSIFICATION

Based on its Morphology:

GINGIVAL POCKET

PERIODONTAL POCKET

COMBINED POCKET

CLASSIFICATION

• Based on its relationship to crestal bone:

Suprabony/Supracrestal/Supra alveolarpocket.

Infrabony/Intrabony/Subcrestal/Intra alveolar pocket.

CLASSIFICATION

• Based on number of surfaces involved:

Simple Pocket.

Compound Pocket.

Complex Pocket.

CLASSIFICATION

• Based on soft tissue wall of the pocket:

Edematous pocket

Fibrotic Pocket

CLASSIFICATION

• Based on the disease activity:

Active Pocket.

Inactive Pocket.

GINGIVAL POCKET

• Formed by gingival enlargement without destruction of underlying periodontal tissues.

• The sulcus is deepened because of the increased bulk of the gingiva.

PERIODONTAL POCKET

• It occurs due to destruction of the supporting periodontal tissues.

It can be of two types • Suprabony pocket• Infrabony pocket

SUPRABONY POCKET

• Also know as Supracrestal or Supra alveolar.

• The base of the pocket is coronal to the level of underlying bone.

• Bone loss is horizontal

INFRABONY POCKET

• Also known as Infrabony or subcrestal or intra alveolar pocket.

• The base of the pocket is apical to the level of adjacent bone

• Bone loss is vertical.

Classification based on involved tooth surfaces.

• SIMPLE POCKET:Involving one tooth surface.

• COMPOUND POCKET:Involving two or more tooth surfaces.

• COMPLEX POCKET/SPIRAL POCKET:Here the base of the pocket is not in direct communication with gingival margin.

PATHOGENESIS.

• Accumlation of micro organisms on the supragingival toothsurface and its extension into gingival sulcus.

• Inflammatory changes in the connective tissue wall of the gingival sulcus.

• Cellular & fluid inflammatory exudate causes degeneration of the connective tissue including the gingival fibers.

• Collagen fibers gets destroyed apical to the junctional epithelium and the area becomes occupied by inflammatory cells and edema.

• The coronal portion of the junctional epithelium detaches from the root as the apical portion migrates.

• Polymorphonuclear neutrophils invade the coronal end of the junctional epithelium in increasing numbers.

• With continued inflammation the gingiva increases in bulk and the crest of the gingival margin extends coronally.

• The junctional epithelium continues to migrate along the root and separate from the root.

Diagrammatic Illustration:

Mechanism Of Collagen Loss:• There are two mechanisms involved:

• FIRST MECHANISM:

Collagenases and other enzymes secreted by fibroblasts, polymorphonuclear leukocytes ,and macrophages.

These enzymes degrade the collagen and other matrix macromolecules into small peptides which are called as matrix metalloprotinases.

• SECOND MECHANISM :

Fibroblasts phagocytize collagen fibers by extending cytoplasmic processes to the ligament -cementum interface and degrade the inserted collagen fibrils and the fibrils of the cementum matrix.

HISTOPATHOLOGYEPITHELIAL CHANGES:• Epithelium becomes degenerated

and atrophied.

• Inner aspect of the pocket wall becomes ulcerated.

• Pus occurs in the pocket with suppurative inflammation of the inner wall.

HISTOPATHOLOGYCONNECTIVE TISSUE CHANGES:• The connective tissue is edematous

and densely infiltrated with plasma cells,lymphocytes,and pmn’s.

• Blood vessels are increased in number,dilated and engorged in subepithelial connective tissue layer.

• Single or multiple necrotic foci are present in the connective tissue.

• Proliferation of endothelial cells,with newly formed capillaries ,fibroblasts,and collagen fibers.

BIBLIOGRAPHY

• Carranza’s Clinical Periodontology Tenth Edition : “Chapter 27”

• Website : http://www.ncbi.nlm.nih.gov/pubmed

THANK YOU!