Periodontal Pockets: Definition, Causes, Symptoms and Classification

Periodontal Pocket

Define and classify periodontal pocket.

Periodontal pocket can be defined as pathological deepening of gingival sulcus.

Classification of Periodontal Pocket

Depending upon Periodontal Pocket morphology

• Gingival/false pocket: Deepening of gingival sulcus mainly owing to increase in size of gingiva without any appreciable loss of underlying tissue or apical migration of junctional epithelium. It is known as false pocket.
• Periodontal/true pocket: It is formed by pathological deepening of gingival sulcus due to destruction of supporting tissues of periodontium and apical proliferation of epithelial attachment.
• Combined pocket.

Depending upon Periodontal Pocket relationship to crestal bone

• Supra-bony/Supra-alveolar pocket: Base of the pocket is coronal to the crest of alveolar bone. Bone loss is horizontal
• Infra-bony/Intra-alveolar pocket: Base of the pocket is apical to the crest of alveolar bone. Bone loss is vertical.

Depending upon the number of surface involved

• Simple pocket: It involves one tooth surface
• Compound pocket: This type of pocket involves two or more tooth surfaces. Base of the pocket is in direct contact with gingival margin along each of involved surface.
• Complex pocket: It originates on one tooth surface and twists around the tooth to involve one or more additional surfaces. Only communication with gingival margin is at surface where pocket originates. It is common in furcation areas.

Read And Learn More: Periodontics Question And Answers

Depending upon the nature of soft tissue wall of the pocket

• Edematous pocket: It contains more cellular exudates and inflammatory infitrate and pocket wall appears bluish red, soft friable with smooth shiny surface.
• Fibrotic pocket: It contains more connective tissue fibers and pocket wall appears pink and relatively firm.

Depending upon the disease activity:

• Active pocket: It consists of more of inflammatory content and is marked by spontaneous bleeding or bleeding on slight provocation.
• Inactive pocket: It consists of less inflammatory contents and show no signs of attachment loss or bone loss.

Periodontal Pocket Clinical Features

Periodontal Pocket  Clinical Signs

• Enlarge bluish red marginal gingiva with a rolled edge separated from tooth surface.
• Shiny discolored and puffy gingiva associated with exposed tooth surface.
• Gingival bleeding, purulent exudate from the gingival margin.
• Mobility, extrusion and migration of teeth.
• Development of diastema may present.

Periodontal Pocket  Clinical Symptoms

• Foul taste in localized area.
• Tendency of material to stick in inter proximal space.
• Feeling of itching in gums.
• Sensitivity to heat and cold.
• Radiating pain.
• Sensation of pressure in gingiva after eating which gradually diminish.
• Symptom of localized pain is present.

Periodontal Pocket  Pathogenesis/Etiopathogenesis

• Pocket formation starts with the laying down of gram-positive bacteria over the supragingival tooth surface and its extension into the gingival sulcus.
• Periodontal pockets are caused by microorganisms as well as their products, which produce pathologic changes that lead to the deepening of the gingival sulcus.
• Since there is an occurrence of inflammation, following changes are observed in the junctional epithelium:
  • Junctional epithelium starts proliferating along the root which is in the form of finger-like projections.
  • Coronal portion of junctional epithelium detaches from the root as the apical migration takes place. The epithelial cell detachment can take place due to:
    • Enzymes produced by the bacteria.
    • Physical force applied by speedly growing bacteria.
    • Bacteria can also interfere with growth as well as synthetic activities of junctional epithelial cells and also with the normal maintenance of the attachment lamina.
    • Exudate which is associated with the advancing bacteria can also be important. Now the sulcus base shift apically and this will be replaced by pocket epithelium.
    • In normal circumstances, the neutrophils emigrates from the vessels of the gingival plexus via the junctional epithelium inside the gingival sulcus and oral cavity. Most of the bacteria produce substances which attact the neutrophils. Chemotactic agents occur across normal, intact junctional epithelium and connective tissue. Neutrophils which leave the blood vessels are guided by chemical gradient toward the gingival margin and inside the gingival sulcus. In normal circumstances, the transmigrating cells leave no trace of their passage and produce no damage. Neutrophils are the primary and fist line of defense around the teeth while the epithelial barrier is the second.
  • As plaque extends subgingivally this causes an increase in the transmigrating neutrophils which can be due to the increased concentration of chemotactic factors and other inflammation-induced substances derived from the bacteria. Such substances lead to vasculitis. Neutrophils get adhere to the endothelial lining and migrate inside the connective tissue, but they still do not accumulate there and they rapidly pass through the junctional or pocket epithelium and form a thick layer which covers the surface of the subgingival plaque. On arrival at the plaque surface, neutrophils are viable partly, and not become completely functional. Neutrophils limit further extension and spread of bacteria by phagocytosis and killing. This can be inhibited by lipopolysaccharides and leukotoxin. The normal neutrophil activities are sufficient to limit the extension of plaque, however, increasing growth rate of bacteria, swamps the neutrophil system and permits tissue destruction to occur.
  • As the pocket formation proceed either due to aggressive growth and action of bacteria or due to ever increasing number of neutrophils which transmigrate through the junctional epithelium and pocket epithelium leads to open communication between the pocket and connective tissue. Occurrence of ulceration of this type is the second major event in pocket formation. As the epithelial barrier gets breached, the gradient of chemotactic agents produced by pocket bacteria can be disrupted. Now the neutrophils have no longer a guidance system for directing them from the blood vessels through tissues inside the pocket. Neutrophils remain in connective tissue and move randomly. Due to rupture of epithelial barrier, connective tissue gets flooded with the bacterial substances and bacteria can now enter the connective tissue.
  • Neutrophils within the connective tissue encounter these substances. Neutrophils become activated and undergo phagocytosis with release of lysosomal enzymes, collagenases and other substances prostaglandin E2 which lead to high tissue damage. As the bacterial substances enter the connective tissue, many systems other than neutrophils are activated such as macrophages, lymphocytes and complement system.
  • As epithelial barrier again gets re-established the chemotactic gradient is created again and the destructive process subsides. If epithelial barrier does not get re-established the tissue destruction continues and alveolar bone is resorbed. A periodontal pocket is established.

Histopathological Features

Changes in Soft Tissue Wall

• Blood vessels are engorged and are dilated.
• Connective tissue become edematous and is densely infitrated with plasma cells, lymphocytes and a scattring of PMN leucocytes.
• Junctional epithelium at base of the pocket is shorter than the normal sulcus.
• Most of the degenerative changes occur along the lateral wall of the pocket. Following are the changes in lateral wall of the pocket:
  • Epithelium at the lateral wall of the pocket show striking proliferative and degenerative changes.
  • Epithelial projection extend deep in connective tissue and extend further apically than junctional epithelium.
  • Epithelium is infitrated with leucocytes and various other inflammatory cells.
  • Degeneration and necrosis of epithelium causes ulceration of epithelium and exposure of underlying connective tissue.
  • Bacterial invasion is present along lateral and apical areas of pocket. Some bacteria traverse basement membrane and invade subepithelial connective tissue.

Changes in Root Surface Wall

• Structural changes:
  • Presence of pathologic granules
  • Areas of increased mineralization
  • Areas of demineralization
• Chemical changes: Mineral content of exposed cementum is increased
• Cytotoxic changes: Bacterial penetration in cementum is found as deep as cementodentinal junction. Bacterial products such as endotoxins are also seen.