Periodontal Pocket Question And Answers

Periodontal Pocket

Terminologies

Junctional epithelium is a band of epithelial cells that begins at the base of the gingival crevice, approximately 20–30 layers thick, and tapers to a few cells at the cemento enamel junction in health.

• Epithelial attachment refers to the structural apparatus or biological mechanism that unites the junctional epithelial cell to the tooth surface through hemi-desmosomes and the internal basal lamina.
• Connective tissue attachment refers to the insertion of collagen fibers of the gingival connective tissue into the cementum coronal to crest of the alveolar bone.
• Connective tissue attachment loss is defined as the pathological detachment of the gingival connective tissue from the cemental surface with the concomitant apical migration of the junctional epithelium on the root surface.

Read And Learn More: Periodontology Important Question And Answers

• It represents the histological events in connective tissue destruction.
• Connective tissue attachment loss should be used rather than the term clinical attachment loss as connective tissue destruction is a histological event.
• Clinical attachment level (CAL) is the distance from the cementoenamel junction to the most apical extent of the periodontal probe penetration.
• It is the clinical approximation of the level of the soft tissue attachment (junctional epithelium) to the tooth surface.
• CAL gives information on the level of the tissue attachment to the tooth and is not synonymous with connective tissue attachment loss.

Question 1: Define periodontal pocket. Add a note on this classification.
Answer:

A periodontal pocket is considered to be one of the hall marks of periodontal disease.

It may be defined as;

1. A pathological deepened gingival sulcus (Carranza).
2. A pathological fissure between the tooth and the crevicular (sulcular) epithelium limited at its apex by the junctional epithelium.
3. It is an abnormal apical extension of the gingival crevice caused by migration of the junctional epithelium along the root surface as gingival connective tissue attachment and the periodontal ligament are detached by a disease process.

Classification Of Periodontal Pocket

• Depending on the presence or absence of attachment loss.
• Clinically pockets can be classified as gingival and periodontal pockets.
  • Gingival pocket (pseudopocket): Deepening of the gingival sulcus occurs by gingival enlargement without loss of connective tissue attachment.
  • Periodontal pocket: This type of pocket occurs due to apical migration of junctional epithelium and connective tissue attachment loss (destruction of the supporting periodontal tissue).
• Depending on the position of the base of periodontal pocket with respect to the alveolar bone.
  • Suprabony (supracrestal or supraalveolar): Th bottom of the pocket is coronal to the crest of the underlying alveolar bone. Occurs in cases of horizontal bone loss.
  • Intrabony (infra bony, subcrustal, or interalveolar): Th bottom of the pocket is apical to the crest of the adjacent alveolar bone. Occurs in cases of vertical bone loss.

• Depending on the involved tooth surfaces.
  • Simple pocket: One surface of the affected teeth is involved.
  • Compound pocket: Two surfaces of the affected teeth is involved.
  • Complex pocket: More than two surfaces of the affected teeth is involved. Seen in spiral pockets in furcation areas.
• Depending on the consistency of the soft tissue wall of the pocket.
  • Edematous pocket wall: In edematous pocket wall, the inflammatory and cellular fluid
    predominate resulting in a bluish red, spongy, and shiny smooth surface.
  • Fibrotic pocket wall: The fibrotic pocket wall is firm and pink as newly formed connective tissue predominates.
• Depending on the periodontal disease activity (progressive deepening of the pocket).
  • Active pocket: Th pocket is undergoing connective tissue destruction resulting in deepening of the probing pocket depth of around 2 mm over a period of time.
  • Inactive pocket: There is a presence of a pocket but showing no increase in probing depth over a period of time.

Question 2: Describe the pathogenesis of pocket formation.
Answer:

Dental plaque is a prerequisite for periodontal pocket formation. The pocket formation begins with the colonization of the micro-organisms on the tooth surface and gingival inflammation.

• If left untreated gingivitis may progress to periodontitis in 15 to 16% of the cases. For pocket formation to occur, therefore, gingival inflammation with all its features must have already occurred.

Breakdown of Connective Attachment and Apical Migration of the Junctional Epithelium

The bacteria and their virulence factors do not by themselves cause tissue destruction but induce the inflammatory cells like polymorphonuclear leukocytes, macrophages to release excessive amounts of pro inflammatory cytokines, prostanoids, and matrix metalloproteinases (MMP).

• The overproduction of these host derived IL-1, IL-6, prostaglandin E2 (PGE2), tumor necrosis factor alpha (TNF-α), MMP’s result in an imbalance between tissue formation and destruction.
• This disruption leads to the soft and hard tissue damage observed in periodontal disease. MMP’s and other proteases degrade the surrounding connective tissue including the gingival fibers just apical to the junctional epithelium.
• Following this, the apical cells of the junctional epithelium proliferate along the roots by extending fingerlike projections two to three cells thick.
• Simultaneously, the coronal portion of the junctional epithelium detaches from the root surface, due to the increased infiltration of neutrophils (60% or more) and loss of cohesiveness (intraepithelial cleavage). The base of the sulcus, therefore, shifts apically and the pocket is formed.
• The soft tissue wall may be edematous or fibrotic depending on the nature of inflammation. As the inflammation progresses apically and approaches the alveolar bone, there is an imbalance in the osteoclast and osteoblast activity as well.
• Pro-inflammatory mediators such as IL-1, IL-6, PGE2, TNF-α, and lipopolysaccharides activate the osteoclastogenesis by affecting the RANK-RANKL pathway, resulting in bone resorption.
• The distance between the apical extent of plaque and the alveolar crest in the periodontal pocket (radius of section) is constant is about 1.97 mm on an average.

Question 3: What are the clinical signs and symptoms associated with a periodontal pocket?
Answer:

Signs

1. Enlarged bluish-red rolled-out marginal gingiva. The bluish-red color is due to circulatory stagnation.
2. The reddish-blue vertical zone which extends from the marginal gingiva into the attached gingiva.
3. Gingival bleeding on probing. This occurs due proliferation of vessels and the engorgement of the veins along with thinning and degeneration of the epithelium.
4. Faciolingual discontinuity of the interdental papilla.
5. Smooth, shiny, and soft surface. This is due to the degeneration of collagen and atrophy of the epithelium along with edema.
6. Purulent exudates may occur due to suppurative inflammation of the inner wall of the pocket.
7. Loosening and shifting of teeth and development of diastema in the anterior due to weakening of the periodontal support.

Signs Symptoms

• Localized type of pain, especially after eating or pain deep in the bone. Pain relieved after inducing bleeding. Pain may be due to ulceration of the sulcular epithelium and also by the release of chemical mediators of inflammation.
• Food impaction, foul odor, and taste in the mouth.

Question 4: Describe the changes happening at the soft tissue wall and root surface of a periodontal pocket.
Answer:

The anatomy of the pocket wall is constantly changing and is dictated by the quasi-static equilibrium between the bacterial invasion and the host response. Seven zones of reference on the gingival wall of the periodontal pocket have been identified by electron microscopic means. These include

1. Zone of quiescence: Flat gingival wall surface with a few mounds of cells or depressions with occasional shedding of cells.
2. Zone of bacterial accumulation: Depressions on the epithelial surface with abundant debris and clumps of cocci, rods, filaments, and spirochetes penetrating the open intercellular spaces.
3. Zone of leukocyte emergence: Areas of emergence of diapedetic leukocytes from within the intercellular spaces.
4. Zone of leukocyte bacterial interaction: Demonstration of phagocytotic activity by leukocytes.
5. Zone of intense epithelial desquamation: Semi-attached or folded epithelial debris partially covered by organized plaque.
6. Zone of ulceration: Areas showing loss of epithelial continuity and exposure of connective tissue.
7. Zones of hemorrhage: Areas showing numerous erythrocytes.

Microtopography of the Root Surface Wall of the Periodontal Pocket

The root surface wall of the periodontal pocket is composed of cementum which in effect is a very permeable and adsorbing surface. The root cementum in periodontitis undergoes structural, chemical, and cytotoxic changes and by its permeability and adsorbing characteristic perpetuates the periodontal infection.

1. Presence of pathologic granules: Representing areas of poorly mineralized collagen fibrils
2. Zones of increased mineralization: The exposure of the root cementum to the oral environment and the saliva may initiate mineralization of the exposed cementum with the supersaturated saliva or the deposition of organic materials of exogenous origin.
3. Zones of demineralization: Areas representing softening of the cementum by exogenous chelating agents or the acid demineralizing effect of cariogenic plaque constituents.
4. Bacteria can readily permeate demineralized cementum and enter the dentinal tubules with resultant loss of the dentin. Large chunks of cementum can become necrotic and detach from the tooth.
5. Zone of calculus
6. Zone of attached plaque
7. Apical zone of unattached plaque
8. Attachment area of the junctional epithelium—reduced to about 100 microns from 500 microns in health
9. Zone of semi-destroyed connective tissue fibers. The root surface also demonstrates changes in the ionic content of various minerals such as calcium, magnesium, phosphorous, and fluoride.
10. Diseased root surfaces adsorb bacterial toxins and other chemical mediators of inflammation and negate the effects of gingival fibroblasts from attaching freely to the surface of the root.

Microtopography Conclusion

A periodontal pocket is a pathognomonic sign of periodontitis. Early diagnosis of periodontal pocket formation and prompt institution of therapy is a prerequisite for successful management of Periodontitis.