P2-PERIO CHAPTER 22

A pathologically deepened gingival sulcus

What is a periodontal pocket?

It is an important clinical feature of periodontal diseases

Why is the periodontal pocket important clinically?

Tissue changes in periodontal pocket, mechanisms of tissue destruction, healing mechanisms.

What do all types of periodontitis share?

Etiology, natural history, progression, and response to therapy.

How do different types of periodontitis differ?

Coronal movement of gingival margin, apical displacement of gingival attachment, or both.

What causes deepening of the gingival sulcus?

• Gingival enlargement without destruction of underlying periodontal tissues; deepening due to increased gingival bulk.

What is a gingival pocket (pseudo-pocket)?

Formed by loss of periodontal attachment; may cause loosening and exfoliation of teeth.

What is a periodontal pocket?

Suprabony and Intrabony.

What are the two types of periodontal pockets based on relation to alveolar bone?

Coronal to the alveolar bone.

Where is the bottom of a suprabony pocket located?

• Apical to the alveolar bone, with lateral pocket wall between tooth and bone.

Where is the bottom of an intrabony pocket located?

Pockets originating on one surface, twisting around tooth to involve additional surfaces (common in furcation areas).

What are spiral pockets?

Bluish-red thickened marginal gingiva, bluish-red vertical zone, gingival bleeding and suppuration, tooth mobility, diastema formation, localized pain.

: What are signs suggesting periodontal pockets?

PRobing gingival margin along each tooth surface.

What is the only reliable method of diagnosing periodontal pockets?

Space between the neck of the tooth and circumferential gingival tissue

What is the gingival sulcus?

Gingival inflammation in response to bacterial challenge.

What is the first lesion in periodontal pocket formation?

Healthy gingiva: coccoid cells & straight rods; Diseased gingiva: spirochetes & motile rods.

How does dental plaque microbiota change from health to disease?

• As inflammatory change in connective tissue wall of gingival sulcus.

How does pocket formation start?

Destroyed apical to junctional epithelium, replaced by inflammatory cells and edema.

What happens to collagen fibers in pocket formation?

Host immune-inflammatory response to persistent bacterial attack destroys collagen and bone.

What is the current concept of tissue destruction in periodontal disease?

IL-1 and TNF-α

: Which proinflammatory cytokines are strongly implicated in progression?

IL-4 and IL-10.

Which cytokines counteract proinflammatory effects?

Enzymatic degradation and phagocytosis by fibroblasts.

What are the two main mechanisms of collagen loss?

• Matrix metalloproteinases (MMPs).

Which enzymes degrade collagen and ECM?

22. Tissue Inhibitors of Metalloproteinases (TIMPs).

What controls MMP activity?

Apical cells proliferate along root surface forming finger-like projections

How does loss of collagen affect junctional epithelium?

Loss of cohesiveness, detachment when PMNs reach ~60%.

What happens when PMNs invade junctional epithelium?

Requires healthy epithelial cells; necrosis leads to ulcer formation instead.

Why is apical extension of junctional epithelium along root necessary

Gingival enlargement, apical migration of junctional epithelium, bulbous lateral wall epithelium, degeneration, and necrosis.

: What happens with continued inflammation?

• A site where plaque removal is impossible.

What does sulcus → pocket transformation create?

plasma cells, lymphocytes, PMNs (~80%).

What cells dominate connective tissue infiltration?

Increased, dilated, engorged blood vessels.

What are vascular changes in periodontal pockets?

degenerative + proliferative changes, epithelial buds, leukocyte infiltration, vesicles, ulceration, suppuration.

What changes occur in lateral wall epithelium?

Tooth (internal basal lamina) and connective tissue (external basal lamina).

What does junctional epithelium attach to?

High permeability and high cellular proliferation/turnover.

What are the permeability and turnover features of junctional epithelium?

Porphyromonas gingivalis, Prevotella intermedia, Aggregatibacter actinomycetemcomitans.

Which bacteria invade pocket walls?

Intercellular spaces, under exfoliating epithelial cells, between deeper epithelial cells, on basement lamina, into connective tissue.

Where can bacteria be located in pocket walls?

Bacterial plaque → inflammatory response.

What triggers tissue destruction in periodontal pockets?

Neutrophils, macrophages, fibroblasts, epithelial cells.

Which host cells produce destructive mediators?

Proteinases, cytokines, prostaglandins

What mediators are produced by host cells?

Relative quiescence

bacterial accumulation

leukocyte emergence

leukocyte–bacteria interaction

epithelial desquamation

ulceration

hemorrhage.

Proteinases, cytokines, prostaglandins

Chronic inflammatory lesions with continuous repair + degeneration.

What are periodontal pockets considered?

Bluish-red, soft, spongy, friable, shiny.

What are the features of an edematous pocket wall?

49. Firm, pink, collagen-rich.

What are the features of a fibrotic pocket wall?

• Microorganisms, enzymes, endotoxins, metabolites, gingival fluid, food, mucin, desquamated cells, leukocytes.

What debris is found in pockets?

usually plaque-covered, projecting from the tooth.

How does calculus appear in a pocket?

Living/dead leukocytes, bacteria, serum, fibrin.

What is purulent exudate (pus) composed of?

No, it is a secondary sign only.

Does pus indicate pocket depth or tissue destruction?

Ultrafiltrate of blood present in the gingival sulcus space

What is gingival crevicular fluid?

Bacterial degradation products, host tissue degradation products, inflammatory mediators.

What does GCF contain?

Easy to collect; used as biomarkers of periodontal disease.

Why is GCF clinically important?

Periimplant sulcular fluid (PISF

What is the implant equivalent of GCF?

They are destroyed in cementum.

What happens to Sharpey fibers as pocket deepens?

Becomes exposed to oral environment and susceptible to bacterial penetration.

What happens to exposed cementum?

62. Cemento-dentinal junction and dentinal tubules.

To what depths can bacterial penetration reach?

Endotoxins (LPS).

What bacterial product is detected in cementum wall?

• Irreversible morphologic changes, prevent fibroblast attachment, induce inflammatory response.

What effects do diseased root fragments cause in tissue culture?

Softened; usually asymptomatic but can cause pain when probed.

What is the condition of cementum surface in periodontal disease?

Exposure of dentin → sensitivity to cold until secondary dentin forms.

What can scaling/root planing cause

Exchange of minerals and organic components at cementum–saliva interface.

What causes increased mineralization of cementum?

Generally 10–20 μm, up to 50 μm.

What is the thickness of the mineralized superficial layer seen under microradiography?

Root caries due to exposure to oral fluids and bacterial plaque.

What causes cementum demineralization?

Yellowish/light brown, covered by plaque, softened/leathery.

What are active root caries lesions like?

Darker, smooth, hard surface

What are inactive root caries lesions like?

• Actinomyces viscosus.

What is the dominant microorganism in root caries?

Often painless, defect felt with probe, sometimes pain, may lead to pulpitis, sensitivity, severe pain, or pulp exposure

What are symptoms of root caries?

• Isolated cavitations penetrating dentin, clear-cut outline, hard surface.

Often painless, defect felt with probe, sometimes pain, may lead to pulpitis, sensitivity, severe pain, or pulp exposure

• Cementum covered by calculus

• attached plaque

• unattached plaque

• junctional epithelium attachment zone

• semidestroyed connective tissue fibers.

What are the five zones in the bottom of a periodontal pocket?

• Zones 3, 4, 5.

Which zones are considered the plaque-free zone?

Reduced inflammatory response, little/no attachment loss.

What occurs during quiescence?

• Buildup of gram-negative, motile, anaerobic plaque → bone and connective tissue loss.

What occurs during exacerbation (activity

Spontaneous/probing bleeding, increased gingival exudate

What are clinical features of active periods?

Thin, ulcerated pocket epithelium with plasma cell/PMN infiltrate

What are histologic features of active periods?

Destruction affects a few teeth or aspects of teeth at a time

What does site specificity mean in periodontitis?

By development of new sites or breakdown of existing sites.

How does severity increase?

Distance from base of pocket to crest of gingival margin

How is pocket depth measured?

Location of base of pocket on root surface.

How is attachment loss measured?

Base of pocket apical to alveolar bone crest; wall between tooth and bone; vertical bone loss

What is an infrabony pocket?

• Base of pocket coronal to alveolar bone crest; wall coronal to bone; horizontal bone loss.

Q: What is a suprabony pocket?

Suprabony = horizontal; Infrabony = oblique.

How are suprabony vs infrabony fiber directions different?

Resective procedures (gingivectomy, osseous surgery

What approaches are used for suprabony pockets?

egenerative procedures (multiple walls, contained defects).

What approaches are used for infrabony defects?

Localized purulent inflammation in periodontal tissues.

What is a periodontal abscess?

Lateral abscess or parietal abscess

What are other names for periodontal abscess?

1) Extension from pocket,

2) Lateral extension into connective tissue,

3) Tortuous pocket course,

4) Incomplete calculus removal,

5) Trauma or lateral wall perforation.

What are five causes of periodontal abscess formation?

Uncommon lesion causing localized destruction of periodontal tissues along lateral root surface.

What is a lateral periodontal cyst?

Mandibular canine–premolar area.

What is the most common site for lateral periodontal cyst?

Rests of Malassez or proliferating odontogenic rests.

What is the origin of lateral periodontal cyst?

Usually asymptomatic, may appear as localized, tender swelling

What are clinical features of lateral periodontal cyst?

Inflammatory response to bacterial biofilm → destruction of PDL fibers + bone loss.

How does periodontitis cause bone loss?

Bacterial mediated and host mediated.

What two categories of factors cause bone destruction

Prostaglandins, IL-1α, IL-1β, TNF-α.

What host factors mediate bone resorption?

Induces bone resorption even without inflammatory cells

What is the role of Prostaglandin E2 (PGE2)?

Adjacent to resorption sites and trabecular surfaces away from inflammation.

Where is new bone formation seen?

Reinforcement of remaining bone during disease

Wat is buttressing bone formation?

Outgrowths of bone, varied size and shape.

What are exostoses?

Horizontal bone loss.

What is the most common bone loss pattern?

Invasion of bifurcation/trifurcation of multirooted teeth.

What is furcation involvement?

Most = mandibular first molars; Least = maxillary premolars.

Which teeth are most and least affected by furcation involvement?

• Nabers probe.

What probe is used to detect furcation involvement?