Pathogenesis of Periodontitis revision notes quiz

Pathogenesis of Periodontitis

• Chemical Mediators: Cytokines, prostaglandins, matrix metalloproteinases.
• Cytokines: Small proteins controlling immune cell growth and activity, signaling the immune system.
• Action of Cytokines in Periodontitis: Release pro-inflammatory cytokines in response to pathogens, accelerating periodontal tissue destruction.
• Prostaglandins: Produced during inflammation, contributing to bone resorption, chemotaxis, and vascular changes.
• Matrix Metalloproteinases (MMPs): Enzymes degrading connective tissue and extracellular matrix components, part of the inflammatory response.
• Polymorphonuclear Leukocytes (PMNs): White blood cells, the body's first line of defense against pathogens, including neutrophils, eosinophils, basophils, and mast cells.
• Bacteria Involved in Periodontitis & Virulence Factors:
• P. gingivalis: Gingipains (for nutrient uptake); carbohydrate capsule (resists host defenses).
• T. denticola: Adherence mechanisms (bind to fibroblasts); degrades cytokines, disrupting host defense.
• T. forsythia: Proteases and apoptotic factors (cause cell death to immune cells).
• A. actinomycetemcomitans: Leukotoxin (destroys white blood cells, inhibits immune response); proteases and toxins (destroy and invade host epithelial cells).

Initial Lesion (2-4 Days After Plaque Biofilm Accumulation)

• Bacterial Features: Bacteria colonize tooth surfaces.
• Cellular Features: Junctional epithelial cells release inflammatory mediators; polymorphonuclear leukocytes (PMNs) are recruited to the area; PMNs migrate into the sulcus, phagocytosing bacteria, and releasing cytokines that can damage healthy gingival connective tissue.
• Tissue Level Features: Plaque biofilm localized supragingivally; vascular dilation in the dentogingival complex (junctional, sulcular, and oral epithelium, connective tissue); gingival crevicular fluid increases in volume, attracting inflammatory cells.
• Clinical Features: Clinically, gingiva appears healthy.
• Host Response: Successful host response if bacteria are effectively cleared and the damage is repairable. Body repair is possible if the bacteria and infection are controlled.

Early Lesion (4-7 Days After Plaque Biofilm Accumulation)

• Bacterial Features: Plaque biofilm accumulation continues and matures; toxins and byproducts penetrate junctional epithelium.
• Cellular Features: PMNs migrate toward the inflammation site, cytokines released by the junctional epithelium increase bacterial defenders; increased blood vessel permeability allows for more PMNs to migrate through tissue near the infection site.
• Tissue Level: Sulcular epithelium and surrounding connective tissue are affected, collagen loss occurs; junctional epithelium cells begin to proliferate, forming epithelial ridges; inflammation is present.
• Clinical Features: Edema (fluid build-up), inflammation, redness of the gingival marginal tissue are observed clinically.

Established Lesion (21 Days After Plaque Biofilm Accumulation)

• Bacterial Features: Plaque biofilm extends subgingivally; disrupts attachment of coronal portion of junctional epithelium from tooth surface.
• Cellular Features: Migration of additional cellular defenders to the site of infection (e.g., PMNs, macrophages, lymphocytes, plasma cells produce antibodies); immune cells increase to fight bacteria, and more toxic chemicals and collagen destruction occur.
• Tissue Level: Epithelial ridges extend deeper into gingival connective tissue; junctional epithelium loosens and transforms into pocket epithelium; more collagen degradation occurs.
• Clinical Features: All features of gingivitis are more evident at this point.

Advanced Lesion: Periodontitis

• Bacterial Features: Plaque biofilm grows laterally and apically along the root surface; periodontal pockets provide a great environment for continued subgingival bacterial growth.
• Cellular Features: Host response intensifies, with bacterial infection becoming chronic, and the inflammation in the periodontium (cementum, PDL, alveolar bone, and gingiva). Increased cellular defenders; immune system releases excessive chemicals that damage periodontal tissues.
• Tissue Level: Destruction of periodontal tissue continues; junctional epithelium cells migrate apically, forming a periodontal pocket; gingival fibroblasts are involved in this tissue degradation.
• Clinical Features: Periodontal pocketing, bleeding on probing, loss of alveolar bone, furcation involvement, and tooth mobility are observed.
• Host Response: Chronic inflammation damages periodontium more than the infection itself; abnormal PMN function, presence of bacterial virulence factors, and systemic factors (e.g., smoking, diabetes) can influence host response.