Pathogenesis of Periodontal Disease

Vocabulary flashcards reviewing the pathogenesis, stages, microbial virulence factors, and host inflammatory mediators of periodontal disease.

Pathogenesis

The origination and development of a disease, or the mechanism by which a causative factor causes disease.

Gingivitis

An inflammatory lesion that is confined to the gingiva.

Periodontitis

Inflammatory processes that extend beyond the gingiva to additionally affect the PDL and the alveolar bone.

Junctional Epithelium

Nonkeratinized tissue forming the epithelial attachment between gingiva and tooth, measuring 15 to 30 cells thick at the sulcus floor and tapering apically to 3 to 4 cells thick.

Initial Lesion

The stage of periodontal pathogenesis occurring after 2 to 4 days of plaque accumulation, characterized by slightly elevated vascular permeability, vasodilation, GCF outflow, and migration of neutrophils.

Early Lesion

The stage occurring after about 1 week of plaque accumulation, characterized by marginal erythema, edema, bleeding on probing, deeper sulcus, and an inflammatory infiltrate dominated by lymphocytes.

Established Lesion

The stage occurring after about 2-3 weeks of plaque accumulation, characterized by chronic gingivitis, a bluish hue, pocket formation, deep rete pegs, and a cellular infiltrate predominated by plasma cells and B-cells.

Advanced Lesion

The stage representing the transition from gingivitis to periodontitis, characterized by apical migration of junctional epithelium, deepening pockets, alveolar bone loss, and PDL damage.

Lipopolysaccharide (LPS)

Large endotoxin molecules in the outer membrane of gram-negative bacteria composed of lipid A and polysaccharide components that elicit strong immune responses.

Lipoteichoic Acid

A component of gram-positive bacterial cell walls that stimulates inflammatory responses in tissues, though it is less potent than lipopolysaccharide.

Butyric Acid

A short-chain carboxylic acid produced by subgingival bacteria that causes cell apoptosis.

Proteases

Bacterial enzymes that break down host structural components including collagen, elastin, and fibronectin.

Fimbriae

Microbial structures that stimulate immune responses such as IL-6 release and can inhibit IL-12 secretion.

Cytokines

Soluble proteins produced by infiltrating leukocytes and resident periodontal cells that signal, broadcast, and amplify immune responses.

Prostaglandin E2 (PGE2)

An arachidonic acid derivative that causes vasodilation, induces cytokine and MMP production, and results in osteoclastic bone resorption.

Matrix Metalloproteinases (MMPs)

A group of host enzymes that break down structural proteins of the body, including collagenases like MMP-8 and MMP-9.

MMP-8

A key matrix metalloproteinase involved in periodontitis, also known as neutrophil collagenase.

MMP-9

A key matrix metalloproteinase involved in periodontitis, also known as gelatinase B.

TNF-alpha

A cytokine that increases neutrophil activity, induces MMP secretion, stimulates osteoclast development, and limits tissue repair by inducing apoptosis in fibroblasts.

Interleukin-6 (IL-6)

A cytokine secreted by osteoblasts and other cells that stimulates bone resorption and osteoclast development.

Chemokines

Molecules that direct the chemotactic migration of neutrophils and other immune cells through periodontal tissues toward the site of bacterial challenge.

IL-10 Family

A group of anti-inflammatory cytokines possessing pleiotropic effects and immunosuppressive properties.