Periodontal Pathogenesis and Host Response Flashcards

The 'ecological plaque hypothesis' (Marsh, 1994) proposes that periodontal disease is caused by:

Answer: Environmental shifts in the subgingival niche that select for a dysbiotic, disease-promoting microbiome

The ecological plaque hypothesis holds that disease-associated bacteria are present in health but environmental changes (inflammation, anaerobiosis, nutrient availability) select for their overgrowth, transitioning health-compatible communities to dysbiotic ones.

In Page and Schroeder's histopathological stages of the periodontal lesion, the 'established lesion' is characterized by predominance of:

Answer: Plasma cells and B lymphocytes with possible pocket formation

The established lesion (corresponding to chronic gingivitis) is dominated by plasma cells secreting immunoglobulins and B lymphocytes; importantly, the lesion is not yet destructive — that distinguishes the advanced lesion.

The IL-1 gene cluster polymorphism (composite genotype +) is clinically significant in periodontology because carriers demonstrate:

Answer: Elevated IL-1α and IL-1β production, increasing susceptibility to severe periodontitis

The IL-1 composite genotype (polymorphisms at IL-1A +4845 and IL-1B +3954) results in hyper-secretion of IL-1α and IL-1β, which drives exaggerated RANKL-mediated bone resorption and increases periodontitis risk — especially in smokers.

Epigenetic modifications implicated in periodontal pathogenesis alter gene expression WITHOUT changing the DNA nucleotide sequence through mechanisms such as:

Answer: DNA methylation, histone modification, and microRNA regulation

Epigenetic mechanisms — CpG methylation silencing anti-inflammatory genes, histone acetylation/deacetylation regulating cytokine expression, and microRNAs controlling post-transcriptional output — all contribute to the persistent pro-inflammatory phenotype seen in periodontitis.

In response to bacterial challenge in periodontitis, the junctional epithelium undergoes which critical pathological change?

Answer: Conversion to pocket epithelium and apical migration along the root surface

Bacterial products and inflammatory mediators cause junctional epithelium proliferation, ulceration, and apical migration, converting it to a non-adherent pocket epithelium with increased permeability that deepens the sulcus into a true periodontal pocket.

Neutrophil extracellular traps (NETs) in the context of periodontal disease:

Answer: Can cause collateral tissue damage and perpetuate inflammation while targeting bacteria

While NETs trap and kill periodontal pathogens, the citrullinated histones, DNA scaffolds, and granule proteins they release also damage host tissue, activate the complement system, and sustain chronic inflammation.

The 'keystone pathogen hypothesis' (Hajishengallis & Lamont) best explains why P. gingivalis causes severe disease at low abundance because:

Answer: P. gingivalis disables complement and neutrophil function, enabling outgrowth of the entire dysbiotic community

P. gingivalis acts as a keystone pathogen by cleaving C5a with gingipains, hijacking complement for nutrients, and paralyzing neutrophil IL-8 production, allowing the broader polymicrobial community to thrive and driving community-wide virulence.