Etiology and Pathogenesis of Periodontal Disease
Etiology and Pathogenesis of Periodontal Disease
Questions here test the biofilm–host interaction, the evolution of plaque hypotheses, and the risk factors that shift a gingivitis case into progressive periodontitis.
Biofilm and virulent species
- Plaque is a structured multi-species biofilm; the ecologic plaque hypothesis (Marsh) frames disease as dysbiosis driven by environmental change, not by a single pathogen.
- The red complex - Porphyromonas gingivalis, Tannerella forsythia, Treponema denticola - is associated with, not diagnostic of, disease; P. gingivalis behaves as a keystone pathogen, subverting complement and neutrophil function.
- Virulence factors: LPS, fimbriae, gingipains (cysteine proteases), leukotoxin. Calculus is always covered by biofilm and is a retention factor, not the cause.
Host response and lesion stages
Page and Schroeder: initial (2–4 days, PMN), early (4–7 days, T lymphocytes), established (2–3 weeks, plasma cells, B cells), advanced (bone loss via RANKL/OPG imbalance, MMPs, IL-1, IL-6, TNF-α, PGE2).
Risk factors
Smoking (vasoconstriction masks bleeding while increasing bone loss), poorly controlled diabetes, genetic susceptibility, stress, obesity, medications; local factors include overhangs, open contacts, root grooves and furcation involvement.
Worked example
A 40-year-old smoker with 6 mm pockets shows almost no bleeding. Absence of BOP does not mean absence of disease; reduced gingival blood flow and impaired neutrophil function suppress the sign while accelerating attachment loss - monitor with CAL and radiographs, not bleeding alone.
Traps
Equating gingivitis with periodontitis (gingivitis is reversible and never involves attachment loss); treating the red complex as a diagnostic test; attributing disease to calculus alone; missing smoking as an effect modifier.