Etiology
Chronic periodontitis is initiated by subgingival dental biofilm (plaque dysbiosis) but its extent and severity are modulated by the host immune-inflammatory response, genetic susceptibility, and systemic risk factors.
KEY PATHOGENS — the 'red complex' (Socransky 1998): Porphyromonas gingivalis (key virulence: gingipains, LPS, fimbriae — subverts complement via C3 cleavage, classified as a 'keystone pathogen'), Treponema denticola (motile spirochete, dentilisin protease), Tannerella forsythia (BspA surface protein). The orange complex (Fusobacterium nucleatum, Prevotella intermedia) bridges early colonisers to red complex.
SYSTEMIC RISK FACTORS: Diabetes mellitus (HbA1c >7% correlates with 3× more severe periodontitis — bidirectional relationship); smoking (nicotine impairs neutrophil function, reduces gingival blood flow masking BOP — a critical diagnostic pitfall); stress (elevated cortisol → immunosuppression); genetic polymorphisms (IL-1α/β positive genotype = 2–4× more severe disease).