Pathogenesis
Pathogenic cascade: subgingival biofilm dysbiosis → innate immune activation (complement, TLRs on sulcular epithelium) → pro-inflammatory cytokines (IL-1β, TNF-α, IL-6, IL-17) → matrix metalloproteinases (MMP-8, MMP-13) and RANKL/OPG imbalance → collagen degradation → osteoclast activation → alveolar bone resorption.
RANKL/OPG axis is central: RANKL (produced by fibroblasts, T-cells) stimulates osteoclastogenesis; OPG decoys RANKL, preventing bone resorption. In periodontitis, RANKL/OPG shifts dramatically toward osteoclast activation. The junctional epithelium migrates apically as the PDL is destroyed, forming pathological pockets that trap anaerobic bacteria in a self-amplifying cycle.
Bone loss patterns: horizontal (uniform level loss — most common); vertical/angular infrabony defects (associated with more virulent pathogens). Furcation involvement (Class I–III) indicates multi-rooted tooth bone loss around the furcation — critical prognostic determinant.