Pathogenesis
Pathogenesis
Initial lesion (0–4 days): bacterial products activate Toll-like receptors on gingival fibroblasts and keratinocytes, triggering IL-8 and other chemokines. Neutrophils migrate through junctional epithelium into the gingival crevice (sulcus). Complement activation, vasodilation, and increased vascular permeability occur. No clinical signs yet.
Early lesion (4–7 days): neutrophil infiltration intensifies. Macrophages and T lymphocytes accumulate. Collagen fibers adjacent to the junctional epithelium begin to degrade (MMP-mediated). The junctional epithelium proliferates. Clinically: slight erythema and edema become detectable.
Established lesion (21+ days): the classic gingivitis stage. Plasma cells predominate, producing local antibody. B and T cell populations persist. Collagen loss continues in the immediate peri-junctional area, though the alveolar bone crest remains intact. The junctional epithelium is ulcerated, allowing bacterial antigens direct access to connective tissue. Clinical signs fully developed: erythema, edema, BOP, altered gingival contour.
Advanced lesion: transition to periodontitis. Inflammation extends apically, destroying periodontal ligament and alveolar bone. This stage is irreversible. The triggers for transition from established gingivitis to periodontitis are not completely understood but involve dysbiosis shifts to more anaerobic, proteolytic organisms and potentially systemic immune permissiveness.