Pathogenesis
Pre-ulceration phase: mononuclear cell infiltrate appears in the lamina propria before clinical ulceration, with CD4+ T cells and activated macrophages predominating.
Ulceration phase: cytotoxic CD8+ T cells and NK cells destroy epithelial cells, creating the ulcer. TNF-α, IFN-γ, and IL-12 maintain the inflammatory microenvironment and prevent healing.
The pseudomembrane covering the ulcer is composed of fibrin, necrotic epithelial cells, neutrophils, and bacteria — it is not infectious but protective.
Healing phase: anti-inflammatory cytokines (IL-10, TGF-β) gradually suppress the immune response; re-epithelialization occurs from the ulcer margins inward, typically completing in 7-14 days for minor aphthae.