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Key pathophysiologic mechanisms include: Mucosal barrier dysfunction: Impaired epithelial tight junctions allow bacterial translocation, triggering innate immune activation T-helper cell dysregulation: Predominantly Th1 and Th17 pathways drive chronic inflammation via TNF-α, IL-12, IL-23 — the basis for biologic therapy targets Transmural inflammation: Unlike UC (mucosal only), CD involves all layers: mucosa → submucosa → muscularis propria → serosa Granuloma formation: Non-caseating granulomas are pathognomonic but present in only ~30–50% of biopsies Fibrosis and stricture: Chronic inflammation activates myofibroblasts → collagen deposition → luminal narrowing → obstructive symptoms Fistula formation: Transmural ulcers penetrate serosa → form sinus tracts → connect to adjacent bowel, bladder, vagina, or skin 7
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