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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-, 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 ~3050% 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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Jia, D., Taguchi, M
Other normal purging signs include mild dryness or flaking as dead cells shed more rapidly, temporary sensitivity that remains manageable, and brief periods of dullness before radiance emerges
Randomized trial of fenretinide to prevent second breast malignancy in women with early breast cancer
Castren E, Rantamaki T
