Saneto RP et al
PRP can be useful in selected patients when the protocol is consistent
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
Thereby, the subsequent burn studies were on the burns covering 20% of total body area on the back of mice, open flame for 5 or 7 s (Mikus et al., 2001
It's a combination that holds immense theoretical promise for researchers looking to explore the frontiers of tissue regeneration and healing
From a pharmacokinetic perspective, topical GHK-Cu has a distinct advantage: it acts locally rather than systemically