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In bone healing, nitric oxide plays a specific role: NO promotes osteoblast differentiation and inhibits osteoclastogenesis at physiological concentrations NO-mediated vasodilation enhances blood flow to the fracture haematoma, improving nutrient and progenitor cell delivery eNOS-derived NO activates VEGF expression in endothelial cells, amplifying the angiogenic cascade within the fracture callus BPC-157s activation of the NO pathway therefore supports bone healing through at least three parallel mechanisms: pro-osteoblastic signalling, anti-osteoclastic effects, and enhanced fracture callus vascularisation each measurable as an independent endpoint in research studies

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