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Researchers created segmental bone defects in rabbits, essentially removing a section of bone to create a gap that would not heal on its own

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Upon release by the endothelium, NO stimulates the soluble guanylate cyclase (sGC) in vascular muscle cells, leading to a rise in the intracellular concentration of cyclic guanosine 3,5-monophosphate (cGMP) and relaxation

Given that implanted chondrocytes are responsible for the generation of new cartilage in the defect site, it is not surprising that the quality of these cells critically affects the reparative results of ACI treatment (Davies and Kuiper, 2019)