PRP has long been defined as autologous plasma that has a concentration of platelets much higher than in normal blood.The effects of PRP rely on the unique biological activity of platelets and their involvement in the wound healing cascade. The main role of platelets is to create a hemostatic plug and to promote fibrin generation and blood clotting to prevent blood loss. However, they are also a vital part of the innate immune response. They combat infection and modulate inflammation, they promote cell chemotaxis and proliferation, and they promote wound healing, angiogenesis,and bone formation.
Within platelets, the most abundant source of secreted proteins is the α-granule. Secreted proteins can be grouped in different families based on their biological activity. Factors such as PDGF, IGF-1, VEGF,and several other chemokines and cytokines favor wound healing and promote angiogenesis in cooperation with proangiogenic mediators such as SDF-1, MMP-1, MMP-2, MMP-9, and angiopoietin that are also present. FGF-2 is a mitogenic factor as well as TGF-β1 that is also known to recruit inflammatory cells to the wound.IGF-1 stimulates matrix formation.Adhesion proteins which can act as cell adhesion molecules thereby mediating cell migration are also released by platelets.
The proinflammatory molecule CD40 ligand present on platelet membranes is believed to play an important role in stimulating angiogenesis by promoting endothelial cell proliferation. BMP-2, BMP-4, and BMP-6 are synthesized by megakaryocytes and released by platelets in the acidic hypoxic environment of bone fracture. Indeed, it has been suggested that PRP stimulates osteoblastic differentiation of myoblasts and osteoblasts in the presence of BMP-2, BMP-4, BMP-6, and BMP-7 possibly by playing a potentiating role in BMP-dependent osteoblastic differentiation.
Post time: Oct-13-2022