Physiological basis of platelet rich plasma therapy Dr. Raj Selvaratnam School of Medical Sciences University of Auckland

PLATELETS

PLATELET PRIMARY FUNCTION

ADHESION Prevented by nitric oxide & PGl2 Anchored to collagen by von Willebrand factor (VWF)

ACTIVATION Inhibited by ADPase & PGl2 released by endothelium low Ca2+ via cAMP activated pump in platelets PGl2 decreases Ca2+ by increasing cAMP ADP increases Ca2+ decreasing cAMP ADP increases Ca2+ increasing IP3 Calcium induces platelet activation

COLLAGEN TRIGGER Binding with platelets activates PLC system Increases Ca2+ Increases production of Thromboxane2 Decreases PGl2 Via PLA, COX1 & TXA synthase Initiate aggregation

GRANULES a, d, g & l granules secrete their content when activated a granules contain growth factors d granules contain ADP or ATP, Adenosine, Calcium, Serotonin and Histamine

a-GRANULES

d-GRANULES

d-GRANULES Adenosine Serotonin Histamine ATP & ADP Acts on Macrophages to produce pro- and anti- inflammatory effects acting via cytokines Serotonin Increases capillary permeability and interacts with Macrophages Histamine Increases perfusion via dilation and permeability. Strong activator of Macrophages ATP & ADP Promotes Platelet activation and aggregation

PDGF in muscle healing Myoblast have PDGF receptors In humans mainly the b-isoform Activation increases DNA synthesis Cell density Leads to muscle development & regeneration

TGF-b in muscle healing Inhibits muscle differentiation Down-regulates RNA Interacts with PDGF to increase cell density and retain muscle type

IGF in muscle healing Increases Muscle mass and strength Satellite cell activation Increases protein synthesis