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

2. PLATELETS

3. PLATELET PRIMARY FUNCTION

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

5. 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

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

7. 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

8. a-GRANULES

9. d-GRANULES

10. 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

11. 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

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

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