What is PRP ?

That is the question so many people have been asking. PRP is an achronym for Platelet Rich Plasma. Essentially, PRP increases the concentration of platelets to an injured site. In an acute injury, platelets normally activate during the inflammatory phase to begin healing. The addition of PRP in the acute injury increases the concentration of platelets at the local tissue above the baseline.

Chronic injuries that have failed conservative therapies presumably have ceased the inflammatory phase. In these situations, PRP would provide two beneficial results. First, the simple act of injecting PRP for tendon, ligament or muscle injuries will stimulate the tissue and restart the inflammatory process. This makes the chronic injury into a “new” acute injury.

Second, the addition of autologous concentrations of platelets theoretically augments the healing process. This new injury now has a known starting point and one can place the injury in a controlled post-injection environment such as immobilization, bracing or
non-weightbearing. During this time, the use of anti-inflammatory medications and therapies is restricted so as not to reverse the desired effect.

Platelets are a major player in the clotting cascade. They are colorless, non-nucleated fragments of cells that are derived from megakaryocytes within the bone marrow. They contain cytokines and granules (a, d, ?). Out of these, a cytokines and granules are the most important as they contain more than 30 proteins that play a pivotal role in soft tissue healing and hemostasis.1

Within minutes of the aggregation of the platelets, the a granules generate and secrete several proteins. Platelet-derived growth factor (PDGF), insulin-like growth factor (IGF), vascular endothelial growth factor (VEGF), epidermal growth factor (EGF), epithelial cell growth factor, osteocalcin, fibrinogen and fibronectin are some of the secretions from the a granules. These growth factors directly affect their target cells by initiating their growth, morphogenesis and differentiation. Examples of target cells are osteoblasts, fibroblasts, endothelial cells, epidermal cells and mesenchymal stem cells.1-3

The normal three phases of wound healing are inflammation, proliferation and remodeling. At the moment of tissue injury, the inflammatory phase, platelets activate and begin to secrete their proteins (cytokines and growth factors) through the granules. They also produce bioactive factors like serotonin, histamine, dopamine, calcium and adenosine. The serotonin and histamine will act to increase permeability of the capillaries and facilitate more of these products being delivered to the wound site. Platelets normally do not aggregate together unless there is a stimulant present.

Once there is tissue injury, a cellular mix of proteins allows the platelets to initiate clotting and the thrombus process.4 Fibronectin, laminins, collagen, von Willebrand factor and other proteins activate the platelets. Even the platelet’s own secretions like serotonin and adenosine diphosphate will trigger platelet aggregation and activation. Once activated, the platelets will begin to form the fibrin clot.2,5

The determination of the appropriate concentration of PRP for clinical use is difficult. The normal concentration of platelets in blood ranges from 150,000/µL to 350,000/µL. Research has shown that a level of at least 1,000,000/µL is necessary to promote an increase in healing.6 Most PRP contains a three- to fivefold level over baseline. However, other studies have suggested efficacy at levels of two- to 8.5-fold.3

References

1. Harrison P, Cramer EM. Platelet alpha-granules. Blood Rev. 1993;7(1):52-62.

2. Broughton G II, Janis JE, Attinger CE. Wound healing: an overview. Plastic Reconstruction Surgery. 2006;117(suppl):12S-32eS.

3. Smith SE, Roukis TS. Bone and wound healing augmentation with platelet-rich plasma. Clin Podiatric Med Surg. 2009;26(4):559-588.

4. Plow EF, Abrams CS. The Molecular basis for platelet function. In: Hoffman R, ed. Hematology: basic principles and practice, 4th edition Philadelphia: Elsevier, Churchill, Livingstone; 2005, pp. 1881-1898.

5. Witte M, Barbul A. General principles of wound healing. Surg Clin North Am. 1997;77(3):509-528.

6. Marx RE. Platelet-rich plasma (PRP): what is PRP and what is not PRP? Implant Dent. 2001;10(4):225-228.