Platelet Rich Plasma inhibits Macrophages

It is clear that PRP induces increased proliferation in a variety of cell types including fibroblasts and mesenchymal stem cells. This recently published paper discusses how PRP may inhibit macrophage proliferation at least initially. This has broad implications for wound and tissue healing. Further research into these findings should be available soon.

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Cellular effects of platelet rich plasma: a study on HL-60 macrophage-like cells.
Woodall J Jr, Tucci M, Mishra A, Benghuzzi H.
Biomed Sci Instrum. 2007;43:266-71.

Healing injured tissue in the body is a complex process which consists of four distinct phases: hemostasis, inflammation, proliferation, and remodeling. Each of these phases is coordinated by growth factor release and cell to cell interactions. Platelet rich plasma (PRP) is a fraction of plasma that has been isolated and used to enhance regeneration in bone and soft tissues. The healing potential of PRP has been attributed to the release of multiple growth factors from the highly concentrated platelets. While there is strong evidence of the pro-stimulatory effect on the cellular proliferation phase of healing, there is little evidence of the effects of PRP on the inflammatory phase of healing. In this study we investigate the effect that PRP has on macrophage cells in culture and the implications this has on the healing process. We investigate specifically the effects of the separate cellular components of PRP, as a whole and individually, on cell proliferation in human macrophage cells in culture. In contrast to the pro-stimulatory effect that PRP has on cells such as osteoblasts, fibroblasts, and tendon cells; our results show a suppression of macrophages by PRP as early as 24 hours after treatment. This suppression was statistically significant (p=0.002) and continued to be significant for the duration of the study. The cell viability results of PRP compared to platelet poor plasma (PPP) and individual components of PRP showed that PRP resulted in a steady increase in viability following the initial insult to the macrophage cells, while the viability of other treatment groups seemed to plateau.