title: Cellular effects of platelet rich plasmainterleukin1 release from prp treated macrophages.
abstract: The therapeutic use of Platelet Rich Plasma (PRP) as a biological tool to enhance soft tissue and bone healing has recently yielded encouraging results in many areas of clinical medicine. PRP is a specific portion of whole blood that contains a high concentration of platelets. The local treatment of bone and soft tissue injuries with this autologous blood product has become increasingly common in recent years. There is still little known about the mechanism by which PRP acts at the cellular level. The macrophage cell has been shown to be critical in the healing of tissues. In this study the macrophage release of a specific pro-inflammatory factor, interleukin-1 (IL-1), was evaluated in macrophage cells activated and treated with platelets as compared to control macrophages in culture. The results show that platelets caused an initial suppression of IL-1 release from activated macrophage compared to controls. The initial suppression was followed by an increase in IL-1 release at day seven over control and activated macrophages that had ceased release of IL-1 at day seven. The initial suppression of the inflammatory response to activation during days 1, 2 and 3 could have broad implications in the explanation of a mechanism by which PRP acts. If PRP can truly be used as a transient anti-inflammatory agent that initially suppresses inflammation and then stimulates a late healing response, then indications for use of PRP may expand beyond the current scope of treatment.
authors.affiliation: Department of Orthopedic Surgery and Rehabilitation, University of Mississippi Medical Center, Jackson, MS, 39216, USA. jwoodall@orthopedics.umsmed.edu.
authors.forename: James
authors.initials: J
authors.lastname: Woodall
authors.forename: Michelle
authors.initials: M
authors.lastname: Tucci
authors.forename: Allan
authors.initials: A
authors.lastname: Mishra
authors.forename: Ayman
authors.initials: A
authors.lastname: Asfour
authors.forename: Hamed
authors.initials: H
authors.lastname: Benghuzzi