title: Subcutaneous injections of platelet-rich plasma into skin flaps modulate proangiogenic gene expression and improve survival rates.
abstract: BACKGROUND
  Flap necrosis remains a major complication of reconstructive surgery. To improve skin flap survival, various treatments with vasodilators, antiplatelet drugs, or the local administration of growth factors have been performed. However, the sufficient prevention of skin necrosis is not well established. Platelet-rich plasma has been used as an autologous factor and includes various growth factors. The authors evaluated whether or not platelet-rich plasma can improve skin flap survival in an experimental rat model.
  
  
  METHODS
  Cranially based dorsal cutaneous flaps were elevated in 48 rats. The animals received subcutaneous injections of either platelet-rich plasma (100 μl) or platelet-poor plasma (100 μl). The rats were divided into three groups: the platelet-rich plasma group (n = 16), the platelet-poor plasma group (n = 16), and the nontreatment group (n = 16). Flap survival was measured and histologic specimens were collected on day 7. Real-time polymerase chain reaction specimens were collected after 8 hours, 24 hours, 3 days, and 7 days.
  
  
  RESULTS
  Platelet-rich plasma significantly improved flap survival rates (61.2 percent) compared with the platelet-poor plasma treatment (35.8 percent) and nontreatment groups (28.0 percent). A histologic analysis showed that significantly fewer inflammatory cells and an increased blood vessel density were observed in the platelet-rich plasma rats versus the platelet-poor plasma or nontreatment rats. In addition, platelet-rich plasma treatment significantly increased the mRNA levels of vascular endothelial growth factor and platelet-derived growth factor.
  
  
  CONCLUSIONS
  Platelet-rich plasma modulates the genes involved in angiogenesis and improves skin flap survival.
authors.affiliation: Tokyo, Japan From the Department of Orthopaedic Surgery and the Developmental Division of Advanced Orthopaedic Therapeutics, Graduate School, Tokyo Medical and Dental University.
authors.forename: Weiwei
authors.initials: W
authors.lastname: Li
authors.forename: Mitsuhiro
authors.initials: M
authors.lastname: Enomoto
authors.forename: Madoka
authors.initials: M
authors.lastname: Ukegawa
authors.forename: Takashi
authors.initials: T
authors.lastname: Hirai
authors.forename: Shinichi
authors.initials: S
authors.lastname: Sotome
authors.forename: Yoshiaki
authors.initials: Y
authors.lastname: Wakabayashi
authors.forename: Kenichi
authors.initials: K
authors.lastname: Shinomiya
authors.forename: Atsushi
authors.initials: A
authors.lastname: Okawa
mesh_terms: D043925:Angiogenesis Inducing Agents / Q000032:analysis; D000818:Animals; D000077214:Becaplermin; D005782:Gels; D015870:Gene Expression; D006085:Graft Survival; D007279:Injections, Subcutaneous; D036341:Intercellular Signaling Peptides and Proteins / Q000008:administration & dosage* / Q000032:analysis / Q000235:genetics; D008297:Male; D055806:Microvessels / Q000378:metabolism / Q000473:pathology; D009336:Necrosis; D018919:Neovascularization, Physiologic / Q000235:genetics*; D053657:Platelet-Rich Plasma / Q000737:chemistry; D020574:Proto-Oncogene Proteins c-sis / Q000032:analysis; D051381:Rats; D017208:Rats, Wistar; D013524:Surgical Flaps / Q000098:blood supply* / Q000473:pathology; D053773:Transforming Growth Factor beta1 / Q000032:analysis; D014841:von Willebrand Factor / Q000032:analysis
chemical_list: D043925:Angiogenesis Inducing Agents; D005782:Gels; D036341:Intercellular Signaling Peptides and Proteins; D020574:Proto-Oncogene Proteins c-sis; D053773:Transforming Growth Factor beta1; D014841:von Willebrand Factor; D000077214:Becaplermin