Effects of platelet-rich plasma on angiogenesis and osteogenesis-associated factors in rabbits with avascular necrosis of the femoral head

OBJECTIVE: Platelet-rich plasma (PRP) contains various growth factors and cytokines that can enhance the recovery of the damaged tissues. The present study aimed to examine the effects of PRP on the recovery of avascular necrosis of the femoral head (ANFH), and to provide novel insights into the clinical treatment of this disease. MATERIALS AND METHODS: A total of 24 New Zealand white rabbits were randomly divided into the normal control group, ANFH model and PRP-treated groups (n = 1 2 each). Blood samples were extracted from the auricular vein at 4, 8 and 12 weeks after establishing the model to determine the hemorheological indexes, as well as the content of serum osteocalcin bone Gla-protein (BGP) and vascular endothelial growth factor (VEGF). In addition, femoral head tissue was collected, with part of it used for hematoxylin and eosin (HE) staining to observe the histological changes. The remaining was used to detect the mRNA expression levels of alkaline phosphatase (AKP), basic fibroblast growth factor (bFGF), transforming growth factor-beta 1 (TGF-beta 1), bone morphogenetic protein 2 (BMP-2) and platelet-derived growth factor B (PDGF-B) by reverse transcription-polymerase chain reaction. RESULTS: Compared with the model group, PRP treatment significantly improved the hemorheological indexes, as well as significantly increased the contents of BGP and VEGF. In the PRP group, the expression levels of TGF-beta 1, bF-GF, BMP-2 and PDGF-B were significantly upregulated, while AKP expression was downregulated compared with the model group. Furthermore, PRP evidently improved the histological structure of the ANFH tissue. CONCLUSIONS: PRP was able to improve the hemorheological indexes following femoral neck fracture, repair the local blood vessels, and promote the expression of osteoblast-associated and angiogenesis-associated factors, which suggested a high efficiency in repairing ANFH.