The molecular mechanism of platelet lysate promotes transformation of non-union cells into osteoblasts

Platelet lysate (PL) was a liquid component obtained from whole blood by density gradient centrifugation to concentrate platelets, and then passed through three times freeze-thaw to lyse platelets (1). PL was characterized by the removal of platelet membranes and other cell debris, in order to reduce immunogenicity and retain many of the cell growth factors, which could create conditions for allogeneic or xenogeneic transplantation (2,3). In recent years, PL had been applied to the research of bone tissue engineering, and significantly promoted bone regeneration and repair. PL is administered to treat many diseases such as bone regeneration, oral mucositis, osteoarthritis, and ocular diseases (4). The injectable tissue-engineered bone, which could improve the osteogenesis rate of osteogenic traction, was constituted by PL, autologous bone, allogeneic bone or hydroxyapatite, and autologous bone matrix stem cells. In addition to procoagulant effects, PL also had the function of promoting tissue wound repair. PL contained many important cell growth factors and was removed of platelet surface antigens. Cell growth factors could promote the division and proliferation of various cells, collagen synthesis, stimulate the growth of blood vessel and induce cell differentiation, which were essential for bone repair and regeneration (5). When PL is activated to gelate by thrombin, cell growth factors are released. PL is a solution saturated by proteins, growth factors and chemokines. PL mainly contains cell growth factors, such as platelet derived growth factor (PDGF), transforming growth factor-β (TGF-β), insulin-like growth factor (IGF), vascular endothelial growth factor (VEGF) and epidermal growth factor (EGF), etc. (6). In recent years, studies had shown that RANKL/RANK/OPG played an important role in bone metabolism (7). RANK was a receptor of RANKL, which involved in the differentiation of osteoclasts and promoting bone resorption. OPG was another receptor for RANKL, which inhibited osteoclast development and bone resorption (8)