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Background Different systems for preparation of platelet-rich plasma are commercially available, but data for comparison of these systems have not been published so far. Materials and Methods We investigated the performance of Vivostat PRF Preparation Kit®, PCCS Platelet Concentrate Collection System®, Harvest® SmartPReP 2 APC 60 Process, and Fibrinet® Autologous Fibrin & Platelet System. The preparations provided by these systems are platelet concentrates with high numbers of platelets in a small volume of plasma and PDGF-AB is released continuously during the 5 days after preparation. Results Vivostat PRF Preparation Kit, PCCS Platelet Concentrate Collection System, Harvest SmartPReP 2 APC 60 Process are comparable in platelet yield and total amount of released PDGF-AB after 120 h while with Fibrinet the lowest platelet yield and PDGF-AB content of supernatant was achieved. The ability of growth factor release was equal in all four systems. Conclusion In conclusion, all four systems for preparation of platelet-rich plasma investigated result in considerable growth factor release. In what extent the total content of PDGF-AB as a consequence of platelet yield has an impact on wound healing has to be further investigated [ABSTRACT FROM AUTHOR]

Platelets are activated at fracture sites or upon the insertion of implants as a consequence of vascular disruption and secrete the contents of their granules into the developing hematoma. The regeneration of injured tissue requires bone remodeling and the resorbing activity of osteoclasts. To test our hypothesis that platelets can stimulate osteoclastogenesis, we examined the effects of supernatants released from thrombin-activated platelets on osteoclast-like cell formation in murine bone marrow cultures. Histochemical analysis indicated the presence of bone-resorbing, tartrate-resistant acid phosphatase (TRAP)-positive multinucleated cells. Transcripts that are characteristically expressed in native osteoclasts were increased in these cultures, as determined by semiquantitative reverse transcription-polymerase chain reaction (RT-PCR) analysis. The inhibition of both cyclooxygenases with indomethacin, as well as the addition of the cyclooxygenase-2 (COX-2)-selective antagonist, NS398, completely blocked osteoclast-like cell formation and decreased endogenous prostaglandin E2 production. Platelet-released supernatants stimulated the expression of receptor activator of NF-κB ligand (RANKL), whereas mRNA levels of osteoprotegerin (OPG) were decreased. The formation of osteoclast-like cells was prevented by recombinant OPG. Our results suggest that COX-2 activity is necessary for osteoclast-like cell formation in response to platelet-released supernatants, and that endogenously produced prostaglandin E2 can, in turn, increase the RANKL:OPG ratio, indicating that platelets can contribute to bone remodeling by stimulation of osteoclastogenesis. [Copyright &y& Elsevier]

Agis H, Stampfl B, Watzek G, Gruber R. Activated platelets increase proliferation and protein synthesis of human dental pulp–derived cells. International Endodontic Journal, 43, 115–124, 2010. Aim To evaluate the impact of activated platelets on the mitogenic expansion of human dental pulp–derived cells (DPC) in vitro. Methodology The effect of supernatants released from activated platelets (PRS) and the corresponding platelet membranes (MEM) on proliferation and protein synthesis of DPC was evaluated. The contributions of the phosphoinositide 3-kinase (PI3K)/AKT and mitogen-activated protein kinase (MAPK) pathways to the response of DPC were assessed using kinase inhibitors. Also examined was whether the presence of calcium hydroxide or the inflammatory mediators tumour necrosis factor alpha, interleukin-1, interleukin-6 and lipopolysaccharide of Escherichia coli modulated the expansion of DPC. Results Physiologic concentrations of PRS and MEM stimulated proliferation and protein synthesis by 18.4-fold ( P < 0.01) and 2.9-fold ( P < 0.01), respectively. This mitogenic expansion was paralleled by activation of AKT and the MAP kinases extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK) and p38. Inhibitor studies revealed that the mitogenic response of DPC involved PI3K/AKT, JNK and p38 signalling ( P < 0.05). Calcium hydroxide and inflammatory factors did not significantly modulate the mitogenic response of DPC to PRS and MEM. Conclusion Supernatants released from activated platelets and the corresponding platelet membranes stimulated DPC proliferation and protein synthesis involving PI3K/AKT and MAPK signalling. These findings may serve as a basis for preclinical studies that address the role of activated platelets in dental pulp repair. [ABSTRACT FROM AUTHOR]