Osteolysis is the main limiting cause for the survival of an orthopedic prosthesis and is accompanied by an enhancement in osteoclastogenesis and inflammation, due by wear debris formation. Unfortunately therapeutic treatments, besides revision surgery, are not available.The aim of the present study was to evaluate the effects of Pulsed ElectroMagnetic Fields (PEMFs) and platelet rich plasma (PRP), alone or in combination, in an in vitro model of osteolysis. Rats peripheral blood mononuclear cells were cultured on Ultra High Molecular Weight Polyethylene particles and divided into 4 groups of treatments: 1) PEMF stimulation (12 hours/day, 2.5 mT, 75Hz, 1.3 ms pulse duration); 2) 10% PRP; 3) combination of PEMFs and PRP; 4) no treatment. Treatments were performed for 3 days and cell viability, osteoclast number, expression of genes related to osteoclastogenesis and inflammation and production of pro-inflammatory cytokines were assessed up to 14 days.PEMF stimulation exerted best results because it increased cell viability at early time points and counteracted osteoclastogenesis at 14 days. On the contrary, PRP increased osteoclastogenesis and reduced cell viability in comparison to PEMFs alone. The combination of PEMFs and PRP increased cell viability over time and reduced osteoclastogenesis in comparison to PRP alone. However, these positive results did not exceed the level achieved by PEMF alone. At longer time points PEMF could not counteract osteoclastogenesis increased by PRP.Regarding inflammation, all treatments maintained the production of pro-inflammatory cytokines at low level, although PRP increased the level of interleukin 1 beta. This article is protected by copyright. All rights reserved.
- platelet rich plasma
- pulsed electromagnetic fields
- wear mediatedperiprosthetic osteolysis
Tschon, M., Veronesi, F., Contartese, D., Sartori, M., Martini, L., Vincenzi, F., Ravani, A., Varani, K., & Fini, M. (2018). Effects of pulsed electromagnetic fields and platelet rich plasma in preventing osteoclastogenesis in an in vitro model of osteolysis. Journal of Cellular Physiology, 233(3), 2645-2656. https://doi.org/10.1002/jcp.26143