Lange, TobiasTobiasLangeSchilling, Arndt F.Arndt F.SchillingPeters, FabianFabianPetersHaag, FriedrichFriedrichHaagMorlock, MichaelMichaelMorlockRueger, Johannes M.Johannes M.RuegerAmling, MichaelMichaelAmling2024-03-142024-03-142009-10-01Biomaterials 30 (29): 5312–5318 (2009)https://hdl.handle.net/11420/46532Particulate wear debris can activate defence cells and osteoclasts at the bone-implant interface possibly leading to bone resorption and implant failure. Cellular responses and inflammatory effects have been reported for particulate hydroxyapatite (HA). However, the immunological effects of particulate beta-tricalciumphosphate (beta-TCP) have not been studied and the question of whether beta-TCP is more biocompatible in this regard as is HA remains to be determined. Therefore the present work investigates effects of endotoxin-free HA and beta-TCP particles of the same size (d50 = 1 μm) and dose (SAR 10:1) on human peripheral blood mononuclear cells in vitro. The production of proinflammatory cytokines (TNF-alpha, IL-1beta, IL-8) and cytokines connected to osteoclast and dendritic cell differentiation (OPG, RANKL, M-CSF, GM-CSF) was determined by ELISA. After 6 and 18 h of incubation HA and beta-TCP caused a quite similar induction of TNF-alpha, IL-1beta and IL-8. Effects of particles on the production of M-CSF and OPG were not detectable. However, in sharp contrast to HA, beta-TCP caused less induction of GM-CSF and not any of RANKL, both known for promoting dendritic cells and osteoclastogenesis respectively. Therefore these in vitro data suggest that wear debris of beta-TCP poses lesser risk of the detrimental effects of osteoclast induction known from HA.en0142-961220092953125318ElsevierBeta-TCPDendritic cellsHuman PBMCHydroxyapatiteInflammationOsteoclastogenesisMedicine, HealthJournal Article10.1016/j.biomaterials.2009.06.023Journal Article