Osteoclast induction from bone marrow cells is due to pro-inflammatory mediators from macrophages exposed to polyethylene particles: a possible mechanism of osteolysis in failed THA.

摘要: Polyethylene debris from joint replacements may be transported in synovial fluid and phagocytosed by macrophages. The activation migration of macrophages play important roles osteolysis implant loosening. Tissues the bone–implant interface do not always contain wear debris, which mean that require direct contact with debris. We hypothesized release polyethylene implants induces macrophage space. Then activated humoral factors, such as inflammatory cytokines, into fluid. These cytokines to bone marrow tissues around where they stimulate differentiation cells osteoclasts. Finally, osteoclasts resorb surrounding bone. To test this hypothesis, were stimulated particles. levels interleukin-6 (IL-6) tumor necrosis factor-alpha (TNF-α) determined enzyme-linked immunosorbent assay increased significantly. interaction between bone-marrow cells, a co-culture system was used an vitro model. With system, two kinds can cultured together without cell types having each other. 5 μm particles observed whether differentiated numbers assessed using tartrate-resistant acid phosphatase (TRAP) staining. TRAP-positive particle-stimulated group higher than control group. ability confirmed dentine pit formation assay. results study support our hypothesis suggest one mechanism failed arthroplasty is more distant effects pro-inflammatory cytokine on osteoclast and/or activity. © 2001 John Wiley & Sons, Inc. J Biomed Mater Res 56: 177–183,