Cobalt-chromium particles inducing preosteoblasts may aggravate periprosthetic inflammation
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BACKGROUND: Arthroplasty has been the most effective treatment for the end-stage osteoarthritis. However, aseptic loosening is the main long-term complication of arthroplasty. How to ameliorate aseptic loosening is an issue of concern. OBJECTIVE: To investigate the biological behavior of preosteoblasts induced with cobalt-chromium particles during aseptic loosening process. METHODS: (1) In vitro experiment: preosteoblasts were cultured in an osteoblast-induction medium and induced with different doses (0.3 or 1.25 g/L) of cobalt-chromium particles. (2) In vivo experiment: titanium screws were implanted to proximal tibia of server combined with immune-deficiency mice to simulate knee joint arthroplasty. Cobalt-chromium particles inducing MC3T3-E1 (5X105) were intra-articularly injected into the implanted knee at 1 week after surgery. Stable group (n=6): screw implanted mice without local particle insertion and cells transfusion; loosening group (n=6): mice were given an intra-articular injection of cobalt-chromium particles (4X104) before screw implantation; cobalt-chromium group: mice were given an intra-articular injection of preosteoblasts induced by cobalt-chromium particles and cobalt-chromium particles (4x1 o4) before screw implantation. RESULTS AND CONCLUSION: (1) In vitro experiment: with the increasing of cobalt-chromium particles, alkaline phosphatase and osteogenic gene expression was decreasing. (2) In vivo experiment: intra-articular injection of cobalt-chromium particles inducing MC3T3-E1 cells resulted in thicker peri-implant pseudomembrane, reduced the shear strength of bone-implant, decreased bone mineral density and bone volume, and increased the number of positive cells for tartrate-resistant acid phosphatase. (3) These results indicate that cobalt-chromium particles inhibit the growth, maturation and functions of preosteoblastic cells. Cobalt-chromium particles inducing preosteoblasts may aggravate periprosthetic inflammation and promote osteoclastogenesis.