## Abstract Aseptic implant loosening of total joint replacements often results from particle‐mediated bone loss, which may be a combined effect of osteolysis and suppressed bone formation. Bone regeneration in the prosthetic bed depends on the activity of osteoblasts and their differentiation from
Polymethylmethacrylate particles inhibit osteoblastic differentiation of MC3T3-E1 osteoprogenitor cells
✍ Scribed by Richard Chiu; Ting Ma; R. Lane Smith; Stuart B. Goodman
- Publisher
- Elsevier Science
- Year
- 2008
- Tongue
- English
- Weight
- 250 KB
- Volume
- 26
- Category
- Article
- ISSN
- 0736-0266
No coin nor oath required. For personal study only.
✦ Synopsis
Abstract
Orthopedic wear debris has been implicated as a significant inhibitory factor of osteoblast differentiation. Polymethylmethacrylate (PMMA) particles have been previously shown to inhibit the differentiation of osteoprogenitors in heterogeneous murine marrow stromal cell cultures, but the effect of PMMA particles on pure osteoprogenitor populations remains unknown. In this study, we challenged murine MC3T3‐E1 osteoprogenitor cells with PMMA particles during their initial differentiation in osteogenic medium. MC3T3‐E1 cultures challenged with PMMA particles showed a gradual dose‐dependent decrease in mineralization, cell number, and alkaline phosphatase activity at low particle doses (0.038–0.150% v/v) and complete reduction of these outcome parameters at high particle doses (≥0.300% v/v). MC3T3‐E1 cultures challenged with a high particle dose (0.300% v/v) showed no rise in these outcome parameters over time, whereas cultures challenged with a low particle dose (0.075% v/v) showed a normal or reduced rate of increase compared to controls. Osteocalcin production was not significantly affected by particles at all doses tested. MC3T3‐E1 cells grown in conditioned medium from particle‐treated MC3T3‐E1 cultures showed a significant reduction in mineralization only. These results indicate that direct exposure of MC3T3‐E1 osteoprogenitors to PMMA particles results in suppression of osteogenic proliferation and differentiation. © 2008 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 26:932–936, 2008
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