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Type: Journal article
Title: Prosthetic particles modify the expression of bone-related protiens by human osteoblastic cells in vitro
Author: Zreiqat, H.
Crotti, T.
Howlett, C.
Capone, M.
Markovic, B.
Haynes, D.
Citation: Biomaterials, 2003; 24(2):337-346
Publisher: Elsevier Sci Ltd
Issue Date: 2003
ISSN: 0142-9612
Statement of
H. Zreiqat, T. N. Crotti, C. R. Howlett, M. Capone, B. Markovic and D. R. Haynes
Abstract: Loss of bone near joint prostheses is thought to be caused by activation of recruited osteoclasts by osteolytic mediators induced by wear particles. It is proposed that particles inhibit osteogenesis during bone remodelling causing a reduction in the levels of peri-implant bone. This study explores whether prosthetic particles modulate bone formation by affecting osteoblastic bone-related mRNAs (alkaline phosphatase, pro-collagen Iα1, osteopontin, osteonectin, osteocalcin, bone sialoprotein and thrombospondin) or their translated proteins using titanium alloy, commercially pure titanium, and cobalt–chrome particles. The direct effect of the particles revealed no change to the expression of the bone-related mRNAs in human bone-derived cells (HBDC) at the time points investigated; although non-collagenous translated proteins expressed by these HBDC were significantly effected (p<0.05). Different patterns of expression for bone-related proteins were induced by the different particles both directly and indirectly. Inflammatory mediators (interleukin-1β, tumor necrosis factor α, interleukin-6, and prostaglandin E2) had similar effects on HBDC to the media obtained from monocytes incubated with particles. This study shows that prosthetic wear particles can significantly modify the expression of bone-related proteins by osteogenic cells in vitro. These alterations in osteogenic activity at the interface of the implant and bone may be an important factor in the failure of many orthopaedic implants.
Keywords: Wear particles; Osteoblasts; Titanium; Cobalt–chrome; Monocytes; Cytokines
Rights: Copyright © 2002 Elsevier Science Ltd.
RMID: 0020031537
DOI: 10.1016/S0142-9612(02)00324-1
Appears in Collections:Pathology publications

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