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REGULATION OF BONE CELLS BY PARTICLE-ACTIVATED MONONUCLEAR PHAGOCYTES

D. R. Haynes, PhD, Research Officer1; S. J. Hay, BAppSci, Research Assistant2; S. D. Rogers, BSc, Research Assistant2; S. Ohta, MD, PhD, Visiting Fellow2; D. W. Howie, PhD, FRACP, Professor2; and S. E. Graves, DPhil, FRACP, Senior Lecturer2

1 Department of Pathology, University of Adelaide, Adelaide, South Australia 5005, Australia.
2 Department of Orthopaedics and Trauma, Royal Adelaide Hospital, Adelaide, South Australia 5000, Australia.

Correspondence should be sent to Dr D. R. Haynes.

Bone loss around replacement prostheses may be related to the activation of mononuclear phagocytes (MNP) by prosthetic wear particles. We investigated how osteoblast-like cells were regulated by human MNP stimulated by particles of prosthetic material.

Particles of titanium-6-aluminium-4-vanadium (TiAlV) stimulated MNP to release interleukin (IL)-1ß, tumour necrosis factor (TNF){alpha}, IL-6 and prostaglandin E2 (PGE2). All these mediators are implicated in regulating bone metabolism. Particle-activated MNP inhibited bone cell proliferation and stimulated release of IL-6 and PGE2. The number of cells expressing alkaline phosphatase, a marker associated with mature osteo-blastic cells, was reduced. Experiments with blocking antibodies showed that TNF{alpha} was responsible for the reduction in proliferation and the numbers of cells expressing alkaline phosphatase. By contrast, IL-1ß stimulated cell proliferation and differentiation. Both IL-1ß and TNF{alpha} stimulated IL-6 and PGE2release from the osteoblast-like cells.

Our results suggest that particle-activated mono-nuclear phagocytes can induce a change in the balance between bone formation and resorption by a number of mechanisms.






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Hip, Knee, Trauma, Upper limb, Foot & Ankle, Paediatrics, Oncology, Spine, Arthroplasty, General