Neovascularisation and the induction of cell adhesion molecules in response to degradation products from orthopaedic implants.

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Abstract
OBJECTIVES--To characterise the cellular interactions and the mechanisms involved in the recruitment of inflammatory macrophages and T cells to the bone implant interface in 30 patients with aseptically loosened orthopaedic prostheses. METHODS--Cell adhesion molecules E-selectin, VCAM-1, ICAM-1 and the receptors LFA-1 and CR3 were immunolocalised on cryostat sections of the bone-implant interface obtained during revision arthroplasty. The percentage of expression on vascular endothelium was determined on serial sections. RESULTS--E-selectin was upregulated on different vessels in 21 patients. Its expression correlated strongly with the presence of metal wear debris. VCAM-1 was detected on vessels in six patients only, and was coexpressed with E-selectin in three patients with metal debris. VCAM-1 was more frequently observed in the lining cells on the implant side. ICAM-1 was upregulated on vessels on the bone side only in 13 patients, and was more strongly expressed on aggregates of macrophages and multinucleated giant cells on the implant side. These macrophage aggregates coexpressed both ICAM-1 and CR3. CONCLUSION--Our findings implicate the contribution of three different pathways in the recruitment of inflammatory cells to the joint in response to orthopaedic implant wear particles. The association of E-selectin expression and metal debris may suggest hypersensitivity reactions. Finally, the simultaneous expression of ICAM-1 and CR3 on the same macrophages on the implant side may predict an additional function of these molecules in homotypic adhesion/cell aggregation that precede differentiation of phagocytes to multinucleated giant cells.

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