Aseptic loosening of orthopaedic implants has a major financial impact on the Health Service. The process is thought to be caused by wear particles that are phagocytosed by macrophages and hence stimulate bone resorption via a cytokine response. Previous work suggests that factors inhibiting or enhancing bone resorption act through regulation of the OPG and RANK-L mechanism. The objective of this study was to identify the role of RANK-L and OPG within the cytokine response leading to orthopaedic implant loosening.

Ten samples of cellular membrane obtained during revision arthroplasty surgery were analysed with basic histological staining, immunohistology and polymerase chain reaction (PCR). In vitro studies were also carried out using explanted cancellous bone, to which PMMA particles were added and bone resorbing osteoclastic cells were identified by their Tartrate-Resistant Acid Phosphatase (TRAP) activity.

PCR identified the presence of OPG in all of the periprosthetic samples, with RANK-L shown in 40% of the specimens. Immunoreactivity was shown for CD3, CD68 and RANK-L. In vitro studies confirm that there is an initial burst of inflammatory cytokine activity that then subsequently plateaus.

A balance of RANK-L and OPG regulates bone resorption at the bone/implant interface of implants by stimulating a significant initial inflammatory response which leads to loosening.