Localized Osteolysis after Joint Replacement Surgery

Abstract

Osteolysis is currently the most common cause of failure of total joint replacements [1–4]. Numerous in vitro and in vivo studies have investigated and elucidated the cellular mechanisms involved in periprosthetic osteolysis, and particulate wear debris from materials used in the prostheses is believed to be the causative agent [2,5–9]. Among the types of wear debris, ultrahigh-molecular-weight polyethylene (UHMWPE) from the acetabular liner is particularly implicated, since billions of submicrometer-sized UHMWPE particles are released into the joint cavity each year [3,6,10]. While macrophages are able to clear modest amounts of wear debris via the lymphatic system, large amounts of debris overwhelm the clearance capacity, resulting in a local accumulation of the debris [11]. Macrophages are then stimulated to release lysosomal enzymes and inflammatory mediators such as prostaglandin E2 (PGE2), interleukin (IL)-1, tumor necrosis factor (TNF) and IL-6 [8, 12–16] which stimulate osteoclasts to resorb the surrounding bone, causing loosening of the prosthesis, which in turn necessitates revision surgery to replace the components (Fig. 40.1).