Potential pharmacological treatments of prosthetic joint loosening

We are beginning to understand the biological events that lead to aseptic loosening of total joint prostheses. Particles of wear, mostly liberated from the articulating surfaces of implants, are phagocytosed by macrophages and induce the release of inflammatory mediators (such as interleukin-1, tumour necrosis factor, interleukin-6 and prostaglandin E₂) or cause cell death. These biological responses are thought to cause the bone loss that leads to prosthetic loosening. Drugs that suppress inflammatory mediators are successfully used to treat inflammatory diseases. Certain drugs can also reduce the corrosion of metal wear particles inside macrophages which enhances mediator release or cell death. Here we consider the prospect that these pharmacological treatments may enhance the long-term survival of implants.