Role of polyethylene particles in peri-prosthetic osteolysis: A review

Abstract

There is convincing evidence that particles produced by the wear of joint prostheses are causal in the peri-prosthetic loss of bone, or osteolysis, which, if it progresses, leads to the phenomenon of aseptic loosening. It is important to fully understand the biology of this bone loss because it threatens prosthesis survival, and loosened implants can result in peri-prosthetic fracture, which is disastrous for the patient and presents a difficult surgical scenario. The focus of this review is the bioactivity of polyethylene (PE) particles, since there is evidence that these are major players in the development and progression of osteolysis around prostheses which use PE as the bearing surface. The review describes the biological consequences of interaction of PE particles with macrophages, osteoclasts and cells of the osteoblast lineage, including osteocytes. It explores the possible cellular mechanisms of action of PE and seeks to use the findings to date to propose potential non-surgical treatments for osteolysis. In particular, a non-surgical approach is likely to be applicable to implants containing newer, highly cross-linked PEs (HXLPEs), for which osteolysis seems to occur with much reduced PE wear compared with conventional PEs. The caveat here is that we know little as yet about the bioactivity of HXLPE particles and addressing this constitutes our next challenge.

Keywords: Aseptic loosening; Osteolysis; Peri-prosthetic; Polyethylene; Wear particle.

Figure 1

Multi-cellular effects of polyethylene wear particles, following their release from the bearing surface, resulting in osteolysis. Polyethylene (PE) engulfment by monocytes and macrophages, and possibly other cells including fibroblasts, as described in the text, causes their activation and release of pro-inflammatory cytokines, prostaglandins and matrix degrading enzymes. These and other factors promote differentiation of macrophages into bone resorbing osteoclasts. PE effects on osteoblastic lineage cells (osteoblasts, lining cells and potentially osteocytes) following contact with and/or engulfment of particles include promotion of a catabolic phenotype, up-regulation of potent chemotactic agents for osteoclast precursors and osteoclastogenic mediators. The responses in each cell type are indicated by boxed arrows. RANKL:receptor activator of nuclear factor-κB ligand; OPG: osteoprotegerin; M-CSF: macrophage colony stimulating factor; MMPs: Matrix metalloproteinases.