The Basic Science of Periprosthetic Osteolysis*†

Abstract

Total joint replacement has been very successful and cost-effective in restoring function and mobility to millions of patients worldwide since its advent more than thirty years ago. With improvements in prophylaxis against infection, the fatigue strength of the components, and skeletal fixation, wear and its sequelae have become the primary limitation to joint replacement longevity1. Initially termed "cement disease,"2 osteolysis is believed to be a biological response not only to polymethylmethacrylate but also to a variety of particles that may originate at several locations around a joint replacement. These include the articulating surfaces, modular component interfaces, fixation surfaces, and devices used for adjuvant fixation3. Recent research has been directed at understanding the biological cascade of events that is initiated by particulate debris and results in periprosthetic bone loss. Clinically, periprosthetic osteolysis can lead to aseptic loosening of components, massive bone loss that renders revision surgery substantially more complex, and periprosthetic pathological fracture (Fig. 1). We present the current understanding of osteolysis with regard to the sources of wear, the morphology of wear particles, and the biological response to wear particles according to findings reported in cell-culture, tissue-explant, and animal studies. The generation of particulate debris after total joint arthroplasty can occur as a result of two processes: wear and corrosion. Wear has been defined as the removal of material from the prosthesis in the form of debris4. The fundamental mechanisms of wear include adhesion, abrasion, and fatigue5. The mechanical conditions under which the prosthesis is functioning when wear occurs have been classified as modes of wear4. Mode 1 refers to the generation of wear debris that occurs with motion between the two bearing surfaces as intended by the designers. Mode 2 refers to a primary bearing surface rubbing against a secondary surface in a manner not intended by the designers (for example, a femoral head articulating with an acetabular shell following wear-through of the polyethylene). Mode 3 refers to two primary bearing surfaces with interposed third-body particles (such as bone, cement, metal, and so on). Mode 4 refers to two nonbearing surfaces rubbing together (such as back-sided wear of an acetabular liner, fretting of the Morse taper, stem-cement fretting, and so on)3. While several modes of wear often occur simultaneously, mode 1 accounts for the majority of wear in well functioning hip or knee replacements5. Corrosion is an electrochemical process in which metal ions are released from an implant surface. Corrosion products can be generated from any metal surface, but they most commonly originate from metal-on-metal modular interfaces, such as the head-neck junction in both mixed-metal or similar-metal femoral stems in total hip replacements6(Figs. 2-A and 2-B). The particles are metal-salt precipitates of these ions that form in the surrounding aqueous environment. Fine particulate debris of chromium phosphate corrosion products is often observed in the periprosthetic tissues of specimens retrieved at revision6. Chromium phosphate corrosion products from the modular junction have been found in sites remote from the hip joint as well6. The most common particle in the periprosthetic tissues is polyethylene, which is predominantly generated by means of mode-1 wear. The remaining particles in the periprosthetic tissues include polymethylmethacrylate, cobalt-alloy, and titanium-alloy particles. In much smaller volumes, silicates and stainless-steel particles are also seen; these most likely represent contaminants from surgical tools, supplemental fixation wires, or remnants from surface processing. Wear debris can gain access to all periprosthetic regions that are accessible to joint fluid7,8.