ABSTRACT
Orthopedic implants (composed of metallic, polymeric, or ceramic biomaterials) play a major role in the clinical implant industry with the U.S. orthopedic implant market projected to rise to US$23 billion by the year 2012 (Freedonia Group 2008). Despite the great advances in orthopedic biomaterials research during the past 75 years or so, the holy grail of a long-lasting orthopedic joint implant in a young active individual has yet to be achieved. One of the leading issues that adversely aŽects the longevity of current total joint arthroplasty (TJA) is aseptic loosening of an implant due to periprosthetic osteolysis (Hallab and Jacobs 2009; Wang 2011). Periprosthetic osteolysis arises from a local inšammatory reaction of the host immune system toward the wear particles and corrosion products from the implants. …e host response to the wear particles, ranging in size from nanometers to millimeters, involves a local immune reaction that is predominantly mediated by macrophages. Figure 7.1 is a schematic showing the macrophage-mediated wear particle-induced inšammation around the implant leading to local tissue damage. Briešy, biomaterial wear particles induce monocyte-macrophage activation and secretion of proinšammatory cytokines such as interleukin (IL)-1β, IL-1α, tumor necrosis factor α (TNF-α), IL-6, IL-18, prostaglandin 2 (PGE2), and IL-8. Many of these cytokines are known to stimulate differentiation of osteoclast precursors to mature osteoclasts, which leads to increased bone resorption and decreased bone deposition, which results in bone loss at the tissue-implant interface and subsequent implant loosening (Hallab and Jacobs 2009; Beck et al. 2012).
