THE EFFECTS OF COBALT-CHROMIUM UPON MACROPHAGES

The purpose of this study was to elucidate the mechanisms by which cob alt chromium particulate wear debris contribute to the aseptic looseni ng of total joint prostheses. Incubation of macrophages with cobalt ch romium led to release of tumor necrosis factor-alpha (TNF-alpha) and p rostaglandin E-2 (PGE2), but did not lead to release of interleukin-1 beta (IL-1 beta) or interleukin 6 (IL-6). Exposure oi macrophages cocu ltured with osteoblasts to cobalt chromium also led to significant rel ease of TNF-alpha and PGE, but did not lead to significant IL-6 or IL- 1 beta production. The release of PGE(2) in the coculture system was g reater than that detected when macrophages were exposed to cobalt chro mium without the osteoblast contribution. Exposure of radiolabeled cal varia to media from macrophages incubated with cobalt chromium in cocu lture with osteoblasts led to release of Ca-45. in contrast, exposure of radiolabeled calvaria to media from isolated macrophages incubated with these particles did not result in release of Ca-45. Exposure of m acrophages to cobalt chromium was toxic, as reflected by release of th e intracellular enzyme lactate dehydrogenase. Macrophages play a role in the initiation of bone resorption at the interface through the phag ocytosis of cobalt chromium particles and subsequent release of TNF-al pha and PGE(2). The presence of osteoblasts at the interface may be re quired for amplification of the inflammatory response and ultimately f or bone resorption. (C) 1998 John Wiley & Sons, Inc.