MACROPHAGE ACTIVATION AND MIGRATION IN INTERFACE TISSUE AROUND LOOSENING TOTAL HIP-ARTHROPLASTY COMPONENTS

The bone-cement interface tissue of failed total hip arthroplasty (THA ) has inflammatory characteristics, such as the presence of prostaglan din E-2 and interleukin 1 (IL-1). We considered that the bone-cement i nterface tissue could be the site of granulomatous inflammation caused by a foreign-body reaction. It has been demonstrated that inflammator y cytokines and chemokines have an important role in granulomatous inf lammation. Bone-cement interface tissue was obtained at revision from nine patients with failed cemented THA, and the role of macrophages wa s assessed by immunohistochemistry, electron microscopy, and molecular biological techniques. We used the reverse-transcriptional polymerase chain reaction to examine the expression of mRNA for IL-1 alpha, IL-1 beta, tumor necrosis factor alpha (TNF alpha), macrophage inflammator y protein (MIP)-1 alpha, MIP-1 beta, IL-8, and monocyte chemoattractan t protein. Polyethylene debris surrounded by macrophages and phagocyto sis of debris by macrophages was frequently observed in the interface tis sue. Macrophage activation and the production of inflammatory cyto kines such as IL-1 and TNF alpha might induce the development of inter face tissue. Expression of chemokine mRNAs was also commonly seen, sug gesting that this led to recruitment of macrophages into the bone-ceme nt interface tissue. Debris released from implants appears to cause ac tivation of macrophages and the production of inflammatory cytokines a nd chemokines that induce cellular recruitment into interface tissue. This mechanism might form a vicious cycle that aggravates THA loosenin g. (C) 1997 John Wiley & Sons, Inc.