title: Macrophage activation and migration in interface tissue around loosening total hip arthroplasty components.
abstract: The bone-cement interface tissue of failed total hip arthroplasty (THA) has inflammatory characteristics, such as the presence of prostaglandin E2 and interleukin 1 (IL-1). We considered that the bone-cement interface tissue could be the site of granulomatous inflammation caused by a foreign-body reaction. It has been demonstrated that inflammatory cytokines and chemokines have an important role in granulomatous inflammation. Bone-cement interface tissue was obtained at revision from nine patients with failed cemented THA, and the role of macrophages was 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 inflammatory protein (MIP)-1 alpha, MIP-1 beta, IL-8, and monocyte chemoattractant protein. Polyethylene debris surrounded by macrophages and phagocytosis of debris by macrophages was frequently observed in the interface tissue. Macrophage activation and the production of inflammatory cytokines such as IL-1 and TNF alpha might induce the development of interface tissue. Expression of chemokine mRNAs was also commonly seen, suggesting that this led to recruitment of macrophages into the bone-cement interface tissue. Debris released from implants appears to cause activation of macrophages and the production of inflammatory cytokines and chemokines that induce cellular recruitment into interface tissue. This mechanism might form a vicious cycle that aggravates THA loosening.
authors.affiliation: Department of Orthopedic Surgery, Nagoya University School of Medicine, Showa-ku, Japan.
authors.forename: N
authors.initials: N
authors.lastname: Ishiguro
authors.forename: T
authors.initials: T
authors.lastname: Kojima
authors.forename: T
authors.initials: T
authors.lastname: Ito
authors.forename: S
authors.initials: S
authors.lastname: Saga
authors.forename: H
authors.initials: H
authors.lastname: Anma
authors.forename: K
authors.initials: K
authors.lastname: Kurokouchi
authors.forename: Y
authors.initials: Y
authors.lastname: Iwahori
authors.forename: T
authors.initials: T
authors.lastname: Iwase
authors.forename: H
authors.initials: H
authors.lastname: Iwata
mesh_terms: D000368:Aged; D001843:Bone Cements; D002465:Cell Movement; D018932:Chemokine CCL2 / Q000096:biosynthesis; D054407:Chemokine CCL4; D016207:Cytokines / Q000096:biosynthesis*; D005260:Female; D006622:Hip Prosthesis; D006801:Humans; D007375:Interleukin-1 / Q000096:biosynthesis; D016209:Interleukin-8 / Q000096:biosynthesis; D008262:Macrophage Activation; D019402:Macrophage Inflammatory Proteins / Q000096:biosynthesis; D008264:Macrophages / Q000502:physiology* / Q000648:ultrastructure; D008297:Male; D008768:Methylmethacrylates; D008854:Microscopy, Electron; D008875:Middle Aged; D010587:Phagocytosis; D016133:Polymerase Chain Reaction; D011475:Prosthesis Failure; D012333:RNA, Messenger / Q000096:biosynthesis; D014158:Transcription, Genetic; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis
chemical_list: D001843:Bone Cements; D018932:Chemokine CCL2; D054407:Chemokine CCL4; D016207:Cytokines; D007375:Interleukin-1; D016209:Interleukin-8; D019402:Macrophage Inflammatory Proteins; D008768:Methylmethacrylates; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha