title: Production of cytokines around loosened cemented acetabular components. Analysis with immunohistochemical techniques and in situ hybridization.
abstract: The chronic inflammatory response to wear particles from orthopaedic joint implants is believed to cause osteolysis and to contribute to prosthetic loosening. Previous in vitro experiments have demonstrated that particulate debris from joint implants causes cells in culture to release products that have been implicated in this pathological bone resorption. The purpose of the current study was to investigate the in vivo features of this complex process in patients who had had a total hip replacement. Membraneous tissue was obtained from the cement-bone interface of ten polyethylene acetabular components that had been revised for aseptic loosening in ten patients. The immunoperoxidase technique, which involves the use of specific antibodies for each cell type, showed that macrophages were the predominant cellular constituents but also that fibroblasts, many of which were not identified on plain histological study, were present and were actively producing collagen. T lymphocytes were present variably, but they generally composed less than 10 percent of the cells. Particulate debris (polyethylene, methylmethacrylate, and metal) was present in all membrane specimens but was intracellular only in macrophages and multinucleated giant cells. 35S-labeled nucleic-acid probes, complementary to human interleukin-1-beta and to platelet-derived growth-factor-2 messenger RNA (mRNA), were hybridized with serial tissue sections. Hybridization demonstrated interleukin-1-beta mRNA predominantly in macrophages, and not in fibroblasts or in T lymphocytes to any major extent. In contrast, immunolocalization demonstrated interleukin-1-beta protein on both macrophages and fibroblasts, suggesting that macrophages release interleukin-1-beta, which then binds to both fibroblasts and macrophages. Platelet-derived growth-factor transcripts were found in both macrophages and fibroblasts.
authors.affiliation: Orthopaedic Biomechanics Laboratory, Massachusetts General Hospital, Boston 02114.
authors.forename: W A
authors.initials: WA
authors.lastname: Jiranek
authors.forename: M
authors.initials: M
authors.lastname: Machado
authors.forename: M
authors.initials: M
authors.lastname: Jasty
authors.forename: D
authors.initials: D
authors.lastname: Jevsevar
authors.forename: H J
authors.initials: HJ
authors.lastname: Wolfe
authors.forename: S R
authors.initials: SR
authors.lastname: Goldring
authors.forename: M J
authors.initials: MJ
authors.lastname: Goldberg
authors.forename: W H
authors.initials: WH
authors.lastname: Harris
mesh_terms: D000368:Aged; D002484:Cementation; D005260:Female; D005347:Fibroblasts / Q000378:metabolism; D006622:Hip Prosthesis; D006801:Humans; D007150:Immunohistochemistry; D017403:In Situ Hybridization; D007375:Interleukin-1 / Q000096:biosynthesis* / Q000235:genetics; D008214:Lymphocytes / Q000378:metabolism; D008264:Macrophages / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D010982:Platelet-Derived Growth Factor / Q000096:biosynthesis* / Q000235:genetics; D011475:Prosthesis Failure; D012333:RNA, Messenger / Q000378:metabolism
chemical_list: D007375:Interleukin-1; D010982:Platelet-Derived Growth Factor; D012333:RNA, Messenger