Modulation of the phenotypic and functional properties of phagocytic macrophages by wear particles from orthopaedic implants

An attempt was made to assess the local chronic inflammatory response in patients with failed orthopaedic implant that is clinically associated with osteolysis, bone and bone marrow necrosis. The main objective was to analyse the heterogeneity of the macrophage functional subsets in the bone–implant interface membrane and to evaluate their possible role in the development of an erosive inflammatory lesion within the bone. Immunohistology was performed on 21 specimens of the bone–implant interface obtained from 17 patients during revision arthroplasty, and synovial membranes from rheumatoid (RA, n=4), and osteoarthritis (OA, n=4) patients. Three well-characterized monoclonal antibodies (MAb) recognizing antigenic determinants on specific functional subsets of macrophages (Mφ) were used. RFD1 (interdigitating reticulum cells/antigen presenting cells, (APC), RFD7 (mature phagocytic macrophages), and RFD9 epithelioid cells and foreign body giant cells (FBGC). RFD1 was expressed on a variable number of perivascular and synovial lining Mφ in both RA and OA synovia, at a frequency of 25%–40%. In cases with total joint replacements, the interface showed a marked increase in the expression of RFD1 (20%–90%). A considerably greater percentage of RFD1 positive Mφ and FBGC was noted in the interfaces from cases with a high level of detectable metal particulate wear debris (mean 80%, range 60%–90%) than in cases with polyethylene wear debris (mean 30%, range 0%–50%), p 0.0001. RFD7 labelled most tissue Mφ in each group. Immunoreactivity for RFD9 was restricted to FBGC in all cases analysed. The finding of elevated expression of RFD1 on metal-containing Mφ and FBGC in the bone-implant interface suggests an increase in antigen-presenting phenotype and indicates that metal particles have more impact in the induction of immune-mediated responses. Such responses are characterized by sustained cellular hyperreactivity and phenotypic changes in Mφ subsets.

[1]  T. Bauer,et al.  Regional dissemination of wear debris from a total knee prosthesis. A case report. , 1993, The Journal of bone and joint surgery. American volume.

[2]  G. Janossy,et al.  Discrimination of Human Macrophages and Dendritic Cells by Means of Monoclonal Antibodies , 1986, Scandinavian journal of immunology.

[3]  Kathleen Gillespie,et al.  Compounds that induce autoimmunity in the Brown Norway rat sensitize mast cells for mediator release and interleukin‐4 expression , 1995, European journal of immunology.

[4]  C. Case,et al.  Widespread dissemination of metal debris from implants. , 1994, The Journal of bone and joint surgery. British volume.

[5]  J. Saurat,et al.  Nickel and skin irritants up-regulate tumor necrosis factor-alpha mRNA in keratinocytes by different but potentially synergistic mechanisms. , 1995, International immunology.

[6]  G. Janossy,et al.  Separate ontogeny of two macrophage-like accessory cell populations in the human fetus. , 1986, Journal of immunology.

[7]  J. Galante,et al.  Release and excretion of metal in patients who have a total hip-replacement component made of titanium-base alloy. , 1991, The Journal of bone and joint surgery. American volume.

[8]  S. Santavirta,et al.  Aggressive granulomatous lesions associated with hip arthroplasty. Immunopathological studies. , 1990, The Journal of bone and joint surgery. American volume.

[9]  H. Yoshikawa,et al.  Inguinal lymphadenopathy due to metal release from a prosthesis. A case report. , 1993, The Journal of bone and joint surgery. British volume.

[10]  S. Goerdt,et al.  Nickel chloride and cobalt chloride, two common contact sensitizers, directly induce expression of intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and endothelial leukocyte adhesion molecule (ELAM-1) by endothelial cells. , 1993, The Journal of investigative dermatology.

[11]  D. Campbell,et al.  Monoclonal antibodies distinguish macrophages and epithelioid cells in sarcoidosis and leprosy. , 1987, Clinical and experimental immunology.

[12]  S. W. Clarke,et al.  Cell-mediated immunity in pigeon breeders' lung: the effect of removal from antigen exposure. , 1989, The European respiratory journal.

[13]  O. Söder,et al.  Mercury induces in vivo and in vitro secretion of interleukin-1 in mice. , 1994, Immunopharmacology.

[14]  P. Revell,et al.  Assessment of the role of GM-CSF in the cellular transformation and the development of erosive lesions around orthopaedic implants. , 1996, American journal of clinical pathology.

[15]  D. Macdonald,et al.  The simultaneous presence of Langerhans' cell and interdigitating cell antigenic markers on inflammatory dendritic cells. , 1986, Clinical and experimental immunology.

[16]  W H Harris,et al.  The synovial-like membrane at the bone-cement interface in loose total hip replacements and its proposed role in bone lysis. , 1983, The Journal of bone and joint surgery. American volume.

[17]  A. Saoudi,et al.  Mercuric chloride, a chemical responsible for T helper cell (Th)2-mediated autoimmunity in brown Norway rats, directly triggers T cells to produce interleukin-4. , 1995, The Journal of clinical investigation.

[18]  P. Revell,et al.  Neovascularisation and the induction of cell adhesion molecules in response to degradation products from orthopaedic implants. , 1995, Annals of the rheumatic diseases.

[19]  P. Revell,et al.  Interleukin-1 production by activated macrophages surrounding loosened orthopaedic implants: a potential role in osteolysis. , 1994, British journal of rheumatology.

[20]  P. D. Wilson,et al.  Metallic wear in failed titanium-alloy total hip replacements. A histological and quantitative analysis. , 1988, The Journal of bone and joint surgery. American volume.

[21]  A. Yau,et al.  The effect of age on the change in deformity after radical resection and anterior arthrodesis for tuberculosis of the spine. , 1994, The Journal of bone and joint surgery. American volume.

[22]  M. Spiteri,et al.  Phenotypic and functional changes in alveolar macrophages contribute to the pathogenesis of pulmonary sarcoidosis. , 1988, Clinical and experimental immunology.

[23]  E. Wiley,et al.  Sinus Histiocytosis of Pelvic Lymph Nodes after Hip Replacement: A Histiocytic Proliferation Induced by Cobalt‐Chromium and Titanium , 1994, The American journal of surgical pathology.

[24]  N. Hogg,et al.  Monoclonal antibodies specific for human monocytes, granulocytes and endothelium. , 1984, Immunology.

[25]  L. Poulter,et al.  Changes in phenotypically distinct mucosal macrophage populations may be a prerequisite for the development of inflammatory bowel disease , 1991, Clinical and experimental immunology.

[26]  C. Frampton,et al.  The incidence of cancer following total hip replacement. , 1988, The Journal of bone and joint surgery. British volume.

[27]  G. Möller,et al.  In vitro effects of HgCl2 on murine lymphocytes. I. Preferable activation of CD4+ T cells in a responder strain. , 1995, Journal of immunology.

[28]  M. Waters,et al.  The involvement of dendritic cells in the cutaneous lesions associated with tuberculoid and lepromatous leprosy. , 1985, Clinical and experimental immunology.

[29]  U. Pazzaglia,et al.  Fractured femoral shaft through an osteolytic lesion resulting from the reaction to a prosthesis. A case report. , 1984, The Journal of bone and joint surgery. British volume.

[30]  F. Sinigaglia.  The molecular basis of metal recognition by T cells. , 1994, The Journal of investigative dermatology.

[31]  C. Kirkpatrick,et al.  The role of metal corrosion in inflammatory processes: induction of adhesion molecules by heavy metal ions , 1994 .

[32]  P. Revell,et al.  The expression of osteoclast markers on foreign body giant cells. , 1994, Bone and mineral.

[33]  F. Breedveld,et al.  Dendritic cells and high endothelial venules in the rheumatoid synovial membrane. , 1990, The Journal of rheumatology.