C Wagner1, G M Hänsch, A Wentzensen, V Heppert. 1. Klinik für Unfall- und Wiederherstellungschirurgie, Berufsgenossenschaftliche Unfallklinik, Ludwig-Guttmann-Strasse 13, 67071 Ludwigshafen, Deutschland. christof.wagner@urz.uni-heidelberg.de
Abstract
BACKGROUND: Formation of bacterial biofilms on implants is a severe complication following orthopaedic surgery. In the present study we addressed the role of the immune response, particularly with regard to the pathogenesis of the disease. METHODS: In a prospective study comprising 74 patients with implant-associated post-traumatic osteomyelitis, peripheral blood cells as well as cells recovered from the infected site during surgery were characterised phenotypically and functionally. RESULTS: We found massive infiltration of polymorphonuclear neutrophils (PMN), which were highly activated, particularly regarding their bactericidal potential, such as increased production of superoxides and upregulation of activation-associated surface receptors. CONCLUSION: PMN are activated in response to the implant-associated osteomyelitis; they also infiltrate the infected tissue, but cannot control the infection. By release of their cytotoxic entities they could contribute to tissue destruction and eventually to osteolysis.
BACKGROUND: Formation of bacterial biofilms on implants is a severe complication following orthopaedic surgery. In the present study we addressed the role of the immune response, particularly with regard to the pathogenesis of the disease. METHODS: In a prospective study comprising 74 patients with implant-associated post-traumatic osteomyelitis, peripheral blood cells as well as cells recovered from the infected site during surgery were characterised phenotypically and functionally. RESULTS: We found massive infiltration of polymorphonuclear neutrophils (PMN), which were highly activated, particularly regarding their bactericidal potential, such as increased production of superoxides and upregulation of activation-associated surface receptors. CONCLUSION: PMN are activated in response to the implant-associated osteomyelitis; they also infiltrate the infected tissue, but cannot control the infection. By release of their cytotoxic entities they could contribute to tissue destruction and eventually to osteolysis.
Authors: Carl L Nelson; Alex C McLaren; Sandra G McLaren; Jeffrey W Johnson; Mark S Smeltzer Journal: Clin Orthop Relat Res Date: 2005-08 Impact factor: 4.176
Authors: A Moghaddam-Alvandi; E Dremel; F Güven; V Heppert; C Wagner; S Studier-Fischer; P A Grützner; B Biglari Journal: Unfallchirurg Date: 2010-04 Impact factor: 1.000