title: In vitro and in vivo activation of polymorphonuclear leukocytes in response to particulate debris.
abstract: The host inflammatory response to particulate wear debris has been implicated as a principal cause of osteolysis and aseptic loosening following total joint arthroplasty. While it has long been assumed that this inflammatory response is mediated solely by a chronic process, there has been evidence to suggest that an acute response to particulate debris may be important in initiating the chronic response. We studied the in vitro and in vivo acute inflammatory responses mediated by polymorphonuclear leukocytes (PMNs) to both retrieved particulate from a catastrophically failed uncemented metal-backed acetabular component and to commercially pure particulate (polyethylene, cobalt-chrome, and titanium). Isolated, nonactivated human PMNs in vitro exhibited both a dose- and time-dependent degranulation response to opsonized particulate debris, as evidenced by release of both specific (increased lysozyme activity) and azurophilic (increased beta-glucuronidase activity) granule contents. In the rat subcutaneous pouch model in vivo, PMNs were recruited within 3-6 h after exposure to particulate debris and were noted to phagocytize particulate and subsequently degranulate, as evidenced by increased beta-glucuronidase and PMN-specific myeloperoxidase (azurophilic granule enzymes) activities. This response peaked within the first 6 h and gradually declined by 24 h. The results of this study demonstrate the presence of an acute inflammatory response mediated by PMNs both in vitro and in vivo to particulate debris, which may be important in the sequence of events that lead to the macrophage-dominated chronic inflammatory process culminating in osteolysis and aseptic loosening of total joint arthroplasties.
authors.affiliation: Musculoskeletal Research Center, Department of Orthopaedic Surgery, Hospital for Joint Diseases Orthopaedic Institute, 301 East 17(th) St., New York, NY 10003, USA.
authors.forename: F S
authors.initials: FS
authors.lastname: Chen
authors.forename: D M
authors.initials: DM
authors.lastname: Scher
authors.forename: R M
authors.initials: RM
authors.lastname: Clancy
authors.forename: A
authors.initials: A
authors.lastname: Vera-Yu
authors.forename: P E
authors.initials: PE
authors.lastname: Di Cesare
mesh_terms: D000818:Animals; D019644:Arthroplasty, Replacement, Hip; D015550:Cell Degranulation / Q000502:physiology; D002499:Centrifugation, Density Gradient; D002858:Chromium Alloys; D005966:Glucuronidase / Q000378:metabolism; D006801:Humans; D007249:Inflammation / Q000201:enzymology / Q000473:pathology; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D008855:Microscopy, Electron, Scanning; D009113:Muramidase / Q000378:metabolism; D018375:Neutrophil Activation / Q000187:drug effects / Q000502:physiology*; D009504:Neutrophils / Q000201:enzymology / Q000473:pathology; D009895:Opsonin Proteins; D020959:Polyethylene; D011475:Prosthesis Failure; D051381:Rats; D014025:Titanium
chemical_list: D002858:Chromium Alloys; D009895:Opsonin Proteins; D020959:Polyethylene; D014025:Titanium; D007770:L-Lactate Dehydrogenase; D009113:Muramidase; D005966:Glucuronidase