Innate immune reactions in septic and aseptic osteolysis around hip implants.
According to the long-standing definition, septic and aseptic total joint replacement loosening are two distinct conditions with little in common. Septic joint replacement loosening is driven by bacterial infection whereas aseptic loosening is caused by biomaterial wear debris released from the bearing surfaces. However, recently it has been recognized that the mechanisms that drive macrophage activation in septic and aseptic total joint replacement loosening resemble each other. In particular, accumulating evidence indicates that in addition to mediating bacterial recognition and the subsequent inflammatory reaction, toll-like receptors (TLRs) and their ligands, pathogen-associated molecular patterns (PAMPs) and danger-associated molecular patterns (DAMPS), play a key role in wear debris-induced inflammation and macrophage activation. In addition, subclinical bacterial biofilms have been identified from some cases of seemingly aseptic implant loosening. Furthermore, metal ions released from some total joint replacements can activate TLR signaling similar to bacterial derived PAMPs. Likewise, metal ions can function as haptens activating the adaptive immune system similar to bacterial derived antigens. Thus, it appears that aseptic and septic joint replacement loosening share similar underlying pathomechanisms and that this strict dichotomy to sterile aseptic and bacterial-caused septic implant loosening is somewhat questionable. Indeed, rather than being two, well-defined clinical entities, peri-implant osteolysis is, in fact, a spectrum of conditions in which the specific clinical picture is determined by complex interactions of multiple local and systemic factors.
Department of Medicine, Institute of Clinical Medicine, Helsinki University Central Hospital, 00029 HUS, Finland; Department of Orthopaedic Surgery, Stanford Medical Center, Stanford CA 94305-5341 , USA.
Jukka
J
Pajarinen
Department of Medicine, Institute of Clinical Medicine, University of Helsinki and Helsinki University Central Hospital, Helsinki, Finland.
Eemeli
E
Jamsen
Department of Clinical Medicine, University of Helsinki and ORTON Orthopaedic Hospital of the Invalid Foundation, Helsinki, Finland.
Yrjo T
YT
Konttinen
Department of Orthopaedic Surgery Stanford University Medical Center Redwood City, CA.
Stuart B
SB
Goodman
D019644:Arthroplasty, Replacement, Hip; D016764:Cell Polarity; D006622:Hip Prosthesis / Q000009:adverse effects*; D006801:Humans; D007113:Immunity, Innate / Q000502:physiology*; D008262:Macrophage Activation; D010014:Osteolysis / Q000503:physiopathology*; D018805:Sepsis / Q000276:immunology*; D051193:Toll-Like Receptors / Q000378:metabolism
D051193:Toll-Like Receptors