Official websites use. Share sensitive information only on official, secure websites. 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.
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.
According to the long-standing definition, septic and aseptic loosening of total joint replacements TJRs are two distinct conditions that, excluding the accompanying peri-implant bone loss, have little in common.
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Septic loosening of TJRs may present as a rapidly developing acute condition that is driven by a fulminant infection of the artificial components by a highly virulent bacteria such as Staphylococcus aureus. The bacteria gain access to the implant either directly during primary surgery causing early postoperative infection developing within some days or a few weeks after the initial surgery.
