title: Mediators of the inflammatory response to joint replacement devices.
abstract: Joint replacement surgery is one of the success stories of modern medicine, restoring mobility, diminishing pain and improving the overall quality of life for millions of people. Unfortunately, wear of these prostheses over time generates debris, which activates an innate immune response that can ultimately lead to periprosthetic resorption of bone (osteolysis) and failure of the implant. Over the past decade, the biological interactions between the particulate debris from various implant materials and the immune system have begun to be better understood. The wear debris induces a multifaceted immune response encompassing the generation of reactive oxygen species and damage-associated molecular patterns, Toll-like receptor signaling and NALP3 inflammasome activation. Acting alone or in concert, these events generate chronic inflammation, periprosthetic bone loss and decreased osteointegration that ultimately leads to implant failure.
authors: Department of Orthopedic Surgery, Montefiore Medical Center, 1250 Waters Place, New York, NY 10461, USA.
authors: Neil
authors: N
authors: Cobelli
authors: Brian
authors: B
authors: Scharf
authors: Giovanna M
authors: GM
authors: Crisi
authors: John
authors: J
authors: Hardin
authors: Laura
authors: L
authors: Santambrogio
mesh_terms: D002352:Carrier Proteins / Q000378:metabolism; D005549:Foreign-Body Reaction / Q000276:immunology*; D006801:Humans; D007595:Joint Prosthesis / Q000009:adverse effects*; D000071199:NLR Family, Pyrin Domain-Containing 3 Protein; D010014:Osteolysis / Q000276:immunology* / Q000517:prevention & control; D011474:Prosthesis Design; D011475:Prosthesis Failure / Q000209:etiology*; D051193:Toll-Like Receptors / Q000378:metabolism
chemical_list: D002352:Carrier Proteins; D000071199:NLR Family, Pyrin Domain-Containing 3 Protein; C453881:NLRP3 protein, human; D051193:Toll-Like Receptors