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Mediators of the inflammatory response to joint replacement devices
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Journal Article
Mediators of the inflammatory response to joint replacement devices
2011
Overview
Periprosthetic osteolysis is a common reason for failure or revision of joint replacement surgery, and is a result of the inflammatory reaction to debris particles generated by wearing of the implant over time. In this Review, the authors describe the cellular and molecular mediators of this process and how it might be prevented or treated.
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.
Key Points
Wear debris is generated by the movements of the articulating surfaces of a joint replacement under load
Microparticle wear debris induces “frustrated phagocytosis” and multinucleated giant cell fusion
Nanoparticle wear debris induces endosomal destabilization and NALP3 inflammasome activation
Ultra-high-molecular-weight polyethylene polymeric wear debris and damage-associated molecular patterns induce activation of Toll-like receptors 2 and 4
Metal wear debris and metal ions can induce a type IV hypersensitivity reaction
The multifaceted myelomonocytic inflammatory response induced by wear debris increases osteoclastogenesis and promotes periprosthetic osteolysis
Publisher
Nature Publishing Group UK,Nature Publishing Group
Subject
/ Carrier Proteins - metabolism
/ Complications and side effects
/ Foreign-Body Reaction - immunology
/ Humans
/ Joint Prosthesis - adverse effects
/ Medicine
/ Nickel
/ NLR Family, Pyrin Domain-Containing 3 Protein
/ Osteolysis - prevention & control
/ Prosthesis Failure - etiology
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