TY - JOUR
T1 - Mediators of the inflammatory response to joint replacement devices
AU - Cobelli, Neil
AU - Scharf, Brian
AU - Crisi, Giovanna M.
AU - Hardin, John
AU - Santambrogio, Laura
N1 - Funding Information:
This work was supported by the generous donation of Arnold Penner and the Jabez and Helen Hardin Foundation. We would like to thank Paolo Verzani for assistance with Figure 1 and Figure 2.
PY - 2011/10
Y1 - 2011/10
N2 - 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.
AB - 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.
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U2 - 10.1038/nrrheum.2011.128
DO - 10.1038/nrrheum.2011.128
M3 - Review article
C2 - 21894210
AN - SCOPUS:80053925867
SN - 1759-4790
VL - 7
SP - 600
EP - 608
JO - Nature Reviews Rheumatology
JF - Nature Reviews Rheumatology
IS - 10
ER -