The Pathology of Orthopedic Implant Failure Is Mediated by Innate Immune System Cytokines
All of the over 1 million total joint replacements implanted in the US each year are expected to eventually fail after 15–25 years of use, due to slow progressive subtle inflammation at the bone implant interface. This inflammatory disease state is caused by implant debris acting, primarily, on inna...
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| Format: | Article |
| Language: | English |
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Wiley
2014-01-01
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| Series: | Mediators of Inflammation |
| Online Access: | http://dx.doi.org/10.1155/2014/185150 |
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| author | Stefan Landgraeber Marcus Jäger Joshua J. Jacobs Nadim James Hallab |
| author_facet | Stefan Landgraeber Marcus Jäger Joshua J. Jacobs Nadim James Hallab |
| author_sort | Stefan Landgraeber |
| collection | DOAJ |
| description | All of the over 1 million total joint replacements implanted in the US each year are expected to eventually fail after 15–25 years of use, due to slow progressive subtle inflammation at the bone implant interface. This inflammatory disease state is caused by implant debris acting, primarily, on innate immune cells, that is, macrophages. This slow progressive pathological bone loss or “aseptic loosening” is a potentially life-threatening condition due to the serious complications in older people (>75 yrs) of total joint replacement revision surgery. In some people implant debris (particles and ions from metals) can influence the adaptive immune system as well, giving rise to the concept of metal sensitivity. However, a consensus of studies agrees that the dominant form of this response is due to innate reactivity by macrophages to implant debris where both danger (DAMP) and pathogen (PAMP) signalling elicit cytokine-based inflammatory responses. This paper discusses implant debris induced release of the cytokines and chemokines due to activation of the innate (and the adaptive) immune system and the subsequent formation of osteolysis. Different mechanisms of implant-debris reactivity related to the innate immune system are detailed, for example, danger signalling (e.g., IL-1β, IL-18, IL-33, etc.), toll-like receptor activation (e.g., IL-6, TNF-α, etc.), apoptosis (e.g., caspases 3–9), bone catabolism (e.g., TRAP5b), and hypoxia responses (Hif1-α). Cytokine-based clinical and basic science studies are in progress to provide diagnosis and therapeutic intervention strategies. |
| format | Article |
| id | doaj-art-2b48a4a6515944299cdec5febb1a98bc |
| institution | Kabale University |
| issn | 0962-9351 1466-1861 |
| language | English |
| publishDate | 2014-01-01 |
| publisher | Wiley |
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| series | Mediators of Inflammation |
| spelling | doaj-art-2b48a4a6515944299cdec5febb1a98bc2025-02-03T01:00:53ZengWileyMediators of Inflammation0962-93511466-18612014-01-01201410.1155/2014/185150185150The Pathology of Orthopedic Implant Failure Is Mediated by Innate Immune System CytokinesStefan Landgraeber0Marcus Jäger1Joshua J. Jacobs2Nadim James Hallab3Department of Orthopaedics, University Hospital Essen, University of Duisburg-Essen, Hufelandstraße 55, 45122 Essen, GermanyDepartment of Orthopaedics, University Hospital Essen, University of Duisburg-Essen, Hufelandstraße 55, 45122 Essen, GermanyDepartment of Orthopedics, Rush University Medical Center, 1735 W Harrison MC107, Chicago, IL 60612, USADepartment of Orthopedics, Rush University Medical Center, 1735 W Harrison MC107, Chicago, IL 60612, USAAll of the over 1 million total joint replacements implanted in the US each year are expected to eventually fail after 15–25 years of use, due to slow progressive subtle inflammation at the bone implant interface. This inflammatory disease state is caused by implant debris acting, primarily, on innate immune cells, that is, macrophages. This slow progressive pathological bone loss or “aseptic loosening” is a potentially life-threatening condition due to the serious complications in older people (>75 yrs) of total joint replacement revision surgery. In some people implant debris (particles and ions from metals) can influence the adaptive immune system as well, giving rise to the concept of metal sensitivity. However, a consensus of studies agrees that the dominant form of this response is due to innate reactivity by macrophages to implant debris where both danger (DAMP) and pathogen (PAMP) signalling elicit cytokine-based inflammatory responses. This paper discusses implant debris induced release of the cytokines and chemokines due to activation of the innate (and the adaptive) immune system and the subsequent formation of osteolysis. Different mechanisms of implant-debris reactivity related to the innate immune system are detailed, for example, danger signalling (e.g., IL-1β, IL-18, IL-33, etc.), toll-like receptor activation (e.g., IL-6, TNF-α, etc.), apoptosis (e.g., caspases 3–9), bone catabolism (e.g., TRAP5b), and hypoxia responses (Hif1-α). Cytokine-based clinical and basic science studies are in progress to provide diagnosis and therapeutic intervention strategies.http://dx.doi.org/10.1155/2014/185150 |
| spellingShingle | Stefan Landgraeber Marcus Jäger Joshua J. Jacobs Nadim James Hallab The Pathology of Orthopedic Implant Failure Is Mediated by Innate Immune System Cytokines Mediators of Inflammation |
| title | The Pathology of Orthopedic Implant Failure Is Mediated by Innate Immune System Cytokines |
| title_full | The Pathology of Orthopedic Implant Failure Is Mediated by Innate Immune System Cytokines |
| title_fullStr | The Pathology of Orthopedic Implant Failure Is Mediated by Innate Immune System Cytokines |
| title_full_unstemmed | The Pathology of Orthopedic Implant Failure Is Mediated by Innate Immune System Cytokines |
| title_short | The Pathology of Orthopedic Implant Failure Is Mediated by Innate Immune System Cytokines |
| title_sort | pathology of orthopedic implant failure is mediated by innate immune system cytokines |
| url | http://dx.doi.org/10.1155/2014/185150 |
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