Aseptic loosening

Wooley, PH; Schwarz, E M

doi:10.1038/sj.gt.3302202

Cited by 195 publications

(173 citation statements)

References 83 publications

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“…The inability to process UHMWPE particles resulting from a lack of appropriate enzymes and resistance of the material to the acidic environment of the phagosome may lead to broad cellular activation in the macrophage population [16]. Phagocytic cells may acquire an activated macrophage phenotype, leading to a release of proinflammatory cytokines (notably interleukin-1b and tumor necrosis factor-a) and inflammatory mediators (prostaglandins and chemokines) that create an inflammatory tissue environment [24,62,78,83]. Necrotic cell death may follow macrophage frustration, heightening deleterious tissue effects and failing to alleviate the debris load.…”

Section: Discussionmentioning

confidence: 99%

“…Crosstalk between macrophages and osteoclasts through inflammatory cytokines will accelerate osteoclastogenesis, leading to the potential for osteolysis and implant loosening. The precise pathways in this process have been well studied [8,26,34,78] but a number of recent papers indicate that the molecular processes involved in the response to conventional UHMWPE may be broader than originally appreciated.…”

Section: Discussionmentioning

confidence: 99%

“…Studies have also shown a variety of cell signaling pathways are involved in the cellular response to debris. These include mitogenactivated protein kinase activation [1], induction of granulocyte macrophage colony-stimulating factor [6], C-C chemokine expression [55], matrix metalloproteinase induction [56], NFkB activation [59,66,72], nitric oxide elicitation [45,64,75], induction of apoptosis [74], cytokine activation [43,78], and direct activation of cyclooxygenase-2 [82]. Although most studies on the etiology of aseptic loosening have been focused on macrophage as the central cell of interest, there is recent interest in examining the role of the fibroblasts in the MMPs 56 UHMWPE = ultrahigh-molecular-weight polyethylene; IL = interleukin; TNF = tumor necrosis factor; GM-CSF = granulocyte macrophage colony-stimulating factor; MMPs = matrix metalloproteinases.…”

Section: Search Strategy and Criteriamentioning

confidence: 99%

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How Has the Introduction of New Bearing Surfaces Altered the Biological Reactions to Byproducts of Wear and Modularity?

Wooley

2014

Clin Orthop Relat Res

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Background Biological responses to wear debris were largely elucidated in studies focused on conventional ultrahigh-molecular-weight polyethylene (UHMWPE) and some investigations of polymethymethacrylate cement and orthopaedic metals. However, newer bearing couples, in particular metal-on-metal but also ceramic-on-ceramic bearings, may induce different biological reactions. Questions/purposes Does wear debris from the newer bearing surfaces result in different biological responses compared with the known responses observed with conventional metal-on-UHMWPE bearings?Methods A Medline search of articles published after 1996 supplemented by a hand search of reference lists of included studies and relevant conference proceedings was conducted to identify the biological responses to orthopaedic wear debris with a focus on biological responses to wear generated from metal-on-highly crosslinked polyethylene, metal-on-metal, ceramic-on-ceramic, and ceramicon-polyethylene bearings. Articles were selected using criteria designed to identify reports of wear debris particles and biological responses contributing to prosthesis failure. Case reports and articles focused on either clinical outcomes or tribology were excluded. A total of 83 papers met the criteria and were reviewed in detail.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Search Strategy and Criteriamentioning

confidence: 99%

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How Has the Introduction of New Bearing Surfaces Altered the Biological Reactions to Byproducts of Wear and Modularity?

Wooley

2014

Clin Orthop Relat Res

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“…2,4,24 We developed a SCID-human tissue chimera model to study the in Figure 1. MTT proliferation assay to assess the in vitro activation of blood monocytes with particulate PMMA and Ti-6Al-4V.…”

Section: Discussionmentioning

confidence: 99%

“…1,2 Investigations have suggested that interaction of prosthetic wear debris particles with cells at or around the periprosthetic margin play critical roles in the periprosthetic osteolysis and implant failure. 2,3 A layer of pseudosynovial tissue is often present between failed implant components and the surrounding bone during revision surgery for aseptic loosening. Numerous polymeric and/ or metallic wear debris particles are present in these vascularized granulomatous tissues, and many of them are engulfed by or in close contact with macrophages and other inflammatory cells.…”

mentioning

confidence: 99%

Polymethylmethacrylate and titanium alloy particles activate peripheral monocytes during periprosthetic inflammation and osteolysis

Yang

Zhang

Bai

et al. 2010

Journal Orthopaedic Research

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ABSTRACT:We investigated the interactions of particulate PMMA or titanium alloy, patient blood monocytes, and periprosthetic tissues using a SCID-hu model of aseptic loosening. Periprosthetic tissues and bone chips obtained at revision surgery for loosening were transplanted into muscles of SCID mice. Peripheral blood monocytes (PBMCs) isolated from the same donors were fluorescently labeled and cocultured with PMMA or Ti-6Al-4V particles before intraperitoneal injection. Control mice with periprosthetic tissue or non-inflammatory ligament xenografts received naive PBMCs transfusion. Mice were euthanized 2 weeks after PBMC transfusion. The human tissues were well accepted in SCID mice. Transfused fluorescent-labeled PBMCs were markedly accumulated in transplanted periprosthetic tissues. Multinucleated osteoclast-like cells were commonly seen within retrieved xenograft tissue, and focal bone erosions were ubiquitous. Total cell densities and CD68þ cells within the xenograft were significantly increased in mice transfused with PMMA and Ti-provoked PBMCs compared to the naÿ ve PBMC animals ( p < 0.05). Immunohistochemical staining identified much stronger positive IL-1 and TNF stains in xenografts from either PMMA or Ti-stimulated monocytes transfusion groups ( p < 0.05). TRAPþ cells were found around bone chips in both activated-PBMCs groups, although markedly more aggregated TRAPþ cells in the PMMA-challenged group than in the titanium group ( p < 0.05). MicroCT assessment confirmed the significant decrease of bone mineral density in chips interacted with activated-monocytes/ osteoclasts. In conclusion, PMMA or titanium particles readily activate peripheral monocytes and promote the cell trafficking to the debriscontaining prosthetic tissues. Particles-provoked PBMCs participated in and promoted the local inflammatory process, osteoclastogenesis, and bone resorption. ß

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Titania Thin Films in Biocompatible Matals and Medical Implants

Variola

Nanci

2011

Oxide Ultrathin Films

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Aseptic loosening

Cited by 195 publications

References 83 publications

How Has the Introduction of New Bearing Surfaces Altered the Biological Reactions to Byproducts of Wear and Modularity?

How Has the Introduction of New Bearing Surfaces Altered the Biological Reactions to Byproducts of Wear and Modularity?

Polymethylmethacrylate and titanium alloy particles activate peripheral monocytes during periprosthetic inflammation and osteolysis

Titania Thin Films in Biocompatible Matals and Medical Implants

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