Orthopedic implant cobalt‐alloy particles produce greater toxicity and inflammatory cytokines than titanium alloy and zirconium alloy‐based particles<i>in vitro</i>, in human osteoblasts, fibroblasts, and macrophages

Dalal, Ali; Pawar, V. D.; McAllister, Kyron; Weaver, C. L.; Hallab, Nadim J.

doi:10.1002/jbm.a.34122

Cited by 109 publications

(104 citation statements)

References 77 publications

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“…27 Although both particulate debris and ions promoted preosteoblasts to upgrade inflammatory gene expressions such as MCP-1, TNF and IL-6; it appeared that the particles exhibited much more chemotactic ability than ions, exhibiting significantly higher expression of MCP-1 that may explain the thicker pseudo-membranes at bone-implant interface following particle-challenged cell injection. The data complements a previous report 34 that orthopedic implant cobalt-alloy particles resulted in greater inflammatory cytokines than titanium and zirconium alloy-based particles on human osteoblasts, fibroblasts and macrophages.…”

Section: Discussionsupporting

confidence: 89%

Particulate and ion forms of cobalt–chromium challenged preosteoblasts promote osteoclastogenesis and osteolysis in a murine model of prosthesis failure

Yang

Zhang

Jiang

et al. 2018

J Biomedical Materials Res

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This study investigated the interactive behavior of the particulate and ion forms of Cobalt-Chromium (Co-Cr) alloy challenged preosteoblasts during the process of prosthetic implant loosening. Preosteoblasts were challenged with Co-Cr particles or Co(II) ions for 72 hours, followed by the proliferation and PCR assays. For in vivo test, a titanium-pin was implanted into proximal tibia of SCID mice to mimic knee replacement. Co-Cr particles or Co(II) ion challenged preosteoblasts (5×105) were intra-articularly injected into the implanted knee. The animals were sacrificed 5 weeks post-op, and the prosthetic knees were harvested for biomechanical pin-pullout testing, histological evaluations, and microCT assessment. In vitro study suggested that Co-Cr particles and Co(II) ions significantly suppressed the proliferation of preosteoblasts in a dose-dependent manner. RT-PCR data on the challenged cells indicated over-expression of receptor activator of nuclear factor kappa-B ligand (RANKL) and inhibited osteoprotegerin (OPG) gene expression. Introduction of the differently challenged preosteoblasts to the pin-implant mouse model resulted in reduced implant interfacial shear strength, thicker peri-implant soft-tissue formation, more TRAP+ cells, lower bone mineral density and bone volume fraction. In conclusion, both Co-Cr particles and Co(II) ions interfered with the growth, maturation and functions of preosteoblasts, and provides evidence that the metal ions as well play an important role in effecting preosteoblasts in the pathogenesis of aseptic loosening.

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Section: Discussionsupporting

confidence: 89%

Particulate and ion forms of cobalt–chromium challenged preosteoblasts promote osteoclastogenesis and osteolysis in a murine model of prosthesis failure

Yang

Zhang

Jiang

et al. 2018

J Biomedical Materials Res

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“…But they are different than the well established long term (>15 years), mechanisms by which particulate plastic and metal debris cause failure by inducing a subtle but persistent innate macrophage inflammatory responses (i.e. granulomas) that invades the bone-implant interface and leads to bone resorption and eventual aseptic loosening of the implant [4]–[7].…”

Section: Introductionmentioning

confidence: 96%

Cobalt-Alloy Implant Debris Induce HIF-1α Hypoxia Associated Responses: A Mechanism for Metal-Specific Orthopedic Implant Failure

et al. 2013

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The historical success of orthopedic implants has been recently tempered by unexpected pathologies and early failures of some types of Cobalt-Chromium-Molybdenum alloy containing artificial hip implants. Hypoxia-associated responses to Cobalt-alloy metal debris were suspected as mediating this untoward reactivity at least in part. Hypoxia Inducible Factor-1α is a major transcription factor involved in hypoxia, and is a potent coping mechanism for cells to rapidly respond to changing metabolic demands. We measured signature hypoxia associated responses (i.e. HIF-1α, VEGF and TNF-α) to Cobalt-alloy implant debris both in vitro (using a human THP-1 macrophage cell line and primary human monocytes/macrophages) and in vivo. HIF-1α in peri-implant tissues of failed metal-on-metal implants were compared to similar tissues from people with metal-on-polymer hip arthroplasties, immunohistochemically. Increasing concentrations of cobalt ions significantly up-regulated HIF-1α with a maximal response at 0.3 mM. Cobalt-alloy particles (1 um-diameter, 10 particles/cell) induced significantly elevated HIF-1α, VEGF, TNF-α and ROS expression in human primary macrophages whereas Titanium-alloy particles did not. Elevated expression of HIF-1α was found in peri-implant tissues and synovial fluid of people with failing Metal-on-Metal hips (n = 5) compared to failed Metal-on-Polymer articulating hip arthroplasties (n = 10). This evidence suggests that Cobalt-alloy, more than other metal implant debris (e.g. Titanium alloy), can elicit hypoxia-like responses that if unchecked can lead to unusual peri-implant pathologies, such as lymphocyte infiltration, necrosis and excessive fibrous tissue growths.

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“…However, immune rejection can occur after dental implant materials are placed into the body. Neutrophil and macrophage accumulation can appear in the tissue around the implant materials for wound repair, leading to a local inflammatory response (Dalal et al, 2012;Cachinho et al, 2013). Macrophages are the main phagocytes in the early stages of inflammation when the body contacts the implant material.…”

Section: Introductionmentioning

confidence: 99%

Macrophage proinflammatory response to the titanium alloy equipment in dental implantation

X¹,

Li²,

Yin³

et al. 2015

Genet. Mol. Res.

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ABSTRACT. Titanium alloy and stainless steel (SS) had been widely used as dental implant materials because of their affinity with epithelial tissue and connective tissue, and good physical, chemical, biological, mechanical properties and processability. We compared the effects of titanium alloy and SS on macrophage cytokine expression as well as their biocompatibility. Mouse macrophage RAW264.7 cells were cultured on titanium alloy and SS surfaces. Cells were counted by scanning electron microscopy. A nitride oxide kit was used to detect released nitric oxide by macrophages on the different materials. An enzyme linked immunosorbent assay was used to detect monocyte chemoattractant protein-1 levels. Scanning electron microscopy revealed fewer macrophages on the surface of titanium alloy (48.2 ± 6.4 x 10 3 cells/cm 2 ) than on SS (135 ± 7.3 x 10 3 cells/cm 2 ). The nitric oxide content stimulated by titanium alloy was 22.5 mM, which was lower than that stimulated by SS (26.8 mM), but the difference was not statistically significant (P = 0.07). The level of monocyte chemoattractant protein-1 released was significantly higher in the SS group (OD value = 0.128) than in the titanium alloy group (OD value = 0.081) (P = 9156 X. Chen et al.©FUNPEC-RP www.funpecrp.com.br Genetics and Molecular Research 14 (3): 9155-9162 (2015) 0.024). The transforming growth factor-b1 mRNA expression levels in macrophages after stimulation by titanium alloy for 12 and 36 h were significantly higher than that after stimulation by SS (P = 0.31 and 0.25, respectively). Macrophages participate in the inflammatory response by regulating cytokines such as nitric oxide, monocyte chemoattractant protein-1, and transforming growth factor-b1. There were fewer macrophages and lower inflammation on the titanium alloy surface than on the SS surface. Titanium alloy materials exhibited better biological compatibility than did SS.

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Orthopedic implant cobalt‐alloy particles produce greater toxicity and inflammatory cytokines than titanium alloy and zirconium alloy‐based particlesin vitro, in human osteoblasts, fibroblasts, and macrophages

Cited by 109 publications

References 77 publications

Particulate and ion forms of cobalt–chromium challenged preosteoblasts promote osteoclastogenesis and osteolysis in a murine model of prosthesis failure

Particulate and ion forms of cobalt–chromium challenged preosteoblasts promote osteoclastogenesis and osteolysis in a murine model of prosthesis failure

Cobalt-Alloy Implant Debris Induce HIF-1α Hypoxia Associated Responses: A Mechanism for Metal-Specific Orthopedic Implant Failure

Macrophage proinflammatory response to the titanium alloy equipment in dental implantation

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