No description available.

In modular hip implants, micro-motion, which leads to fretting corrosion at the head/neck and neck/stem interfaces, has been identified as a major cause of early revision in hip implants, particularly those with heads larger than 32mm. It has been found that the type of fluid used to simulate the fretting corrosion of biomedical materials is crucial for the reliability of laboratory tests. Therefore, to properly understand and effectively design against fretting corrosion damage in modular hips, there is the need to replicate the human body environment as closely as possible during in-vitro testing and validation. In this work, corrosion behavior of CoCrMo in 0.14 M NaCl, phosphate buffered saline (PBS) and clinically relevant simulated body fluid (sbf) is carried out. Also, fretting corrosion studies of the CoCrMo alloy in a clinically relevant novel simulated body fluid (sbf) environment is studied. The presence of phosphate ions in PBS accounted for the higher corrosion rate when compared with 0.14 M NaCl and sbf environment. Despite the low and comparable corrosion rates in 0.14 M NaCl and sbf, the nature of the protective passive film formed in sbf shows the suitability of the novel sbf for future corrosion and fretting corrosion analysis. Finally, the influence of micro-motion at the modular head/neck and neck/stem interfaces on the concentration of metallic ions that goes into the synovial fluid and surrounding tissues is reported.

No description available.

Orthopedic metal implant materials may mediate a variety of adverse tissue reactions by releasing ions through corrosion. Adverse tissue reactions include inflammation, fibrosis and hypersensitivity. All of these reactions eventually lead to implant failure. The goal of this study was to provide a better understanding of the cellular-material interaction at the metal surface. The hypotheses were that 1. the attachment of cells and their released reactive inflammatory compounds (e.g. hydrogen peroxide H2O2, superoxide O2. and nitric oxide NO.) on the surfaces alter the alloys? corrosion and surface properties and 2. the changes in corrosion and chemical properties of the surfaces affect cell behavior. To evaluate the hypotheses, a custom-made electrochemical corrosion cell was used to evaluate how cell culture medium, macrophage cells and macrophage cells activated to simulate inflammation affected the corrosion and surface properties of Co-Cr-Mo and Ti-6Al-4V alloys and how released alloy corrosion products affected cell behaviors. The macrophage cell line used was known to produce reactive species H2O2, O2. and NO. when activated by antigen and interferon. The alloy corrosion properties were enhanced by observing the open circuit potential (OCP), charge transfer, metal ion release, and changes in surface oxides. Proliferation, viability and metabolism were used to evaluate effects of corrosion on the cells. The OCP of Co-Cr-Mo remained unchanged whereas that of Ti-6Al-4V increased over three days for all three test conditions. Both alloys cultured with medium had the lowest OCP among all conditions. With activated macrophage cells, both alloys had the lowest total charge transfer and concentrations of metal ion released. This improved corrosion resistance was mostly due to an enhancement of the surface oxide due to the reactive species released from activated cells, as indicated from the surface analyses. Both alloys were found to have increased percentage (in peak intensity) of O and Ti or Cr peaks, which indicated an increase of Ti and Cr oxides on Ti-6Al-4V and Co-Cr-Mo alloys respectively. The improved corrosion properties resulted in less metal ion release than those without enhanced surface oxides, thus alloys did not further activate cell immune responses in the three day period. The non-activated or activated cells with released metal ions did not exhibit any degradation in their viability, intracellular ATP, NO and IL-1b release as compared to controls. This is consistent with the generally accepted good biocompatibility of these alloys.

Because of their excellent mechanical, tribological, and electrochemical properties, Cobalt Chromium Molybdenum alloys have been used as the material for both the stem and head of modular hip implants. Corrosion is one mechanism by which metal debris, from these implants, is generated, which can lead to adverse events that requires revision surgery. Manufacturing process such as wrought, as-cast, and powder metallurgy influences the microstructure, material properties, and performance of these implants The current research focuses on analyzing the microstructure of CoCrMo alloys from retrieved hip implants with optical and scanning electron microscopy. Additionally, energy disperse spectroscopy was utilized to determine weight composition of cobalt, chromium, and molybdenum in solution. Potentiodynamic polarization was used as an accelerated corrosion testing method to determine the electrochemical behavior of the different microstructures. In agreement with prior literature, it was found that Low Carbon Wrought CoCrMo Alloys have the best corrosion resistance properties.

Despite the high success rates of hip replacements, implant-wear mediated periprosthetic osteolysis remains the most prominent cause of long-term implant failure. Other adverse tissue reactions including hypersensitivity reactions and pseudotumors have also recently been reported as a cause for short-term implant failures. The objectives of this thesis were: 1.) To analyze the effects of Co2+ and Cr3+ released from CoCrMo alloys used in hip implants on macrophage chemokine release; 2.) To determine if Co2+, Cr3+, and the chemokines in cultures of macrophages exposed to Co2+ and Cr3+ can induce migration of T and B lymphocytes; and 3) To analyze the potential modulation of macrophage response to Cr3+ using simvastatin as an anti-inflammatory agent. Results showed that the release of TNF–α and CC chemokines were ion-specific and dose-dependent. Results also suggested that Co2+ and Cr3+ may be capable of directly stimulating the migration of T cells, but not that of B cells, suggesting the potential of these ions to create a micro-environment that would favour a T cell-mediated response in vivo. Results also showed that simvastatin was capable of decreasing chemokine release in macrophages exposed to Cr3+, suggesting its potential to modulate the Cr3+-induced inflammatory response. Together, these studies improve the understanding of the role metal ions play in ion-mediated adverse tissue reactions and potential therapies that may modulate the immune response to metal ions.

Wear particles and ions from cobalt-chromium-molybdenum (CoCrMo)-based implants have been shown to cause adverse immune responses, including periprosthetic osteolysis leading to aseptic loosening, the main cause of implant failure. Previous studies have shown that these wear and corrosion products can lead to the release of inflammatory cytokines, including interleukin-1β (IL-1β), suggesting the involvement of the NLRP3 inflammasome. However, the mechanisms leading to IL-1β release have not been fully elucidated. The primary objectives of this thesis were to determine if, in murine macrophages, IL-1β release induced by micrometre-size CoCrMo particles and nanometre-size chromium oxide (Cr2O3) particles is: 1. Caspase-1-dependent; 2. Reduction-oxidation (redox)-dependent; and 3. NLRP3 inflammasome-dependent. Additionally, the effects of metal ions (Co2+, Cr3+, and Ni2+) on NLRP3 inflammasome activation and the effects of matrix metalloproteinase (MMP) inhibition on IL-1β release induced by CoCrMo particles were analyzed. Results showed that IL-1β release induced by CoCrMo particles was partly caspase-1-, redox-, and MMP-dependent, but NLRP3 inflammasome-independent. On the other hand, IL-1β release induced by Cr2O3 particles appeared to be NLRP3 inflammasome-dependent. Finally, IL-1β release induced by Cr3+, but not Co2+, appeared to be NLRP3 inflammasome-dependent, while Ni2+-induced IL-1β release appeared to be only partially NLRP3 inflammasome-dependent, suggesting that other pathways may also be involved. These findings, which provide additional insights into the mechanisms leading to IL-1β release induced by wear particles and ions from CoCrMo-based implants, may help the future development of therapeutic treatments to modulate wear product-induced inflammation and increase implant longevity.

Highly corrosion-resistant alloys are used in sensitive environments such as the human body and food environments. However, even tiny amounts of released metals from these surfaces could potentially cause adverse effects. It is hence important to study the biointerface between corrosion-resistant alloys and protein-rich environments. This licentiate thesis focused on the metal release processes for stainless steels and cobalt-chromium-molybdenum (CoCrMo) alloys in different protein-rich environments. It aimed at investigating the effect of protein displacement (Vroman effect), gamma irradiation, and friction on the metal release processes. Trace metal analysis was the main tool, combined with other solution analytical tools, electrochemical methods, and surface sensitive techniques. The effect of gamma irradiation, of relevance for cancer radiotherapy, on metal release from CoCrMo and stainless steel 316L was investigated in Paper I. The effect was minor, however the released amount of metals increased after irradiation causing an enhanced surface passivation effect. Whether the displacement of surface proteins (Vroman effect) was playing a role on the metal release and corrosion processes of stainless steels 316L and 303, and of CoCrMo, was investigated in Papers II and III. A Vroman effect influencing the metal release could be observed for stainless steel 316L, but not for CoCrMo and stainless steel grade 303. However, the displacement of the smaller protein bovine serum albumin (BSA) from the surface by the larger protein fibrinogen (Fbn) was observed for both stainless steel grades. The Vroman effect also caused a higher corrosion susceptibility of stainless steel 303, probably due to a thicker layer or patches of adsorbed Fbn. Most probably, protein aggregation and precipitation caused an underestimation of the extent of metal release, especially in the case of CoCrMo. Protein aggregation and precipitation were significantly observed in all studies, especially for solutions with high protein concentrations (Papers II-IV). The effect of friction, by using different setups (stirring with physical contact and sliding in a pin-on-disk machine), on metal release from stainless steel 316L and CoCrMo was investigated in Papers II and IV. Friction induced an increased extent of metal release, increased protein aggregation and precipitation, and enhanced metal precipitation. A combined friction and complexation effect was observed for stainless steel 316L, resulting in an etching effect and relatively high amounts of released metals. Due to enhanced precipitation effects and the experimental setup, it is recommended to strongly consider protein aggregation and metal precipitation events in systems where this could be expected and where friction is present. Otherwise, there is a risk to strongly underestimate the extent of metal release in these protein-rich environments. / <p>QC 2020-09-28</p>

No description available.

Corrosion and metal release mechanisms of CoCrMo alloys are at human biological conditions not fully understood. The main objective of this master thesis was to investigate whether the Vroman effect influences the extent of metal release from CoCrMo alloy in mixed protein solutions. The project focuses on the corrosion properties and release of cobalt (Co), chromium (Cr) and molybdenum (Mo) from a CoCrMo alloy into simulated physiological solutions of pH 7.2-7.4 in the presence of proteins. The metal release study was performed in phosphate buffered saline (PBS) for 4 and 24 h at 37 °C with and without different concentration of proteins (bovine serum albumin-BSA and fibrinogen-Fbn from bovine plasma). In order to investigate whether any Vroman effect could affect the extent of released metals in solutions, sequential tests were performed by sampling after 1, 4, 6 and 24 h in solutions that were partially replenished after 5 h. Significant metal-induced protein aggregation and precipitation were observed in solutions of physiologically-relevant protein concentrations (40 g/L BSA and 2.67 g/L Fbn). Cr was strongly enriched in the surface oxide of CoCrMo after exposure in all solutions. This was for all solutions accompanied by metal release processes dominated by Co. Based on electrochemical investigations, the electrochemical activity did not increase, but rather decreased, in protein-containing solutions as compared to PBS alone. This could possibly be explained by blocking of cathodic areas as a result of protein adsorption.