Interactions between stainless steel, shear stress, and monocytes

Messer, Regina L. W.; Mickalonis, J.I.; Lewis, Jill B.; Omata, Yo; Davis, Cortney M.; Brown, Yolanda; Wataha, John C.

doi:10.1002/jbm.a.31730

Cited by 10 publications

(10 citation statements)

References 42 publications

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“…Many studies have reported that proteins may increase or decrease or do not affect the corrosion rates of various materials. 21‐28, 32‐34, 37, 39, 40, 42, 50 The interaction between materials and proteins, cells, or their by‐products is dependent on several factors including surface charge, roughness, and composition of the material as well as shape, charge, and binding affinities of the molecule 50. Proteins may increase corrosion by proteins binding and carrying away metal ions from the alloy surface, encouraging further corrosion; proteins limiting oxygen at the surface do discourage passivation as the oxide layer forms or when it is disturbed 32, 37.…”

Section: Discussionmentioning

confidence: 99%

“…Protein adsorption alters corrosion depending on pH, the type of alloy, surface condition of the alloy, the presence of other metal ions, and the nature of protein adsorption onto the alloy 21–28. Other studies have assessed the effects of hydrogen peroxide,29–31 proteins,22‐24, 26, 28, 32 mechanical stress,33–36 wear/fretting,37, 38 and cells31, 33, 34, 39‐42 on implant material corrosion properties and have used animal models to correlate metal ions release to in vitro corrosion testing 43, 44. However, these studies generally have been restricted to the use of flat or cylindrical “bulk” samples in commercial electrolytes (i.e., saline, serum, or artificial saliva) 19, 38, 42, 45–50.…”

Section: Introductionmentioning

confidence: 99%

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Corrosion of machined titanium dental implants under inflammatory conditions

et al. 2008

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The effects of hyperglycemia, altered cell function, or inflammatory mediators on implant corrosion are not well studied; yet, these effects are critical to implant biocompatibility and osseointegration. Because implant placement is burgeoning, patients with medically compromising systemic conditions such as diabetes are increasingly receiving implants, and the role of other inflammatory diseases on implant corrosion also needs investigation. In the current study, the corrosion properties of commercially available, machined titanium implants were studied in blood, cultures of monocytic cells, and solutions containing elevated dextrose concentrations. Implant corrosion was estimated by open circuit potentials, linear polarization resistance, and electrical impedance spectroscopy (EIS) for 26 h. In selected samples, THP1 monocytic cells were activated for 2 h with Lipopolysaccharide prior to implant exposure, and IL-1beta secretion was measured to assess the affect of the implants on monocyte activation. Implants under conditions of inflammatory stress exhibited more negative E(corr) values, suggesting an increased potential for corrosion. Linear polarization measurements detected increased corrosion rates in the presence of elevated dextrose conditions over PBS conditions. EIS measurements suggested that implants underwent surface passivation reactions that may have limited corrosion over the short term of this test. This result was supported by cyclic polarization tests. IL-1beta secretion was not altered under conditions of corrosion or implant exposure. The results suggest that inflammatory stress and hyperglycemia may increase the corrosion of dental endosseous titanium-based implants, but that longer, more aggressive electrochemical conditions may be necessary to fully assess these effects.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Corrosion of machined titanium dental implants under inflammatory conditions

et al. 2008

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“…Indeed, the prolonged application of high fluid shear to human chondrocytes in vitro recapitulates the gene expression profiles associated with OA in vivo (7). As shown in Table 1, the levels of IL‐1β (44–46), IL‐6 (10, 13, 44, 46, 47), IL‐8 (45), IL‐10 (44), and TNF‐α (48) are significantly elevated in different shear‐activated human cell lines (Table 1). More interestingly, these shear‐induced PICs are similarly regulated in OA cartilage (Table 1).…”

Section: Fluid Shear Stress Reveals the Mechanisms By Which Oa Inducementioning

confidence: 99%

“…These data demonstrate that fluid shear stress is an appropriate in vitro model for OA investigation and emphasize the importance of shear stress in the pathogenesis of OA. Moreover, three additional genes, CXCL1 (45), CCL1 (45), and MCP‐1 (45, 49), are up‐regulated in shear‐activated human THP1 monocytes and human umbilical vein endothelial cells (HUVECs; Table 1). Although we could find no similar reports for OA‐activated cells, the same family of proteins, including CXCL2 (17) and CCL3 (17), has been found to be up‐regulated in human OA cartilage.…”

Section: Fluid Shear Stress Reveals the Mechanisms By Which Oa Inducementioning

confidence: 99%

Fluid shear stress‐induced osteoarthritis: roles of cyclooxygenase‐2 and its metabolic products in inducing the expression of proinflammatory cytokines and matrix metalloproteinases

Wang¹,

Guan²,

Guo

et al. 2013

FASEB j.

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The mechanical overloading of cartilage is involved in the pathophysiology of osteoarthritis (OA) by both biochemical and mechanical pathways. The application of fluid shear stress to chondrocytes recapitulates the earmarks of OA, as evidenced by the release of proinflammatory cytokines (PICs), matrix metalloproteinases (MMPs), and apoptotic factors. Dysregulations or mutations in these genes might directly cause OA in addition to determining the stage at which OA becomes apparent, the joint sites involved, and the severity of the disease and how rapidly it progresses. However, the underlying mechanisms remain unknown. In this review, we propose that the dysregulation of cyclooxygenase-2 (COX-2) is associated with fluid shear stress-induced OA via its metabolic products at different stages of the disease. Indeed, high fluid shear stress rapidly induces the production of PICs and MMPs via COX-2-derived prostaglandin (PG)E2 at the early stage of OA. In contrast, prolonged shear exposure (>12 h) aggravates the condition by concurrently up-regulating the expression of proapoptotic genes and down-regulating the expression of antiapoptotic genes in a 15-deoxy-Δ (12,14)-prostaglandin J2 (15d-PGJ2)-dependent manner at the late stage of disease. These observations may help to resolve long-standing questions in OA progression and provide insight for development of strategies to treat and combat OA.

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“…10 The corrosion process within the body is due to the presence of proteins and shearing stresses along the stent surface. 12,13 In addition to inflammation, nickel particles have been implicated as potentially carcinogenic. 13 The corrosion process starts within days of implantation and can potentially lead to loss of arterial structural integrity.…”

Section: Introductionmentioning

confidence: 99%

Corrosion resistance improvement for 316L stainless steel coronary artery stents by trimethylsilane plasma nanocoatings

Jones

Chen

2014

J Biomed Mater Res

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To improve their corrosion resistance and thus long-term biocompatibility, 316L stainless steel coronary artery stents were coated with trimethylsilane (TMS) plasma coatings of 20–25 nm in thickness. Both direct current (DC) and radio-frequency (RF) glow discharges were utilized for TMS plasma coatings and additional NH3/O2 plasma treatment to tailor the surface properties. X-ray photoelectron spectroscopy (XPS) was used to characterize the coating surface chemistry. It was found that both DC and RF TMS plasma coatings had Si- and C-rich composition, and the O-and N-contents on the surfaces were substantially increased after NH3/O2 plasma treatment. Surface contact angle measurements showed that DC TMS plasma nanocoating with NH3/O2 plasma treatment generated very hydrophilic surface. The corrosion resistance of TMS plasma coated stents was evaluated through potentiodynamic polarization and electro-chemical impedance spectroscopy (EIS) techniques. The potentiodynamic polarization demonstrated that the TMS plasma coated stents imparted higher corrosion potential and pitting potential, as well as lower corrosion current densities as compared with uncoated controls. The surface morphology of stents before and after potentiodynamic polarization testing was analyzed with scanning electron microscopy, which indicated less corrosion on coated stents than uncoated controls. It was also noted that, from EIS data, the hydrophobic TMS plasma nanocoatings showed stable impedance modulus at 0.1 Hz after 21 day immersion in an electrolyte solution. These results suggest improved corrosion resistance of the 316L stainless steel stents by TMS plasma nanocoatings and great promise in reducing and blocking metallic ions releasing into the bloodstream.

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Interactions between stainless steel, shear stress, and monocytes

Cited by 10 publications

References 42 publications

Corrosion of machined titanium dental implants under inflammatory conditions

Corrosion of machined titanium dental implants under inflammatory conditions

Fluid shear stress‐induced osteoarthritis: roles of cyclooxygenase‐2 and its metabolic products in inducing the expression of proinflammatory cytokines and matrix metalloproteinases

Corrosion resistance improvement for 316L stainless steel coronary artery stents by trimethylsilane plasma nanocoatings

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