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Wear Debris (wear + debris)
Terms modified by Wear Debris Selected AbstractsA method for the tribological testing of thin, hard coatingsLUBRICATION SCIENCE, Issue 2 2002R. Michalczewski Abstract A new method has been developed for tribological testing of thin, hard antiwear coatings, using a ball-on-disc tribosystem, under conditions of dry sliding. In this, an Al2O3 ball is pressed against a coated steel disc. Wear debris is removed from the contact zone by a stream of dry argon in this novel method. This improves the stability of the tribological properties and the repeatability of the test results. All test conditions are precisely defined, in particular: the type of motion, air relative humidity, ambient temperature, sliding speed, load, tribosystem spatial configuration, substrate material, substrate hardness and roughness, and coating thickness. The method developed has been used to test various physical vapour deposition coatings (deposited by the vacuum arc method), i. e., single-layer TiN, Ti(C,N), CrN, and Cr(C,N), and multilayer Cr(C,N)/CrN/Cr and Cr(C,N)/(CrN+Cr2N)/CrN/Cr. It is shown that CrN coatings exhibit the best antiwear properties, and Ti(C,N) the worst. Friction coefficients for CrN and Cr(C,N) coatings are much lower than for the more commonly used TiN. Multilayer coatings have better antiwear properties than single-layer ones. [source] Ratcheting and fatigue-led wear in rail,wheel contactFATIGUE & FRACTURE OF ENGINEERING MATERIALS AND STRUCTURES, Issue 10 2003F. J. FRANKLIN ABSTRACT A computer model, which simulates the ratcheting wear of a ductile material subject to repeated loading, is presented and discussed in detail. Variation of material properties is a feature of the model, failure by ductility exhaustion occurring at isolated points or extending regions of failure. Such regions form crack-like features. Mechanisms for removal of weakened material from the surface as wear debris are described. The wear process causes a degree of surface roughness. The simplicity of the model enables simulation of millions of load cycles in only a few hours' computer time. The computer model is used to study the effect of partial slip on wear rate. When creepage is relatively low, the wear rate increases sharply with creepage. When creepage is relatively high, the wear rate is largely insensitive to the creepage. [source] Modeling UHMWPE wear debris generationJOURNAL OF BIOMEDICAL MATERIALS RESEARCH, Issue 2 2007H. Baudriller Abstract It is widely recognized that polyethylene wear debris is one of the main causes of long-term prosthesis loosening. The noxious bioreactivity associated with this debris is determined by its size, shape, and quantity. The aim of this study was to develop a numerical tool that can be used to investigate the primary polyethylene wear mechanisms involved. This model illustrates the formation of varying flow of polyethylene debris with various shapes and sizes caused by elementary mechanical processes. Instead of using the classical continuum mechanics formulation for this purpose, we used a divided materials approach to simulate debris production and release. This approach involves complex nonlinear bulk behaviors, frictional adhesive contact, and characterizes material damage as a loss of adhesion. All the associated models were validated with various benchmark tests. The examples given show the ability of the numerical model to generate debris of various shapes and sizes such as those observed in implant retrieval studies. Most of wear mechanisms such as abrasion, adhesion, and the shearing off of micro-asperities can be described using this approach. Furthermore, it could be applied to study the effects of friction couples, macroscopic geometries, and material processing (e.g. irradiation) on wear. © 2006 Wiley Periodicals, Inc. J Biomed Mater Res Part B: Appl Biomater, 2007 [source] Standardized analysis of UHMWPE wear particles from failed total joint arthroplastiesJOURNAL OF BIOMEDICAL MATERIALS RESEARCH, Issue 5 2002Jay D. Mabrey Abstract Periprosthetic tissue obtained at revision surgery from eight total hip replacement cases was hydrolyzed, and polyethylene debris particles were isolated from each case. Individual particles were analyzed by scanning electron microscopy (SEM) and computerized image analysis in accordance with ASTM F1877-98, a standard for quantitative description of wear debris. For comparison, periprosthetic tissues from eight total knee revision and four total shoulder revision cases were processed and analyzed with identical methods. A total of 2599 hip, 4345 knee, and 1200 shoulder particles were analyzed. The morphologies of the isolated polyethylene particles from the total hip specimens were distinctly different from the total knee and total shoulder particles. The mean equivalent circle diameter (ECD) for hip particles was 0.694 ,m ± 0.005; knee particles measured 1.190 ,m ±0.009; and shoulder particles 1.183 ,m ± 0.017. The ECD was significantly different between hip particles and those from the shoulder and knee. The mean aspect ratio (AR) for the hip particles was 1.626 ± 0.015, compared to the knee particles at 1.935 ± 0.015 and shoulder particles at 2.082 ± 0.033. The AR was statistically different among all three groups. Other descriptors from the ASTM standard, elongation (E), form factor (FF), and roundness (R) were all significantly different among the three groups of joints. This study demonstrates the utility of ASTM F1877-98 in differentiating wear debris particles from different sources. © 2002 Wiley Periodicals, Inc. J Biomed Mater Res (Appl Biomater) 63: 475,483, 2002 [source] Expression profiling reveals alternative macrophage activation and impaired osteogenesis in periprosthetic osteolysisJOURNAL OF ORTHOPAEDIC RESEARCH, Issue 1 2008Panagiotis Koulouvaris Abstract Interactions between periprosthetic cells and prosthetic wear debris have been recognized as an important event in the development of osteolysis and aseptic loosening. Although the ability of wear debris to activate pro-inflammatory macrophage signaling has been documented, the full repertoire of macrophage responses to wear particles has not been established. Here, we examined the involvement of alternative macrophage activation and defective osteogenic signaling in osteolysis. Using real-time RT-PCR analysis of periprosthetic soft tissue from osteolysis patients, we detected elevated levels of expression of alternative macrophage activation markers (CHIT1, CCL18), chemokines (IL8, MIP1 ,) and markers of osteoclast precursor cell differentiation and multinucleation (Cathepsin K, TRAP, DC-STAMP) relative to osteoarthritis controls. The presence of cathepsin K positive multinuclear cells was confirmed by immunohistochemistry. Reduced expression levels of the osteogenic signaling components BMP4 and FGF18 were detected. Expression levels of TNF-,, IL-6, and RANKL were unchanged, while the anti-osteoclastogenic cytokine OPG was reduced in osteolysis patients, resulting in elevated RANKL:OPG ratios. In vitro studies confirmed the role of particulate debris in alternative macrophage activation and inhibition of osteogenic signaling. Taken together, these results suggest involvement in osteolysis of alternative macrophage activation, accompanied by elevated levels of various chemokines. Increased recruitment and maturation of osteoclast precursors is also observed, as is reduced osteogenesis. These findings provide new insights into the molecular pathogenesis of osteolysis, and identify new potential candidate markers for disease progression and therapeutic targeting. © 2007 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 26:106,116, 2008 [source] Role of fibroblasts and fibroblast-derived growth factors in periprosthetic angiogenesisJOURNAL OF ORTHOPAEDIC RESEARCH, Issue 10 2007Miklos Tunyogi-Csapo Abstract The periprosthetic granulomatous soft tissue [designated iterfacial membrane (IFM) in this study] exhibits heterogeneous histopathological features, in which highly vascularized areas with dense cellularity alternate with fibrotic and pseudocapsule-like tissue structures. Although macrophage/monocyte activation is a prominent event in the periprosthetic environment, fibroblasts also phagocytose particulate wear debris both in vivo and in vitro. Particulate wear debris and/or cytokines/growth factors alone or in combination (e.g., in conditioned media of explant cultures of IFMs) stimulated normal synovial and IFM fibroblasts to express inflammatory mediators and growth factors such as interleukin (IL)-1,, IL-6, IL-8, three isoforms of vascular endothelial growth factor (VEGF), monocyte/macrophage chemoattractant protein-1 (MCP-1), macrophage-colony-stimulating factor (M-CSF), cycloxygenases (Cox-1 and Cox-2), acid- and basic-fibroblast growth factors (FGF-1 and FGF-2), leukemia inhibitory factor-1 (LIF-1), transforming growth factor ,-1 (TGF-,1), receptor activator of nuclear factor-kappa B ligand (RANKL), and osteoprotegerin (OPG). Thus, the fibroblast is capable of expressing a wide array of angiogenic and osteoclastogenic factors which are involved in the detrimental processes of the periprosthetic osteolysis. © 2007 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 25:1378,1388, 2007 [source] Involvement of complement receptor 3 (CR3) and scavenger receptor in macrophage responses to wear debrisJOURNAL OF ORTHOPAEDIC RESEARCH, Issue 11 2006Diptendu S. Rakshit Abstract The ability of prosthetic wear debris to induce pro-inflammatory responses in macrophages is widely appreciated, but little is known about the molecular mechanisms involved in particle recognition. Specifically, the nature of the cell surface receptors that interact with wear debris is poorly understood. Elucidating the identities of these receptors and how they interact with different types of wear debris are critical to understanding how wear debris initiates periprosthetic osteolysis. We examined the involvement of opsonization, complement receptor 3 (CR3), and scavenger receptor A (SRA), in responses to polymethylmethacrylate (PMMA) and titanium wear particles. Serum dependence of pro-inflammatory responses to PMMA and titanium was tested, and serum proteins that adhered to these two types of particles were identified. Several serum proteins, including known opsonins such as C3bi and fibronectin, adhered to PMMA but not titanium, and serum was required for pro-inflammatory signaling induced by PMMA, but not by titanium. Phagocytosis of PMMA and titanium by macrophages was demonstrated by flow cytometry. Blocking CR3 specifically inhibited phagocytosis of PMMA by macrophages, whereas blocking SRA specifically inhibited titanium uptake. Direct involvement of CR3 and SRA in cell,particle interaction was assessed by expression of these receptors in nonphagocytic HEK293 cells. CR3 specifically induced cell binding to PMMA particles and adhesion to PMMA-coated plates, while SRA specifically induced binding to titanium particles and adhesion to titanium-coated plates. Taken together, these results suggest involvement of opsonization, complement, and integrin receptors, including CR3 and fibronectin receptors, in PMMA action, and an involvement of scavenger receptors in responses to titanium. © 2006 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 24:2036,2044, 2006 [source] The entrapment of corrosion products from CoCr implant alloys in the deposits of calcium phosphate: A comparison of serum, synovial fluid, albumin, EDTA, and waterJOURNAL OF ORTHOPAEDIC RESEARCH, Issue 8 2006A. C. Lewis Abstract Physical wear of orthopedic implants is inevitable. CoCr alloy samples, typically used in joint reconstruction, corrode rapidly after removal of the protective oxide layer. The behavior of CoCr pellets immersed in human serum, foetal bovine serum (FBS), synovial fluid, albumin in phosphate-buffered saline (PBS), EDTA in PBS, and water were studied using X-ray Photoelectron Spectroscopy (XPS) and Time-of-Flight Secondary Ion Mass Spectroscopy (ToF-SIMS). The difference in the corrosive nature of human serum, water, albumin in PBS and synovial fluid after 5 days of immersion was highlighted by the oxide layer, which was respectively 15, 3.5, 1.5, and 1.5 nm thick. The thickness of an additional calcium phosphate deposit from human serum and synovial fluid was 40 and 2 nm, respectively. Co and Cr ions migrated from the bulk metal surface and were trapped in this deposit by the phosphate anion. This may account for the composition of wear debris from CoCr orthopedic implants, which is known to consist predominantly of hydroxy-phosphate compounds. Known components of synovial fluid including proteoglycans, pyrophosphates, phospholipids, lubricin, and superficial zone protein (SZP), have been identified as possible causes for the lack of significant calcium phosphate deposition in this environment. Circulation of these compounds around the whole implant may inhibit calcium phosphate deposition. © 2006 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 24:1587,1596, 2006 [source] Chemokine IL-8 induction by particulate wear debris in osteoblasts is mediated by NF-,BJOURNAL OF ORTHOPAEDIC RESEARCH, Issue 6 2005Elizabeth A. Fritz Abstract Chemokines, or chemotactic cytokines, are major regulators of the inflammatory response and have been identified as pathogenic factors in the periprosthetic soft tissue. Particulate wear debris induced NF-kB activation, the major transcriptional regulator of IL-8 and MCP-1 pro-inflammatory genes and, indeed, both IL-8 and MCP-1 chemokine gene expressions were upregulated in titanium particulate-stimulated human osteoblasts. Here, we demonstrate that phagocytosed particles activate the IL-8 gene promoter via a NF-kB-mediated mechanism. Transfection of a dominant negative mutant IkB, protein that cannot be serine phosphorylated led to suppression of IL-8 promoter activity. The p65/RelA NF-kB subunit activity was affected in both a time- and titanium particle concentration-dependent fashion. Titanium particles led to increased ERK, JNK, and p38 activation in MG-63 osteoblast cells, and IL-8 protein release was suppressed by specific inhibitors of the ERK and p38 MAPK pathways. Together, our results suggest that wear debris particles induce chemokine expression in osteoblasts via NF-kB-mediated transcriptional activation, which is controlled by the MAPK signal transduction pathway. © 2005 Orthopaedic Research Society. Published by Elsevier Ltd. All rights reserved. [source] New insight into the mechanism of hip prosthesis loosening: Effect of titanium debris size on osteoblast functionJOURNAL OF ORTHOPAEDIC RESEARCH, Issue 2 2004Daniel T. O'Connor Abstract The incidence of rheumatoid arthritis and osteoarthritis is on the rise due to our expanding elderly population. Total joint arthroplasty is the most successful, prevalent treatment modality for these and other degenerative hip conditions. Despite the wide array of prosthetic devices commercially available, hip prostheses share a common problem with a gradual and then accelerating loss of bone tissue and bone,implant interface integrity, followed by implant instability and loosening. Implant failure is largely the result of inevitable wear of the device and generation of wear debris. To provide information for the development of improved prosthetic wear characteristics, we examined the effects of size-separated titanium particles on bone forming cell populations. We demonstrate unequivocally that particle size is a critical factor in the function, proliferation, and viability of bone-forming osteoblasts in vitro. In addition, we have elucidated the time-dependent distribution of the phagocytosed particles within the osteoblast, indicating an accumulation of particles in the perinuclear area of the affected cells. The report finds that particle size is a critical factor in changes in the bone formation-related functions of osteoblasts exposed to simulate wear debris, and that 1.5,4 ,m titanium particles have the greatest effect on osteoblast proliferation and viability in vitro. The size of titanium particles generated through wear of a prosthetic device may be an important consideration in the development of superior implant technology. © 2003 Orthopaedic Research Society. Published by Elsevier Ltd. All rights reserved. [source] The effectiveness of polyethylene versus titanium particles in inducing osteolysis in vivo,JOURNAL OF ORTHOPAEDIC RESEARCH, Issue 2 2004Marius von Knoch Abstract Bearing surface wear and periprosthetic osteolysis due to wear particles are among the most common reasons for joint replacement failure. A murine calvarial model of wear particle-induced osteolysis has been used to identify different biologic factors associated with this problem and to test nonsurgical methods of modulating the host response to particulate debris. This model has utilized titanium particles, however, in clinical practice the most common source of particulate debris is polyethylene particles from bearing surface wear. We now report a calvarial model of wear particle-induced osteolysis based on commercially available polyethylene particles. We found that compared to sham surgery osteoclast recruitment and bone resorption can be induced by introduction of the titanium particles or polyethylene particles. However, bone resorption was significantly higher with polyethylene particles compared to titanium particles (p = 0.02). We consider the polyethylene based murine calvarial model of wear particle-induced osteolysis a reliable and clinically relevant tool to understand the host factors and potential pharmacologic interventions that can influence wear debris generated osteolysis. This model might serve as an extension of the well-established titanium based bone resorption model. © 2003 Orthopaedic Research Society. Published by Elsevier Ltd. All rights reserved. [source] Use of volumetric computerized tomography as a primary outcome measure to evaluate drug efficacy in the prevention of peri-prosthetic osteolysis: A 1-year clinical pilot of etanercept vs. placeboJOURNAL OF ORTHOPAEDIC RESEARCH, Issue 6 2003Edward M. Schwarz Although total hip replacement (THR) is amongst the most successful and beneficial medical procedures to date, long-term outcomes continue to suffer from aseptic loosening secondary to peri-prosthetic osteolysis. Extensive research over the last two decades has elucidated a central mechanism for osteolysis in which wear debris generated from the implant stimulates inflammatory cells to promote osteoclastogenesis and bone resorption. The cytokine tumor necrosis factor alpha (TNF,) has been demonstrated to be central to this process and is considered to be a leading target for intervention. Unfortunately, even though FDA approved TNF antagonists are available (etanercept), currently there are no reliable outcome measures that can be used to evaluate the efficacy of a drug to prevent peri-prosthetic osteolysis. To the end of developing an effective outcome measure, we evaluated the progression of lesion size in 20 patients with established peri-acetabular osteolysis (mean = 29.99 cm3, range = 2.9,92.7 cm3) of an uncemented primary THR over 1-year, using a novel volumetric computer tomography (3D-CT) technique. We also evaluated polyethylene wear, urine N-telopeptides and functional assessments (WOMAC, SF-36 and Harris Hip Score) for comparison. At the time of entry into the study baseline CT scans were obtained and the patients were randomized to etanercept (25 mg s.q., twice/week) and placebo in a double-blinded fashion. CT scans, urine and functional assessments were also obtained at 6 and 12 months. No serious adverse drug related events were reported, but one patient had to have revision surgery before completion of the study due to aseptic loosening. No remarkable differences between the groups were observed. However, the study was not powered to see significant drug effects. 3D-CT data from the 19 patients was used to determine the mean increase in lesion size over 48 weeks, which was 3.19 cm3 (p < 0.0013). Analysis of the urine N-telopeptides and functional assessment data failed to identify a significant correlation with wear or osteolysis. In conclusion, volumetric CT was able to measure progression of osteolysis over the course of a year, thus providing a technology that could be used in therapeutic trials. Using the data from this pilot we provide a model power calculation for such a trial. © 2003 Orthopaedic Research Society. Published by Elsevier Science Ltd. All rights reserved. [source] Four-year study of cobalt and chromium blood levels in patients managed with two different metal-on-metal total hip replacementsJOURNAL OF ORTHOPAEDIC RESEARCH, Issue 2 2003Christian Lhotka Abstract Background: Metal-on-metal total hip prostheses will produce a certain amount of wear debris. This results in increased whole-blood metal levels, which may cause adverse effects. It is not known to what extent the problem has been overcome by advances in alloy technology. Methods: In 259 patients who with total hip replacement, blood cobalt and chromium concentrations were measured with atomic absorption spectrophotometry over a period of four years after arthroplasty. Of the patients enrolled in the study, 131 had been managed with a METASUL® cobalt-chromium alloy metal-on-metal bearing combination, while 128 had been given a SIKOMET®-SM21® cobalt-chromium alloy metal-on-metal combination. The control group consisted of 31 age- and gender-matched subjects. Results: Compared with the controls, all the patients had higher cobalt and chromium levels. Cobalt concentrations were up to 50 times higher, while chromium concentrations were up to 100 times higher. Conclusions: Both systems showed evidence, in the whole-blood samples, of wear debris production by the implants. Therefore, patients managed with metal-on-metal bearing combinations should be carefully monitored in order to ensure that any local or systemic complications are detected early on. © 2002 Orthopaedic Research Society. Published by Elsevier Science Ltd. All rights reserved. [source] Efficacy of ex vivo OPG gene therapy in preventing wear debris induced osteolysisJOURNAL OF ORTHOPAEDIC RESEARCH, Issue 2 2002J. Jeffrey Goater Aseptic loosening of prosthetic implants remains a serious orthopaedic problem and the greatest limitation to total joint arthroplasty. Central to the etiology of aseptic loosening is periprosthetic osteolysis at the bone-implant interface, which is caused by wear debris-induced inflammation. This inflammation produces the critical osteoclast differentiation factor RANKL, which directly stimulates osteoclastogenesis and osteoclastic bone resorption. A dominant factor known to counteract this process is the natural RANKL receptor antagonist protein OPG. Here we explore the potential of ex vivo OPG gene therapy for aseptic loosening by evaluating the efficacy of stably transfected fibroblast-like synoviocytes (FLS) expressing OPG in preventing wear debris-induced osteoclastogenesis, in a mouse calvaria model. Although the stably transfected fibroblasts produced small amounts of OPG (0.3 ng/ml/72 h/106 cells), this protein was very effective in preventing osteoclastic resorption as determined in a bone wafer assay. More importantly, implantation of 107 FLS,OPG, together with 30 mg of Ti wear debris, onto the calvaria of mice, completely inhibited osteoclastogenesis 3 days after surgery. Animals given FLS-LacZ control cells, which persisted for 3 days as determined by X-gal staining, together with the Ti particles, had a 6-fold increase in osteoclastogenesis compared to controls without Ti. This increased osteoclastogenesis was completely inhibited by the FLS-OPG, as osteoclast numbers in the calvaria of these animals were similar to that seen in the SHAM controls. © 2002 Orthopaedic Research Society. Published by Elsevier Science Ltd. All rights reserved. [source] Reciprocative sliding friction and wear properties of electrical discharge machined ZrO2 -based compositesLUBRICATION SCIENCE, Issue 9 2009Koenraad Bonny Abstract Hot-pressed, laboratory-made, ZrO2 -based composites with 40 vol. % WC, TiCN or TiN were surface finished by electrical discharge machining in order to compare their reciprocating sliding friction and wear response against WC,6wt%Co cemented carbide in unlubricated conditions. Sliding experiments were performed using a Plint TE77 pin-on-flat wear test rig, revealing a strong impact of the secondary phase on the tribological behaviour of the ZrO2 -based composites. The worn surfaces and wear debris were characterised by scanning electron microscopy, energy dispersive X-ray analysis and surface topography scanning, pointing out abrasion, polishing and adhesion as main wear mechanisms. The most favourable friction and wear characteristics were encountered with ZrO2,WC composites compared to the other grades with equal amount of volumetric secondary phase. Copyright © 2009 John Wiley & Sons, Ltd. [source] Osteopontin deficiency impairs wear debris,induced osteolysis via regulation of cytokine secretion from murine macrophagesARTHRITIS & RHEUMATISM, Issue 5 2010Sadanori Shimizu Objective To investigate the molecular mechanisms underlying particle-induced osteolysis, we focused on osteopontin (OPN), a cytokine and cell-attachment protein that is associated with macrophage chemoattractant and osteoclast activation. Methods We compared OPN protein levels in human periprosthetic osteolysis tissues with those in osteoarthritis (OA) synovial tissues. To investigate the functions of OPN during particle-induced osteolysis in vivo, titanium particles were implanted onto the calvaria of OPN-deficient mice and their wild-type (WT) littermates. Mice were killed on day 10 and evaluated immunohistologically. The effects of OPN deficiency on the secretion of inflammatory cytokines were examined using cultured bone marrow,derived macrophages (BMMs). BMMs from OPN-deficient and WT mice were cultured with titanium particles for 12 hours, and the concentrations of inflammatory cytokines in the conditioned media were measured by enzyme-linked immunosorbent assay. Results Expression of OPN protein was enhanced in human periprosthetic osteolysis tissues as compared with OA synovial tissues. In the particle-induced model of osteolysis of the calvaria, bone resorption was significantly suppressed by OPN deficiency via inhibition of osteoclastogenesis, whereas an inflammatory reaction was observed regardless of the genotype. Results of immunostaining indicated that OPN protein was highly expressed in the membrane and bone surface at the area of bone resorption in WT mice. When BMMs were exposed to titanium particles, the concentration of proinflammatory cytokines, such as tumor necrosis factor ,, interleukin-1, (IL-1,), IL-1,, and IL-6, as well as chemotactic factors, such as monocyte chemoattractant protein 1 and macrophage inflammatory protein 1,, in the conditioned medium were significantly reduced by OPN deficiency. Whereas phagocytic activity of BMMs was not attenuated by OPN deficiency, phagocytosis-mediated NF-,B activation was impaired in OPN-deficient BMMs. These data indicated that OPN was implicated in the development of particle-induced osteolysis via the orchestration of pro-/antiinflammatory cytokines secreted from macrophages. Conclusion OPN plays critical roles in wear debris,induced osteolysis, suggesting that OPN is a candidate therapeutic target for periprosthetic osteolysis. [source] | ||||||||||