Titanium Alloy Particles Research Articles

Nano-sized titanium alloy particles inhibit the proliferation and promote the apoptosis of bone marrow mesenchymal stem cells invitro.

Aseptic loosening of artificial joints is the leading cause of failure for patients who receive total joint arthroplasty. Prior reports indicate that bone marrow mesenchymal stem cells (BSMC) are critical in the stabilization of implanted artificial joints, and that deregulated interaction between BMSCs and artificial joint derived particles is a risk factor for aseptic loosening with an unknown mechanism. In the present study, the pathomechanisms whereby titanium and its alloy derived particles facilitate aseptic loosing were investigated in vitro. It was demonstrated that nano-sized titanium alloy particles significantly inhibited the proliferation of BMSCs in a time and concentration dependent manner. Furthermore, it was demonstrated that the particles promoted the apoptosis of BMSCs in the same manner. Bax and Caspase-3 expression of BMSCs were elevated when cultured with the particles. As BMSCs exhibit a critical role in the stabilization of artificial joints, the results of the present study may provide a novel direction for the management of aseptic loosening in clinics.

In vitro cytotoxicity and surface topography evaluation of additive manufacturing titanium implant materials.

Custom-designed patient-specific implants and reconstruction plates are to date commonly manufactured using two different additive manufacturing (AM) technologies: direct metal laser sintering (DMLS) and electron beam melting (EBM). The purpose of this investigation was to characterize the surface structure and to assess the cytotoxicity of titanium alloys processed using DMLS and EBM technologies as the existing information on these issues is scarce. "Processed" and "polished" DMLS and EBM disks were assessed. Microscopic examination revealed titanium alloy particles and surface flaws on the processed materials. These surface flaws were subsequently removed by polishing. Surface roughness of EBM processed titanium was higher than that of DMLS processed. The cytotoxicity results of the DMLS and EBM discs were compared with a "gold standard" commercially available titanium mandible reconstruction plate. The mean cell viability for all discs was 82.6% (range, 77.4 to 89.7) and 83.3% for the control reconstruction plate. The DMLS and EBM manufactured titanium plates were non-cytotoxic both in "processed" and in "polished" forms.

Excessive Anteversion Leads to Failure at 3 Years Due to Impingement as Evidenced by Twin Notches in Ti6A4V Stem

A 63-year old female with bilateral hip replacements was referred to our clinic for pain and elevated metal ions. Her left hip had been revised earlier. The right hip had an SROM Ti6Al4V stem implanted with a 28mm head, a 28mm CoCr liner and Pinnacle Ti6Al4V shell. The patient reported pain, numbness, tingling, and repeated clicking and popping sensations with gait. She specifically noted that her hip would freeze while walking and could pop rising from a chair. Repeated metal ion levels showed Co (blood)17ppb, Cr (serum) 21ppb, and Ti (blood) at 69ppb. CT-images of right hip revealed femoral stem anteversion was 43° and cup anteversion was 40°, for a combined anteversion of 83°. The right hip was revised 3.5 years postoperatively for persistent pain and elevated metal ions. At surgery, large twin notches were evident on her posterior femoral neck and 10mm-wide scalloped damage was evident in the rim of the Ti6A4V shell. SEM-imaging revealed contaminating layers on CoCr head containing elements Al, V and Ti. These indicated that titanium-alloy particles liberated by cup-to-neck impingements had transferred to the CoCr bearings. Our intent in this case was not to document that a MOM bearing produced impingement damage, because this case clearly implicated adverse surgical positioning. Rather, the intent was to document sequelae likely in a THA case that has a metal cup impinging on a metal femoral neck. In particular, twin notches on the femoral neck indicated that this patient was routinely impinging her Ti6Al4V shell against the Ti6Al4V neck and also subluxing her femoral head out of the cup. These signs are a clear indication that one or both components must be revised, as opposed to simply replacing the CoCr liner with a revision polyethylene liner.

Friction-stir welding of titanium/aluminum dissimilar alloys: Joint configuration design, as-welded interface characteristics and tensile properties

Ti-6Al-4V titanium alloy and 5A06 aluminum alloy were successfully butt-joined by friction-stir welding method utilizing a special design of butt-joint configuration. The tool-pin was bias placed toward the aluminum butt-side, accompanying with an excess plunge value of tool shoulder into the top surface of aluminum sheet. The as-welded interface characteristics, joining mechanisms and tensile properties of the modified titanium/aluminum dissimilar butt-joint were performed. Experimental results indicated that the defect-free butt-joints with good formation quality were obtainable when the rotation speed of 1200 r/min, the travel speed of 60 mm/min and the pin offset of 0.5 mm were tailored. The stir nugget zone in joints exhibited a composite-like structure of titanium-alloy particles distributed in aluminum-alloy matrix, with an obvious so-called onion-ring morphology. The energy-dispersive X-ray spectroscopy detections showed that no bulky intermetallic compounds were formed at the titanium/aluminum as-welded interface. The maximum tensile strength of the joint was 265 MPa, which generally reached 84.13% of that of the parent 5A06 aluminum alloy.

Effective two-step method for producing Ti–6Al–4V alloy particles with various morphologies

Magnesium was used as a reductant for the direct combustion synthesis of titanium alloy particles (Ti–6Al–4V) from titanium oxide (TiO2). The feed material (TiO2) and reductant (Mg) were mixed with Al (or AlCl3·6H2O), vanadium pentoxide (V2O5), and calcium hydroxide (Ca(OH)2), and the reaction mixture was combusted under pressurized argon. Temperature–time profiles were intermittently measured during combustion to analyze the combustion temperatures and wave velocities. The combustion product was subsequently acid-leached to eliminate secondary phases (MgO, MgCl2, CaO) and produce Ti–6Al–4V alloy particles whose oxygen content was ~1.3%. Further the content of oxygen was decreased to 0.2wt.% by deoxidizing the Ti–6Al–4V alloy particles with calcium in the range 850–900°C. The AlCl3·6H2O affected the particle morphology more than the Al metal did; i.e. the Al-doped alloy particles were porous and consisted of relatively small agglomerated particles whereas using AlCl3·6H2O produced dense, round particles. Pilot-scale production experiments revealed that Ti–6Al–4V alloy particles can be efficiently produced using our method.

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

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.

Titanium particle-challenged osteoblasts promote osteoclastogenesis and osteolysis in a murine model of periprosthestic osteolysis

The current study investigates the interactive behavior of titanium alloy particle-challenged osteoblastic bone marrow stromal cells (BMSCs) and macrophage lineage cells in a murine knee-prosthesis failure model. BMSCs were isolated from male BALB/c mice femurs and induced in osteogenic medium. At 24h after isolation, BMSCs in complete induction medium were challenged with 1, 3 or 5mgml−1 titanium particles for 7days. Culture media were collected at 2, 4 and 6days and cells were harvested at 7days for alkaline phosphatase (ALP) assay/stains. Cell proliferation in the presence of Ti particles was periodically evaluated by MTT assay. Mice implanted with titanium-pin tibial implants were given an intra-articular injection of 50μl medium containing 5×105 Ti particles-challenged bone-marrow-derived osteoblastic cells, followed by a repeat injection at 2weeks post-operation. Control mice with titanium-pin implants received a naïve osteoblastic cell transfusion. After sacrifice at 4weeks, the implanted knee joint of each group was collected for biomechanical pin-pullout testing, histological evaluation and reverse transcriptase polymerase chain reaction analysis of mRNA extracted from the joint tissues. Ti particles significantly stimulated the proliferation of BMSC-derived osteoblastic cells at both high and low particle concentrations (p<0.05), with no marked differences between the particle doses. ALP expression was diminished following Ti particle interactions, especially in the high-dose particle group (p<0.05). In addition, the culture media collected from short-term challenged (48h) osteoblasts significantly increased the numbers of TRAP+ cells when added to mouse peripheral blood monocytes cultures, in comparison with the monocytes cells receiving naïve osteoblasts media (p<0.05). Intra-articular introduction of the osteoblastic cells to the mouse pin-implant failure model resulted in reduced implant interfacial shear strength and thicker peri-implant soft-tissue formation, suggesting that titanium particles-challenged osteoblasts contributed to periprosthetic osteolysis. Comparison of the gene expression profiles among the peri-implant tissue samples following osteoblast injection did not find significant difference in RunX2 or Osterix/Sp7 between the groups. However, MMP-2, IL-1, TNF-α, RANKL, and TRAP gene expressions were elevated in the challenged-osteoblast group (p<0.05). In conclusion, titanium alloy particles were shown to interfere with the growth, maturation, and functions of the bone marrow osteoblast progenitor cells. Particle-challenged osteoblasts appear to express mediators that regulate osteoclastogenesis and peri-prosthetic osteolysis.

Quantifying subtle but persistent peri-spine inflammation in vivo to submicron cobalt–chromium alloy particles

We evaluated the consequences of cobalt-chromium alloy (CoCr) wear debris challenge in the peri-spine region to determine the inflammation and toxicity associated with submicron particulates of CoCr-alloy and nickel on the peri-spine. The lumbar epidural spaces of (n = 50) New Zealand white rabbits were challenged with: 2.5 mg CoCr, 5.0 mg CoCr, 10.0 mg CoCr, a positive control (20.0 mg of nickel) and a negative control (ISOVUE-M-300). The CoCr-alloy and Ni particles had a mean diameter of 0.2 and 0.6 μm, respectively. Five rabbits per dose group were studied at 12 and 24 weeks. Local and distant tissues were analyzed histologically and quantitatively analyzed immunohistochemically (TNF-α and IL-6). Histologically, wear particles were observed in all animals. There was no evidence of toxicity or local irritation noted during macroscopic observations in any CoCr-dosed animals. However, Ni-treated control animals experienced bilateral hind leg paralysis and were euthanized at Day 2. Histopathology of the Ni particle-treated group revealed severe neuropathy. Quantitative immunohistochemistry demonstrated a CoCr-alloy dose-dependent increase in cytokines (IL-6, TNF-α, p < 0.05) at 12 and 24 weeks. Subtle peri-spine inflammation associated with CoCr-alloy implant particles was dose dependent and persistent. Neuropathy can be induced by highly reactive Ni particles. This suggests peri-spine challenge with CoCr-alloy implant debris (e.g., TDA) is consistent with past reports using titanium alloy particles, i.e., mild persistent inflammation.

Effects of titanium allov particles on cell Proliferation and expression of receptor activator of nuclear factor-κB ligand gene in osteoblasts of mice

Objective To observe the effect of titanium alloy particles on the cell proliferation and the expression of gene receptor activator of nuclear factor-κB (NF-κB) ligand (RANKL) in osteoblasts of mice,and to investigate the mechanism of periprosthetic osteolysis.Methods Osteoblasts were cultured in 10％ serum medium containing different concentrations of titanium alloy particles.The cells were randomly divided into four groups.In the experimental groups A,B and C,osteoblasts were cultured with 0.01％,0.10％ and 1.00％ concentrations of titanium alloy particles,respectively; in the control group,no titanium alloy particles were given.Cell Counting Kit-8 (CCK-8) test was used to assess the cell proliferation at 24,48,96,168 h,respectively.At 24 and 48 h,reverse transcription-polymerase chain reaction (RTPCR) and enzyme linked immunosorbent assay (ELISA) were performed to detect the RANKL expression in osteoblasts and the intensity of the concentrations of RANKL in the supernatant of medium,respectively.Results The proliferation of osteoblasts had no differences between experimental groups A or B and control group at 48 h (P ＞ 0.05).The proliferation of osteoblasts in the experimental group C was significantly reduced as compared with other groups at 48 h (P ＜ 0.01 ).Meanwhile the titanium alloy particles up-regulated the mRNA and protein expression of RANKL ( P ＜ 0.01 ).Conclusion The proliferation of osteoblasts is decreased with exposure to titanium particles and different concentrations of titanium alloy particles could up-regulate the mRNA and protein expression of RANKL,which may be one of the mechamisms for the periprosthetic osteolysis. Key words: Titanium alloy particles; Osteoblast; Nuclear factor-κB; Osteolysis

Low-Dose Captopril Inhibits Wear Debris-Induced Inflammatory Osteolysis

The role of captopril in titanium alloy particle-induced inflammatory osteolysis was investigated. BALB/c mice (n = 32) were divided into four groups, an untreated control group and three treatment groups given 12.5, 25 or 50 mg/kg per day captopril. Intraperitoneal injections of either 0.9% saline (control) or captopril began 2 days before the introduction of titanium alloy particles and calvaria bone from a syngeneic mouse into established air pouches. Mice were sacrificed 10 days after bone/titanium alloy implantation, and pouch membranes and implants were collected for histological and molecular analysis. Low-dose captopril (12.5 mg/kg per day) was found to inhibit titanium particle-induced tissue inflammation and inflammatory osteolysis. Pouch membrane thickness and inflammatory cellular infiltration were significantly reduced relative to controls. Captopril also inhibited production of the inflammatory cytokines tumour necrosis factor-α, interleukin-1β and receptor activator of nuclear factor-κB ligand compared with controls. This study provides evidence that a low-dose of captopril can inhibit titanium particle-induced inflammatory osteolysis.

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

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 co-cultured 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 CD68+ cells within the xenograft were significantly increased in mice transfused with PMMA and Ti-provoked PBMCs compared to the naïve 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). TRAP+ cells were found around bone chips in both activated-PBMCs groups, although markedly more aggregated TRAP+ 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 debris-containing prosthetic tissues. Particles-provoked PBMCs participated in and promoted the local inflammatory process, osteoclastogenesis, and bone resorption.

Tribochemical Component of Oxidizing Stress Development at Joint Replacement. Part I. Determination of Radical-Forming Ability of Wear Particles from Various Orthopaedic Materials

Using the model reaction of cumene oxidation the radical-forming ability of wear particles of some orthopaedic alloys and corundum ceramics were studied. It was revealed that wear particles from different alloys catalyzed cumene oxidation whereas particles of corundum ceramics were inert. Cobalt alloy wear particles were much more active as compared with the titanium alloy and stainless steel particles. Production of cobalt alloy by laser sintering reduced the radical-forming ability of its wear particles. Activity of cobalt wear particles was preserved for a long time after their formation and could considerably strengthen the development of oxidizing stress at joint arthroplasty. Detection of catalytic activity of orthopaedic alloys' wear particles requires studying of the influence of free radicals generated by tribochemical reaction upon implant components and biological tissues.

Transforming growth factor‐β activated kinase 1 signaling pathways regulate TNF‐α production by titanium alloy particles in RAW 264.7 cells

Implant particles may induce inflammatory response by activating the nuclear factor kappaB (NFkappaB) and mitogen activated protein kinases (MAPK). Previous studies have shown that these signaling pathways are involved in the transforming growth factor-beta activated kinase 1 (TAK1) in signaling cascades induced by the receptor activator of NFkappaB ligand (RANKL) and tumor necrosis factor-alpha (TNF-alpha) as well as interleukin-1beta (IL-1beta). In this study, the roles of the TAK1 pathway in the production of the pro-inflammatory cytokine TNF-alpha in RAW 264.7 cells exposed to titanium alloy particles were investigated. Endogenous TAK1 was phosphorylated upon simulating RAW 264.7 cells by titanium alloy particles. The critical role for TAK1 in p38MAPK and NFkappaB activation was as well confirmed by the inhibition of p38MAPK and NFkappaB activity following 5Z-7-oxozeaenol, a selective inhibitor of TAK1. Furthermore, it was found that TNF-alpha was completely blocked by 5Z-7-oxozeaenol in RAW 264.7 cells. These results suggest that the TAK1-MAPK-NFkappaB signaling pathways may be a potential pharmacological target that can prevent instability for arthroplasty prosthesis.

Locally administered lentivirus-mediated siRNA inhibits wear debris-induced inflammation in murine air pouch model

Lentivirus(LV)-mediated small interfering RNA (siRNA) targeting tumor necrosis factor-alpha (TNF-alpha) was locally administered into the air pouch of mice to inhibit inflammation induced by titanium alloy particles. The lentiviral vector expressed green fluorescent protein (GFP) as a reporter gene. Down-regulation of TNF-alpha in pouch area was confirmed by real-time PCR and ELISA, resulting in significantly decreased local inflammatory responses (P < 0.01). This approach was proven safe by localized GFP fluorescence and invariant TNF-alpha expression in peripheral blood, liver, spleen, kidney, lung and brain of mouse. In conclusion, locally administered siRNA provides an effective and safe method for inhibiting particle-induced inflammation.

The spinal cord dura mater reaction to nitinol and titanium alloy particles: a 1-year study in rabbits

This investigation was undertaken to simulate in an animal model the particles released from a porous nitinol interbody fusion device and to evaluate its consequences on the dura mater, spinal cord and nerve roots, lymph nodes (abdominal para-aortic), and organs (kidneys, spleen, pancreas, liver, and lungs). Our objective was to evaluate the compatibility of the nitinol particles with the dura mater in comparison with titanium alloy. In spite of the great use of metallic devices in spine surgery, the proximity of the spinal cord to the devices raised concerns about the effect of the metal debris that might be released onto the neural tissue. Forty-five New Zealand white female rabbits were divided into three groups: nitinol (treated: N = 4 per implantation period), titanium (treated: N = 4 per implantation period), and sham rabbits (control: N = 1 per observation period). The nitinol and titanium alloy particles were implanted in the spinal canal on the dura mater at the lumbar level L2-L3. The rabbits were sacrificed at 1, 4, 12, 26, and 52 weeks. Histologic sections from the regional lymph nodes, organs, from remote and implantation sites, were analyzed for any abnormalities and inflammation. Regardless of the implantation time, both nitinol and titanium particles remained at the implantation site and clung to the spinal cord lining soft tissue of the dura mater. The inflammation was limited to the epidural space around the particles and then reduced from acute to mild chronic during the follow-up. The dura mater, sub-dural space, nerve roots, and the spinal cord were free of reaction. No particles or abnormalities were found either in the lymph nodes or in the organs. In contact with the dura, the nitinol elicits an inflammatory response similar to that of titanium. The tolerance of nitinol by a sensitive tissue such as the dura mater during the span of 1 year of implantation demonstrated the safety of nitinol and its potential use as an intervertebral fusion device.

Effects of titanium alloy particle on the expression of OPG in human osteoblasts in vitro

目的 研究钛合金颗粒对体外培养条件下的成骨细胞骨保护素(OPG)基因表达的影响,探讨人工关节假体松动中磨损颗粒导致的骨溶解机制.方法分别将不同浓度的钛合金颗粒(1、0.1、0.01 mg/mL)与第3～5代成骨细胞共同培养3、6、9 d,用RT-PCR方法半定量测定OPG基因mRNA的表达.结果不同浓度的钛合金颗粒均抑制成骨细胞OPG基因表达,各组与空白对照组比较差异有显著性意义(P＜0.01);存在一定的剂量、时间-效应关系,随时间延长,钛合金颗粒对OPG基因作用逐渐降低.结论 钛合金颗粒使成骨细胞OPG基因表达下降,使破骨细胞分化、活化功能增强,这可能是导致假体松动的骨溶解机制之一。

The impact of nanocolloidal wear‐particles on human mononuclear cells

AbstractThis article investigates the effects of metallic wear‐medium prepared from 316L stainless steel and titanium alloy (TiAl6V4) in vitro. Wear was generated by a tribometer, under sterile conditions, disc‐on‐pin submersed in cell culture medium. Wear medium was separated into a particle fraction (&gt;200 nm) and a nanocolloidal fraction (&lt; 200 nm). A standardized cell culture model was employed using isolated mononuclear cells from peripheral human blood cells were incubated with increasing amounts of wear medium containing particles or nanocolloids. Vitality was assayed using MTT and inflammatory reactions were measured by TNF‐α ELISA. In a second step wear‐medium was aged over two weeks in an incubator to simulate passivation of the implant / particle surfaces.Dose dependant toxic reactions induced by nanocolloids from titanium alloy and even more from stainless steel were identified with the vitality decreasing to 50 % compared to untreated cells. Nanocolloids did not induce inflammatory effects. Particles had no apparent toxic effects on cells. On the other hand, particles from titanium alloy induced a higher secretion of TNF‐α in the supernatants than 316L.Aged nanocolloids lost their toxic potential, but aged particles did still show a strong inflammatory reaction with titanium alloy being the stronger inflammatory agent.This study demonstrates that particles from titanium alloy can not be assumed as to be an inert biomaterial. In fact, titanium alloy particles induced a stronger inflammatory reaction rather than stainless steel. We conclude that both particles and nanocolloids show specific interactions with mononuclear cells in a sense of toxicity and inflammation. Furthermore, it seems to be of great importance to critically consider fabrication processes and age of particles used for cell culture settings in future research.

Does endotoxin contribute to aseptic loosening of orthopedic implants?

Aseptic loosening of orthopedic implants caused by wear particles is a major clinical problem. This review examines the hypothesis that bacterial endotoxin contributes to aseptic loosening. Clinical findings support this hypothesis: bacterial biofilms exist on many implants from patients with aseptic loosening and antibiotics in bone cement reduce the rate of aseptic loosening. Three approaches were used to demonstrate that adherent endotoxin increases bioactivity of titanium particles. These experiments measured cytokine production and osteoclast differentiation in vitro and murine calvarial osteolysis in vivo. First, removal of >99.9% of the adherent endotoxin from titanium particles significantly ablates their biological activity. Second, adding lipopolysaccharide back to these "endotoxin-free" particles restores their biological activity. Third, cells or mice that are genetically hyporesponsive to endotoxin are significantly less responsive to titanium particles than are wild-type controls. Other investigators have confirmed and extended these results to include virtually all orthopedically relevant types of particles, including authentic titanium alloy particles retrieved from patients with loosening. Our recent studies suggest that adherent endotoxin on orthopedic implants may also inhibit initial osseointegration of the implants. Taken together, these studies suggest that bacterial endotoxin may have a significant role in induction of aseptic loosening.

The role of implant alignment on stability and particles on periprosthetic osteolysis--A rabbit model of implant failure.

The study objective was to determine the tissue response to polyethylene and/or titanium particles and the role that these play in peri-prosthetic osteolysis in a rabbit model of implant failure. Twenty-two mature rabbits were used. Unilateral tibial arthroplasty was performed on all of them. The test animals received implants that were intentionally rotationally unstable with reference to the host tibia in order to create a model of failure. The test rabbits were divided into three groups. Group 1 consisted of seven rabbits in which only the carrier was implanted. Group 2 consisted of seven rabbits that received only polyethylene particles suspended in the carrier. Group 3 consisted of eight rabbits that received a mixture of polyethylene and titanium alloy particles suspended in the carrier. The rabbits were sacrificed at 6 months post surgery. The entire knee, together with the immediately surrounding soft tissue, was retrieved. The position of the implant in each rabbit was assessed with reference to its alignment to the tibia. The number of inflammatory, foreign-body reactive cells, the presence of neovascularization, edema, and necrosis in the periprosthetic zones were recorded and assessed in a qualitative and semiquantitative manner. Quantitative histomorphometry was used to determine the proportion of implant surface that interfaced with osseous or fibrous tissue. Also assessed was the thickness and maturity of the fibrous tissue and the endosteal remodeling activity in the peri-implant bone counting both osteoclastic and osteoblastic activity. The results showed that implanted particles and misalignment of the implants combined to produce peri-prosthetic bone resorption. Bone resorption was found to be proportional to the degree of misalignment. The animals that received combined polyethylene/titanium particles had a greater degree of foreign-body and inflammatory response with osteolysis than the other groups. The combination of bio-material particles (polyethylene and titanium alloy) produced a greater degree of bone resorption than the single biomaterial particles (polyethylene). The amount of bone resorption surrounding the implant was directly proportional to the degree of misalignment of the implant.

93. Spinal cord reaction to nitinol and titanium alloy particles: a 1-year study in rabbits

93. Spinal cord reaction to nitinol and titanium alloy particles: a 1-year study in rabbits