scholarly journals The Role of TLR and Chemokine in Wear Particle-Induced Aseptic Loosening

2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Qiaoli Gu ◽  
Qin Shi ◽  
Huilin Yang
Keyword(s):  
Inflammatory Response ◽  
Aseptic Loosening ◽  
Osteoclast Differentiation ◽  
Adaptor Protein ◽  
Wear Particle ◽  
Cellular Migration ◽  
Cellular Interaction ◽  
Wear Particles ◽  
Orthopaedic Implants ◽  
Inhibitory Protein

Wear particle-induced periprosthetic osteolysis remains the principal cause of aseptic loosening of orthopaedic implants. Monocytes/macrophages phagocytose wear particles and release cytokines that induce inflammatory response. This response promotes osteoclast differentiation and osteolysis. The precise mechanisms by which wear particles are recognized and induce the accumulation of inflammatory cells in the periprosthetic tissue have not been fully elucidated. Recent studies have shown that toll-like receptors (TLRs) contribute to the cellular interaction with wear particles. Wear particles are recognized by monocytes/macrophages through TLRs coupled with the adaptor protein MyD88. After the initial interaction, wear particles induce both local and systemic migration of monocytes/macrophages to the periprosthetic region. The cellular migration is mediated through chemokines including interleukin-8, macrophage chemotactic protein-1, and macrophage inhibitory protein-1 in the periprosthetic tissues. Interfering with chemokine-receptor axis can inhibit cellular migration and inflammatory response. This paper highlights recent advances in TLR, and chemokine participated in the pathogenesis of aseptic loosening. A comprehensive understanding of the recognition and migration mechanism is critical to the development of measures that prevent wear particle-induced aseptic loosening of orthopaedic implants.

scholarly journals The Recombinant Protein EphB4-Fc Changes the Ti Particle-Mediated Imbalance of OPG/RANKL via EphrinB2/EphB4 Signaling Pathway and Inhibits the Release of Proinflammatory Factors In Vivo

2020 ◽  
Vol 2020 ◽  
pp. 1-15
Author(s):  
Yu-Wei Ge ◽  
Kai Feng ◽  
Xiao-Liang Liu ◽  
Hong-Fang Chen ◽  
Zhen-Yu Sun ◽  
...  
Keyword(s):  
Recombinant Protein ◽  
Inflammatory Response ◽  
Signaling Pathway ◽  
Osteoclast Differentiation ◽  
Wear Particle ◽  
Enzyme Linked Immunosorbent Assay ◽  
Tartrate Resistant Acid Phosphatase ◽  
Wear Particles ◽  
Proinflammatory Factors

Aseptic loosening caused by wear particles is one of the common complications after total hip arthroplasty. We investigated the effect of the recombinant protein ephB4-Fc (erythropoietin-producing human hepatocellular receptor 4) on wear particle-mediated inflammatory response. In vitro, ephrinB2 expression was analyzed using siRNA-NFATc1 (nuclear factor of activated T-cells 1) and siRNA-c-Fos. Additionally, we used Tartrate-resistant acid phosphatase (TRAP) staining, bone pit resorption, Enzyme-linked immunosorbent assay (ELISA), as well as ephrinB2 overexpression and knockdown experiments to verify the effect of ephB4-Fc on osteoclast differentiation and function. In vivo, a mouse skull model was constructed to test whether the ephB4-Fc inhibits osteolysis and inhibits inflammation by micro-CT, H&E staining, immunohistochemistry, and immunofluorescence. The gene expression of ephrinB2 was regulated by c-Fos/NFATc1. Titanium wear particles activated this signaling pathway to the promoted expression of the ephrinB2 gene. However, ephrinB2 protein can be activated by osteoblast membrane receptor ephB4 to inhibit osteoclast differentiation. In in vivo experiments, we found that ephB4 could regulate Ti particle-mediated imbalance of OPG/RANKL, and the most important finding was that ephB4 relieved the release of proinflammatory factors. The ephB4-Fc inhibits wear particle-mediated osteolysis and inflammatory response through the ephrinB2/EphB4 bidirectional signaling pathway, and ephrinB2 ligand is expected to become a new clinical drug therapeutic target.

scholarly journals Novel biological strategies for treatment of wear particle-induced periprosthetic osteolysis of orthopaedic implants for joint replacement

2014 ◽  
Vol 11 (93) ◽  
pp. 20130962 ◽  
Author(s):  
S. B. Goodman ◽  
E. Gibon ◽  
J. Pajarinen ◽  
T.-H. Lin ◽  
M. Keeney ◽  
...  
Keyword(s):  
Pathologic Fracture ◽  
Wear Particle ◽  
Wear Particles ◽  
Implant Loosening ◽  
Orthopaedic Implants ◽  
Periprosthetic Osteolysis ◽  
Joint Replacements ◽  
Local Inhibition ◽  
Tissue Healing ◽  
Chronic Inflammatory Reaction

Wear particles and by-products from joint replacements and other orthopaedic implants may result in a local chronic inflammatory and foreign body reaction. This may lead to persistent synovitis resulting in joint pain and swelling, periprosthetic osteolysis, implant loosening and pathologic fracture. Strategies to modulate the adverse effects of wear debris may improve the function and longevity of joint replacements and other orthopaedic implants, potentially delaying or avoiding complex revision surgical procedures. Three novel biological strategies to mitigate the chronic inflammatory reaction to orthopaedic wear particles are reported. These include (i) interference with systemic macrophage trafficking to the local implant site, (ii) modulation of macrophages from an M1 (pro-inflammatory) to an M2 (anti-inflammatory, pro-tissue healing) phenotype in the periprosthetic tissues, and (iii) local inhibition of the transcription factor nuclear factor kappa B (NF-κB) by delivery of an NF-κB decoy oligodeoxynucleotide, thereby interfering with the production of pro-inflammatory mediators. These three approaches have been shown to be viable strategies for mitigating the undesirable effects of wear particles in preclinical studies. Targeted local delivery of specific biologics may potentially extend the lifetime of orthopaedic implants.

STAT3/IL-6 dependent induction of inflammatory response in osteoblast and osteoclast formation in nanoscale wear particle-induced aseptic prosthesis loosening

2021 ◽  
Author(s):  
Zhantao Deng ◽  
Ruiying Zhang ◽  
Mengyuan Li ◽  
Shuai Wang ◽  
Guangtao Fu ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Inflammatory Responses ◽  
Wear Particle ◽  
Osteoclast Formation ◽  
Wear Particles ◽  
Rankl Expression ◽  
Prosthesis Loosening ◽  
Aseptic Prosthesis Loosening ◽  
Nanoscale Wear

Our study demonstrated wear particles, which are generated by the abrasion of implanted prostheses, could induced STAT3 activation in osteoblasts. And further, inflammatory responses and RANKL expression would activate osteoclasts and cause osteolysis.

scholarly journals Lipopolysaccharide induces neuroinflammation in microglia by activating the MTOR pathway and downregulating Vps34 to inhibit autophagosome formation

2020 ◽  
Vol 17 (1) ◽  
Author(s):  
Xiaoxia Ye ◽  
Mingming Zhu ◽  
Xiaohang Che ◽  
Huiyang Wang ◽  
Xing-Jie Liang ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Microglial Activation ◽  
Adaptor Protein ◽  
Mtor Pathway ◽  
Microglial Cells ◽  
Inflammatory Factors ◽  
Intraventricular Injection ◽  
Enzyme Linked Immunosorbent Assay ◽  
Autophagic Flux

Abstract Background Microglial activation is a prominent feature of neuroinflammation, which is present in almost all neurodegenerative diseases. While an initial inflammatory response mediated by microglia is considered to be protective, excessive pro-inflammatory response of microglia contributes to the pathogenesis of neurodegeneration. Although autophagy is involved in the suppression of inflammation, its role and mechanism in microglia are unclear. Methods In the present study, we studied the mechanism by which lipopolysaccharide (LPS) affects microglial autophagy and the effects of autophagy on the production of pro-inflammatory factors in microglial cells by western blotting, immunocytochemistry, transfection, transmission electron microscopy (TEM), and real-time PCR. In a mouse model of neuroinflammation, generated by intraventricular injection of LPS (5 μg/animal), we induced autophagy by rapamycin injection and investigated the effects of enhanced autophagy on microglial activation by enzyme-linked immunosorbent assay (ELISA) and immunohistochemistry. Results We found that autophagic flux was suppressed in LPS-stimulated N9 microglial cells, as evidenced by decreased expression of the autophagy marker LC3-II (lipidated form of MAP1LC3), as well as increased levels of the autophagy adaptor protein SQSTM1. LPS significantly decreased Vps34 expression in N9 microglial cells by activating the PI3KI/AKT/MTOR pathway without affecting the levels of lysosome-associated proteins and enzymes. More importantly, overexpression of Vps34 significantly enhanced the autophagic flux and decreased the accumulation of SQSTM1 in LPS-stimulated N9 microglial cells. Moreover, our results revealed that an LPS-induced reduction in the level of Vps34 prevented the maturation of omegasomes to phagophores. Furthermore, LPS-induced neuroinflammation was significantly ameliorated by treatment with the autophagy inducer rapamycin both in vitro and in vivo. Conclusions These data reveal that LPS-induced neuroinflammation in N9 microglial cells is associated with the inhibition of autophagic flux through the activation of the PI3KI/AKT/MTOR pathway, while enhanced microglial autophagy downregulates LPS-induced neuroinflammation. Thus, this study suggests that promoting the early stages of autophagy might be a potential therapeutic approach for neuroinflammation-associated diseases.

Brake Wear Particle Size and Shape Analysis of Non-Asbestos Organic (NAO) and Semi Metallic Brake Pad

2014 ◽  
Vol 71 (2) ◽  
Author(s):  
Hussain, S. ◽  
M.K Abdul Hamid ◽  
A.R Mat Lazim ◽  
A.R. Abu Bakar
Keyword(s):  
Particle Size ◽  
Wear Particle ◽  
Brake Disc ◽  
Wear Particles ◽  
Brake Pad ◽  
Brake Pads ◽  
Size And Shape ◽  
Brake Wear Particles ◽  
Brake Wear ◽  
Particle Size And Shape

Brake wear particles resulting from friction between the brake pad and disc are common in brake system. In this work brake wear particles were analyzed based on the size and shape to investigate the effects of speed and load applied to the generation of brake wear particles. Scanning electron microscopy (SEM) with energy-dispersive X-ray spectroscopy (EDX) was used to identify the size, shape and element compositions of these particles. Two types of brake pads were studied which are non-asbestos organic and semi metallic brake pads. Results showed that the size and shape of the particles generatedvary significantly depending on the applied brake load, and less significantly on brake disc speed. The wear particle becomes bigger with increasing applied brake pressure. The wear particle size varies from 300 nm to 600 µm, and contained elements such as carbon, oxygen, magnesium, aluminum, sulfur and iron.

scholarly journals A simple method of suspending implant wear particles for more physiological modelling of cell-particle interactions in vitro

2021 ◽  
Author(s):  
Christine Poon
Keyword(s):  
Wear Debris ◽  
Culture Media ◽  
Polymeric Materials ◽  
Wear Particle ◽  
Physicochemical Characteristics ◽  
Wear Particles ◽  
Simple Method ◽  
Implant Wear

AbstractArthroplasty implants e.g. hip, knee, spinal disc sustain relatively high compressive loading and friction wear, which lead to the formation of wear particles or debris between articulating surfaces. Despite advances in orthopaedic materials and surface treatments, the production of wear debris from any part of a joint arthroplasty implant is currently unavoidable. Implant wear debris induces host immune responses and inflammation, which causes patient pain and ultimately implant failure through progressive inflammation-mediated osteolysis and implant loosening, where the severity and rate of periprosthetic osteolysis depends on the material and physicochemical characteristics of the wear particles. Evaluating the cytotoxicity of implant wear particles is important for regulatory approved clinical application of arthroplasty implants, as is the study of cell-particle response pathways. However, the wear particles of polymeric materials commonly used for arthroplasty implants tend to float when placed in culture media, which limits their contact with cell cultures. This study reports a simple means of suspending wear particles in liquid medium using sodium carboxymethyl cellulose (NaCMC) to provide a more realistic proxy of the interaction between cells and tissues to wear particles in vivo, which are free-floating in synovial fluid within the joint cavity. Low concentrations of NaCMC dissolved in culture medium were found to be effective for suspending polymeric wear particles. Such suspensions may be used as more physiologically-relevant means for testing cellular responses to implant wear debris, as well as studying the combinative effects of shear and wear particle abrasion on cells in a dynamic culture environments such as perfused tissue-on-chip devices.

Autophagy inhibitors 3-MA and LY294002 repress osteoclastogenesis and titanium particle-stimulated osteolysis

2021 ◽  
Author(s):  
Weishen Chen ◽  
Guoyan Xian ◽  
Minghui Gu ◽  
Baiqi Pan ◽  
Xiaoyu Wu ◽  
...  
Keyword(s):  
Aseptic Loosening ◽  
Joint Replacement ◽  
Revision Surgery ◽  
Wear Particle ◽  
Common Complication ◽  
Titanium Particle ◽  
Inflammation Response

Aseptic loosening caused by peri-implant osteolysis (PIO) is a common complication after joint replacement, and there is still no better treatment than revision surgery. The wear particle-induced inflammation response, especially...

scholarly journals IL-17B Can Impact on Endothelial Cellular Traits Linked to Tumour Angiogenesis

2010 ◽  
Vol 2010 ◽  
pp. 1-5 ◽  
Author(s):  
Andrew J. Sanders ◽  
Xiaoxia Guo ◽  
Malcolm D. Mason ◽  
Wen G. Jiang
Keyword(s):  
Rheumatoid Arthritis ◽  
Endothelial Cell ◽  
Inflammatory Response ◽  
Cellular Migration ◽  
Tumour Angiogenesis ◽  
Tubule Formation ◽  
Founding Member ◽  
Cell Matrix ◽  
Cell Matrix Adhesion

IL-17B is a member of the IL-17 cytokine family which have been implicated in inflammatory response and autoimmune diseases such as rheumatoid arthritis. The founding member of this family, IL-17 (or IL-17A), has also been implicated in promoting tumour angiogenesis through the induction of other proangiogenic factors. Here we examine the potential of recombinant human IL-17B to contribute to the angiogenic process. In vitro rhIL-17B was able to inhibit HECV endothelial cell-matrix adhesion and cellular migration and also, at higher concentrations, could substantially reduce tubule formation compared to untreated HECV cells in a Matrigel tubule formation assay. This data suggests that IL-17B may act in an antiangiogenic manner.

scholarly journals Magnetic Properties of Ferromagnetic Particles under Alternating Magnetic Fields: Focus on Particle Detection Sensor Applications

Sensors ◽  
2018 ◽  
Vol 18 (12) ◽  
pp. 4144 ◽  
Author(s):  
Ran Jia ◽  
Biao Ma ◽  
Changsong Zheng ◽  
Liyong Wang ◽  
Xin Ba ◽  
...  
Keyword(s):  
Magnetic Energy ◽  
Coupling Effect ◽  
Interparticle Distance ◽  
Magnetic Coupling ◽  
Wear Particle ◽  
Effective Field ◽  
Wear Particles ◽  
Force Output ◽  
Field Frequency ◽  
Sensor Applications

The electromagnetic wear particles detection sensor has been widely studied due to its ability to monitor the wear status of equipment in real time. To precisely estimate the change of the magnetic energy of the sensor coil caused by the wear particles, the magnetic property models of wear particles under the alternating magnetic field was established. The models consider the hysteresis effect and the eddy current effect of the wear particles. The analysis and experimental results show that with the increase of the effective field frequency, the change of the magnetic energy caused by the wear particles gradually decrease, which makes the induced electromotive force output by the sensor reduce with the decrease of the particle speed, so a signal compensation method is presented to obtain a unified signal when the same wear particle passing through the sensor in different speeds. The magnetic coupling effect between the two adjacent wear particles is analyzed. The result illustrates that the change of the magnetic energy caused by the dual wear particles system is larger than the sum of the energy variation caused by two independent wear particles, and with the increase of the interparticle distance, the magnetic coupling effect gradually weakens and disappears.

Biological reaction to debris in relation to joint prostheses

1997 ◽  
Vol 211 (2) ◽  
pp. 187-197 ◽  
Author(s):  
P A Revell ◽  
N AL-Saffar ◽  
A Kobayashi
Keyword(s):  
Bone Resorption ◽  
Bone Loss ◽  
Inflammatory Response ◽  
Joint Replacement ◽  
Total Joint Replacement ◽  
Wear Particles ◽  
Cellular Reaction ◽  
Biological Reaction ◽  
Joint Prostheses

Bone loss induced by the inflammatory response to wear particles is a major cause of long-term failure of total joint replacement. This review describes the cellular reaction occurring in response to these particles and what is currently known about the inflammatory mechanisms contributing to bone resorption.

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