This paper investigates the self-loosening of threaded fasteners subjected to dynamic shear load. Three kinds of typical coatings, PTFE, MoS_2, and TiN applied to bolts and nuts, are tested in this investigation. The ...This paper investigates the self-loosening of threaded fasteners subjected to dynamic shear load. Three kinds of typical coatings, PTFE, MoS_2, and TiN applied to bolts and nuts, are tested in this investigation. The study experimentally examines the loosening mechanisms of fasteners and assesses the anti-loosening performance of the three tested coatings based on their tightening characteristics, loosening curves, and the damage of thread surface. Additionally, the anti-loosening performance of the three coatings is compared under different load forms. The results indicate that the PTFE and MoS_2 coatings have significant anti-loosening effect, whereas the anti-loosening performance of Ti N coating is not satisfactory. It is also found that an appropriate increase of the initial tightening torque can significantly improve the anti-loosening effect. In addition, the microscopic analyses of PTFE and MoS2 coating reveal that a reduced initial tightening torque leads to fretting wear on the thread contact surfaces of fasteners, thereby aggravating the damage.展开更多
为改善振动条件下螺纹紧固件抵抗松动能力,在紧固件横向振动试验装置上,测试了微粒子喷丸未处理及处理镀锌紧固件的抗松动能力,使用扫描电镜观察测量了试验前、后螺纹面磨损形貌和尺寸,建立了考虑螺纹面磨损深度的紧固件刚度模型,利用...为改善振动条件下螺纹紧固件抵抗松动能力,在紧固件横向振动试验装置上,测试了微粒子喷丸未处理及处理镀锌紧固件的抗松动能力,使用扫描电镜观察测量了试验前、后螺纹面磨损形貌和尺寸,建立了考虑螺纹面磨损深度的紧固件刚度模型,利用该模型计算分析了磨损深度改变对预紧力的影响.结果表明:未喷丸紧固件预紧力耐久极限为2.8 k N,喷丸紧固件为2.0 k N,未喷丸紧固件抗松动能力低于喷丸紧固件,未喷丸紧固件螺纹面发生严重磨损,喷丸紧固件螺纹面磨损轻微;螺纹面磨损深度随着滑移距离的增加而增加,紧固件预紧力随着螺纹面磨损深度的增加先呈线性降低,随后降低速度逐渐加快.螺纹面磨损降低了紧固件抵抗松动的能力.展开更多
There is convincing evidence that particles produced by the wear of joint prostheses are causal in the periprosthetic loss of bone,or osteolysis,which,if it progresses,leads to the phenomenon of aseptic loosening.It i...There is convincing evidence that particles produced by the wear of joint prostheses are causal in the periprosthetic loss of bone,or osteolysis,which,if it progresses,leads to the phenomenon of aseptic loosening.It is important to fully understand the biology of this bone loss because it threatens prosthesis survival,and loosened implants can result in peri-prosthetic fracture,which is disastrous for the patient and presents a difficult surgical scenario.The focus of this review is the bioactivity of polyethylene(PE)particles,since there is evidence that these are major players in the development and progression of osteolysis around prostheses which use PE as the bearing surface.The review describes the biological consequences of interaction of PE particles with macrophages,osteoclasts and cells of the osteoblast lineage,including osteocytes.It explores the possible cellular mechanisms of action of PE and seeks to use the findings to date to propose potential nonsurgical treatments for osteolysis.In particular,a nonsurgical approach is likely to be applicable to implants containing newer,highly cross-linked PEs(HXLPEs),for which osteolysis seems to occur with much reduced PE wear compared with conventional PEs.The caveat here is that we know little as yet about the bioactivity of HXLPE particles and addressing this constitutes our next challenge.展开更多
Historically, the most common mechanism of total kneearthroplasty(TKA) failures included aseptic loosening, instability and malalignment. As polyethylene production improved, modes of failure from polyethylene wear an...Historically, the most common mechanism of total kneearthroplasty(TKA) failures included aseptic loosening, instability and malalignment. As polyethylene production improved, modes of failure from polyethylene wear and subsequent osteolysis became less prevalent. Newer longitudinal studies report that infection has become the primary acute cause of failure with loosening and instability remaining as the overall greatest reasons for revision. Clinical database and worldwide national registries confirm these reports. With an increasing amount of TKA operations performed in the United States, and with focus on value-based healthcare, it is imperative to understand why total knees fail.展开更多
Aseptic prosthesis loosening(APL)is one of the most prevalent complications associated with arthroplasty.The main cause is the periprosthetic osteolysis induced by wear particles.However,the specific mechanisms of cro...Aseptic prosthesis loosening(APL)is one of the most prevalent complications associated with arthroplasty.The main cause is the periprosthetic osteolysis induced by wear particles.However,the specific mechanisms of crosstalk between immune cells and osteoclasts/osteoblasts during osteolysis are unclear.In this study,we report the role and mechanism of macrophage-derived exosomes in wear particle-induced osteolysis.The results of exosomes up-taken experiments revealed that osteoblast and mature osteoclasts capture macrophage-derived exosomes(M-Exo).Next-generation sequencing and RT-qPCR on M-Exo revealed that exosomal microRNA miR-3470b was downregulated in wear particle-induced osteolysis.The results of analysis on Luciferase reporter assays/fluorescence in situ hybridization(FISH)/immunofluorescence(IF)/immunohistochemistry(IHC)and co-culture experiments demonstrated that wear particles induced osteoclast differentiation by increasing the expression of NFatc1 via M-Exo miR-3470b targeting TAB3/NF-κB signaling.We also illustrate that engineered exosomes enriching miR-3470b facilitated to suppressed the osteolysis;the microenvironment enriching with miR-3470b could suppress wear particle-induced osteolysis via inhibition of TAB3/NF-κB in vivo.In summary,our findings indicate that macrophage-derived exosomes transfer to osteoclasts to induce osteolysis in wear particle-induced APL.Engineering exosomes enriching with miR-3470b might be a novel strategy for the targeting treatment of bone resorption-related diseases.展开更多
基金the financial support provided by the National Science Funds for Distinguished Young Scholars(No.51025519)the Changjiang Scholarships and Innovation Team Development Plan(No.IRT1178)the Self-Topic Fund of Traction Power State Key Laboratory(No.2016TPL-Z03)
文摘This paper investigates the self-loosening of threaded fasteners subjected to dynamic shear load. Three kinds of typical coatings, PTFE, MoS_2, and TiN applied to bolts and nuts, are tested in this investigation. The study experimentally examines the loosening mechanisms of fasteners and assesses the anti-loosening performance of the three tested coatings based on their tightening characteristics, loosening curves, and the damage of thread surface. Additionally, the anti-loosening performance of the three coatings is compared under different load forms. The results indicate that the PTFE and MoS_2 coatings have significant anti-loosening effect, whereas the anti-loosening performance of Ti N coating is not satisfactory. It is also found that an appropriate increase of the initial tightening torque can significantly improve the anti-loosening effect. In addition, the microscopic analyses of PTFE and MoS2 coating reveal that a reduced initial tightening torque leads to fretting wear on the thread contact surfaces of fasteners, thereby aggravating the damage.
文摘为改善振动条件下螺纹紧固件抵抗松动能力,在紧固件横向振动试验装置上,测试了微粒子喷丸未处理及处理镀锌紧固件的抗松动能力,使用扫描电镜观察测量了试验前、后螺纹面磨损形貌和尺寸,建立了考虑螺纹面磨损深度的紧固件刚度模型,利用该模型计算分析了磨损深度改变对预紧力的影响.结果表明:未喷丸紧固件预紧力耐久极限为2.8 k N,喷丸紧固件为2.0 k N,未喷丸紧固件抗松动能力低于喷丸紧固件,未喷丸紧固件螺纹面发生严重磨损,喷丸紧固件螺纹面磨损轻微;螺纹面磨损深度随着滑移距离的增加而增加,紧固件预紧力随着螺纹面磨损深度的增加先呈线性降低,随后降低速度逐渐加快.螺纹面磨损降低了紧固件抵抗松动的能力.
文摘There is convincing evidence that particles produced by the wear of joint prostheses are causal in the periprosthetic loss of bone,or osteolysis,which,if it progresses,leads to the phenomenon of aseptic loosening.It is important to fully understand the biology of this bone loss because it threatens prosthesis survival,and loosened implants can result in peri-prosthetic fracture,which is disastrous for the patient and presents a difficult surgical scenario.The focus of this review is the bioactivity of polyethylene(PE)particles,since there is evidence that these are major players in the development and progression of osteolysis around prostheses which use PE as the bearing surface.The review describes the biological consequences of interaction of PE particles with macrophages,osteoclasts and cells of the osteoblast lineage,including osteocytes.It explores the possible cellular mechanisms of action of PE and seeks to use the findings to date to propose potential nonsurgical treatments for osteolysis.In particular,a nonsurgical approach is likely to be applicable to implants containing newer,highly cross-linked PEs(HXLPEs),for which osteolysis seems to occur with much reduced PE wear compared with conventional PEs.The caveat here is that we know little as yet about the bioactivity of HXLPE particles and addressing this constitutes our next challenge.
文摘Historically, the most common mechanism of total kneearthroplasty(TKA) failures included aseptic loosening, instability and malalignment. As polyethylene production improved, modes of failure from polyethylene wear and subsequent osteolysis became less prevalent. Newer longitudinal studies report that infection has become the primary acute cause of failure with loosening and instability remaining as the overall greatest reasons for revision. Clinical database and worldwide national registries confirm these reports. With an increasing amount of TKA operations performed in the United States, and with focus on value-based healthcare, it is imperative to understand why total knees fail.
基金supported by the National Natural Science Foundation of China[grant numbers 82172405,81972050,81802179].
文摘Aseptic prosthesis loosening(APL)is one of the most prevalent complications associated with arthroplasty.The main cause is the periprosthetic osteolysis induced by wear particles.However,the specific mechanisms of crosstalk between immune cells and osteoclasts/osteoblasts during osteolysis are unclear.In this study,we report the role and mechanism of macrophage-derived exosomes in wear particle-induced osteolysis.The results of exosomes up-taken experiments revealed that osteoblast and mature osteoclasts capture macrophage-derived exosomes(M-Exo).Next-generation sequencing and RT-qPCR on M-Exo revealed that exosomal microRNA miR-3470b was downregulated in wear particle-induced osteolysis.The results of analysis on Luciferase reporter assays/fluorescence in situ hybridization(FISH)/immunofluorescence(IF)/immunohistochemistry(IHC)and co-culture experiments demonstrated that wear particles induced osteoclast differentiation by increasing the expression of NFatc1 via M-Exo miR-3470b targeting TAB3/NF-κB signaling.We also illustrate that engineered exosomes enriching miR-3470b facilitated to suppressed the osteolysis;the microenvironment enriching with miR-3470b could suppress wear particle-induced osteolysis via inhibition of TAB3/NF-κB in vivo.In summary,our findings indicate that macrophage-derived exosomes transfer to osteoclasts to induce osteolysis in wear particle-induced APL.Engineering exosomes enriching with miR-3470b might be a novel strategy for the targeting treatment of bone resorption-related diseases.
