Wear particles induce a new macrophage phenotype with the potential to accelerate material corrosion within total hip replacement interfaces

Bijukumar, Divya; Salunkhe, Shruti; Zheng, Guoxing; Barba, Mark; Hall, D. W.; Pourzal, Robin; Mathew, Mathew T.

doi:10.1016/j.actbio.2019.10.039

Cited by 42 publications

(23 citation statements)

References 52 publications

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“…Bijukumar et al in a recent study also indicate the presence of similar features with a similar size distribution within head-neck tapers on retrieved devices. 41 In future work, retrieved devices with well-preserved biological material can be analyzed through sputter-coated SEM analysis 42 or Fourier transform infra-red spectroscopy (FTIR). 43 Scharf et al published findings from periprosthetic retrieved tissue histology that show corrosion debris phagocytosed by a macrophage cell.…”

Section: Discussionmentioning

confidence: 99%

Nontribological corrosion modes dominate wrought CoCrMo acetabular taper corrosion: A retrieval study

2021

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Corrosion of modular metal-on-metal acetabular tapers in total hip arthroplasty (THA) systems is often attributed to mechanically driven processes. Recent findings suggest that mechanically assisted crevice corrosion (MACC) might not be the dominant cause of corrosion in shell-liner tapers. This study aims to document and present the corrosion modes observed in metal-metal acetabular liners. Twenty-one retrieved wrought CoCrMo liners were examined using digital optical microscopy (DOM), scanning electron microscopy (SEM) and energy dispersive x-ray spectroscopy (EDS). Corrosion-related damage was documented in nonengagement taper regions, outside of direct taper contact. Within engagement regions, nonmechanically driven corrosion features (pitting, intergranular corrosion) were observed adjacent to fretting and material transfer, which rely on mechanical contact; corrosion independent of MACC was observed even in contact regions. Corrosion types observed included intergranular corrosion (IGC), pitting attack, phase boundary dissolution, all both outside and inside of taper junctions, and MACC within contact regions of the taper. Typical fretting scars associated with MACC were mostly absent, and were not always associated with corrosion damage where present. Finally, hard phase particles (Mo-Si-O) released from the wrought CoCrMo microstructure had redeposited within regions with material loss. Acetabular taper corrosion modes differ significantly from those in head-neck tapers and are dominated by electrochemically driven processes, not mechanical processes, as indicated by corrosion in noncontact regions. With greater prevalence of dual mobility hip implants, acetabular taper corrosion processes must be understood in order to limit their impact on device performance.

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Section: Discussionmentioning

confidence: 99%

Nontribological corrosion modes dominate wrought CoCrMo acetabular taper corrosion: A retrieval study

2021

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“…Macrophages in areas of inflammatory tissue are derived from monocytes in the bloodstream. Activated macrophages can be categorized into the M1 phenotype (classically activated macrophage phenotype) and the M2 phenotype (alternative activated macrophage phenotype) [ 22 ]. In the presence of interferon γ (IFN- γ ) and lipopolysaccharide (LPS), macrophages polarize toward the M1 phenotype.…”

Section: Exosomes and Macrophage Polarizationmentioning

confidence: 99%

Exosome: Function and Application in Inflammatory Bone Diseases

Wang

Chen

et al. 2021

Oxidative Medicine and Cellular Longevity

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In the skeletal system, inflammation is closely associated with many skeletal disorders, including periprosthetic osteolysis (bone loss around orthopedic implants), osteoporosis, and rheumatoid arthritis. These diseases, referred to as inflammatory bone diseases, are caused by various oxidative stress factors in the body, resulting in long-term chronic inflammatory processes and eventually causing disturbances in bone metabolism, increased osteoclast activity, and decreased osteoblast activity, thereby leading to osteolysis. Inflammatory bone diseases caused by nonbacterial factors include inflammation- and bone resorption-related processes. A growing number of studies show that exosomes play an essential role in developing and progressing inflammatory bone diseases. Mechanistically, exosomes are involved in the onset and progression of inflammatory bone disease and promote inflammatory osteolysis, but specific types of exosomes are also involved in inhibiting this process. Exosomal regulation of the NF-κB signaling pathway affects macrophage polarization and regulates inflammatory responses. The inflammatory response further causes alterations in cytokine and exosome secretion. These signals regulate osteoclast differentiation through the receptor activator of the nuclear factor-kappaB ligand pathway and affect osteoblast activity through the Wnt pathway and the transcription factor Runx2, thereby influencing bone metabolism. Overall, enhanced bone resorption dominates the overall mechanism, and over time, this imbalance leads to chronic osteolysis. Understanding the role of exosomes may provide new perspectives on their influence on bone metabolism in inflammatory bone diseases. At the same time, exosomes have a promising future in diagnosing and treating inflammatory bone disease due to their unique properties.

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“…At present, a growing body of evidence indicates that the functional polarization of macrophages into either M1 or M2 phenotype is a multifactorial process involving a large number of factors, which produces different activation scenarios [ 22 ]. Once macrophages adopt a specific phenotype, it will keep changing in order to adapt the new environment [ 23 ]. The reversible polarization exhibits certain therapeutic potential, particularly in diseases caused by the imbalance of M1/M2 macrophages [ 24 ].…”

Section: Discussionmentioning

confidence: 99%

LncRNA MEG8 sponging miR-181a-5p contributes to M1 macrophage polarization by regulating SHP2 expression in Henoch-Schonlein purpura rats

et al. 2021

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Background Long noncoding RNAs (LncRNAs) are regulatory molecules that play important roles in various biological and pathological processes. Herein, we aimed to explore whether maternally expressed gene 8 (MEG8) promotes M1 macrophage polarization among Henoch-Schonlein purpura (HSP) rats, and to investigate the underlying mechanism. Methods Relative mRNA expression of MEG8, miR-181a-5p and suppressor of SH2 domain-containing tyrosine phosphatase 2 (SHP2) were examined using quantitative reverse transcription polymerase chain reaction. Furthermore, expression of SHP2 and the Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) pathway-related proteins was identified using western blot. Luciferase activity assay was conducted to evaluate whether miR-181a-5p could bind to MEG8 or SHP2. The macrophage phenotype was determined using flow cytometry and enzyme-linked immunosorbent assay. Results We observed macrophage polarization towards the M2 phenotype in the peripheral blood of HSP rats. Furthermore, MEG8 and SHP2 expression were down-regulated, while miR-181a-5p was up-regulated in monocyte-derived macrophages from the HSP rats compared to the control group. Furthermore, MEG8 functioned as a sponge for miR-181a-5p in order to facilitate SHP2 expression. Moreover, miR-181a-5p mimic and SHP2 knockdown significantly reversed the MEG8 overexpression-mediated suppression of JAK2/STAT3 signalling, and promotion of M1 polarization. Conclusions The lncRNA MEG8 sponged miR-181a-5p, which contributes to M1 macrophage polarization by regulating SHP2 expression in HSP rats. Key Messages LncRNA MEG8 downregulation and M2 polarization in Henoch Schonlein purpura rats. MEG8 upregulation enhances M1 polarization and suppresses JAK2/STAT3 pathway. MEG8 sponges miRNA-181a-5p to regulate SHP2 expression. MiRNA-181a-5p upregulation reverses lncRNA MEG8-mediated enhancement of M1 polarization and inhibition of JAK2/STAT3 pathway. SHP2 downregulation reverses lncRNA MEG8-mediated enhancement of M1 polarization and inhibition of JAK2/STAT3 pathway.

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Wear particles induce a new macrophage phenotype with the potential to accelerate material corrosion within total hip replacement interfaces

Cited by 42 publications

References 52 publications

Nontribological corrosion modes dominate wrought CoCrMo acetabular taper corrosion: A retrieval study

Nontribological corrosion modes dominate wrought CoCrMo acetabular taper corrosion: A retrieval study

Exosome: Function and Application in Inflammatory Bone Diseases

LncRNA MEG8 sponging miR-181a-5p contributes to M1 macrophage polarization by regulating SHP2 expression in Henoch-Schonlein purpura rats

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