Nanochannels formed on TiZr alloy improve biological response

Ion, Raluca; Stoian, Andrei Bogdan; Dumitriu, Cristina; Grigorescu, Sabina; Mazare, Anca; Cîmpean, Anișoara; Demetrescu, Ioana; Schmuki, Patrik

doi:10.1016/j.actbio.2015.06.016

Cited by 40 publications

(37 citation statements)

References 50 publications

(73 reference statements)

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“…This effect causes the risk of aseptic inflammation, which may result in implant loosening. Based on multiple retrieval studies, macrophages can play significant roles in determining the duration and intensity of the inflammatory response and in the mechanism behind implant failure [11][12][13]. Many coating materials and bone substitute materials can activate macrophages at the bone-implant interface, possibly leading to bone resorption and implant failure [14,15].…”

Section: Introductionmentioning

confidence: 99%

Exposure of the murine RAW 264.7 macrophage cell line to dicalcium silicate coating: assessment of cytotoxicity and pro-inflammatory effects

Chen

Liu

Wei

et al. 2016

J Mater Sci: Mater Med

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Inflammatory effects are significant elements of the immune response to biomaterials. Previously, we reported inflammatory effects in response to dicalcium silicate (Ca2SiO4, C2S) particles. However, the immunological effects of C2S coatings have not been studied. C2S often used as coatings materials in orthopedic and dentistry applications. It may have different effect from C2S particles. Further, it remains unclear whether C2S coating is equally biocompatible as 45S5 coating. The aim of this study was to test the cytotoxicity and pro-inflammatory effects of C2S coating on RAW 264.7 macrophages. C2S and 45S5 coatings were characterized using scanning electron microscopy (SEM), atomic force microscopy (AFM), energy dispersive analysis (EDS) and X-ray diffraction (XRD). inductively coupled plasma optical emission spectroscopy (ICP-OES) was used to detect ionic concentrations after soaking coated discs in medium. The cytotoxicity of C2S and 45S5 coatings against RAW 264.7 macrophages was measured using the LDH Cytotoxicity Assay Kit, Cell Counting Kit-8 (CCK-8) assays and flow cytometry for apoptosis assays. The gene and protein expression of TNF-α, IL-6 and IL-1β were detected using RT-q PCR and ELISA, respectively. The tested coating materials are not cytotoxic to macrophages. The C2S-coated surface stimulated macrophages to express pro-inflammatory mediators, such as TNF-α, IL-6 and IL-1β, and C2S coating caused less IL-6 but greater IL-1β production than the 45S5 coating. C2S coating have no cytotoxicity when directly cultured with macrophages. C2S and 45S5 coatings both have the potential to induce pro-inflammatory effects, and the biocompatibility of C2S is similar to that of 45S5.

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Section: Introductionmentioning

confidence: 99%

Exposure of the murine RAW 264.7 macrophage cell line to dicalcium silicate coating: assessment of cytotoxicity and pro-inflammatory effects

Chen

Liu

Wei

et al. 2016

J Mater Sci: Mater Med

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“…4,[26][27][28] Studies investigating the surface-dependent inflammatory responses have shown that nanostructured surfaces are able to mitigate the activation of macrophages by reducing the secretion of the pro-inflammatory mediators. [29][30][31][32][33][34] Moreover, surface nanostructuring of Ti (or Ti alloys) can be easily performed by electrochemical anodization, resulting in nanotubular structures directly coated on the Ti substrate. 35 For TiO 2 nanotubes, the activation of macrophages was shown to depend on the nanotopography, that is the diameter of the nanotubes is the key morphological parameter influencing inflammatory responses (from diameters ranging from 30 to 100 nm, the 70 nm showed the weakest inflammatory response).…”

Section: Introductionmentioning

confidence: 99%

Attenuation of the macrophage inflammatory activity by TiO2 nanotubes via inhibition of MAPK and NF-κB pathways

Neacsu¹,

Mazare²,

Schmuki³

et al. 2015

IJN

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Biomaterial implantation in a living tissue triggers the activation of macrophages in inflammatory events, promoting the transcription of pro-inflammatory mediator genes. The initiation of macrophage inflammatory processes is mainly regulated by signaling proteins of mitogen-activated protein kinase (MAPK) and by nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) pathways. We have previously shown that titania nanotubes modified Ti surfaces (Ti/TiO 2 ) mitigate the immune response, compared with flat Ti surfaces; however, little is known regarding the underlying mechanism. Therefore, the aim of this study is to investigate the mechanism(s) by which this nanotopography attenuates the inflammatory activity of macrophages. Thus, we analyzed the effects of TiO 2 nanotubes on the activation of MAPK and NF-κB signaling pathways in standard and lipopolysaccharide-evoked conditions. Results showed that the Ti/TiO 2 significantly reduce the expression levels of the phosphorylated forms of p38, ERK1/2, c-Jun NH 2 -terminal kinase (JNK), IKKβ, and IkB-α. Furthermore, a significant reduction in the p65 nuclear accumulation on the nanotubular surface was remarked. Following, by using specific MAPK inhibitors, we observed that lipopolysaccharide-induced production of monocyte chemotactic protein-1 and nitric oxide was significantly inhibited on the Ti/TiO 2 surface via p38 and ERK1/2, but not via JNK. However, the selective inhibitor for JNK signaling pathway (SP600125) was effective in reducing tumor necrosis factor alpha release as well as monocyte chemotactic protein-1 and nitric oxide production. Altogether, these data suggest that titania nanotubes can attenuate the macrophage inflammatory response via suppression of MAPK and NF-κB pathways providing a potential mechanism for their anti-inflammatory activity.

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“…Nanochannels were formed on TiZr alloy pieces (2 cm × 2 cm) containing 50 wt % Ti and 50 wt % Zr (from ATI Wah Chang Co., Albany, OR, USA) as previously described [18]. Briefly, prior to anodization, TiZr pieces were chemically etched in a cold acid mixture (HNO 3 :HF:H 2 O in a 3:1:2 ratio) for 10 s, rinsed with deionized water (DI) and dried in a N 2 stream.…”

Section: Samples Preparation and Characterizationmentioning

confidence: 99%

“…The morphological and chemical characterization of the nanochannelar surface used in the present work was previously described [18]. Briefly, the morphology of nanochannels consists of~35 nm diameter and 3.2 ± 0.6 µm length (the top morphology is shown in Figure 1); note that the needle-like microstructure of the alloy is also transferred to the nanostructure.…”

Section: Materials Characterizationmentioning

confidence: 99%

“…On the other hand, micrometer thicknesses can be grown without observing a drop in the growth rate with time. In our previous study [18], we reported a simple, inexpensive method for the generation of mesoporous structures, i.e., aligned oxide nanochannels, on Ti50Zr alloy, by anodization in hot glycerol-phosphate electrolytes. Initial cell characterization revealed a reduced number of metabolically-active macrophages on nanochannels, a low potential to induce macrophage fusion into foreign body giant cells, and a low concentration of pro-inflammatory cytokines in the culture medium.…”

Section: Introductionmentioning

confidence: 99%

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Nanochannelar Topography Positively Modulates Osteoblast Differentiation and Inhibits Osteoclastogenesis

et al. 2018

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Based on previously reported findings showing reduced foreign body reactions on nanochannelar topography formed on TiZr alloy, this study explores the in vitro effects of such a nanostructured surface on cells relevant for implant osseointegration, namely osteoblasts and osteoclasts. We show that such nanochannelar surfaces sustain adhesion and proliferation of mouse pre-osteoblast MC3T3-E1 cells and enhance their osteogenic differentiation. Moreover, this specific nanotopography inhibits nuclear factor kappa-B ligand (RANKL)-mediated osteoclastogenesis. The nanochannels’ dual mode of action on the bone-derived cells could contribute to an enhanced bone formation around the bone implants. Therefore, these results warrant further investigation for nanochannels’ use as surface coatings of medical implant materials.

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Nanochannels formed on TiZr alloy improve biological response

Cited by 40 publications

References 50 publications

Exposure of the murine RAW 264.7 macrophage cell line to dicalcium silicate coating: assessment of cytotoxicity and pro-inflammatory effects

Exposure of the murine RAW 264.7 macrophage cell line to dicalcium silicate coating: assessment of cytotoxicity and pro-inflammatory effects

Attenuation of the macrophage inflammatory activity by TiO2 nanotubes via inhibition of MAPK and NF-κB pathways

Nanochannelar Topography Positively Modulates Osteoblast Differentiation and Inhibits Osteoclastogenesis

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Nanochannels formed on TiZr alloy improve biological response

Cited by 40 publications

References 50 publications

Exposure of the murine RAW 264.7 macrophage cell line to dicalcium silicate coating: assessment of cytotoxicity and pro-inflammatory effects

Exposure of the murine RAW 264.7 macrophage cell line to dicalcium silicate coating: assessment of cytotoxicity and pro-inflammatory effects

Attenuation of the macrophage inflammatory activity by TiO2 nanotubes via inhibition of MAPK and NF-&kappa;B pathways

Nanochannelar Topography Positively Modulates Osteoblast Differentiation and Inhibits Osteoclastogenesis

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Attenuation of the macrophage inflammatory activity by TiO2 nanotubes via inhibition of MAPK and NF-κB pathways