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In vivo immunomodulatory effects of different modified surfaces in a DM model. (A) Schematic representation of the animal modeling and experimental treatment workflow. (B, C) hematoxylin and eosin staining of the peri-implant tissues in the femurs of DM rats 1 week after implantation, accompanied by quantitative analysis of the fibrous capsule thickness (scale bar = 100 μm, n = 5). (D–G) Immunofluorescence staining evaluating the polarization state of macrophages surrounding the implants (green: macrophage marker cluster of differentiation (CD) 68; red: M1 marker CD86 and M2 marker CD206; blue: nuclei), along with corresponding quantitative analysis of the fluorescence signals (scale bar = 100 μm, n = 5). (H–K) Immunohistochemical staining assessing the expression of the pro-inflammatory marker <t>tumor</t> <t>necrosis</t> <t>factor-α</t> and the anti-inflammatory marker interleukin-10 in the peri-implant area, with quantitative results of the positive staining areas (scale bar = 100 μm, n = 5). Data are expressed as the mean ± standard deviation, with statistical analysis performed using one-way ANOVA and Tukey's post-hoc test. ∗p < 0.05, ∗∗p < 0.01, and ∗∗∗p < 0.001 indicate statistical significance.
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AMOA promotes osteoclast and inflammatory remodeling in periodontal area. (a) Representative images of immunohistochemical staining <t>for</t> <t>CTSK,</t> <t>TNF‐α,</t> IL‐1β. CTSK staining at the periodontal ligament‑alveolar bone interface. Scale bar: 100 µm(CTSK), 20 µm(TNF‐α), and 20 µm(IL‐1β). (b) Statistics of numbers of CTSK positive cells in the alveolar bone and percentage of TNF‐α, IL‐1β positive cells per field in the periodontal ligament of the first molar. Mean ± SD. n = 4. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.001. (c) Diagram of the possible mechanism by which static magnetic field accelerates orthodontic tooth movement.
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AMOA promotes osteoclast and inflammatory remodeling in periodontal area. (a) Representative images of immunohistochemical staining <t>for</t> <t>CTSK,</t> <t>TNF‐α,</t> IL‐1β. CTSK staining at the periodontal ligament‑alveolar bone interface. Scale bar: 100 µm(CTSK), 20 µm(TNF‐α), and 20 µm(IL‐1β). (b) Statistics of numbers of CTSK positive cells in the alveolar bone and percentage of TNF‐α, IL‐1β positive cells per field in the periodontal ligament of the first molar. Mean ± SD. n = 4. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.001. (c) Diagram of the possible mechanism by which static magnetic field accelerates orthodontic tooth movement.
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AMOA promotes osteoclast and inflammatory remodeling in periodontal area. (a) Representative images of immunohistochemical staining <t>for</t> <t>CTSK,</t> <t>TNF‐α,</t> IL‐1β. CTSK staining at the periodontal ligament‑alveolar bone interface. Scale bar: 100 µm(CTSK), 20 µm(TNF‐α), and 20 µm(IL‐1β). (b) Statistics of numbers of CTSK positive cells in the alveolar bone and percentage of TNF‐α, IL‐1β positive cells per field in the periodontal ligament of the first molar. Mean ± SD. n = 4. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.001. (c) Diagram of the possible mechanism by which static magnetic field accelerates orthodontic tooth movement.
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AMOA promotes osteoclast and inflammatory remodeling in periodontal area. (a) Representative images of immunohistochemical staining <t>for</t> <t>CTSK,</t> <t>TNF‐α,</t> IL‐1β. CTSK staining at the periodontal ligament‑alveolar bone interface. Scale bar: 100 µm(CTSK), 20 µm(TNF‐α), and 20 µm(IL‐1β). (b) Statistics of numbers of CTSK positive cells in the alveolar bone and percentage of TNF‐α, IL‐1β positive cells per field in the periodontal ligament of the first molar. Mean ± SD. n = 4. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.001. (c) Diagram of the possible mechanism by which static magnetic field accelerates orthodontic tooth movement.
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AMOA promotes osteoclast and inflammatory remodeling in periodontal area. (a) Representative images of immunohistochemical staining <t>for</t> <t>CTSK,</t> <t>TNF‐α,</t> IL‐1β. CTSK staining at the periodontal ligament‑alveolar bone interface. Scale bar: 100 µm(CTSK), 20 µm(TNF‐α), and 20 µm(IL‐1β). (b) Statistics of numbers of CTSK positive cells in the alveolar bone and percentage of TNF‐α, IL‐1β positive cells per field in the periodontal ligament of the first molar. Mean ± SD. n = 4. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.001. (c) Diagram of the possible mechanism by which static magnetic field accelerates orthodontic tooth movement.
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Image Search Results


In vivo immunomodulatory effects of different modified surfaces in a DM model. (A) Schematic representation of the animal modeling and experimental treatment workflow. (B, C) hematoxylin and eosin staining of the peri-implant tissues in the femurs of DM rats 1 week after implantation, accompanied by quantitative analysis of the fibrous capsule thickness (scale bar = 100 μm, n = 5). (D–G) Immunofluorescence staining evaluating the polarization state of macrophages surrounding the implants (green: macrophage marker cluster of differentiation (CD) 68; red: M1 marker CD86 and M2 marker CD206; blue: nuclei), along with corresponding quantitative analysis of the fluorescence signals (scale bar = 100 μm, n = 5). (H–K) Immunohistochemical staining assessing the expression of the pro-inflammatory marker tumor necrosis factor-α and the anti-inflammatory marker interleukin-10 in the peri-implant area, with quantitative results of the positive staining areas (scale bar = 100 μm, n = 5). Data are expressed as the mean ± standard deviation, with statistical analysis performed using one-way ANOVA and Tukey's post-hoc test. ∗p < 0.05, ∗∗p < 0.01, and ∗∗∗p < 0.001 indicate statistical significance.

Journal: Bioactive Materials

Article Title: Integrated apoptotic extracellular vesicle-recruitment peptide coating reprograms the diabetic bone microenvironment and orchestrates enhanced implant osseointegration

doi: 10.1016/j.bioactmat.2026.05.059

Figure Lengend Snippet: In vivo immunomodulatory effects of different modified surfaces in a DM model. (A) Schematic representation of the animal modeling and experimental treatment workflow. (B, C) hematoxylin and eosin staining of the peri-implant tissues in the femurs of DM rats 1 week after implantation, accompanied by quantitative analysis of the fibrous capsule thickness (scale bar = 100 μm, n = 5). (D–G) Immunofluorescence staining evaluating the polarization state of macrophages surrounding the implants (green: macrophage marker cluster of differentiation (CD) 68; red: M1 marker CD86 and M2 marker CD206; blue: nuclei), along with corresponding quantitative analysis of the fluorescence signals (scale bar = 100 μm, n = 5). (H–K) Immunohistochemical staining assessing the expression of the pro-inflammatory marker tumor necrosis factor-α and the anti-inflammatory marker interleukin-10 in the peri-implant area, with quantitative results of the positive staining areas (scale bar = 100 μm, n = 5). Data are expressed as the mean ± standard deviation, with statistical analysis performed using one-way ANOVA and Tukey's post-hoc test. ∗p < 0.05, ∗∗p < 0.01, and ∗∗∗p < 0.001 indicate statistical significance.

Article Snippet: For IHC analysis, sections underwent heat-induced antigen retrieval and blocking prior to incubation with antibodies against TNF-α (GB11188, Servicebio, China), IL-10 (GB11534, Servicebio, China), and VEGF (GB15165, Servicebio, China) to identify differences in local inflammatory and angiogenic profiles.

Techniques: In Vivo, Modification, Staining, Immunofluorescence, Marker, Fluorescence, Immunohistochemical staining, Expressing, Standard Deviation

AMOA promotes osteoclast and inflammatory remodeling in periodontal area. (a) Representative images of immunohistochemical staining for CTSK, TNF‐α, IL‐1β. CTSK staining at the periodontal ligament‑alveolar bone interface. Scale bar: 100 µm(CTSK), 20 µm(TNF‐α), and 20 µm(IL‐1β). (b) Statistics of numbers of CTSK positive cells in the alveolar bone and percentage of TNF‐α, IL‐1β positive cells per field in the periodontal ligament of the first molar. Mean ± SD. n = 4. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.001. (c) Diagram of the possible mechanism by which static magnetic field accelerates orthodontic tooth movement.

Journal: Advanced Science

Article Title: Arrayed Magnetic Accelerator Synergistically Enhances Orthodontic Tooth Movement via Microtubule Assembly‐Mediated Periodontal Remodeling

doi: 10.1002/advs.77447

Figure Lengend Snippet: AMOA promotes osteoclast and inflammatory remodeling in periodontal area. (a) Representative images of immunohistochemical staining for CTSK, TNF‐α, IL‐1β. CTSK staining at the periodontal ligament‑alveolar bone interface. Scale bar: 100 µm(CTSK), 20 µm(TNF‐α), and 20 µm(IL‐1β). (b) Statistics of numbers of CTSK positive cells in the alveolar bone and percentage of TNF‐α, IL‐1β positive cells per field in the periodontal ligament of the first molar. Mean ± SD. n = 4. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.001. (c) Diagram of the possible mechanism by which static magnetic field accelerates orthodontic tooth movement.

Article Snippet: Primary antibodies against rat CTSK (Proteintech, 11239‐1‐AP, 1:200), TNF‐α (Proteintech, 60291‐1‐Ig, 1:200) and IL‐1β (Proteintech, 26048‐1‐AP, 1:200) were used.

Techniques: Immunohistochemical staining, Staining

SMFs enhance orthodontic mechano‐transduction via activation in microtubule‐integrin assembly of PDLCs. (a) Heat map for cluster analysis of differentially expressed genes (DEGs). (b) Bubble plot of GO enrichment results of DEGs. (c) Bubble plot of KEGG enrichment results of DEGs. (d) Relative FPKM values of ITGB1, ITGB7, ITGB9, CCL7, TNF and IL6 from RNA‐seq data. Mean ± SD. n = 3. ** p < 0.01, *** p < 0.001. (e) 12h and 24h Relative gene expression of ITGB1, ITGB2, ITGB3, IFNG, MCSF and TNF from qRT‐PCR. Mean ± SD. n = 3. ** p < 0.01, *** p < 0.001, **** p < 0.0001. (f) Representative immunofluorescence images of α‐Tubulin (green), Integrin‐β1 (red) (merged yellow) and nuclei (blue) in mechanical force applied PDLCs without and with SMFs. Scale bar: 10 µm. (g) Pearson's coefficient and Manders’ overlap coefficient (M1) for the colocalization analysis between α‐Tubulin and Integrin‐β1. Mean ± SD. n = 30. **** p < 0.0001.

Journal: Advanced Science

Article Title: Arrayed Magnetic Accelerator Synergistically Enhances Orthodontic Tooth Movement via Microtubule Assembly‐Mediated Periodontal Remodeling

doi: 10.1002/advs.77447

Figure Lengend Snippet: SMFs enhance orthodontic mechano‐transduction via activation in microtubule‐integrin assembly of PDLCs. (a) Heat map for cluster analysis of differentially expressed genes (DEGs). (b) Bubble plot of GO enrichment results of DEGs. (c) Bubble plot of KEGG enrichment results of DEGs. (d) Relative FPKM values of ITGB1, ITGB7, ITGB9, CCL7, TNF and IL6 from RNA‐seq data. Mean ± SD. n = 3. ** p < 0.01, *** p < 0.001. (e) 12h and 24h Relative gene expression of ITGB1, ITGB2, ITGB3, IFNG, MCSF and TNF from qRT‐PCR. Mean ± SD. n = 3. ** p < 0.01, *** p < 0.001, **** p < 0.0001. (f) Representative immunofluorescence images of α‐Tubulin (green), Integrin‐β1 (red) (merged yellow) and nuclei (blue) in mechanical force applied PDLCs without and with SMFs. Scale bar: 10 µm. (g) Pearson's coefficient and Manders’ overlap coefficient (M1) for the colocalization analysis between α‐Tubulin and Integrin‐β1. Mean ± SD. n = 30. **** p < 0.0001.

Article Snippet: Primary antibodies against rat CTSK (Proteintech, 11239‐1‐AP, 1:200), TNF‐α (Proteintech, 60291‐1‐Ig, 1:200) and IL‐1β (Proteintech, 26048‐1‐AP, 1:200) were used.

Techniques: Transduction, Activation Assay, Analysis, RNA Sequencing, Gene Expression, Quantitative RT-PCR, Immunofluorescence

Journal: Advanced Science

Article Title: Arrayed Magnetic Accelerator Synergistically Enhances Orthodontic Tooth Movement via Microtubule Assembly‐Mediated Periodontal Remodeling

doi: 10.1002/advs.77447

Figure Lengend Snippet:

Article Snippet: Primary antibodies against rat CTSK (Proteintech, 11239‐1‐AP, 1:200), TNF‐α (Proteintech, 60291‐1‐Ig, 1:200) and IL‐1β (Proteintech, 26048‐1‐AP, 1:200) were used.

Techniques: Sequencing