Journal
SCIENCE ADVANCES
Volume 7, Issue 14, Pages -Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/sciadv.abf6654
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Funding
- National Key R&D Program of China [2018YFA0703100]
- General Research Fund of Hong Kong Research Grant Council [17207719, 17214516]
- Hong Kong Health and Medical Research Fund [19180712]
- National Science Fund for Distinguished Youth Scholar [51925104]
- Shenzhen Science and Technology [JSGG20180507183242702]
- HKU-SZH Fund for Shenzhen Key Medical Discipline [SZXK2020084]
- Sanming Project of Medicine in Shenzhen Team of Excellence in Spinal Deformities and Spinal Degeneration [SZSM201612055]
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The study showed that reducing the scale of honeycomb-like TiO2 structures can activate anti-inflammatory macrophage phenotype, promoting osteogenesis. Among different scales, the 90-nanometer sample demonstrated the most effective outcomes in both in vitro cell culture and in vivo implantation experiments.
Proper immune responses are critical for successful biomaterial implantation. Here, four scales of honeycomb-like TiO2 structures were custom made on titanium (Ti) substrates to investigate cellular behaviors of RAW 264.7 macro-phages and their immunomodulation on osteogenesis. We found that the reduced scale of honeycomb-like TiO2 structures could significantly activate the anti-inflammatory macrophage phenotype (M2), in which the 90-nanometer sample induced the highest expression level of CD206, interleukin-4, and interleukin-10 and released the highest amount of bone morphogenetic protein-2 among other scales. Afterward, the resulting immune microenvironment favorably triggered osteogenic differentiation of murine mesenchymal stem cells in vitro and subsequent implant-to-bone osteointegration in vivo. Furthermore, transcriptomic analysis revealed that the minimal scale of TiO2 honeycomb-like structure (90 nanometers) facilitated macrophage filopodia formation and up-regulated the Rho family of guanosine triphosphatases (RhoA, Rac1, and CDC42), which reinforced the polarization of macrophages through the activation of the RhoA/Rho-associated protein kinase signaling pathway.
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