<p>Antibacterial and osteogenesis performances of LL37-loaded titania nanopores in vitro and in vivo</p>

Abstract

Background: Many studies have shown that the size of nanotube (NT) can significantly affect the behavior of osteoblasts on titanium-based materials. But the weak bonding strength between NT and substrate greatly limits their application. Purpose: The objective of this study was to compare the stability of NT and nanopore (NP) coatings, and further prepare antibacterial titanium-based materials by loading LL37 peptide in NP structures. Methods: The adhesion strength of NT and NP layers was investigated using a scratch tester. The proliferation and differentiation of MC3T3-E1 cells on different substrates were evaluated in vitro by CCK8, alkaline phosphatase activity, mineralization and polymerase chain reaction assays. The antibacterial rates of NP and NP/LL37 were also measured by spread plate method. Moreover, the osteogenesis around NP and NP/LL373 in vivo was further evaluated using uninfected and infected models. Results: Scratch test proved that the NP layers had stronger bonding strength with the substrates due to their continuous pore structures and thicker pipe walls than the independent NT structures. In vitro, cell results showed that MC3T3-E1 cells on NP substrates had better early adhesion, spreading and osteogenic differentiation than those of NT group. In addition, based on the drug reservoir characteristics of porous materials, the NP substrates were also used to load antibacterial LL37 peptide. After loading LL37, the antibacterial and osteogenic induction abilities of NP were further improved, thus significantly promoting osteogenesis in both uninfected and infected models. Conclusion: We determined that the NP layers had stronger bonding strength than NT structures, and the corresponding NP materials might be more suitable than NT for preparing drug-device combined titanium implants for bone injury treatment.

<p>Macro-Microporous Surface with Sulfonic Acid Groups and Micro-Nano Structures of PEEK/Nano Magnesium Silicate Composite Exhibiting Antibacterial Activity and Inducing Cell Responses</p>

“…Bacterial infection is one of the most serious problems for clinical application of the implantable biomaterials, which is the primary cause of implantation failure. 29 Implantable biomaterials with antibacterial performances can inhibit bacterial infection, and thus maintain long-term stability of the implants. 30 Previous studies have shown that -SO 3 H groups on biomaterials could reduce bacterial adhesion and prevent bacteria from biofilm formation, showing antibacterial performances.…”

Reviewing recently developed technologies to direct cell activity through the control of pore size: From the macro‐ to the nanoscale

“…Indeed, SEM and confocal fluorescence images showed neuron‐like cell shape, with several neuritic extensions, whereas for substrates with larger pores, the cell cytosol appears with no preferred direction. Many studies reported the fabrication of nanopores on the titanium (Ti) surface applied in bone implants (Ketabchi, Komm, Miles‐Rossouw, Cassani, & Variola, ; Louarn, Salou, Hoornaert, & Layrolle, ; Pan et al, ; Schürmann et al, ; Shen et al, ; Sun, Liu, Wu, & Huang, ; Zhuang, Zhou, & Yuan, ). For instance, oxidative nanopatterning (Bellod et al, ; Lauria et al, ) and electron beam lithography (EBL; Garoli et al, ) can be applied to form nanopores on Ti alloys.…”

Human β-defensin 3 gene modification promotes the osteogenic differentiation of human periodontal ligament cells and bone repair in periodontitis

“…Furthermore, it was proven that the p38 MAPK pathway also modulates the proliferation and osteogenic differentiation of human bone-derived marrow mesenchymal stem cells. 28 There are few reports about hBD3 and osteogenesis; however, other cationic antimicrobial peptides, such as LL37, have been found to affect the proliferation and differentiation of MC3T3-E1 cells 29 and to enhance bone regeneration in a rat calvarial bone defect through the p38 MAPK pathway. 30 Therefore, we hypothesized that the p38 MAPK pathway might also modulate the osteogenic process of hBD3 gene-modified hPDLCs.…”