Abstract
Bioprinting has emerged as a novel technological approach with the potential to address unsolved questions in the field of tissue engineering. We have recently shown that Laser Assisted Bioprinting (LAB), due to its unprecedented cell printing resolution and precision, is an attractive tool for the in situ printing of a bone substitute. Here, we show that LAB can be used for the in situ printing of mesenchymal stromal cells, associated with collagen and nano-hydroxyapatite, in order to favor bone regeneration, in a calvaria defect model in mice. Also, by testing different cell printing geometries, we show that different cellular arrangements impact on bone tissue regeneration. This work opens new avenues on the development of novel strategies, using in situ bioprinting, for the building of tissues, from the ground up.
Highlights
Much attention has been drawn to tissue engineering approaches in order to build three-dimensional (3D) constructs to replace or sustain the regeneration of tissues, using a combination of biocompatible and bioactive biomaterials with/or without cells and bioactive factors[1]
Using Laser Assisted Bioprinting (LAB) technology, we focus on the impact of different geometric cell patterning in order to achieve guided regeneration of in vivo bone tissue, following bioprinting
We have previously demonstrated the feasibility of Laser-Assisted Bioprinting (LAB) for the printing of nano-hydroxyapatite, in situ, in a calvaria defect on mice[14]
Summary
Based on the printing designs tested in in vitro conditions, we followed to adapt the same printing geometries to an in vivo defect in mouse calvaria. In order to confine the printed cell spots to the calvaria defect, and to provide an osteoconductive matrix to the printed cells, two nHA-collagen disks were printed before and after the cellularized ink printing (Fig. 3A1 and B1, for ring and disk geometries, respectively). In order to assess the proliferation of the printed cells, using the described printing design, we followed the luciferase signal of luciferase positive D1 cells in the in vivo calvaria model in mice up to 42 days. A consistent signal augmentation can be observed towards time and no significant differences can be observed for both geometries tested
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