As the key to regeneration of oral and maxillofacial tissues such as bone, dental pulp and skin, vascularization has always been the focus of tissue engineering. With the development of three-dimensional (3D) printing in tissue engineering, there are increasing ways to construct vascular structures. However, to achieve the objective of highly simulating vascular structure in morphology and function and promote tissue repair, it is still a major difficulty for 3D bioprinting to construct highly precise and biologically functional simulated vascular structures. This paper summarizes new progress of 3D printing vascular structure, expounds frontier biological manufacturing technologies of vascular and vascularized structure such as suspension printing, coaxial printing, 4D printing, and so on, analyzes its advantages and disadvantages, and discusses its development prospect, in order to provide reference for the application of 3D printing blood vessels in regeneration and repair of oral and maxillofacial tissues.

Bacterial Typing Techniques ; Campylobacter Infections ; microbiology ; Campylobacter fetus ; classification ; isolation & purification ; Humans ; Multilocus Sequence Typing

Graphene family nanomaterials (GFNs) are highly popular in the field of bone tissue engineering because of their excellent mechanical properties, biocompatibility, and ability to promote the osteogenic differentiation of stem cells. GFNs play a multifaceted role in promoting the bone regeneration microenvironment. First, GFNs activate the adhesion kinase/extracellularly regulated protein kinase (FAK/ERK) signaling pathway through their own micromorphology and promote the expression of osteogenesis-related genes. Second, GFNs adapt to the mechanical strength of bone tissue, which helps to maintain osseointegration; by adjusting the stiffness of the extracellular matrix, they transmit the mechanical signals of the matrix to the intracellular space with the help of focal adhesions (FAs), thus creating a favorable physiochemical microenvironment. Moreover, they regulate the immune microenvironment at the site of bone defects, thus directing the polarization of macrophages to the M2 type and influencing the secretion of relevant cytokines. GFNs also act as slow-release carriers of bioactive molecules with both angiogenic and antibacterial abilities, thus accelerating the repair process of bone defects. Multiple types of GFNs regulate the bone regeneration microenvironment, including scaffold materials, hydrogels, biofilms, and implantable coatings. Although GFNs have attracted much attention in the field of bone tissue engineering, their application in bone tissue regeneration is still in the basic experimental stage. To promote the clinical application of GFNs, there is a need to provide more sufficient evidence of their biocompatibility, elucidate the mechanism by which they induce the osteogenic differentiation of stem cells, and develop more effective form of applications.

Human adipose-derived stem cells (hASCs) are a promising cell type for bone tissue regeneration. Circular RNAs (circRNAs) have been shown to play a critical role in regulating various cell differentiation and involve in mesenchymal stem cell osteogenesis. However, how circRNAs regulate hASCs in osteogenesis is still unclear. Herein, we found circ_0003204 was significantly downregulated during osteogenic differentiation of hASCs. Knockdown of circ_0003204 by siRNA or overexpression by lentivirus confirmed circ_0003204 could negatively regulate the osteogenic differentiation of hASCs. We performed dual-luciferase reporting assay and rescue experiments to verify circ_0003204 regulated osteogenic differentiation via sponging miR-370-3p. We predicted and confirmed that miR-370-3p had targets in the 3'-UTR of HDAC4 mRNA. The following rescue experiments indicated that circ_0003204 regulated the osteogenic differentiation of hASCs via miR-370-3p/HDAC4 axis. Subsequent in vivo experiments showed the silencing of circ_0003204 increased the bone formation and promoted the expression of osteogenic-related proteins in a mouse bone defect model, while overexpression of circ_0003204 inhibited bone defect repair. Our findings indicated that circ_0003204 might be a promising target to promote the efficacy of hASCs in repairing bone defects.
Adipose Tissue/metabolism* ; Animals ; Cell Differentiation/genetics* ; Cells, Cultured ; Histone Deacetylases/metabolism* ; Humans ; Mice ; MicroRNAs/metabolism* ; Osteogenesis/genetics* ; RNA, Circular/metabolism* ; Repressor Proteins/metabolism* ; Signal Transduction ; Stem Cells/metabolism*