Sci-Tech

New tissue engineering scaffold assisted in integrated regeneration of soft and hard tissue interfaces

2024-04-12   

Recently, Wu Chengtie, a researcher of the Chinese Academy of Sciences Shanghai Silicate Research Institute, made important progress in the field of immune multicellular scaffold used for tendon bone repair. The relevant research results have recently been published in the journal Scientific Progress, and the team has applied for an invention patent for the results. The tendon bone interface connects tendons and bones, consisting of tendons, bones, and fibrocartilage, with a complex layered structure that includes gradient material components, extracellular matrix, and cell phenotype. There is a gradual and continuous transition between adjacent tissues. This unique interface connects soft and hard tissues, enabling effective mechanical stress transfer, alleviating stress concentration at the soft hard tissue interface, and fully utilizing skeletal muscle function, playing an important role in human motor function. However, due to the poor regeneration ability of multiple tissues at the interface and the complex physiological environment, once damaged, conservative treatment or surgical repair can easily form disorganized fibrous vascular scar tissue in clinical practice, causing poor interface structure and weakened mechanical strength, leading to limited tissue activity in patients after recovery. Developing a tissue engineering scaffold that combines multi tissue regeneration activity and immune regulation function is crucial for the restoration of natural tendon bone structure. Wu Chengtie introduced that tissue engineering scaffolds are an effective treatment method that can promote the repair of damaged tissues, and have attracted widespread attention from relevant researchers in the field of tendon bone injuries. However, traditional biomaterials tend to enhance biological functions directly related to the tendon bone interface, such as osteogenic differentiation or tendon differentiation, while ignoring the influence of the three-dimensional microenvironment around the injury site, especially the inflammatory response triggered by immune cells in the body. In various immune cells, macrophages are receiving increasing attention in tendon bone interface damage due to their close association with tendon fibrosis. Previous studies have shown that by reducing the accumulation of M1 macrophages at the tendon bone interface and inducing polarization of M2 macrophages, better histological and biomechanical properties can be obtained at the tendon bone interface. However, due to factors such as tissue aging, high muscle load, and pressure, the transformation of M1 and M2 in macrophages often occurs at the tendon bone interface, leading to chronic inflammation. As is well known, the immune environment usually determines the outcome of tissue damage repair. Appropriate inflammatory response helps initiate tissue repair, while excessive inflammation can hinder tissue repair progress, leading to pathological fibrosis or scar structure development at the injury site, thereby reducing the expected function of biomaterials. The research team used multicellular 3D printing technology to combine manganese silicate nanoparticles with tendon bone related cells, and designed and constructed a multicellular scaffold with immune regulation function for integrated regeneration of tendon bone interface. Immune regulatory scaffolds not only simulate the phenotypic composition and gradient structure of natural interface cells well, but also exhibit diverse biological activities in vitro. In various animal models of rotator cuff injury, this scaffold has achieved immune regulation, integrated regeneration of multiple tissues, and recovery of motor function. Wu Chengtie said that the research team has constructed an immune multicellular scaffold, in which tendon stem/progenitor cells and bone marrow mesenchymal stem cells are distributed in a layered manner in the scaffold, achieving simulation of the tendon bone interface. Thanks to multicellular distribution and

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