Tissue adhesive, ROS scavenging and injectable PRP-based ‘plasticine’ for promoting cartilage repair

Abstract

Platelet-rich plasma (PRP) that has various growth factors has been used clinically in cartilage repair. However, the short residence time and release time at the injury site limit its therapeutic effect. The present study fabricated a granular hydrogel that assembled from gelatin microspheres and tannic acid (TA) through their abundant hydrogen bonding. Gelatin microspheres with the gelatin concentration of 10 wt% and the diameter distribution of 1–10 μm were used to assemble by TA to form the granular hydrogel, which exhibited elasticity under low shear strain, but flowability under higher shear strain. The viscosity decreased with increase of shear rate. Meanwhile, the granular hydrogel exhibited self-healing feature during rheology test. Thus, granular hydrogel carrying PRP not only exhibited well-performed injectability, but also performed like a “plasticine” that possessed good plasticity. The granular hydrogel showed tissue adhesion ability and reactive oxygen species (ROS) scavenging ability. Granular hydrogel carrying PRP transplanted to full thickness articular cartilage defects could integrate well with native cartilage, resulting in newly formed cartilage articular fully filled in defects and well-integrated with the native cartilage and subchondral bone. The unique feature of the present granular hydrogel, including injectability, plasticity, porous structure, tissue adhesion, and ROS scavenging provided an ideal PRP-carrier towards cartilage tissue engineering.

Exosomes loaded a smart bilayer-hydrogel scaffold with ROS-scavenging and macrophage-reprogramming properties for repairing cartilage defect

“…The chronic inflammatory microenvironment resulting from AC damage is inundated with various activated inflammatory cells and pro-inflammatory mediators, along with reactive oxygen species (ROS) [ 20 , 21 ]. During cartilage injury, overexpressed ROS not only attacks the extracellular matrix (ECM) of the AC directly but also induces lipid peroxidation and DNA cleavage, which destabilizes the microenvironment [ 22 ]. Furthermore, ROS overexpression at cartilage defect sites exacerbates inflammation, thereby creating an intense pro-inflammatory microenvironment, which may compromise downstream cellular functions and lead to impaired healing [ 23 ].…”