The natural reticular hematoma scaffold modulating inflammatory microenvironment and promoting bone regeneration

Abstract

The bone defect causes hematoma, with the degradation of hematoma, the hematoma providing a bridge to the fracture edge and serving as the first scaffold after bone defect. However, there is a paucity of studies exploring the correlation between surface properties of scaffolds and hematoma fibrin network properties as well as immune response. In this study, we manufactured the needle-like crystals calcium magnesium phosphate bone cement (CMPC) by thermodynamic recrystallization. In vitro experiments, the blood cells formed the hematoma on CMPC. With the degradation of hematoma, it showed a fibrin network with the porosity of 70.8±0.03% and the diameter of 0.43±0.02 μm formed on the CMPC surface. Moreover, the degradation of hematoma also promoted the release of growth factors and cell migration. The tibial fracture model and femoral condyle defect model in rats demonstrated that the fibrin networks formed on CMPC after implantation. It promoting bone tissue regeneration by attenuating acute inflammation during the early stage of bone healing, suppressing endoplasmic reticulum stress, and establishing an anti-inflammatory microenvironment.