Deceleration of porous magnesium alloy scaffold degradation and synchronization of bone defect repair by LIPUS-activated piezoelectric mineralization barrier

• Contrary to the ZE21C magnesium alloy, LIPUS promotes the deposition of Ca-P salts and slows down the degradation of coated scaffolds. • Under the intervention of LIPUS, an osteoconductive interface conducive to bone tissue growth appeared around the magnesium scaffolds with coating, promoting bone repair. • The synergistic effect of ultrasound and piezoelectric coating promotes the growth and mineralization of new bone. • This synergistic effect created an anti - inflammatory environment around the scaffold, promoted the expression of osteocalcin (OCN), inhibited the expression of tartrate - resistant acid phosphatase (TRAP), and promoted bone repair. Biodegradable magnesium alloys exhibit significant potential for application in bone defect repair owing to their excellent mechanical properties and biocompatibility. Low-intensity pulsed ultrasonography (LIPUS) is a potential intervention for promoting bone repair. However, when magnesium alloys were used with LIPUS, their degradation was accelerated, which may have a negative impact on bone repair. In this study, a bio-piezoelectric coating was prepared on a porous magnesium alloy scaffold, and the degradation behavior of the porous scaffolds with a bio-piezoelectric coating under LIPUS intervention was studied while evaluating their synergistic effect on bone defect regeneration. In vitro studies revealed that the charge generation induced by the piezoelectric effect accelerated CaP deposition, which in turn decelerated the degradation of the coated scaffold. Meanwhile, the synergistic effect promoted the M2 transformation of macrophages, thereby enhancing osteogenic differentiation. In vivo studies showed that a transition layer of MgO and Mg₃(PO₄)₂ appeared at the bone–scaffold interface, which was beneficial for tissue repair. In addition, a large amount of Ca-P layer above served as an osteoconductive interface to promote tissue repair. Histological staining indicated that this synergistic effect accelerated bone formation and mineral deposition. Immunohistochemical staining demonstrated that the synergistic effect promoted OCN expression while suppressing TRAP expression, thereby promoting bone repair. These findings demonstrate that, under a synergistic effect, new bone formation synchronizes with magnesium degradation, consequently providing an innovative clinical strategy for bone defect regeneration.