Strategy based on liquid crystal elastomer active tensile to accelerate bone repair: Mechanistic analysis of LAMB1-ITGB4 mediated PI3K-AKT signaling.

Mechanical tensile forces play a crucial role in modulating bone tissue behavior and the response of surrounding cells in vivo. During orthodontic tooth movement, tensile stresses within the periodontal ligament on the tension side stimulate bone deposition. Drawing inspiration from this biological process, our work introduces a strategy using mechanically active materials to enhance bone defect healing. We utilize liquid crystal elastomers (LCEs), a class of soft active materials known for excellent actuation performance. LCEs apply stable mechanical forces to target bone tissue, mimicking the traction of the periodontal ligament and actively promoting bone regeneration. By employing a sequential thiol-Michael/thiol-ene click reaction, optimizing component ratios, and utilizing low-temperature crosslinking, the driving temperature of LCE was significantly reduced to 27.3 °C. This advancement eliminates limitations on its medical applications in tissue regeneration. Moreover, both in vitro and in vivo experiments confirm that LCE-induced tensile forces enhance bone regeneration. The LAMB1-ITGB4 signaling axis mediates the process via the PI3K-AKT pathway. This mechanobiological approach opens new avenues for bone defect healing and provides mechanistic insights into how mechanical tensile forces promote bone regeneration.