Regulation Of Orthodontic Alveolar Bone Remodeling By Lamin A/C

Lamin A/C plays a crucial role in the information transmission between the cytoplasm and the nucleus. However, it remains unclear whether it participates in the periodontal tissue remodeling during orthodontic tooth movement (OTM). Therefore, this project aims to explore the role and specific mechanism of Lamin A/C during OTM. In this study, orthodontic models using Wistar rats and in vitro PDLSCs were established. Both in vivo and in vitro experiments were divided into 5 groups, including control, force application, force application + F-actin disruption, force application + F-actin disruption + Lamin A/C overexpression, and force application + F-actin disruption + empty vector. Techniques including laser confocal microscopy, RT-qPCR, WB, IHC, and virus transfection, were utilized to investigate the regulatory effect and mechanism of Lamin A/C during OTM. Both in vivo and in vitro experiments have verified that orthodontic tensile stress upregulated F-actin, Lamin A/C, YAP and osteogenesis-related factors. Disrupting F-actin inhibits the osteogenic effect of tensile stress. However, overexpressing Lamin A/C rescued the nuclear entry level of YAP and osteogenesis. Orthodontic tensile stress can regulate the osteogenic differentiation of PDLSCs through the F-actin/Lamin A/C/YAP signaling axis. This project provides a new molecular mechanism interpretation for OTM, and it is expected that local injection of Lamin A/C in the periodontal tissues can facilitate periodontal tissue remodeling, offering a new theoretical basis and potential therapeutic target for enhancing the efficiency of OTM.