牙周病主要表现为对牙周组织的进行性破坏，是导致成人牙齿丧失的主要原因，牙周组织完全性再生是牙周病治疗的理想目标。最新研究发现，干细胞源性外泌体可诱导自体细胞的募集、增殖及分化，成为组织再生潜在新靶点。目前，尚未见外泌体诱导牙周组织再生的作用机制研究成果。项目组前期发现LIPUS能够促进PDLSCs外泌体诱导分化效应，这一过程与Smad6精氨酸甲基化上调有较强相关性，并可能通过BMP2/Smad1通路发挥调节作用，但具体诱导作用及机制不明。本研究拟利用细胞分子生物学技术、牙周缺损及牙周炎大鼠模型，探讨在LIPUS诱导的PDLSCs外泌体对牙周组织再生作用中，Smad6精氨酸甲基化调控BMP2/Smad1通路的分子机制。该研究将有助于深入理解LIPUS诱导的PDLSCs外泌体对牙周再生的作用，阐明Smad6精氨酸甲基化修饰调控牙周细胞增殖分化的具体机制，为牙周病的治疗提供理论依据和新思路。

Periodontal disease is a progressive disease that affects the periodontium, which is the main cause of adult tooth loss. Periodontal tissue complete regeneration is the optimal goal of related treatment. Recent evidence indicates that stem cell-derived exosomes can induce autologous cell recruitment, proliferation and differentiation, which makes exosomes to be a potential target for regeneration. The role of exosomes in periodontal tissue repair still needs systematic basic research to elucidate the possible mechanism. Our previous study has showed that Low-Intensity Pulsed Ultrasound (LIPUS)-induced Periodontal Ligament Stem Cells (PDLSCs) exosome might promote periodontal regeneration，which corresponded with increasing Smad6 arginine methylation and taking BMP2/Smad1 pathway as the regulator of this process. The exact function and mechanism still remain unclear. Our study will use cellular molecular biology techniques and rat periodontal defect or periodontitis model to explore the possible machanism of Smad6 arginine methylation and BMP2/Smad1 pathway during LIPUS-induced PDLSCs-exosome in periodontal regeneration. The results will help further understand the progress of LIPUS induced PDLSCs exosomes in periodontal regeneration and how Smad6 arginine methylation regulates periodontal cell proliferation and differentiation, which will devote a brand new thought and evidence for periodontal tissue regeneration.