Regulation of Periodontal Ligament Autophagy by Super-Activated Platelet Lysate in a Rat Maxillary Expansion Model

Yang Liu,1– 3 Jianan Li,1 Huiying Lu,4 Xiaoyao Liu,1 Yang Li,4 Yi Zhang,4 Peijun Wang1 1Department of Orthodontics, The First Affiliated Hospital, Harbin Medical University, Harbin, 150001, People’s Republic of China; 2School of Stomatology, Harbin Medical University, Harbin, 150001, People’s Republic of China; 3Department of Stomatology, The Fourth Affiliated Hospital, Harbin Medical University, Harbin, 150001, People’s Republic of China; 4National and Local Joint Stem Cell Research & Engineering Center for Aging Diseases, Tian Qing Stem Cell Co., Ltd., Harbin, 150028, People’s Republic of ChinaCorrespondence: Peijun Wang, Department of Orthodontics, The First Affiliated Hospital, Harbin Medical University, Harbin, 150001, People’s Republic of China, Email 13946027000@163.com Yang Liu, Email 435797399@qq.comPurpose: To investigate the regulatory effect of Super-Activated Platelet Lysate (sPL) on autophagy of periodontal ligament stem cells (PDLSCs) during rat maxillary expansion, with implications for optimizing orthodontic treatment outcomes.Methods: Fifty-four male Sprague-Dawley rats were randomized into control, maxillary expansion model, and sPL-treated groups. After expansion model establishment, arch width was monitored, and maxillary samples were collected on days 3, 7, and 14 post-expansion. Histological staining (H&E, TRAP) and immunological assays (IHC/IF) were performed to evaluate periodontal tissue morphology, osteoclast activity, and autophagy-related marker (LC3B, LAMP2, mTOR) expression.Results: All rats adapted well after expander installation with no mortality. Arch width increased significantly over time. H&E staining showed narrowed periodontal space, disorganized fibers, and localized bone resorption in the model group on days 3 and 7, with stabilization by day 14. The sPL group exhibited improved tissue morphology by day 7 and stabilization by day 14, though with slightly increased osteoclast activity. TRAP staining revealed elevated osteoclast numbers in the model group on days 3 and 7, decreasing by day 14, whereas the sPL group had fewer osteoclasts initially but more by day 14 (all p < 0.05). IHC indicated increased LC3B expression in both groups on day 3, with significant intergroup differences. By day 7, LC3B decreased in the sPL group but remained elevated in the model group. On day 14, the sPL group showed significantly higher LC3B than the model group. LAMP2 expression mirrored LC3B, while mTOR showed an inverse trend. IF confirmed LC3B expression in CD90-positive cells within the periodontal ligament.Conclusion: sPL can modulate PDLSCs autophagy during maxillary expansion, a novel regulatory mechanism that may mitigate alveolar bone complications and shorten orthodontic treatment duration. This finding highlights sPL’s potential as a therapeutic agent in orthodontic practice.Keywords: sPL, autophagy, maxillary expansion, PDLSCs, OTM