Semaphorin 3A regulates alveolar bone remodeling on orthodontic tooth movement

• Published in: Scientific reports Vol. 12; no. 1; p. 9243
• Main Authors: Kamei, Hirokazu, Ishii, Takenobu, Nishii, Yasushi
• Format: Journal Article
• Language: English
• Published: England Nature Publishing Group 02.06.2022; Nature Publishing Group UK; Nature Portfolio
• Subjects: Alveolar bone; Animals; Bone growth; Bone remodeling; Bone Remodeling - physiology; Bone resorption; Bone Resorption - metabolism; Compression; IL-1β; Immunohistochemistry; Inflammation; Interleukin 6; Ligaments; Localization; Mice; Mineralization; Molars; Orthodontics; Osteoblastogenesis; Osteoblasts; Osteoclastogenesis; Osteoclasts; Osteoclasts - metabolism; Osteogenesis; Periodontal ligament; Semaphorin-3A - metabolism; Semaphorins; Teeth; Tension; Tooth Movement Techniques; Tumor necrosis factor-α
• ISSN: 2045-2322; 2045-2322
• DOI: 10.1038/s41598-022-13217-x

Semaphorin 3A (Sema3A) promotes osteoblast differentiation and inhibits osteoclast differentiation. In the present study, we observed the regulation of alveolar bone remodeling by Sema3A during orthodontic tooth movement (OTM). Four inflammatory cytokines (IL-1β, IL-6, TNFα, and INF-γ) involved in OTM were applied to osteoblasts in vitro, and Sema3A expression was determined by reverse-transcription quantitative polymerase chain reaction (RT-qPCR). In vivo, springs were attached to the maxillary first molars of C56BL/6J mice (OTM model) and the localization of Sema3A was confirmed by immunofluorescent. Recombinant Sema3A (rSema3A) was locally injected into the OTM model. Inflammatory cytokine localization in the OTM model was confirmed by immunohistochemistry. In vivo, more Sema3A was observed on the tension side in the OTM group. Injection of rSema3A into the OTM model increased mineralization on the tension side and decreased the number of osteoclasts on the compression side. In vitro, IL-1β significantly increased Sema3A mRNA levels. Immunohistochemistry for IL-1β in vivo showed more concentrated staining in the periodontal ligament on the tension side than on the compression side. In summary, our findings revealed the distribution of Sema3A in the periodontal ligament and demonstrated that rSema3A administration promotes bone formation and inhibits bone resorption during OTM.