Department of Orthodontics, Cranial-Facial Growth and Development Center, Peking University School and Hospital of Stomatology, Haidian District, Beijing, PR China.
National Center of Stomatology & National Clinical Research Center for Oral Diseases & National Engineering Laboratory for Digital and Material Technology of Stomatology & Beijing Key Laboratory for Digital Stomatology & Research Center of Engineering and Technology for Computerized Dentistry Ministry of Health & NMPA Key Laboratory for Dental Materials, Haidian District, Beijing, PR China.
J Dent Res. 2024 Aug;103(9):937-947. doi: 10.1177/00220345241262706. Epub 2024 Aug 5.
Alveolar bone (AB) remodeling, including formation and absorption, is the foundation of orthodontic tooth movement (OTM). However, the sources and mechanisms underlying new bone formation remain unclear. Therefore, we aimed to understand the potential mechanism of bone formation during OTM, focusing on the leptin receptor+ (Lepr+) osteogenitors and periodontal ligament cells (PDLCs). We demonstrated that Lepr+ cells activated by force-induced PDLC apoptosis served as distinct osteoprogenitors during orthodontic bone regeneration. We investigated bone formation both in vivo and in vitro. Single-cell RNA sequencing analysis and lineage tracing demonstrated that Lepr represents a subcluster of stem cells that are activated and differentiate into osteoblasts during OTM. Targeted ablation of Lepr+ cells in a mouse model disrupted orthodontic force-guided bone regeneration. Furthermore, apoptosis and sequential fluorescent labeling assays revealed that the apoptosis of PDLCs preceded new bone deposition. We found that PDL stem cell-derived apoptotic vesicles activated Lepr+ cells in vitro. Following apoptosis inhibition, orthodontic force-activated osteoprogenitors and osteogenesis were significantly downregulated. Notably, we found that bone formation occurred on the compression side during OTM; this has been first reported here. To conclude, we found a potential mechanism of bone formation during OTM that may provide new insights into AB regeneration.
牙槽骨(AB)重塑,包括形成和吸收,是正畸牙齿移动(OTM)的基础。然而,新骨形成的来源和机制仍不清楚。因此,我们旨在了解 OTM 期间骨形成的潜在机制,重点关注瘦素受体+(Lepr+)成骨细胞和牙周膜细胞(PDLCs)。我们证明,力诱导的 PDLC 凋亡激活的 Lepr+细胞在正畸骨再生过程中充当独特的成骨前体细胞。我们在体内和体外研究了骨形成。单细胞 RNA 测序分析和谱系追踪表明,Lepr 代表了一个干细胞亚群,在 OTM 期间被激活并分化为成骨细胞。在小鼠模型中靶向消融 Lepr+细胞会破坏正畸力引导的骨再生。此外,凋亡和连续荧光标记测定表明,PDLC 的凋亡先于新骨沉积。我们发现 PDL 干细胞衍生的凋亡小体在体外激活 Lepr+细胞。在抑制凋亡后,正畸力激活的成骨前体细胞和成骨作用显著下调。值得注意的是,我们发现 OTM 期间骨形成发生在压缩侧;这是首次报道。总之,我们发现了 OTM 期间骨形成的潜在机制,这可能为 AB 再生提供新的见解。