Dental Science Research Institute, School of Dentistry, Chonnam National University, Gwangju, Korea.
Department of Anatomy and Neuroscience, College of Medicine, Eulji University, Daejeon, Korea.
J Clin Periodontol. 2021 Apr;48(4):528-540. doi: 10.1111/jcpe.13416. Epub 2021 Jan 26.
We aimed to identify a key molecule that maintains periodontal tissue homeostasis during biophysical force-induced tooth movement (BTM) by orchestrating alveolar bone (AB) remodelling.
Differential display-PCR was performed to identify key molecules for BTM in rats. To investigate the localization and expression of the identified molecules, immunofluorescence, real-time RT-PCR and Western blotting were performed in rats and human periodontal ligament (PDL) cells. Functional test and micro-CT analysis were performed to examine the in vivo effects of the identified molecules on BTM.
Secretory leucocyte peptidase inhibitor (SLPI) in the PDL was revealed as a key molecule for BTM-induced AB remodelling. SLPI was enhanced in the PDL under both compression and tension, and downregulated by an adenyl cyclases inhibitor. SLPI induced osteoblastogenic genes including runt-related transcription factor 2 (Runx2) and synergistically augmented tension-induced Runx2 expression. SLPI augmented mineralization in PDL cells. SLPI induced osteoclastogenic genes including receptor activator of nuclear factor kappa-Β ligand (RANKL) and synergistically augmented the compression-induced RANKL and macrophage colony-stimulating factor (MCSF) expression. Finally, the in vivo SLPI application into the AB significantly augmented BTM.
SLPI or its inhibitors might serve as a biological target molecule for therapeutic interventions to modulate BTM.
通过协调牙槽骨（AB）重塑，确定在生物物理力诱导的牙齿移动（BTM）过程中维持牙周组织动态平衡的关键分子。
在大鼠中进行差异显示-PCR 以鉴定 BTM 的关键分子。为了研究鉴定分子的定位和表达，在大鼠和人牙周韧带（PDL）细胞中进行免疫荧光、实时 RT-PCR 和 Western blot。进行功能测试和 micro-CT 分析，以检查鉴定分子对 BTM 的体内影响。
在 PDL 中发现分泌白细胞肽酶抑制剂（SLPI）是 BTM 诱导的 AB 重塑的关键分子。SLPI 在压缩和张力下均在 PDL 中增强，并被腺苷酸环化酶抑制剂下调。SLPI 诱导包括 runt 相关转录因子 2（Runx2）在内的成骨基因，并协同增强张力诱导的 Runx2 表达。SLPI 增强了 PDL 细胞中的矿化。SLPI 诱导破骨细胞生成基因，包括核因子 kappa-B 受体激活剂配体（RANKL），并协同增强压缩诱导的 RANKL 和巨噬细胞集落刺激因子（MCSF）表达。最后，AB 内的体内 SLPI 应用显著增强了 BTM。
SLPI 或其抑制剂可能作为治疗干预的生物靶标分子，用于调节 BTM。
