Periodontitis patients are at risk of alveolar bone loss during orthodontic treatment. The aim of this study was to investigate whether intermittent parathyroid hormone (1–34) treatment (iPTH) could reduce alveolar bone loss during orthodontic tooth movement (OTM) in individuals with periodontitis and the underlying mechanism. A rat model of OTM in the context of periodontitis was established and alveolar bone loss was observed. The control, iPTH and iPTH + stattic groups received injections of vehicle, PTH and vehicle, or PTH and the signal transducer and activator of transcription 3 (STAT3) inhibitor stattic, respectively. iPTH prevented alveolar bone loss by enhancing osteogenesis and suppressing bone resorption in the alveolar bone during OTM in rats with periodontitis. This effect of iPTH was along with STAT3 activation and reduced by a local injection of stattic. iPTH promoted osteoblastic differentiation and might further regulate the Wnt/β-catenin pathway in a STAT3-dependent manner. The findings of this study suggest that iPTH might reduce alveolar bone loss during OTM in rats with periodontitis through STAT3/β-catenin crosstalk.

牙周炎患者在正畸治疗期间存在牙槽骨丢失的风险。本研究的目的是调查间歇性甲状旁腺激素 (1-34) 治疗 (iPTH) 是否可以减少牙周炎患者正畸牙齿移动 (OTM) 期间的牙槽骨丢失及其潜在机制。建立牙周炎大鼠OTM模型，观察牙槽骨丢失情况。对照组、iPTH 和 iPTH + stattic 组分别接受载体、PTH 和载体，或 PTH 和信号转导和转录激活剂 3 (STAT3) 抑制剂的注射。iPTH 通过在牙周炎大鼠 OTM 期间增强骨生成和抑制牙槽骨中的骨吸收来预防牙槽骨丢失。iPTH 的这种作用伴随着 STAT3 的激活，并通过局部注射 stattic 降低。iPTH 促进成骨细胞分化，并可能以 STAT3 依赖性方式进一步调节 Wnt/β-catenin 通路。本研究结果表明，iPTH 可能通过 STAT3/β-catenin 串扰减少牙周炎大鼠 OTM 期间的牙槽骨丢失。