目的 探讨局部应用甲状旁腺激素（parathyroid hormone，PTH）能否激活蛋白激酶A（protein kinase A，PKA）/瞬时受体电位香草素4（transient receptor potential vanilloid 4，TRPV4）通路并协同正畸力加速大鼠牙移动及其作用机制。 方法 将48只雄性SD大鼠随机分为空白对照组、单纯牵引组（OTM组）、单纯PTH给药组（PTH组）以及牵引联合PTH给药组（OTM + PTH组），建立大鼠左侧上颌第一磨牙OTM模型，施加0.6 N恒定牵引力，局部隔日注射相应药物。建模后第10天检测牙移动距离、压力侧骨密度、牙周组织病理学改变及PKA、TRPV4、核因子κB受体活化因子配体（RANKL）/OPG的表达。体外培养RAW264.7细胞，用50 ng/mL RANKL诱导破骨分化，分别加入PTH及PKA/TRPV4通路激动剂/抑制剂，检测相关分子表达。 结果 体内实验结果显示OTM + PTH组相较于其他3组牙移动距离显著增加，压力侧骨密度降低，破骨细胞数量增多，PKA、TRPV4及RANKL/OPG比值显著上调（P < 0.05）。体外实验显示，PKA或TRPV4激动剂可增强PTH的促破骨分化效应，抑制剂则可阻断该效应。 结论 局部应用PTH可通过激活PKA/TRPV4信号通路，上调RANKL/OPG比值，协同正畸力共同促进破骨细胞的分化与活化，增强牙槽骨改建效率，从而加速OTM，本研究为临床优化正畸治疗方案提供了新的理论依据。

Objective To investigate whether the local application of parathyroid hormone （PTH） can activate the protein kinase A （PKA）/transient receptor potential vanilloid 4 （TRPV4） pathway to synergistically accelerate orthodontic tooth movement in rats and to explore its mechanism of action. Methods Forty-eight male Sprague-Dawley （SD） rats were randomly divided into four groups： a blank control group， a pure orthodontic tooth movement （OTM） group， a pure PTH administration group （PTH group）， and a combined orthodontic tooth movement and PTH administration group （OTM + PTH group）. A left maxillary first molar orthodontic movement model was established in the rats. A constant traction force of 0.6 N was applied， and the corresponding drugs were injected locally every other day. On the 10th day after model establishment， the tooth movement distance， the bone density on the pressure side， the periodontal histopathological changes， and the expression levels of PKA， TRPV4， and the ratio of receptor activator of nuclear factor-κB ligand （RANKL） to osteoprotegerin （OPG） were measured. RAW264.7 cells were cultured in vitro and induced to differentiate into osteoclasts with 50 ng/mL RANKL. Subsequently， PTH and PKA/TRPV4 pathway agonists or inhibitors were added， and the expression of relevant molecules was detected. Results Compared with the OTM group， the tooth movement distance in the OTM + PTH group was significantly greater. The bone density on the pressure side decreased， the number of osteoclasts increased， and the levels of PKA， TRPV4， and the RANKL/OPG ratio were significantly upregulated （P < 0.05）. In vitro experiments demonstrated that PKA or TRPV4 agonists could enhance the osteoclast-differentiation-promoting effect of PTH， whereas inhibitors could significantly impede this effect. Conclusions Local PTH treatment activates the PKA/TRPV4 signaling pathway， increases the RANKL/OPG ratio， and acts synergistically with orthodontic forces to promote osteoclast differentiation and activation. This enhances the efficiency of alveolar bone remodeling and consequently accelerates orthodontic tooth movement. This study offers a new theoretical foundation for optimizing clinical orthodontic treatment protocols.