This study investigates the effects of parathyroid hormone (PTH) on alveolar bone formation in a rat model of orthodontic treatment, with a specific focus on the non-phospholipase C (PLC)-dependent protein kinase C (PKC) activation pathway. Forty female Sprague-Dawley rats were randomly assigned to either an experimental group receiving daily subcutaneous injections of recombinant human PTH or a control group receiving an equivalent volume of saline. After seven days of pretreatment, an orthodontic tooth movement model was established using a fixed nickel-titanium coil spring exerting 50 g of force to induce mesial displacement of the maxillary first molar. In vitro, MC3T3-E1 osteoblastic cells were divided into five groups to evaluate proliferation and apoptosis under various conditions, including treatment with PTH peptide mimics (G1R19) and the PKC inhibitor Go6983. Histological analysis showed that osteoclast numbers on the pressure side peaked at day 14 in both groups but remained significantly lower in the PTH-treated group across all time points. Dual-energy X-ray absorptiometry demonstrated significantly higher alveolar bone density in the PTH group on days 14, 21, and 28. Although tooth movement distance increased progressively in both groups, no significant difference was observed between them. In vitro, G1R19(1-34) significantly enhanced cell proliferation and reduced apoptosis; these effects were reversed by co-treatment with Go6983, suggesting involvement of a non-PLC-dependent PKC signaling pathway. In conclusion, PTH administration enhances alveolar bone formation, increases bone density, and mitigates root resorption during orthodontic treatment, potentially through activation of a non-PLC-dependent PKC signaling pathway. These findings suggest that PTH or its analogs may serve as effective biological adjuncts in clinical orthodontics to accelerate tooth movement, improve bone health, and minimize treatment-associated complications.
Zhang et al. (Thu,) studied this question.