Parathyroid hormone promotes maxillary expansion and reduces relapse in the repeated activation maxillary expansion rat model by regulating Wnt/β-catenin pathway

Abstract

Background Constricted maxillary bone is a common skeletal deformity, which may lead to crowding and posterior crossbite. Mid-palatal suture expansion is often used to increase the maxillary width, but its skeletal effects are limited and tend to relapse, even with prolonged retention. We hypothesized that parathyroid hormone (PTH) may reduce the relapse of maxillary expansion. Methods We established a novel rat maxillary expansion model using palatal tubes with an insertable “W”-shaped spring which can be repeatedly activated. A total of 32 male healthy Wistar rats were randomly divided into six groups: the control group, the PTH group, the expansion group, the expansion + PTH group, the expansion + relapse group and the expansion + PTH + relapse group. All animals in the first 4 groups were killed after 10 days and the 2 relapse groups were killed after 15 days. The maxillary arch widths and histological staining were used to assess the expansion and relapse effects. The immunohistochemical staining, micro-CT, RT-qPCR and Western blot were used to evaluate the bone remodeling during expansion. Results The suture width was increased by the expansion device, and the repeated activation maxillary expansion rat model showed better expansion effects than the conventional model. PTH significantly promoted the expansion width and reduced the relapse ratio. Meanwhile, in the expansion + PTH group, histological and immunohistochemical staining showed that osteoblasts, osteoclasts, new cartilage and osteoid were significantly increased, micro-CT showed increased bone mass, and PCR and Western blot results confirmed up-regulation of RANKL, β-catenin, type II collagen and OCN. Conclusion The novel repeated activation maxillary expansion rat model has better effects than the conventional model. PTH enhances the maxillary expansion and reduces its relapse by regulating Wnt/β-catenin and RANKL pathways. PTH administration may serve as an adjunctive therapy in addition to mechanical expansion for treatment of maxillary constriction.

Suppressing STAT3 activation impairs bone formation during maxillary expansion and relapse

“…However, the high relapse rate due to insufficient bone formation/mineralization remains a prime concern. To minimize relapse, various interventions have been used in animal models to augment bone formation, such as treatment with parathyroid hormone, 14 Salvia officinalis L. extracts, 15 and salvianolic acid B. 16 These biological factors and drugs should stimulate bone formation in MPS subjected to RME.…”

Extracellular vesicles derived from M1 macrophages enhance rat midpalatal suture expansion by promoting initial bone turnover and inflammation

“…The structure of the palatal suture in the posterior region of rats is similar to that of humans, with secondary cartilage along the palatine bone edges and a thin layer of fibers in the core, with suture-derived stem cells (SuSCs) in the center [ 3 , 32 ]. SuSCs are a unique functional population that possess an intrinsic ability to differentiate into osteoblasts, chondrocytes, and fibroblasts[ 33 ].…”