The objective of this study was to investigate the effects of parathyroid hormone on tooth movement and uncover its mechanism from a metabolic perspective. The influences of parathyroid hormone on PDLCs osteogenic differentiation and monocyte osteoclastic differentiation were investigated. According to the RNA-seq analysis, glucose metabolism has been discussed subsequently. Mouse maxillary first molar mesial movement model was constructed to estimate the effects of parathyroid administration on alveolar bone remodelling and tooth movement. Parathyroid administration accelerated mouse maxillary first molar mesial movement by promoting alveolar bone remodelling. The expression of osteogenic markers and the number and surface of osteoclast cells were promoted. Parathyroid hormone administration facilitates PDLCs osteogenic differentiation and monocytes osteoclastic differentiation synchronously. RNA-seq indicated that parathyroid administration mainly affects the metabolism and cellular signalling of PDLCs. Parathyroid administration enhanced glucose uptake, glucose consumption and aerobic glycolysis of PDLCs while exhibiting no obvious effects on the Krebs cycle and oxidative phosphorylation. Moreover, mitochondrial fission of PDLCs was promoted after parathyroid administration. Furthermore, results indicated that parathyroid administration promoted the expression of GLUT1, HK1 and LDHA. Inhibition of mitochondrial midzone fission partially alleviated the osteo-inductive effects of parathyroid hormone. Collectively, parathyroid hormone regulates PDLCs aerobic glycolysis and mitochondrial fission to promote alveolar bone remodelling, and metabolic reprogramming is of vital importance in the processes of orthodontic tooth movement. This study elucidates the role of metabolites associated with parathyroid hormones in tooth movement, and lays a foundation for regulating the speed of tooth movement by monitoring their activity.
Wu et al. (Wed,) studied this question.