Adjunctive interventions for accelerating orthodontic tooth movement have been a hot topic of interest in orthodontics. Prolonged orthodontic treatment is often associated with multiple potential complications, such as decalcification, caries, root resorption, and gingival inflammation. Therefore, applying adjunctive interventions that accelerate orthodontic tooth movement and reduce the duration of orthodontic treatment can provide patients with numerous benefits that are of profound clinical significance. Currently, adjunctive interventions for accelerating orthodontic tooth movement can be divided into two main categories: surgical and nonsurgical. Surgical interventions, represented by corticotomy and modified corticotomy procedures, are the most common in clinical practice and can minimize the treatment duration, augment alveolar bone, and expand the range of orthodontic tooth movement. However, these procedures are inevitably traumatic and have many risks and limitations that prevent them from being widely used in clinical practice. In recent years, multiple modified corticotomy techniques, such as corticision, piezocision, micro-osteoperforation, and discision, have been proposed; these techniques can reduce soft and hard tissue damage and the incidence of postoperative complications and are relatively easy to perform in the clinic. Corticotomy and other improved surgical techniques can shorten the duration of orthodontic treatment to a certain extent and promote the recovery of periodontal health with no adverse effects on periodontal, dental, or pulp tissues. However, in clinical application, several potential side effects (such as periodontal tissue damage, root resorption, loss of pulp vitality, etc) and shortcomings need further research with long-term follow-up.

Oral potentially malignant disorders (OPMDs) are precursors of oral squamous cell carcinoma (OSCC). Deregulated cellular energy metabolism is a critical hallmark of cancer cells. Peroxisome proliferator-activated receptor-gamma coactivator-1 alpha (PGC1α) plays vital role in mitochondrial energy metabolism. However, the molecular mechanism of PGC1α on OPMDs progression is less unclear. Therefore, we investigated the effects of knockdown PGC1α on human dysplastic oral keratinocytes (DOKs) comprehensively, including cell proliferation, cell cycle, apoptosis, xenograft tumor, mitochondrial DNA (mtDNA), mitochondrial electron transport chain complexes (ETC), reactive oxygen species (ROS), oxygen consumption rate (OCR), extracellular acidification rate (ECAR), and glucose uptake. We found that knockdown PGC1α significantly inhibited the proliferation of DOKs in vitro and tumor growth in vivo, induced S-phase arrest, and suppressed PI3K/Akt signaling pathway without affecting cell apoptosis. Mechanistically, downregulated of PGC1α decreased mtDNA, ETC, and OCR, while enhancing ROS, glucose uptake, ECAR, and glycolysis by regulating lactate dehydrogenase A (LDHA). Moreover, SR18292 (an inhibitor of PGC1α) induced oxidative phosphorylation dysfunction of DOKs and declined DOK xenograft tumor progression. Thus, our work suggests that PGC1α plays a crucial role in cell proliferation by reprograming energy metabolism and interfering with energy metabolism, acting as a potential therapeutic target for OPMDs.