The treatment of bone malocclusion often requires a combination of orthodontics and orthognathic surgery. This surgery mainly involves several types of osteotomies to move the jaw block in order to correct a wide spectrum of dentofacial deformities (Patel & Novia, 2007). These osteotomies inevitably create a wedge-shaped osteotomy gap. Thus, bone gap repair is an important process after surgery. All patients of clinical orthodontic and orthognathic doctors expect an accelerated and well-done stable repair.Bone repair is a multistage and complicated process (Ghiasi et al., 2017) involving osteoclastic bone resorption and osteoblastic

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During the mandibular condylar growth, the absorption of calcified cartilage matrix induced by osteoclasts is crucial for the continuous endochondral osteogenesis. Meanwhile, recent studies showed that subchondral bone resided within the low-oxygen microenvironment, and our previous study revealed that hypoxia-inducible transcription factor 1α (HIF-1α) promoted osteoclastogenesis under hypoxia. However, whether HIF-1α regulates the function of osteoclasts in the mandibular condyle cartilage remains elusive. Our study indicated that severe deformity of the mandibular condyle was displayed in 10-wk-old osteoclast-specific HIF-1α conditional knockout (CKO) mice, accompanied by shortened length of condylar process and disorganized fibrocartilage. In 1-, 2-, and 4-wk-old CKO mice, the size of the hypertrophic layer and chondrocytic layer was significantly thickened. In the chondrocytic layer, chondrocytes were atrophied, showing a form of apoptosis in 4-wk-old CKO mice. Furthermore, an increase in the thickness of the fibrous and proliferating layer was observed in 10-wk-old CKO mice, as well as a significant decrease in that of the chondrocytic and hypertrophic chondrocyte layers. Interestingly, the articular surface of the condylar process abnormally presented a horizontal concave shape, and a disk-like acellular connective tissue appeared. In addition, genetic ablation of HIF-1α blunted cartilage matrix loss by subchondral osteoclast deficiency, resulting in a high subchondral bone mass phenotype, accompanied with a decreased number of blood vessels, alkaline phosphatase staining, and vascular endothelial growth factor (VEGF) expression. Mechanistically, the number of osteoclasts in the center of the condyle in CKO mice was significantly reduced by attenuated expression of adenosine 5′-monophosphate-activated protein kinase (AMPK) signaling. These findings reveal a novel influence of HIF-1α function in osteoclasts on maintenance of osteoclast-induced resorption of calcified cartilage matrix via AMPK signaling, as well as subchondral bone formation through VEGF-dependent angiogenesis in bone marrow.

Background: Osteoclasts, which are multinucleated cells formed by monocyte fusion, play a key role in bone resorption. Hypoxia-inducible factor (HIF)-1α is vital for the development of osteoclasts in hypoxic environments and during bone resorption. However, additional research is required to further study the HIF-1α-dependent regulation of osteoclast differentiation at the genetic level.Methods: In our study, RNA sequencing (RNA-seq) was used to identify the expression profiles of long noncoding RNAs (lncRNAs) and mRNAs in conditional HIF-1α-knockout osteoclasts.Results: A total of 1,320 mRNAs and 95 lncRNAs were differentially expressed. The expression of lncRNAs MSTRG.7566.12 and MSTRG.31769.2 were strongly negatively correlated with that of Mmp9, Ctsk, etc.Conclusion: Our research provides a basis for further understanding the role of mRNAs and lncRNAs in conditional HIF-1α-knockout osteoclasts, and many of these molecules may be potential targets for treating bone diseases related to HIF-1α.

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