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Bone defects are highly prevalent diseases caused by trauma, tumors, inflammation, congenital malformations and endocrine abnormalities. Ideally effective and side effect free approach to dealing with bone defects remains a clinical conundrum. Klotho is an important protein, which plays an essential role in regulating aging and mineral ion homeostasis. More recently, research revealed the function of Klotho in regulating skeleton development and regeneration. Klotho has been identified in mesenchymal stem cells, osteoblasts, osteocytes and osteoclasts in different skeleton regions. The specific function and regulatory mechanisms of Klotho in long bone and craniofacial bone vary due to their different embryonic development, ossification and cell types, which remain unclear and without conclusion. Moreover, studies have confirmed that Klotho is a multifunctional protein that can inhibit inflammation, resist cancer and regulate the endocrine system, which may further accentuate the potential of Klotho to be the ideal molecule in inducing bone restoration clinically. Besides, as an endogenous protein, Klotho has a promising potential for clinical therapy without side effects. In the current review, we summarized the specific function of Klotho in long bone and craniofacial skeleton from phenotype to cellular alternation and signaling pathway. Moreover, we illustrated the possible future clinical application for Klotho. Further research on Klotho might help to solve the existing clinical difficulties in bone healing and increase the life quality of patients with bone injury and the elderly. [ABSTRACT FROM AUTHOR]

The utilization of mobile devices in education is a growing trend in various subjects. We developed the Dental and Maxillofacial Development Teaching Atlas App, and applied it to the learning process of oral histopathology. The aim of the current study was to investigate the educational effects of atlas-based mobile-assisted teaching in the field of dental medicine, and to suggest relevant improvements. The Dental and Maxillofacial Development Teaching Atlas App encompasses a wide range of atlases. It harbors various features, such as terminology definitions, student communications, and teacher–student interactions. By conducting questionnaires (70 students) and a quiz (68 students), we obtained students' feedback, to evaluate the effects and application prospects of the WeChat applet. The questionnaire results indicate that students experienced a high level of satisfaction and support. Additionally, students participated in the quiz, with the experimental group exhibiting significantly higher average scores than the control group. The fill-in-the-blank questions, image recognition questions, and the total score all demonstrated statistically significant differences, while the terminology definition questions did not. The Dental and Maxillofacial Development Teaching Atlas App facilitates students' utilization of fragmented time for learning, and demonstrates positive effects in enhancing students' learning interests and proactiveness. It also holds promising potential for applications in other disciplines in the field of dental education. [ABSTRACT FROM AUTHOR]

Regeneration of orofacial bone defects caused by inflammatory-related diseases or trauma remains an unmet challenge. Parathyroid hormone 1 receptor (PTH1R) signaling is a key mediator of bone remodeling whereas the regulatory mechanisms of PTH1R signaling in oral bone under homeostatic or inflammatory conditions have not been demonstrated by direct genetic evidence. Here we observed that deletion of PTH1R in Gli1+-progenitors led to increased osteogenesis and osteoclastogenesis. Single-cell and bulk RNA-seq analysis revealed that PTH1R suppresses the osteogenic potential of Gli1+-progenitors during inflammation. Moreover, we identified upregulated IGF1 expression upon PTH1R deletion. Dual deletion of IGF1 and PTH1R ameliorated the bone remodeling phenotypes in PTH1R-defienct mice. Furthermore, in vivo evidence revealed an inverse relationship between PTH1R and Hedgehog signaling, which was responsible for the upregulated IGF1 production. Our work underscored the negative feedback between PTH1R and IGF1 in craniofacial bone turnover, and revealed mechanisms modulating orofacial bone remodeling.