In the 1950s, German-American medical scientist Hermann Becks proposed “Oral Biology”, and 30 years later, this discipline was introduced into China. Through the efforts of colleagues in the field of oral medicine, "Oral Biology" emerged as a course in the oral medicine education and teaching system in the 1990s, and the work on textbook compilation was also put on the agenda. The first unified textbook was published in 2000 by Professor Liu Zheng as the chief editor, by the People's Medical Publishing House. Subsequently, a large number of related textbooks emerged continuously, and the course construction achieved great success. In 2010, the Oral Biomedicine Professional Committee of the Chinese Stomatological Association was established in Beijing, followed by the founding of the academic quarterly “Oral Biomedicine”, which greatly promoted the academic progress of oral biology in China. In the new historical period, oral biology should continuously expand in various levels and fields such as talent training, technological innovation, achievement transformation, and clinical application, thereby opening a new era of academic development.

Objective:?Investigating whether apoptotic vesicles (apoVs) derived from stem cells from apical papilla (SCAP) modulate macrophage inflammatory phenotype by influencing glycolysis-associated enzymes, thereby regulating the inflammatory response. Methods:?Human-derived SCAP were cultured and characterized in vitro. Staurosporine induction was employed to obtain apoVs from SCAP, followed by the characterization and identification of the apoVs using scanning electron microscopy, flow cytometry, and other methods. Experimental groups included a blank control group, an inflammation group and an apoVs group. Rat bone marrow-derived macrophages (BMDMs) were treated with PBS, LPS and LPS in conjunction with apoVs. Using flow cytometry to assess the expression of surface markers CD80 and CD86 on pro-inflammatory macrophages; employing Western blot to detect the expression of glycolytic enzymes in macrophages. Results:?ApoVs derived from SCAP can be taken up by macrophages, reducing the expression of pro-inflammatory phenotype markers CD80 and CD86. Additionally, they exert an impact on glycolysis-associated enzymes, with a significant downregulation observed in the expression of GLUT1 and GLUT3 (P<0.05). Conclusions:?ApoVs derived from SCAP regulate the expression of glycolysis-associated enzymes in macrophages, reducing the distribution of pro-inflammatory phenotype macrophages, thereby modulating the inflammatory response.

Objective:To investigate the compatibility of protein retention expansion microscopy (proExM) with mouse mandibular-derived microvesicles (MVs), and to observe the distributions of surface markers on MVs after expansion, as well as to accurately identify their cellular origins. Methods:MVs from mouse mandibles were isolated by differential centrifugation; Transmission electron microscopy, Western blot and Nanoparticle tracking analysis were used to identify the MVs; Immunofluorescence staining was conducted for the surface proteins CD9, CD63, alkaline phosphatase (ALP) and osteoclast associated receptor (OSCAR) of MVs; The proExM was used to amplify the MVs after immunofluorescence staining; The expansion coefficient was measured, and the morphology and fluorescence staining of MVs before and after expansion were observed by confocal microscopy. Results:The MVs isolated from mouse mandibles by differential centrifugation met the identification criteria for MVs; Under the experimental procedure, a 4-fold expansion of mouse mandibular-derived MVs was achieved by expansion of the gel; The fluorescence intensity distributions of CD9 and CD63 on the line profile of MVs after expansion presented multi-peak patterns; After expansion, the variance of mander’s colocalization coefficient (MCC) 1 of MVs increased significantly (P＜0.01), while the variance of MCC2 decreased (P＜0.05), and the variance of pearson correlation coefficient (PCC) increased significantly (P＜0.01); After expansion, accurate identification of MVs secreted by osteoblasts and osteoclasts was achieved; After expansion, it was measured that osteoblast-derived MVs accounted for 11.11% of the CD9+ MVs derived from mouse mandibles, while osteoclast-derived MVs accounted for 3.70%. Conclusions:This experimental procedure could improve the resolution in the observation of mouse mandibular-derived MVs. In this study, a standard experimental procedure was established to reveal the heterogeneity of surface protein distribution of MVs and to achieve the accurate identification of the cell origins of tissue-derived MVs.

Objective: To construct a Sprague Dawley (SD) rat oral submucosal fibrosis model by injecting arecoline solution under the mucosa. Methods: 20 SD rats were randomly divided into an experimental group and a control group. The rats were injected with arecoline solution under the buccal mucosa for modeling in experimental group, while the rats were injected with physiological saline in control group. After 10 weeks of treatment, the oral mucosa color and weight of rats were observed, and the passive mouth opening was measured; hematoxylin-eosin (HE) and Masson staining were used to observe pathological changes in mucosal tissue; Immunohistochemical staining and real-time fluorescence quantitative PCR were used to detect the protein and gene expression levels of α-Smooth muscle action (α- SMA) and platelet endothelial cell adhesion molecule-1 (PECAM-1/CD31) in mucosal tissue. Results: In experimental group, white lesions appeared on the buccal mucosa of the rats, and the mouth opening decreased (P＜0.000 1); epithelial atrophy and deposition of collagen fibers in the lamina propria appeared in mucosal tissue; protein and gene expression levels of α-SMA significantly increased (P＜0.000 1), while the expression levels of CD31 significantly decreased in mucosal tissue (P＜0.000 1). Conclusions: The submucosal injection method of arecoline can construct an OSF rat model with typical symptoms and significant pathological changes.

Objective:To explore the effect of METTL7A on cell senescence and osteogenic/odontogenic differentiation of DPSCs through m6A methylation. Methods:The lentivirus was used to transfect the DPSCs to obtain the DPSCs of METTL7A knockdown. The retrovirus was used to transfect the DPSCs to obtain the DPSCs of METTL7A overexpression. The knockdown and overexpression efficiency was detected by qRT-PCR and western blot assay. On this basis, SA-b-gal staining and quantification of the SA-b-gal staining was used to detect whether METTL7A regulated the cell senescence of DPSCs. Dot hybridization experiments were conducted to determine whether METTL7A regulated m6A methylation levels of DPSCs. After adding the Cyc to the METTL7A overexpression group, the SA-b-gal staining, the quantification of the SA-b-gal staining and ALP activity confirmed that METTL7A regulated cell senescence and osteogenic/odontogenic differentiation of DPSCs through m6A methylation. Results:The lentivirus was used to transfect the DPSCs. Compared with the Consh group, the gene and protein expression of METTL7A in METTL7A knockdown group (METTL7Ash) was significantly decreased (P<0.01). The quantity of positive cells was increased, which was detected by SA-b-gal staining and quantification of the SA-b-gal staining in METTL7Ash group (P<0.05). The retrovirus was used to transfect the DPSCs. Compared with the control group (Vector), the expression of METTL7A in the METTL7A overexpression group (HA-METTL7A) was significantly increased (P<0.01). The quantity of positive cells detected by SA-b-gal staining and quantification of SA-b-gal staining in the HA-METTL7A group was significantly decreased (P<0.01). In addition, compared with the control group, the m6A methylation modification level of DPSCs in the METTL7Ash group was significantly decreased, while the m6A methylation modification level of DPSCs in the METTL7A overexpression group was significantly increased. After adding the Cyc to the METTL7A overexpression group, the quantity of positive cells detected by SA-b-gal staining and quantification significantly increased compared with the METTL7A overexpression group (P<0.01). After adding the Cyc to the METTL7A overexpression group, the ALP activity was significantly inhibited that promoted by METTL7A overexpression (P<0.05). Conclusions: METTL7A may inhibit the cell senescence and promote osteogenic/odontogenic differentiation of DPSCs by regulating m6A methylation levels.

Objective:?To explore the molecular mechanism of ANGPTL4 in the progression and lymph node metastasis of tongue cancer, in order to provide a new molecular target for the treatment of tongue cancer.. Methods:?The ANGPTL4 gene in tongue cancer cells was silenced by small interfering RNA (siRNA). The transfection efficiency was tested by qRT-PCR. The biological behavior of tongue cancer cells after ANGPTL4 silencing was determined by CCK-8, Transwell and scratch experiments. The expressions of epithelial-to-mesenchymal transition（EMT）related markers were detected by reverse transcription polymerase chain reaction and Western blotting. Results:?After silencing ANGPTL4 by siRNA, the proliferation was significantly reduced （P<0.01） and migration ability of tongue cancer cells was weakened (P＜0.05). The expression of downstream related genes of EMT, E-cadherin was up-regulated and DDR1, Vimentin, ZEB-1 were down-regulated. Conclusions:?Silencing ANGPTL4 can enhance the adhesion between tongue cancer cells, thereby reducing the migration and epithelial-mesenchymal transition of tongue cancer cells. ANGPTL4 may be a key target for lymph node metastasis of tongue cancer.

Objective: This study used 3D scanning technology to explore the morphological characteristics of the facial soft tissue in mouth-breathing children. Methods: 81 children aged 10-12 years, 42 children with mouth breathing, and 39 children with nasal breathing, 3dMDFace system was used to obtain three-dimensional facial images, and a total of 18 measurement values were obtained, including linear distances, angles, and ratios. Subjects were grouped by gender, measures were compared using Independent sample t-test and Mann Whitney u test, and binomial logistic regression was used to verify the correlation between facial features and breathing patterns. Results: For males, mouth breathing had significantly smaller nasolabial angle compared with nasal breathing (p<0.05). Regarding the female group, mouth breathing compared to their nasal breathing counterpart had significantly decreased values in the mandibular width; the ratio of the mandibular width to the sum of the upper facial height, and the upper and lower lip height; and the ratio of the mandibular width to the sum of the upper and lower lip height (p<0.01). Besides significantly increased value in the ratio of lip width to mandibular width (p<0.05). Logistic regression results showed that nasolabial angle, and mandibular width were correlated with mouth breathing(p<0.05). Conclusion: Mouth-breathing children showed narrower mandibular width and more protruded upper lip.

Diabetes and periodontitis were chronic inflammatory diseases caused by a variety of complex factors. They were closely related with each other. Both diabetes and periodontitis were urgent health problems that our society is currently grappling with. The high glucose microenvironment will significantly increase the incidence of periodontal disease and accelerate bone loss, hinder periodontal regeneration and bring great challenges to periodontal treatment. Starting from the pathogenesis of periodontal disease, this review introduced the effects of high glucose microenvironment on periodontal tissue cells such as epithelial cells, immune cells and stem cells, and proposed corresponding targeted therapeutic strategies for future periodontal treatment under high glucose microenvironment.

The ultimate goal of periodontal treatment was to reconstruct the structure and function of cementum-periodontal ligament-alveolar bone complex. However, how to precisely regulate the mineralization of different periodontal tissues was the key point and main difficulty in achieving periodontal tissue regeneration. Studies had shown that pyrophosphate (PPi) and its related regularoty factors could regulate the mineralization of alveolar bone, cementum and periodontal ligament. In this review, we analysed and summarized the research progress of the regulation of PPi and its related regulatory factors on periodontal supporting tissue mineralization and try to provide a theoretical basis for periodontal regeneration.

Heterotopic ossification (HO) was the formation of bone outside the skeleton in non bone tissue. Inflammation had a contributory role in the development of HO, and macrophages were key mediators of inflammation. Large numbers of macrophages were recruited to the site of HO and were involved in the molecular mechanisms of osteogenic differentiation of mesenchymal stem cells, angiogenesis, and the hypoxic microenvironment. Influenced by changes in the microenvironment, macrophages were activated and polarized into different subpopulations exercising different functions. Metabolites of the tricarboxylic acid cycle played specific roles for both macrophage activation and homeostatic functions. In this paper, we provided an overview of the reprogramming of glycometabolism in macrophages in HO.