Background: In recent years, annual incidences of adenoid hypertrophy (AH), a highly common tissue lesion in children, have increased. Currently, research on AH has focused on its obstruction of nasal cavity function, and little has been written on its influence on the upper airway’s bone structure. For this reason, our present study seeks to determine the influence of AH on both the morphological development characteristics of the upper airway and the craniofacial features in children, with the goal being to offer more choices for diagnosing and treating the condition in the future. Methods: From June 2019 to December 2020 in Department of Orthodontics, Beijing Stomatological Hospital, Capital Medical University, 38 children with AH admitted to the Department of Otolaryngology [research group (RG)] and 35 children [control group (CG)] who underwent orthodontic treatment over the same time span were selected as the research objects. X-ray examination of the lateral position of the head, observation of the maxillofacial structure, and detection of the children’s height, growth factors, and sleep status, and analysis of the differences between the two groups. Results: The height of RG, insulin-like growth factor-1 (IGF-1) as well as insulin-like growth factor binding protein-3 (IGFBP-3) were all lower than CG (P<0.05), the upper airway became narrower, and the malocclusion was aggravated (P<0.05). Cephalometric measurement showed that the angle between the subspinale and sella at nasion (SNA angle) and the angle between the subspinale and supraemental at nasion (ANB angle) of RG children decreased, and the angle between the supraemental and sella at nasion (SNB angle) increased (P<0.05). In addition, the sleep quality of RG was significantly lower than that of CG (P<0.05). Conclusions: AH can change a child’s breathing mode and function by giving rise to upper airway stenosis, and by inducing deformities of their craniomaxillofacial region and oral cavity, thus disrupting their normal growth and development.

Background: Butyrate is a major subgingival microbial metabolite that is closely related to periodontal disease. It affects the proliferation and differentiation of mesenchymal stem cells. However, the mechanisms by which butyrate affects the osteogenic differentiation of periodontal ligament stem cells (PDLSCs) remain unclear. Here, we investigated the effect of sodium butyrate (NaB) on the osteogenic differentiation of human PDLSCs. Methods: PDLSCs were isolated from human periodontal ligaments and treated with various concentrations of NaB in vitro. The cell counting kit-8 assay and flow cytometric analysis were used to assess cell viability. The osteogenic differentiation capabilities of PDLSCs were evaluated using the alkaline phosphatase activity assay, alizarin red staining, RT-PCR, western blotting and in vivo transplantation. Results: NaB decreased PDLSC proliferation and induced apoptosis in a dose- and time-depend manner. Additionally, 1 mM NaB reduced alkaline phosphatase activity, mineralization ability, and the expression of osteogenic differentiation-related genes and proteins. Treatment with a free fatty acids receptor 2 (FFAR2) antagonist and agonist indicated that NaB inhibited the osteogenic differentiation capacity of PDLSCs by affecting the expression of Smad1. Conclusion: Our findings suggest that NaB inhibits the osteogenic differentiation of PDLSCs by activating FFAR2 and decreasing the expression of Smad1.

Background: MicroRNA-155 (miR-155) is a multifunctional miRNA whose expression is known to be involved in a range of physiological and pathological processes. Its association with several oral diseases has been established. However, the specific role of miR-155 in orthodontic tooth movement remains unclear. In this study, we investigated the impact of miR-155 on osteoclast differentiation and orthodontic tooth movement models, aiming to explore the underlying mechanisms. Methods: In this experiment, we utilized various agents including miR-155 mimic, miR-155 inhibitor, as well as non-specific sequences (NC mimic & NC inhibitor) to treat murine BMMNCs. Subsequently, osteoclast induction (OC) was carried out to examine the changes in the differentiation ability of monocytes under different conditions. To assess these changes, we employed RT-PCR, Western blotting, and TRAP staining techniques. For the orthodontic tooth movement model in mice, the subjects were divided into two groups: the NaCl group (injected with saline solution) and the miR-155 inhibitor group (injected with AntagomiR-155). We observed the impact of orthodontic tooth movement using stereoscopic microscopy, micro-CT, and HE staining. Furthermore, we performed RT-PCR and Western blotting analyses on the tissues surrounding the moving teeth. Additionally, we employed TargetScan to predict potential target genes of miR-155. Results: During osteoclast induction of BMMNCs, the expression of miR-155 exhibited an inverse correlation with osteoclast-related markers. Overexpression of miR-155 led to a decrease in osteoclast-related indexes, whereas underexpression of miR-155 increased those indexes. In the mouse orthodontic tooth movement model, the rate of tooth movement was enhanced following injection of the miR-155 inhibitor, leading to heightened osteoclast activity. TargetScan analysis identified SOCS1 as a target gene of miR-155. Conclusions: Our results suggest that miR-155 functions as an inhibitor of osteoclast differentiation, and it appears to regulate osteoclasts during orthodontic tooth movement. The regulatory mechanism of miR-155 in this process involves the targeting of SOCS1.

Excessive sugar intake has become a major challenge in modern societies. Stevioside is a promising non-calorie sweetener with anti-inflammatory effects; however, its effects on the oral environment and periodontitis remain unclear. Therefore, this study explores the effect of stevioside on periodontitis in mice. Mice were divided into four groups, namely, control, treated with water, and periodontitis models, established using 5 − 0 silk sutures ligation around the second molar then infected the oral cavity with Porphyromonas gingivalis (P. gingivalis) viscous suspension, divided into three groups treated with 0.1% stevioside (P + S), 10% glucose (P + G), or water (P). Micro-CT scanning was used to assess alveolar bone resorption, while RT-PCR was used to evaluate the inflammatory factors expression and P. gingivalis invasion in the gingiva. The composition of the oral bacteria was analysed using 16 S rRNA sequence in the saliva. In addition, P. gingivalis was co-cultured with stevioside at different concentrations in vitro, and bacterial activity was detected via optical density values and live/dead staining. The virulence was detected using RT-PCR, while biofilm formation was detected using scanning electron microscopy. Compared with 10% glucose, treatment with 0.1% stevioside reduced alveolar bone absorption and osteoclasts while decreasing IL-6, TNF-α, IL-1β, and P. gingivalis in the gingiva of periodontitis mice. The CEJ-ABC distance in the P + S group was significantly lower than that in the P and P + G groups (P < 0.05). Moreover, the composition of the oral bacteria in the P + S group was similar to that of the control. In vitro stevioside treatment also reduced the bacterial activity and toxicity of P. gingivalis in a dose-dependent manner and affected its biofilm composition. Our results indicate that, compared with 10% glucose, 0.1% stevioside intake can reduce alveolar bone resorption and inflammation in periodontal tissues in mice; the bacterial composition following 0.1% stevioside intake was similar to that of a healthy environment. In vitro, high concentrations of stevioside reduced P. gingivalis activity, biofilm formation, and virulence expression. Therefore, stevioside is a potential alternative to glucose for patients with periodontitis.