With the increasing proportion of human papilloma virus (HPV) infection in the pathogenic factors of oropharyngeal cancer, a series of changes have occurred in the surgical treatment. While the treatment mode has been improved, there are still many problems, including the inconsistency between diagnosis and treatment modes, the lack of popularization of reconstruction technology, the imperfect post-treatment rehabilitation system, and the lack of effective preventive measures. Especially in terms of treatment mode for early oropharyngeal cancer, there is no unified conclusion whether it is surgery alone or radiotherapy alone, and whether robotic minimally invasive surgery has better functional protection than radiotherapy. For advanced oropharyngeal cancer, there is greater controversy over the treatment mode. It is still unclear whether to adopt a non-surgical treatment mode of synchronous chemoradiotherapy or induction chemotherapy combined with synchronous chemoradiotherapy, or a treatment mode of surgery combined with postoperative chemoradiotherapy. In order to standardize the surgical treatment of oropharyngeal cancer in China and clarify the indications for surgical treatment of oropharyngeal cancer, this expert consensus, based on the characteristics and treatment status of oropharyngeal cancer in China and combined with the international latest theories and practices, forms consensus opinions in multiple aspects of preoperative evaluation, surgical indication determination, primary tumor resection, neck lymph node dissection, postoperative defect repair, postoperative complication management prognosis and follow-up of oropharyngeal cancer patients. The key points include: ① Before the treatment of oropharyngeal cancer, the expression of P16 protein should be detected to clarify HPV status; ② Perform enhanced magnetic resonance imaging of the maxillofacial region before surgery to evaluate the invasion of oropharyngeal cancer and guide precise surgical resection of oropharyngeal cancer. Evaluating mouth opening and airway status is crucial for surgical approach decisions and postoperative risk prediction; ③ For oropharyngeal cancer patients who have to undergo major surgery and cannot eat for one to two months, it is recommended to undergo percutaneous endoscopic gastrostomy before surgery to effectively improve their nutritional intake during treatment; ④ Early-stage oropharyngeal cancer patients may opt for either surgery alone or radiation therapy alone. For intermediate and advanced stages, HPV-related oropharyngeal cancer generally prioritizes radiation therapy, with concurrent chemotherapy considered based on tumor staging. Surgical treatment is recommended as the first choice for HPV unrelated oropharyngeal squamous cell carcinoma (including primary and recurrent) and recurrent HPV related oropharyngeal squamous cell carcinoma after radiotherapy and chemotherapy; ⑤ For primary exogenous T1-2 oropharyngeal cancer, direct surgery through the oral approach or da Vinci robotic surgery is preferred. For T3-4 patients with advanced oropharyngeal cancer, it is recommended to use temporary mandibulectomy approach and lateral pharyngotomy approach for surgery as appropriate; ⑥ For cT1-2N0 oropharyngeal cancer patients with tumor invasion depth >3 mm and cT3-4N0 HPV unrelated oropharyngeal cancer patients, selective neck dissection of levels IB to IV is recommended. For cN+ HPV unrelated oropharyngeal cancer patients, therapeutic neck dissection in regions I-V is advised; ⑦ If PET-CT scan at 12 or more weeks after completion of radiation shows intense FDG uptake in any node, or imaging suggests continuous enlargement of lymph nodes, the patient should undergo neck dissection; ⑧ For patients with suspected extracapsular invasion preoperatively, lymph node dissection should include removal of surrounding muscle and adipose connective tissue; ⑨ The reconstruction of oropharyngeal cancer defects should follow the principle of reconstruction steps, with priority given to adjacent flaps, followed by distal pedicled flaps, and finally free flaps. The anterolateral thigh flap with abundant tissue can be used as the preferred flap for large-scale postoperative defects.

The oral cavity harbors a diverse population of microorganisms, making it one of the most heavily colonized sites in the human body. Maintaining a balanced microecology is crucial for oral health. Ligilactobacillus salivarius as a species of Ligilactobacillus, has good oral colonization ability and potential to improve oral microecology for disease prevention and control. Currently, the application and mechanism of Ligilactobacillus salivarius in oral diseases include several aspects. First, by directly inhibiting the growth of Streptococcus mutans and downregulating the expression of its cariogenic virulence factor, gtfs, the aim is to reduce the number of adherent Streptococcus mutans on the tooth surface, thereby preventing dental caries. Second, reducing the number of keystone taxa in periodontitis, and the virulence factors of Aggregatibacter actinomycetemcomitans, including CdtB and LtxA, can alleviate local stimulation in patients with periodontitis. Additionally, directly inhibiting macrophage MAPK and NF-κB pathway activation suppresses osteoclastogenesis and reduces periodontal bone absorption. In mucosal inflammation, Ligilactobacillus salivarius competes with Candida albicans, inhibits the formation of pathogenic hyphae or germ tubes, and prevents monilial stomatitis. Ligilactobacillus salivarius can also reduce the amount of Staphylococcus aureus and mitigate the activation of the macrophage TLR/PI3K/Akt/mTOR and TLR/PI3K/Akt/IκB/NF-κB pathways induced by S. aureus infections, thus alleviating inflammation in the oral and pharyngeal regions. In vitro studies on oral tumors have revealed that Ligilactobacillus salivarius can downregulate the expression of cancer cell Akt/Cyclin D1, induce direct apoptosis of tumor cells, reduce COX-2 expression, and improve the tumor immune-suppressive microenvironment. Previous studies have revealed considerable variability in Ligilactobacillus salivarius, necessitating more detailed research to clarify its clinical effects, safety, and mechanisms. Despite the emergence of novel microbiological research techniques, their application to Ligilactobacillus salivarius remains relatively limited. One crucial direction for future research is to better utilize these methods to investigate the effects of Ligilactobacillus salivarius on oral diseases. Considering these factors, this study provides a comprehensive review of existing research studies on Ligilactobacillus salivarius in the fields of oral medicine and dentistry, with the aim to serve as a reference and guide for future studies.

The irreversible destruction of periodontal tissue caused by periodontitis is the result of an imbalance between external pathogenic factors and the internal immune response. As human immune cells, macrophages have both pro- and anti-inflammatory roles in the occurrence and development of periodontitis. Pathogenic bacteria, inflammatory cytokines, and neutrophils in the periodontal microenvironment can significantly affect the metabolism and functional status of macrophages, and the status of macrophages can regulate disease processes. By activating the NF-κB signaling pathway, the bacteria cause macrophages to undergo M1 proinflammatory polarization and pyroptosis, forming a microenvironment that induces periodontal tissue destruction. With the development of the disease, numerous apoptotic neutrophils are recognized and phagocytized by macrophages (i.e. efferocytosis), which can both inhibit the NF-κB pathway and activate the nuclear receptors PPAR and LXR, promoting the anti-inflammatory polarization of M2 and further enhancing the efferocytosis activity of macrophages. As a result, these treatments can limit tissue inflammatory damage and promote tissue repair. In recent years, periodontitis treatment strategies focusing on macrophage regulation have received extensive attention, including gene knockout, nanoparticles, exosomes, miRNA, and polyunsaturated fatty acid diets. In this article, we review the specific role of macrophages in periodontitis from three aspects, including macrophage polarization, pyroptosis, and efferocytosis, which may improve our understanding of periodontitis and provide possible directions for periodontitis treatment strategies.

Periodontitis and periapical periodontitis have a high incidence rate and often result in the progressive absorption of alveolar bone. This is one of the main causes of tooth loosening and loss. Prolonged local inflammation leads to the proliferation of capillaries, fibroblasts, and inflammatory cells such as neutrophils and lymphocytes. This process results in the replacement of surrounding bone tissue with inflammatory granulation tissue. Traditionally, it has been advocated that inflammatory granulation tissue is pathological and should be completely removed from the extraction socket to avoid complications such as bleeding, infection, and poor bone healing after tooth extraction. Although the regenerative capacity of inflammatory granulation tissue is reduced, it can be enhanced by increasing the body’s immunity or by eliminating pathogenic stimuli (such as tooth extraction and root canal treatment). As a result, the fibrous components in the inflammatory granulation tissue gradually increase, while infiltrating inflammatory cells gradually decrease. Ultimately, this transformation leads to the formation of reparative granulation tissue, followed by ossification. Furthermore, the use of granulation tissue from the tooth extraction socket for immediate implantation to facilitate wound closure or soft tissue reconstruction has yielded favorable clinical outcomes, and histological studies simultaneously confirmed the presence of mesenchymal stem cells within the inflammatory granulation tissue. Therefore, it is necessary to reconsider the traditional belief that inflammatory granulation tissue must be completely removed. Given the potential of inflammatory granulation tissue to undergo osteogenic transformation under appropriate interventions, regulating the transformation of inflammatory granulation tissue into reparative granulation tissue with osteogenic potential represents a novel strategy for the regenerative treatment of dental alveolar inflammatory lesions. This approach holds broad clinical application prospects and is an important research direction for the future. Reactive oxygen species, NOD-like receptor protein 3, and matrix metalloproteinase K are key regulatory factors involved in the transformation of inflammatory granulation tissue into reparative granulation tissue. Furthermore, bone morphogenetic protein 2 and vascular endothelial growth factor are key regulatory factors involved in the osteogenic regeneration of reparative granulation tissue. However, the molecular mechanisms of these regulatory factors remain unclear; therefore, elucidating their molecular mechanisms will help identify suitable targets for promoting the regeneration of dental alveolar inflammatory lesions. Furthermore, this will contribute to the development of related biological treatment technologies and drugs, which may ultimately provide a more minimally invasive and effective treatment for inflammatory lesions of alveolar bone. However, it is important to note that research in this field is still in its early stages. There is still considerable progress to be made before clinical translation and application can be achieved.

Bacterial overproliferation and virulence factors in plaque biofilms can cause inflammation of soft and hard tissues around the implant, resulting in peri-implantitis. If not well controlled, severe peri-implantitis can lead to failure of implant osseointegration and implant loosening and loss. Currently, peri-implantitis can be treated by surgical and non-surgical treatment such as mechanical debridement and chemotherapy, but there remain problems related to the unpredictable therapeutic effect and high recurrence rate. Therefore, gaining a comprehensive understanding of the relationship between plaque biofilm formation and peri-implantitis is crucial for the prevention and treatment of peri-implantitis. In this article, we comprehensively review current research on the specific composition and formation process of biofilms and the influence of implant material characteristics on biofilm formation. The results of the research review indicated that peri-implantitis biofilms are composed of extracellular matrix, with a predominant population of anaerobic Gram-negative bacteria embedded within. The formation process includes the acquisition of an acquired membrane, microbial adhesion, and biofilm detachment and dispersion. Biofilm formation is primarily influenced by the implant surface roughness, surface free energy (SFE), and material properties. Current strategies for biofilm removal around implants mainly involve implant surface coating techniques, mechanical debridement, chemical agents, laser therapy, and photodynamic therapy; however, the therapeutic outcomes remain uncertain. The future research direction will be based on the characteristics of the plaque biofilm around the implant, combined with cutting-edge methods, such as nanotechnology, immunotherapy, and gene therapy, to continuously prevent the formation of plaque biofilm on the surface of the implant to prevent and treat peri-implantitis.

Objective To explore the influence of apical dense bone islands on tooth movement during orthodontic treatment and its complications, and to provide a reference for orthodontic clinical treatment. Methods This study obtained approval from the hospital ethics committee. A retrospective analysis was conducted on 33 patients with apical dense bone islands who received full-mouth fixed orthodontic treatment in the Orthodontics Department of Huizhou Stomatological Hospital from 2018 to 2022. Cone-beam CT (CBCT) was used to determine the location, distribution, and wrapping severity of the apical dense bone islands before treatment. The number of loose teeth located in the apical dense bone islands and the degree of external apical root resorption in the apical area of teeth were analyzed before treatment, immediately after treatment, and 12 months after treatment. Results There were 33 orthodontic patients (aged 11 to 42 years, with an average age of 16.7 years and a median age of 15 years) included in this study, including 12 males (36.4%) and 21 females (63.6%). All apical dense bone islands involved a single tooth located in the mandible, mainly in the premolar-molar area. No gender differences were present in the location of the dense bone islands (P>0.05). The apical dense bone islands were mildly wrapped in 23 cases (69.7%), moderately wrapped in 10 cases (30.3%), and severely wrapped in no cases. No difficulty in tooth movement or incomplete closure of extraction space was found in the apical dense bone islands with different degrees of wrapping during orthodontic treatment. For teeth located in apical dense bone islands, 1 patient (3.0%) had loose teeth before treatment, 6 patients (18.2%) had loose teeth after treatment, and 2 patients (6.1%) had loose teeth 12 months after treatment. The number of patients with grade I loose teeth increased after treatment and 12 months after treatment. There was a statistically significant difference in the number of loose teeth before and after treatment (P<0.05), no statistically significant difference in the number of loose teeth before treatment and 12 months after treatment (P>0.05), and no statistically significant difference in the number of loose teeth after treatment and 12 months after treatment (P>0.05). After treatment, apical dense bone islands showed mild resorption in 26 cases (78.8%), moderate resorption in 7 cases (21.2%), and severe resorption in no cases. The apical dense bone islands showed mild resorption in 25 cases (75.8%), moderate resorption in 8 cases (24.2%), and severe resorption in no cases 12 months after treatment. For the severity of root resorption, there was a statistically significant difference between before and after treatment (P<0.05) as well as between before treatment and 12 months after treatment (P<0.05). However, no statistically significant difference was observed between after treatment and 12 months after treatment (P>0.05). Conclusion Apical dense bone islands were not found to affect tooth movement during orthodontic treatment. After orthodontic treatment, the number of loose teeth increased and mild-to-moderate tooth external apical root resorption occurred, which may be a potential risk of external apical root resorption. Thus, it is recommended to pay close attention during the orthodontic process.

Inflammatory bowel disease (IBD) is a group of chronic, non-specific inflammatory diseases of the gastrointestinal tract including primarily Crohn’s disease and ulcerative colitis, which are affected by multiple factors. Periodontitis is a type of disease characterized by plaque biofilm as the initiating factor and chronic destruction of alveolar bone via resorption. An increasing number of studies have reported a correlation between periodontitis and IBD, but the relationship between the two remains unclear. In this study, we explore the internal relationships between the two diseases from three dimensions, including epidemiological, biological, and associated treatment evidence. Based on epidemiological evidence, periodontitis was found to be associated with an increased risk of IBD, which also affects periodontal health, although the bidirectional correlation needs to be further studied by expanding the number of data sources. From the biological evidence, both clinical studies and animal experiments show that IBD and periodontitis are interconnected. Based on evidence from association therapy, drugs that are beneficial for the treatment of IBD are also effective in the prevention and treatment of periodontitis. In addition, drugs that are good for improving periodontitis can also significantly alleviate IBD. The interaction mechanism between IBD and periodontitis includes the microbial pathway and the immunization route. The microbial pathway refers to the increase in the probability of intestinal tract ectopic colonization by oral bacteria transmitted through the mouth-gut axis or blood, resulting from the increase in the proportion of opportunistic pathogens in the oral cavity of patients with periodontitis and the influence of IBD on the secretion of gastric juice and the balance of intestinal flora. These microorganisms further aggravate IBD inflammation by releasing virulence factors, destroying the intestinal mucosal barrier, and triggering inflammatory responses. In periodontitis, adaptive immunity is activated in the mouth, leading to the production of a large number of immune cells, including Th17 containing the intestinal homing marker α4β7 integrin on their surface. Increased ligand expression of α4β7 integrin in the intestinal mucosa of patients with IBD accelerates oral Th17 cell transfer to the intestine, thereby worsening intestinal inflammation. In parallel, the abnormal expression of cytokines, such as TNF-α, IL-1β, IL-10, IL-6, IL-21, soluble CD40 ligand (sCD40L), IL-23, and INF-γ, in the oral cavity of patients with IBD was observed, suggesting that IBD may affect periodontitis through immunity. These cytokines represent targets for the treatment of both diseases and provide a research direction for their prevention and treatment in the future.

Antimicrobial photodynamic therapy uses photosensitizers to produce reactive oxygen species under light exposure to inhibit pathogenic bacteria. Although its application in the management of oral infectious diseases has increased over recent years, it is limited by inadequate tissue and biofilm penetration and suboptimal bioavailability exhibited by individual photosensitizers. These challenges can potentially be surmounted through the integration of nanomaterials, such as polymers, metals and metal oxides, metal-organic frameworks, and carbon and silicon nanomaterials. Polymers allow the controlled release of photosensitizers through structural adjustments but have low stability, while metals and metal oxides possess strong antibacterial properties but can be potentially toxic. Meanwhile, metal-organic frameworks have flexible structures and multifunctionality but have low stability and potential toxicity. Moreover, carbon and silicon nanomaterials, despite exhibiting excellent antibacterial properties and biocompatibility, have limited application due to high production costs. Materials with inherent antibacterial properties, such as chitosan and graphene oxide, have broader application prospects, as they can form multimodal antibacterial platforms with photosensitizers, enhancing the antibacterial effects and eliminating infections. Future research could incorporate other functional materials, such as anti-inflammatory agents and immunomodulatory materials, to construct comprehensive therapeutic nanoplatforms for the treatment of oral infectious diseases.

Alzheimer’s disease (AD), a common neurodegenerative disease, has been linked to periodontitis, especially Porphyromonas gingivalis (P. gingivalis) infection. This review summarizes the potential mechanisms and pathways through which P. gingivalis and its virulence factors are involved in AD pathogenesis, aiming to provide the scientific basis for the development of novel prevention and treatment strategies for AD. P. gingivalis can promote AD by exacerbating neuroinflammation, facilitating amyloid beta and Tau deposition, and disrupting the blood-brain barrier. Gingipains, secreted by P. gingivalis, serve as core effector molecules by increasing the blood-brain barrier permeability. The association between P. gingivalis and its effectors and AD pathology has been validated by metagenomic analysis and sample detection, indicating that P. gingivalis may be an environmental susceptibility factor or modifiable risk factor for AD. However, the precise mechanisms by which P. gingivalis influences AD, and its interactions with other potential AD-related factors, remain unclear. Moreover, further research needs to be conducted on the therapeutic potential of P. gingvalis intervention in improving AD.

Exploration of the underlying mechanisms of tumor occurrence and development, as well as evaluation of the efficacy of anticancer drug treatments, relies on various research models both in vivo and in vitro. Over the past few decades, with the rapid advancement of biomedical technology, significant achievements have been made in this field. Gene detection technology has progressed from a single-gene perspective to multi-gene approaches, resulting in rapid development of bioinformatics and transformation of the conceptual understanding of malignant tumors. Moreover, in vitro cell research models have evolved from monolayer two-dimensional and primary cultures to three-dimensional configurations, which better imitate the cellular interactions and functions within tumor tissues. Furthermore, in vivo animal research models have transitioned from traditional carcinogen induction and cell or tissue xenografts to genetically engineered animal models or xenograft models, enabling targeted investigation into the roles of relevant genes in the occurrence and development of tumors. Clinical research has shifted from simple retrospective to prospective studies, including phase Ⅰ/Ⅱ/Ⅲ clinical trials, investigator-initiated clinical trials, and real-world clinical trials. The major shortcomings of current malignant tumor research models include their singularity, insufficient simulation of the tumor microenvironment, disparities between animal models and human tumors, and the lack of consideration for personalized medicine. Further research and optimization of the models are still needed in the future, along with more effective integration of different models to form an optimized comprehensive experimental model system. This review systematically examines and comprehensively overviews the evolution of malignant tumor research models with the aim of providing more references to researchers engaged in oncology research.

Objective To employ next-generation sequencing (NGS) to analyze differentially expressed mRNAs in the gingival tissue of hypertensive rats with or without periodontitis to provide a theoretical basis for the prevention and treatment of hypertension with periodontitis. Methods After obtaining approval from the Animal Experiment Ethics Committee, a hypertensive rat model was established by administering high-salt feed containing 8%（w/w） NaCl, and a periodontitis rat model was established by ligating the first molar of the mandibular region using 3-0 sterile silk thread. Rat models of the normal control (N), hypertension (H), and hypertension with periodontitis (PH) groups were established. The blood pressure, heart rate, alveolar bone resorption, and number of osteoclasts in the alveolar bone were measured, before harvesting the gingival tissues from the three groups for NGS to analyze the expression of significantly different genes. Gene ontology (GO) enrichment analysis was performed for all significantly differentially expressed genes between the H and PH groups. Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis was performed. Key genes were screened by protein-protein interaction (PPI) networks, and the key gene expression in each group was verified using immunohistochemistry (IHC). The expression of key genes in the systemic circulation of each group was analyzed using enzyme-linked immunosorbent assay (ELISA). Results At the end of the experiment (11th week), the blood pressure was higher in both the H and PH groups than that in the N group (P<0.001), but there was no statistically significant difference in blood pressure between the H and PH groups. There was no statistical difference in heart rate among the 3 groups. Micro-CT showed that the distance from the cemento-enamel junction to the alveolar bone crest (CEJ-ABC) of the mandibular first molar in the PH group was significantly higher than that in the N and H groups (P<0.016 7). The number of osteoclasts in the alveolar bone of the PH group was significantly higher than that of the N and H groups (P<0.0167). No common differentially expressed genes were found among the 3 groups. There were 235 significantly differentially expressed genes in the gingival tissue between the H and PH groups, and 137 upregulated genes (e.g., P-selectin, keratin 16, and S100 calcium binding protein A) and 98 downregulated genes (e.g., FK506 binding protein 5, mediator complex subunit 22, zinc finger and BTB domain containing 16) in the PH group compared to the H group. GO analysis showed that the major enriched biological processes (BP) were leukocyte migration, the major cellular component (CC) was complex of collagen trimers, and the significant molecular function (MF) was extracellular matrix structural constituent in the H and PH groups. KEGG pathway analysis showed that signaling pathways such as cytokine-cytokine receptor interaction, IL-17 signaling pathway, and TNF-α signaling pathway were significantly enriched in the H and PH groups. PPI analysis identified four key genes affecting periodontitis in hypertensive conditions, including interleukin-1β (IL-1β), matrix metalloproteinase-9 (MMP-9), collagen type I alpha1 (COL1α1), and chemokine ligand 1 (CXCL1). Compared to the N and H groups, the expressions of IL-1β and TNF-α were all upregulated in the gingival tissue and systemic serum in the PH group (P<0.016 7). Conclusion The differentially expressed mRNAs in hypertension with or without periodontitis included IL-1β and MMP-9, while the differentially expressed signaling pathways were IL-17 and TNF-α. These results provide a theoretical reference for further investigation of the molecular regulatory mechanism of hypertension with periodontitis in the future.

Objective To study the effect of deep learning applied to the assisted diagnosis of radiolucent lesions and radiopaque lesions of the jaws in panoramic radiography and to reduce the missed diagnosis, with early screening to assist doctors to improve the diagnostic accuracy. Methods This study was approved by the Ethics Committee of the West China Stomatological Hospital of Sichuan University. The YOLO v8m-p2 neural network model was constructed with 443 panoramic images as a subject to read. The labeled images were divided into 354 training sets, 45 verification sets, and 44 test sets, which were used for model training, verification, and testing. Accuracy, recall, F-1 score, G score, and mAP50 were used to evaluate the detection performance of the model. Results 443 panoramic images covered the common benign lesions of the jaw, the number of radiolucent lesions of the jaw was 318, containing dentigerous cyst, odontogenic keratocyst, and ameloblastoma. The number of radiopaque lesions was 145, containing idiopathic osteosclerosis, odontoma, cementoma, and cemento-osseous dysplasia; the samples are well representative. The accuracy of the YOLO v8m-p2 neural network model in identifying jaw lesions was 0.887, and the recall, F-1 score, G score, and mAP50 were 0.860, 0.873, 0.873, and 0.863, respectively. The recall rates of dentigerous cyst, odontogenic keratocyst, and ameloblastoma were 0.833, 0.941, and 0.875, respectively. Conclusion YOLO v8m-p2 neural network model has good diagnostic performance in preliminary detection of radiolucent and radiopaque lesions of the jaws in panoramic radiography and multi-classification monitoring of radiolucent lesions of jaws, which can assist doctors to screen jaw diseases in panoramic radiography.

Objective To investigate the clinical characteristics and prognosis of crown fractures in immature permanent incisors due to trauma, and identify factors affecting their prognosisto provide a reference for clinical treatment. Methods This study was approved by the Medical Ethics Committee of West China Stomatology Hospital, Sichuan University. The study subjects were patients admitted to the pediatric stomatology department from December 2011 to December 2021, and a retrospective analysis was conducted on young permanent teeth with anterior crown fracture caused by injury and followed up for at least 1 year, which were diagnosed as enamel fractures, enamel-dentin fractures, and complicated crown fracture and treated by observation, pulpotomy etc. in the first appointment. The age, sex and time elapsed from trauma to baseline visit of the patients and the location, mobility, stage of root development, diagnosis and treatments were collected. The occurrence of pulp infection, pulp necrosis, and other events in the affected tooth is defined as clinical failure. Record whether clinical failure occurred and the timing of their occurrence of the traumatized tooth. Analyze factors related to the prognosis of various types of crown fractures in young permanent incisors and performsurvival analysis on the affected teeth. Results Among 358 cases of young permanent incisors, 50 cases were diagnosed with enamel fracture, 176 cases with enamel-dentin fracture, and 132 cases with complicated crown fracture. The clinical success rate of crown fractures was 73.7% (264/358) in young permanent incisors. The incidence rates of clinical failure cases, including pulp infection and necrosis, were 4% (2/50) for enamel fractures, 33.3% (58/176) for enamel-dentin fractures, and 25.8% (34/132) for complicated crown fractures respectively. The clinical failure rate of enamel-dentin fracture treated with indirect pulp capping and restoration was higher than restoration only and pulpotomy (χ² = 10.077, P = 0.004). The clinical failure rate of complicated crown fractures treated with direct pulp capping was higher than pulpotomy (χ² = 5.501, P = 0.038). The clinical failure rates between observation, smoothing edges and restoration of enamel fractures exhibit no significant differences (χ² = 0.588, P = 0.999). Risk factors for clinical failure in this study population included patient age over 9 years old (HR = 2.11, 95%CI: 1.1-3.9, P = 0.017)、time elapsed from trauma to baseline visit greater than 3 days (HR = 2.3, 95%CI: 1-4.8, P = 0.028), traumatized teeth with mobility (HR = 1.95, 95%CI: 1.2-3, P = 0.004), enamel-dentin fractures treated with restoration (HR = 6.89, 95%CI: 1.6-29.6, P = 0.010), enamel-dentin fractures treated with indirect pulp capping and restoration (HR = 13.8, 95%CI: 3.2-58.3, P<0.001) and complicated crown fractures treated with direct pulp capping (HR = 46.07, 95%CI: 8-263.8, P<0.001). Conclusion Enamel fractures treated by observation, smoothing edges and restoration, and complicated crown fractures treated with pulpotomy generally had a good prognosis in young permanent incisors. Close follow-up was recommended for crown fractures in young permanent incisors with identified risk factors for poor prognosis.

Objective To evaluate the caries excavation efficacy and minimally invasive potential of three dentine caries excavation methods including traditional excavation, chemomechanical excavation, and fluorescence-aided caries excavation using micro-computerized tomography (micro-CT). Methods This study was approved by the Biomedical Research Ethics Committee, and all patients provided informed consent. Thirty molars and premolars with dentin caries were collected and randomly divided into three groups. The samples were obtained by traditional excavation (traditional excavation group), chemomechanical excavation (chemomechanical excavation group), and fluorescence-aided caries excavation (fluorescence-aided caries excavation group), and the operation time for each sample was recorded. Micro-CT was used to scan and record the caries volume and healthy tooth volume of each tooth before and after caries excavation. The caries excavation efficacy and minimally invasive potential of the three caries excavation methods were evaluated based on the caries volume and the healthy tooth volume before and after caries excavation. Results In terms of caries excavation operation time, the chemomechanical excavation group (501.7 s ± 143.6 s) had a longer operation time than the traditional excavation group (263.9 s ± 121.2 s) and the fluorescence-aided caries excavation group (284.2 s ± 135.6 s), with a statistically significant difference (P<0.01); there was no significant difference between the traditional excavation group and the fluorescence-aided caries excavation group. In terms of caries excavation efficacy, the ratio of residual caries volume to initial caries volume was determined in the traditional excavation group (0.087 ± 0.04), followed by the fluorescence-aided caries excavation group (0.36 ± 0.10), and the chemomechanical excavation group was the highest (0.51 ± 0.10); the observed disparity between the groups exhibited statistical significance (P<0.01). In terms of minimally invasive potential, the ratio of the traditional excavation group (0.87 ± 0.05) was lower than the chemomechanical excavation group (0.99 ± 0.01) and fluorescence-aided caries excavation group (0.98 ± 0.01), with statistically significant differences (P<0.01); the difference between the ratio of the chemomechanical excavation group and the fluorescence-aided caries excavation group was not statistically significant. Conclusion The traditional excavation group had the shortest operation time, but the traditional excavation removed too much healthy dentin and demineralized dentin. The chemomechanical excavation group retained demineralized dentin and healthy dentin and had the best minimally invasive potential, but the caries excavation efficacy was poor and the operation time was long. The fluorescence-aided caries excavation preserved part of the demineralized dentin and healthy dentin, had certain minimally invasive potential, and the clinical operation time was moderate.

Objective To investigate the effect of calcium ions on the expression of kallikrein-4 (KLK4) and cell growth of ameloblast, and to provide an experimental basis for calcium ion promoting normal mineralization of enamel. Methods ALC cells were treated with 0, 2.0, 2.5, 3.0, and 3.5 mmol/L CaCl₂ for 24 and 48 h. KLK4 expression was analyzed by qRT-PCR and Western blot analysis. The viability of ALC cells was determined by using CCK-8. AnnexinV-FITC/PI dual staining combined with flow cytometry and Hoechst 33342 staining were used to detect the ALC cell cycle and cell apoptosis. The protein expression level of glucose-regulated protein 78 (GRP78) was measured by Western blot analysis. Results After 24 h of treatment with 2.5, 3.0, and 3.5 mmol/L CaCl₂, the expression of KLK4 mRNA was increased (P<0.05), and after 24 h of treatment with 2.0, 2.5, 3.0, and 3.5 mmol/L CaCl₂, the expression of KLK4 protein was increased (P<0.05). After 48 h of treatment with 3.0 mmol/L and 3.5 mmol/L CaCl₂, the expression of KLK4 mRNA and protein was increased (P<0.05). Compared with the control group, the viability of ALC cells was increased after 24 and 48 h of treatment with 2.0, 2.5, and 3.0 mmol/L CaCl₂ (P<0.05), and the highest cell viability was observed with 2.5 mmol/L CaCl₂. Hoechst 33342 staining results showed that 3.0 mmol/L and 3.5 mmol/L CaCl₂ may promote apoptosis in ALC cells. Flow cytometry showed that the proportion of G2/M phase cells and the apoptosis rate increased after 3.5 mmol /L CaCl₂ treatment for 24 h (P<0.05), compared with the 0, 2.0, 2.5, and 3.0 mmol/L CaCl₂ groups. After 24 h of treatment with 3.0 mmol/L and 3.5 mmol/L CaCl₂, the expression of GRP78 protein was reduced (P<0.05), and after 48 h of treatment with 2.5 mmol/L CaCl₂, the expression of GRP78 protein was reduced (P<0.05). Conclusion Calcium ions can promote the increase of KLK4 expression and cell viability in ALC cells, but a higher concentration of calcium ions can block the G2/M phase of ALC cells, thus inducing apoptosis of ALC cells and reducing the expression of apoptosation-related protein GRP78.

Objective To investigate the effect of the Piezo1 channel on tension-side angiogenesis and osteogenic remodeling during orthodontic tooth movement, so as to provide an experimental basis for accelerating orthodontic periodontal tissue remodeling. Methods This study was approved by the Animal Ethics Committee. Sixty healthy male Sprague-Dawley rats with bilateral maxillary incisors as the anchorage were selected, and nickel titanium tension springs were used to apply 0.5 N of force to the right maxillary first molar of the rats and construct an orthodontic tooth movement model. The rats were randomly divided into three groups (n = 20 per group). On Days 0 and 8 of force application, equal volumes of saline (control group), 100 μmol/L Piezo1 channel agonist (Yoda1 group), and 48 μmol/L Piezo1 channel inhibitor (GsMTx4 group) were injected into the buccal and palatal submucosa of the right maxillary first molar. Tooth movement distances were recorded on Days 1, 3, 7, and 14. Five rats from each group were sacrificed at each time point to obtain maxillary tissue samples. Hematoxylin and eosin (HE) staining was performed to observe the histophysiological changes in the tension-side periodontal tissues. Immunohistochemical staining was used to mark and count CD31-positive cells (microvascular quantification) and to detect the expression of osteocalcin (OCN) in the tension side. Results Measurements of tooth movement distance showed that the Yoda1 group exhibited significantly increased tooth movement distances on Days 3, 7, and 14 (0.238 ± 0.008 mm, 0.406 ± 0.011 mm, and 0.746 ± 0.013 mm, respectively) compared to the control group (P<0.05). In contrast, the GsMTx4 group showed significantly reduced tooth movement distances on Day 7 (0.282 ± 0.011 mm) and Day 14 (0.578 ± 0.008 mm) compared to the control group (P<0.05). HE staining results indicated that the periodontal ligament space on the tension side gradually widened with the duration of force application and then gradually returned to normal, with visible osteoblasts. Quantitative analysis of CD31-positive cells (microvascular quantification) showed that the Yoda1 group had significantly increased numbers of blood vessels on Day 3 (8.027 ± 0.225) and Day 7 (14.320 ± 0.471) compared to the control group (P<0.05), peaking on Day 7 and then gradually decreasing. The GsMTx4 group showed significantly fewer blood vessels in the periodontal ligament on the tension side on Day 3 (6.013 ± 0.177), Day 7 (9.187 ± 0.678), and Day 14 (12.613 ± 0.334) compared to the control group (P<0.05). Immunohistochemical results indicated that the Yoda1 group had significantly increased OCN expression on Days 1, 3, 7, and 14 compared to the control group (P<0.05), while the GsMTx4 group showed reduced OCN expression on Days 7 and 14 (P<0.05). Conclusion Activation of the Piezo1 channel promotes orthodontic tooth movement, tension-side angiogenesis, and osteogenic remodeling, while inhibition of the Piezo1 channel produces the opposite effect.

Objective To investigate the effect of resveratrol (RSV) in the treatment of peri-implantitis in a murine model and its effect on nuclear factor kappa-B (NF-κB) signaling and mitogen-activated protein kinase (MAPKs) signaling. Methods This study has been reviewed and approved by the Ethics. After extracting the right maxillary molars of 40 C57BL/6 mice and allowing them to heal naturally for 8 weeks, implants were implanted at the site of the first molar. The mice were randomly divided into a control group, a mouse peri implantitis model group, a low-dose group of 20 mg/kg resveratrol (RSV-L), and a high-dose group of 40 mg/kg resveratrol (RSV-H). After 4 weeks of implant implantation, a silk thread ligation induced peri implantitis model was established in all mice except for the control group. The model group received intervention with physiological saline by gavage, while the drug group received intervention with resveratrol by gavage for 6 consecutive weeks. After 6-week treatment, observe the swelling of the gums around the implant and measure the bone resorption around the mouse implant using micro CT. Enzyme linked immunosorbent assay (ELISA) was used to detect the levels of tumor necrosis factor alpha (TNF-α) and interleukin-6 (IL-6) in gingival crevicular fluid. HE staining was used to observe the infiltration of inflammatory cells in the surrounding tissues of mouse implants. Protein expression level and phosphorylation level of extracellular regulated protein kinases (ERK), p-ERK, c-Jun N-terminal kinase (JNK), p-JNK, p38 mitogen activated protein kinase (p38 MAPK), p-p38MAPK, nuclear factor kappa-B (NF-κB), p-NF-κB, nuclear factor-κB inhibitory protein (IκΒα), p-IκBα in MAPKs/NF-κB signaling pathway were detected by Western blot (WB). Results Resveratrol group showed reduced tissue edema and decreased alveolar bone resorption. Among them, the high-dose resveratrol group had lighter tissue edema and weaker bone resorption compared to the low-dose group. The micro CT results showed that significant changes in the bone level around the implant were observed in the model group mice at four sites: proximal, distal, buccal, and palatal. High dose resveratrol intervention reduced alveolar bone resorption (P<0.05); compared with the low-dose group, the high-dose group showed a decrease in palatal bone resorption (P<0.05), while there was no significant difference in absorption between the mesial, distal, and buccal sides (P>0.05). The ELISA results showed that compared with the model group, the levels of TNF - α and IL-6 in the gingival crevicular fluid of mice in the low-dose and high-dose resveratrol groups were lower (P<0.05). The IL-6 in the gingival crevicular fluid of mice in the high-dose resveratrol group was lower than that in the low-dose group (P<0.05). However, there was no significant difference in TNF-α levels between the two groups. HE staining showed a decrease in inflammatory cell infiltration in mice after treatment with resveratrol. The WB results showed that compared with the control group, the expression levels of p-Erk, p-JNK, p-p38MAPK, p-IκA, and p-NF-κB phosphorylated proteins in the gingival tissue of the model group mice were significantly increased (P<0.01). The resveratrol treatment group significantly inhibited the phosphorylation of p-Erk, p-JNK, p-p38MAPK, p-IκA, and p-NF-κB proteins. Compared with the low-dose group, the high-dose group inhibited the phosphorylation of MAPKs/NF-κB signaling pathway related proteins more significantly (P<0.05). Conclusion Resveratrol protect ligature induced peri-implantitis murine model, which may be related to its inhibition of phosphorylation of MAPKs/NF-κB pathway.

Objective To compare the accuracy of the original-mirror alignment algorithm and a landmark-independent method in constructing the midsagittal plane (MSP) of the cone beam computed tomography in patients with facial deformities, so as to provide a theoretical basis for symmetric analysis. Methods The study was approved by the hospital ethics committee. Cone beam computed tomography data of 30 patients with facial deformities were obtained, and the output was saved in DICOM format. The scan data were imported into Mimics 21.0; after segmentation, three-dimensional (3D) skull models were reconstructed. Furthermore, the 3D scan data of skulls were transformed into mirror skull models using Geomagic Studio 2014 reverse engineering software. The MSP of each skull was generated using both the original-mirror alignment algorithm and the landmark-independent method. Original-mirror alignment algorithm: the original skull model and its mirror model were combined, and the new data to calculate the MSP (S1) of the original data in Geomagic Studio 2014 were obtained. Landmark-independent method: the following anatomical landmarks were determined using Mimics 21.0: nasion (N), crista galli (CG), sella (S), basion (Ba), vomer (V), posterior nasal spine (PNS), incisive foramen (IF), and anterior nasal spine (ANS). The MSP (S2) of best fit was then found by minimizing the mean square distance of these eight anatomical landmarks to a plane in Geomagic Studio 2014. The results of the S1 and S2 models constructed using the original-mirror alignment algorithm and the landmark-independent method, respectively, were scored subjectively by five senior maxillofacial surgeons, and a paired t-test was performed for the two groups. The internal consistency analysis was performed based on secondary experiments to verify the repeatability of the expert evaluation method. Results The average scores of the S1 and S2 models were 65.73 and 75.90, respectively. The average score of the model constructed using the landmark-independent method was significantly higher than that of the model constructed using the original-mirror alignment algorithm (P<0.01). Furthermore, the results of the internal consistency analysis showed that the expert evaluation method had good reliability and validity. Conclusion In patients with facial deformities, the MSP constructed using the landmark-independent method is superior to that constructed using the original-mirror alignment algorithm. This study provides a theoretical basis for maxillofacial symmetry analysis in clinical settings and is clinically feasible.

Objective To investigate the impact of metabolic labeling on Porphyromonas gingivalis (Pg) and compare the imaging effects of two fluorescent probes. Methods This study was reviewed by the unit Ethics Committee and was approved by the Experimental Animal Welfare Ethics Branch of the Unit Experimental Biomedical Ethics Committee. Pg integrated N-azidoacetylgalactosamine (Ac₄GalNAz) via a bioorthogonal reaction and was labeled with Cy5-DBCO or Cy7-DBCO via a click chemistry reaction. The bacteria were divided into Pg group (control, not fluorescently labeled), Cy5-Pg group (tagged by Cy5-DBCO), and Cy7-Pg group (tagged by Cy7-DBCO). A live/dead staining kit was applied to test the viability of Pg, Cy5-Pg, and Cy7-Pg. The mRNA levels of interleukin-6 (IL-6) and IL-8 and cell proliferation were examined in human gingival fibroblasts (HGFs) after the challenge of Cy5-Pg, Cy7-Pg, or Pg. To investigate the stability of metabolic labeling, Cy5-Pg or Cy7-Pg was cocultured with Escherichia coli (E. coli). Cy5-Pg and Cy7-Pg signal intensity with serial dilutions were examined using an in vivo imaging system (IVIS). Finally, C57BL/6J mice were orally administered Cy5-Pg or Cy7-Pg for IVIS detection, and the signal-to-background ratios were calculated. Results Metabolic labeling could be applied to label live Pg in vitro. The optimal labeling concentrations for Cy5 and Cy7 were 20 μmol/L and 30 μmol/L, respectively. The area ratios of live to dead bacteria were approximately 2.0 in the three groups (F = 0.318, P>0.05). After a 6-h challenge with Cy5-Pg, Cy7-Pg, or Pg, the mRNA levels of HGFs increased by 7.86-, 7.46-, and 6.56-fold for IL-6, respectively (F = 40.886, P<0.001) and 12.43-, 13.03-, and 13.71-fold for IL-8 (F = 18.781, P<0.01), were spectively, compared to that of the Ctrl group, which was not challenged by bacteria, where no significant differences were observed among the three groups (P>0.05). HGFs were further challenged by Cy5-Pg, Cy7-Pg, or Pg at different MOIs, and cell proliferation was significantly inhibited (MOI = 10⁴∶1, F = 153.52, P<0.001; MOI = 10⁵∶1, F = 331.21, P<0.001; MOI = 10⁶∶1, F = 533.65, P<0.001), with no significant differences among the three groups (P>0.05). Within 24 h of co-culturing Cy5-Pg or Cy7-Pg with E. coli, minimal E. coli was detected. The intensities of Cy5 and Cy7 remained stable for 3 h. Additionally, the fluorescence signal intensities of Cy5 and Cy7 were linearly correlated with the concentration (R² = 0.97). After oral gavage of Cy5-Pg or Cy7-Pg in mice for the abdominal region at 1 h and 3 h, the signal-to-background ratios of Cy7-Pg were approximately 4.24-fold (t = 6.893, P<0.01) and 3.77-fold (t = 4.407, P<0.05) higher, respectively, than those of Cy5-Pg. For the isolated gastrointestinal tracts at 3 h, the signal-to-background ratio of Cy7-Pg was 5.19-fold higher than that of Cy5-Pg (t = 4.418, P<0.05). Conclusions Metabolic labeling did not significantly affect viability, immunomodulatory ability, and toxicity. The imaging effect of Cy7 on IVIS was better than that of Cy5. Our study provided experimental evidence for the correlation between periodontitis and overall health.

Bone diseases, such as osteoporosis and osteoarthritis, have emerged as pressing public health concerns requiring immediate attention and resolution. Cellular therapy and tissue engineering techniques are among the most promising therapeutic approaches for such conditions. Human induced pluripotent stem cells (hiPSCs) possess remarkable capacity for indefinite self-renewal in vitro and the ability to differentiate into all somatic cell types originating from the three germ layers, thereby making them a promising source of osteoblasts. Consequently, it is crucial to establish a well-delineated system for osteogenic differentiation of hiPSCs in vitro, with the aim to generate osteoblast-like cells that conform to clinical application standards. Numerous research teams have achieved substantial advancements in both the direct osteogenic differentiation of hiPSCs and the indirect pathway via mesenchymal stem cells. In this article, we provide a comprehensive review of these two osteogenic differentiation pathways and their current applications, with the aim of serving as a valuable reference for bone regeneration technologies. Current research efforts have relied on embryoid body formation and monolayer induction methods utilizing biomaterials to develop a system that facilitates in vitro culture and osteogenic differentiation of hiPSCs. However, the existing research is primarily constrained by unclear system components and low efficiency. Therefore, the development of a stepwise and three-dimensional induction system based on stringent regulation by specific compounds is a primary research direction for the future.

Exosomes (EXOs) are important mediators of intercellular communication that contain a variety of substances, including miRNA, mRNA, DNA, and protein molecules, which can act on target cells and have broad medical prospects as “cell-free therapy”. The inclusion of EXOs varies with the type and state of the donor cell, thus EXOs from different cell types may exhibit different biological effects. Dental mesenchymal stem cell (DMSC)-derived EXOs (DMSC-EXOs) have gained increasing research attention in the fields of tissue regenerative medicine and immune regulation. Current research on EXOs is focused on the homeostasis between proinflammatory (M1)/anti-inflammatory (M2) macrophages and T-helper 17 (Th17)/regulatory T (Treg) cells during periodontal immune regulation. Studies have shown that DMSC-EXOs can promote the transformation of macrophages and T cells and that this function may be dependent on the surrounding microenvironment and the tissue origin of stem cells. For instance, miR-1246 in dental pulp stem cell-derived EXOs promotes M2 macrophage polarization by inhibiting nuclear factor kappa-B (NF-κB) p65. Meanwhile, EXOs derived from stem cells from apical papilla promote DNA demethylase Tet2-mediated demethylation of FoxP3, maintain stable FoxP3 expression, and promote Treg cell transformation, thus alleviating local inflammation in periodontitis. In addition, the immunomodulatory activities of DMSC-EXOs can be affected by inflammatory factors. For example, EXOs derived from lipopolysaccharide-preconditioned dental follicle stem cells can reduce the receptor activator of NF-κB ligand/osteoprotegerin ratio through the reactive oxygen species (ROS)/c-Jun N-terminal kinase signaling pathway and promote M2 macrophage polarization through the ROS/extracellular signal-regulated kinase signaling pathway. Additionally, EXOs derived from gingiva-derived mesenchymal stem cells pretreated with tumor necrosis factor-α and interferon-α proinflammatory cytokines can promote M2 macrophage polarization through high expression of CD73 and CD5L, while EXOs derived from inflammatory periodontal ligament stem cells can promote M1 macrophage polarization. This article reviews the research progress on the immunoregulation and effects of DMSC-EXOs on the homeostasis of M1/M2 macrophages and Th17/Treg cells during periodontal immune regulation and provides a reference for the treatment of periodontitis using DMSC-EXOs.

Objective To investigate the expression of trophoblast cell-surface antigen 2 (TROP2) in salivary adenoid cystic carcinoma (SACC) in order to analyze its relationship with TROP2 expression and clinicopathological features, as well as to clarify the correlation between TROP2 expression and the prognosis of patients with SACC. Methods With approval from the ethics committee, the expression of TROP2 in 85 SACC and paracancer tissue samples was detected by using the immunohistochemical method, and the relationship between TROP2 expression and clinicopathological characteristics was analyzed. The Kaplan-Meier method was used to analyze the relationship between TROP2 protein expression and 5-year disease-free survival (DFS) in 40 patients with SACC. Furthermore, the logistic regression model was used to analyze the prognostic factors of patients with SACC. Results The low or no expression rate of TROP2 in SACC tissues was significantly higher than that in paracancer tissues (P<0.001). Low or no expression of TROP2 was significantly positively correlated with tumor growth and clinical staging in patients with SACC (P<0.05). Kaplan-Meier survival analysis showed that the DFS of patients with SACC with low or no expression of TROP2 protein was significantly lower than those of patients with high expression of TROP2 protein (P<0.05), and the prognosis was poor. The logistic regression model showed that low or no expression of TROP2 protein (OR = 5.37; 95% CI: 1.03-28.08; P = 0.046) and Ⅲ-Ⅳ clinical staging (OR = 6.89; 95%CI: 1.37~34.77; P = 0.019) were risk factors affecting the prognosis of patients with SACC. Conclusion Low or no expression of TROP2 protein in SACC tissues leads to poor prognosis of patients and is positively correlated with tumor growth and clinical staging. In addition, low or no expression of TROP2 can be used as an independent prognostic risk factor for poor prognosis in patients with SACC, and TROP2 is a marker of poor prognosis in patients with SACC.

The source and process of mandible development are significantly different from those of other bones in the body, and abnormal development can lead to various bone-related diseases, seriously affecting the quality of life of patients. In recent years, the role of the Hedgehog signaling pathway in bone development has received increasing attention. The Hedgehog gene includes three subtypes: Sonic Hedgehog (Shh), Indian Hedgehog (Ihh), and Desert Hedgehog (Dhh). Shh and Ihh can participate in bone metabolism regulation through various pathways, with Shh primarily involved in limb development and Ihh playing a key role in endochondral osteogenesis. The Hedgehog signaling pathway includes Hedgehog signaling protein ligands, Patched (Ptch) receptors, Smoothed (Smo) receptors, nuclear transcription factors, glioma-associated oncogene homologues (Gli), and downstream target genes. The activation of typical Hedgehog signaling pathways requires the involvement of Gli, whereas atypical Hedgehog signaling is mainly regulated by Ptch, Smo, and others. Shh regulates various biological behaviors during early vertebrate embryogenesis, such as organ differentiation, neural stem formation, stem cell differentiation and proliferation, limb bone development, and tooth germ development. During the process of bone cell differentiation, Shh, Ptch1, and Gli1 are expressed in osteoblasts, further promoting the differentiation of bone marrow mesenchymal stem cells into osteoblasts and chondrocytes. IHh plays an indispensable functional role in bone growth, development, and homeostasis and participates in the formation of intramembrane bone collars, proliferation, and maturation of chondrocytes. IHh is expressed in mature skull osteoblasts and can act as a promoter of bone factor regulation of Ptch and bone morphogenetic protein (BMP) expression to induce intramembrane ossification. Brain and muscle ARNT-like protein 1 (BMAL1) can regulate the Hedgehog signaling pathway by binding to Ptch1 and Ihh, playing a crucial role in cartilage formation and endochondral osteogenesis in the temporomandibular joint. Hedgehog signal activators can improve the reduction in mandibular bone mass caused by BMAL1 deficiency. Hedgehog signaling imbalance can have a significant impact on bone development and lead to a series of bone diseases, such as abnormal bone development, fractures, osteoporosis, and osteoarthritis. The mechanism of the Hedgehog signaling pathway in relation to mandibular diseases has not been fully elucidated, and future research should seek to further explore Hedgehog signaling as a potential target for treating mandibular developmental-related diseases.

Objective To explore whether the environmental pollutant triclosan (TCS) has negative effects on the various biological characteristics of dental pulp stem cells (DPSCs), as well as the distribution and hazards of TCS in rat dental pulp tissue in vivo, which will provide a basis for the clinical application of DPSCs and the safety of TCS. Methods Tooth collection was approved by the Ethics Committee of Tianyou Hospital Affiliated to Wuhan University of Science and Technology. Human DPSCs were extracted, cultured, and identified. Up to 0.08 mmol/L of TCS was added to the in vitro culture medium of DPSCs. The proliferation ability of DPSCs was detected by CCK-8. The migration ability of DPSCs was detected via scratch assay. The differentiation ability of DPSCs was detected by inducing trilineage differentiation. The gene or protein expression levels of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6), interleukin-10 (IL-10), inducible nitric oxide synthase (iNOS), and transforming growth factor-β (TGF-β) in DPSCs were detected. The level of reactive oxygen species (ROS) generated by DPSCs was analyzed using fluorescence staining. Changes in mitochondrial membrane potential of DPSCs were detected using a fluorescent probe. The activity of PI3K/Akt/mTOR, p38, and JNK pathways of DPSCs were detected. Animal experiments were approved by the Animal Ethics Committee of Wuhan University of Science and Technology. A rat model of short-term oral exposure to 50 mg/kg/d of TCS for 2 months was established, and the TCS concentration in the liver, brain, and dental pulp tissues of rats was detected through liquid chromatography-mass spectrometry. Results TCS at 0.02 mmol/L, 0.04 mmol/L, and 0.08 mmol/L significantly inhibited the proliferation ability of human-derived DPSCs on the 5th and 7th days of contact. TCS at 0.04 mmol/L and 0.08 mmol/L significantly inhibited the migration ability and tri-lineage differentiation ability of DPSCs on the 3rd day of contact. TCS induced the gene or protein expression of proinflammatory factors including TNF-α, IL-1β, IL-6, and iNOS, induced the gene or protein expression of TGF-β, and inhibited the protein expression of anti-inflammatory factor IL-10. On day 1, TCS at 0.04 mmol/L and 0.08 mmol/L induced the production of ROS in DPSCs and reduced the mitochondrial membrane potential of DPSCs. On day 3, TCS at these levels inhibited PI3K/Akt/mTOR pathway activity and enhanced p38 pathway activity of DPSCs, without affecting the pathway activity of JNK. After short-term intragastric exposure of rats to TCS, TCS was detected in liver (430 ng/mL) and brain (41.4 ng/mL) tissues but not in the dental pulp. The TCS concentration was highest in the liver, but no obvious histopathological changes were observed. Conclusion TCS inhibits a variety of biological characteristics of DPSCs and poses a potential risk to the organism. No TCS exists in the dental pulp tissue of rats exposed to TCS for a brief period of time, and the health of the rats is not damaged.

Objective To study the effect of the combinational use of miR-34a-functionalized Bio-Oss^® bone powder with transglutaminase crosslinked gelatin (Col-Tgel) on the osteoblastic differentiation of bone marrow mesenchymal stem cells (BMSCs) and bone defect healing after irradiation. Methods The experiment was approved by the Animal Ethics Committee. BMSCs were isolated from the bone marrow of 2-week-old Sprague-Dawley (SD) rats and identified. After reaching 80% confluence, BMSCs were irradiated with 2 Gy of X-ray radiation to establish a radiation-damaged BMSC model for further experimentation. 2.5 μL or 5 μL of Col-Tgel was mixed with 10 mg of Bio-Oss^® (P) to prepare PG-2.5 and PG-5. The optimal proportion of Bio-Oss^® (P) and Col-Tgel was determined through in vitro and in vivo experiments. Cy3-labeled agomiR-34a, agomiR-34a, or agomiR NC was mixed with lipofectamine 2000 and added to 10 mg of Bio-Oss^® (P). The mixtures were lyophilized, and 2.5 μL Col-Tgel was added to each group of lyophilized Bio-Oss^®/lipofectamine/miRNA complexes or to 10 mg of Bio-Oss^® to obtain PG-Cy3-miR-34a, PG-miR-34a, PG-miR NC, and PG. Irradiated BMSCs were cocultured with PG-Cy3-miR-34a to evaluate cellular uptake of Cy3-agomiR-34a using confocal microscopy. Then, irradiated BMSCs were cocultured with PG-miR-34a, PG-miR NC, and PG. The expression of miR-34a was tested by RT-qPCR and cell proliferation was tested by CCK-8 assay. After 14 days of osteogenic induction, the mRNA expression of Runt-related transcription factor 2 (Runx2), alkaline phosphatase (ALP), and osteocalcin (OCN) was tested by RT-qPCR. The bilateral tibias of 8-week-old SD rats were irradiated with a single dose of 15 Gy of X-ray radiation. Three weeks later, tibial defects with a diameter of 3 mm and a depth of 2 mm were created 2-3 mm below the epiphyseal line in the tibial metaphysis. The composite bone substitute materials of PG-miR-34a, PG-miR NC, and PG were implanted into the defect area. Eight weeks after implantation, the tibias were harvested and evaluated for bone regeneration using micro-CT analysis and HE staining. Results The results demonstrated that 2 Gy irradiation adversely affected the osteogenic differentiation capacity of BMSCs, evidenced by the decreased ALP staining and number of mineralized nodules stained with Alizarin red in the irradiated group compared to the non-irradiated group. The composite material consisting of 10 mg Bio-Oss^® and 2.5 μL Col-Tgel exhibited good osteogenic induction capability and handling properties and was used for subsequent experiments. The PG-Cy3-miR-34a could deliver the loaded Cy3-agomiR-34a into irradiated BMSCs. PG-miR-34a enhanced the expression of miR-34a in irradiated BMSCs without affecting cell proliferation. PG-miR-34a significantly upregulated the expression of osteogenic-related genes, including Runx2, ALP, and OCN. In the experiment of bone defect healing in irradiated tibias, micro-CT analysis showed that PG-miR-34a group had a higher bone volume in the bone defect area compared to other groups. The HE staining results also confirmed that implantation of PG-miR-34a can promote the healing of bone defects in irradiated tibias. Conclusion The combinational use of miR-34a-functionalized Bio-Oss^® bone powder with Col-Tgel could promote the osteogenic differentiation of irradiated BMSCs and enhance bone regeneration in irradiated bone defects.

During orthodontic treatment, clinical monitoring of patients is a crucial factor in determining treatment success. It aids in timely problem detection and resolution, ensuring adherence to the intended treatment plan. In recent years, digital technology has increasingly permeated orthodontic clinical diagnosis and treatment, facilitating clinical decision-making, treatment planning, and follow-up monitoring. This review summarizes recent advancements in digital technology for monitoring orthodontic tooth movement, related complications, and appliance-wearing compliance. It aims to provide insights for researchers and clinicians to enhance the application of digital technology in orthodontics, improve treatment outcomes, and optimize patient experience. The digitization of diagnostic data and the visualization of dental models make chair-side follow-up monitoring more convenient, accurate, and efficient. At the same time, the emergence of remote monitoring technology allows orthodontists to promptly identify oral health issues in patients and take corresponding measures. Furthermore, the multimodal data fusion method offers valuable insights into the monitoring of the root-alveolar relationship. Artificial intelligence technology has made initial strides in automating the identification of orthodontic tooth movement, associated complications, and patient compliance evaluation. Sensors are effective tools for monitoring patient adherence and providing data-driven support for clinical decision-making. The application of digital technology in orthodontic monitoring holds great promise. However, challenges like technical bottlenecks, ethical considerations, and patient acceptance remain.

Objective To explore the effect of a phased rehabilitation training programme to relieve shoulder dysfunction in patients after neck dissection and to provide effective solutions for postoperative shoulder joint function recovery of patients. Methods This study has been reviewed and approved by the Ethics Committee, and informed consent has been obtained from patients. A phased rehabilitaiton training programme for the shoulder after neck dessection was developed through literature review and discussion, and 70 eligible patients from Hospital of Stomatology, Sun Yat-sen University from December 2020 to April 2021 were selected and randomly divided into the test group and control group (35 patients in each group). The control group underwent motor rehabilitation training from 6 weeks postoperative to 1 year after surgery, such as shoulder mobility and coordination training and small range of motion training of the neck, while the test group took part in a rehabilitation training program that included familiarization maneuver training, protective rehabilitation, exercise rehabilitation, and resistance training in the following four stages: preoperative, postoperative general anesthesia and awake until the removal of stitches, the removal of stitches until 6 weeks after surgery, and 6 weeks after surgery until 1 year after surgery. The frequency of training in both groups was at least 3 days per week, and the length of each training session was 10-15 min. The intensity of exercise was 2-3 points on the Borg Conscious Exercise Intensity Scale (i.e., mild-to-moderate tachypnea or fatigue). The neck dissection injury index (NDII) was used to evaluate the quality of life related to shoulder joint function at four time points: preoperative, postoperative 3 months, postoperative 6 months, and postoperative 12 months. The higher the score, the better the quality of life. Results 28 cases in the test group and 32 cases in the control group completed a one-year follow-up. At 3 and 6 months postoperative, the NDII of the test group was significantly higher than that of the control group [3 months postoperative: test group (93.48 ± 9.36) vs. control group (80.00 ± 11.34) (P<0.001), 6 months postoperative: test group (98.21 ± 4.76) vs. control group (90.70 ± 9.12) (P<0.001)]; 12 months after surgery, the NDII of the test group (97.23 ± 4.88) was still higher than that of the control group (96.33 ± 4.49), but the difference was not statistically significant (P = 0.458). The difference in NDII scores among subjects at 3, 6, and 12 months after surgery was statistically significant in each group (P<0.001). Conclusion The application of the phased rehabilitation training method in neck dissection patients has a feasibility and could improve the quality of life of patients' shoulder joint function within 6 months after surgery.

Periodontitis is a chronic inflammatory disease caused by plaque microorganisms, which is the main cause of tooth loss in adults in China. Due to the complexity of periodontitis, their pathogenesis is still unclear. Ferroptosis is a form of iron-dependent regulation of cell death, which affects the function of glutathione peroxidase (GPX4) in the cell through different signaling pathways, thus decreasing antioxidant capacity, accumulation of reactive oxygen species and lipid peroxidation, eventually causing cell and tissue damage. Recent studies have found that iron overload, oxidative stress and lipid peroxidation are closely related to the occurrence and development of periodontitis. This article reviews the characteristics of ferroptosis and the relationship between ferroptosis and inflammatory diseases, especially periodontitis, to provide new ideas for the diagnosis, treatment, and prognosis evaluation of periodontitis. ferroptosis is mainly manifested as the disruption of the body's redox homeostasis, decreased antioxidant capacity, activation of damage related molecular patterns, release of pro-inflammatory mediators, and induction or exacerbation of inflammation. Iron dependent oxidative stress and lipid peroxidation are simultaneously involved in the regulation of ferroptosis and inflammatory diseases. Pathogenic bacteria of periodontitis can induce ferroptosis of periodontal ligament stem cells, thereby activating the release of inflammatory factors such as interleukin-17, tumor necrosis factor alpha, and hypoxia inducible factor-1 alpha, exacerbating periodontitis; In addition, inflammatory factors activated by ferroptosis play an important role in alveolar bone homeostasis, and ferroptosis is involved in the process of lipopolysaccharide induced inflammation of gingival fibroblasts. Future research can focus on exploring the molecular mechanisms and therapeutic targets of ferroptosis in periodontitis, providing new strategies for the prevention and treatment of periodontal disease.

Objective To investigate the expression and role of the DNA repair and recombination protein RAD54-like (RAD54L) in oral squamous cell carcinoma (OSCC). Methods Using OSCC-related data from The Cancer Genome Atlas (TCGA) database, the difference in RAD54L expression between OSCC and control samples was analysed using the Mann-Whitney rank sum test, and the potential value of RAD54L mRNA in OSCC diagnosis was assessed using the receiver operator characteristic curve. The correlation between RAD54L expression levels and clinicopathological data of OSCC patients was analysed using the chi-square test. Once OSCC samples were divided into two groups of high and low expression based on the median value of RAD54L mRNA expression, Cox regression analysis was used to compare the prognostic differences between the two groups. The differentially expressed genes between the groups were subsequently screened using the DESeq2 package, and KEGG pathway enrichment analysis was performed using the clusterProfiler package. The correlation between RAD54L mRNA and gene expression in the homologous recombination repair pathway was demonstrated by Spearman correlation analysis. After clarifying the bioinformatics significance of RAD54L, RAD54L knockdown experiments were performed in human oral squamous carcinoma cell line HSC-3, and the knockdown efficiency was verified through real-time quantitative polymerase chain reaction. After transfection, the changes in proliferation, migration, apoptosis, and cycle of HSC-3 cells were assessed by CCK-8, 5-ethynyl-2'-deoxyuridine (EdU) staining, wound healing, apoptosis, and cell cycle assays. Results Bioinformatics analysis showed that the expression of RAD54L mRNA was higher in OSCC than in normal controls (P<0.001) and had a high value in predicting poor prognosis (AUC = 0.927). The high RAD54L expression group was associated with an increased proportion of male patients (P = 0.032), having a higher T-stage (P = 0.040), clinical stage (P = 0.027), and pathological grading (P = 0.013). Once OSCC samples were divided into two groups of high and low expression using the median value of RAD54L mRNA expression, the prognosis of the group with high expression of RAD54L was poorer than that of the group with low expression (P = 0.049). The differentially expressed genes between the high and low RAD54L expression groups two groups were mainly enriched in neuroactive ligand-receptor interactions, cytokine-cytokine receptor interactions, calcium signaling pathway, cell cycle, gastric cancer, extracellular matrix receptor interactions, chemical carcinogenesis-DNA adducts, DNA replication, homologous recombination, and mismatch repair pathways (P<0.05). In the homologous recombination repair pathway, the expression of RAD54L was positively correlated with the expression of BRCA1, BLM, EME1, XRCC2, POLD1, TOPBP1, RAD51, BRIP1, RAD54B, BRCA2, and SYCP3 (P<0.05), and was strongly positively correlated with the expression of BRCA1, BLM, and EME1 (R>0.8, P<0.05). The results of in vitro experiments showed that RAD54L expression was knocked down to approximately 25% in HSC-3 cells (P<0.001). Compared with the control group, the RAD54L knockdown group showed a lower proliferation rate (P<0.05), a lower proportion of EdU-positive cells (P<0.001), a lower proportion of wound closure (P<0.001), a higher proportion of G1-phase cells (P<0.001), a lower proportion of S-phase cells (P<0.001), and a higher proportion of apoptotic cells (P<0.001). Conclusion RAD54L is highly expressed in OSCC and correlates with poor prognosis. Down-regulation of RAD54L expression inhibits the proliferation and migration of HSC-3 cells, promotes apoptosis, and impedes cell cycle progression.

Neutrophil extracellular traps (NETs) are fibrous web-like structures composed of decondensed chromatin and granular proteins released by neutrophils, with the ability to capture and kill bacteria. Pathogens, such as bacteria and viruses, can trigger the formation of NETs via NETosis, a type of programmed cell death that has two distinct forms: suicidal NETosis and vital NETosis. Numerous studies have found that NETs interact with immune cells in the tumor microenvironment, where they activate macrophages, promote immunosuppressive effects of myeloid-derived suppressor cells, and coat the tumor surface to prevent cytotoxic effects of CD8⁺ T cells and natural killer cells. Recent research has identified a substantial presence of NETs in oral squamous cell carcinoma (OSCC) tissues, indicating a complex relationship between NETs and OSCC development. Depending on the phenotype of neutrophils, NETs may exhibit pro-tumor or anti-tumor effects. For instance, NETs derived from N1-type neutrophils may exert anti-tumor effects, while TGF-β-induced NETs derived from N2-type neutrophils may exert pro-carcinogenic activity, thereby contributing to the development of oral squamous metaplasia. Furthermore, NETs likely play a role in OSCC metastasis by capturing circulating tumor cells and inducing a hypercoagulable state, thereby facilitating tumor-related thrombus formation and hematogenous metastasis. The involvement of NETs in the occurrence and progression of OSCC opens new avenues for anti-tumor therapy and prognostication. Inhibiting NET formation can significantly suppress the development of chemotherapy-induced drug resistance and reduce the risk of thrombosis in OSCC patients, thereby inhibiting tumor metastasis. Currently, multiple prognostic models based on NET-related genes have been constructed and validated for head and neck squamous cell carcinoma, indicating the potential clinical value of NETs. However, the association between NETs and OSCC treatment is still unclear, necessitating further research on its underlying mechanisms and feasibility. This article attempts to review the relationship between NETs and OSCC, aiming to provide novel perspectives for OSCC treatment.

Objective To explore the characteristics and correlation of the chin and airway in females with skeletal Class Ⅱ mandibular retraction for reference for clinical diagnosis and therapy. Methods This study was approved by the hospital Medical Ethics Committee. Forty cases of skeletal Class Ⅱ mandibular retraction adult females with average angle were selected as the research group, and sixty cases of skeletal Class Ⅰ patients with average angle were selected as the control group. Cone-beam computed tomography (CBCT) images for all subjects were analyzed using three-dimensional modeling software. Measurements included the chin morphology, position, and upper airway morphology. Results Compared with skeletal Class I patients, patients with skeletal Class Ⅱ mandibular retraction had smaller anterior chin thickness, base bone volume, chin total volume, and larger chin angle, chin depression, chin curvature, and alveolar area with statistically significant differences (P<0.05). Gn-V, Gn-H, Po-NB distance, and facial angle were smaller, and the Y-axis angle was larger in patients with skeletal Class Ⅱ mandibular retraction with statistically significant differences (P<0.05). Upper airway total volume, transverse and sagittal diameter of the glossopharynx upper boundary were smaller in patients with skeletal Class Ⅱ mandibular retraction with statistically significant differences (P<0.05). The correlation analysis between the morphology and position of the chin and the morphology of the upper airway in patients with Class Ⅱ mandibular retraction showed that there was a negative correlation between chin angle and laryngopharynx length in patients with Class Ⅱ mandibular retraction (r = -0.277, P<0.01). There was a negative correlation between Po-NB distance and palatopharyngeal length (r = -0.222, P<0.05). Chin height (r = -0.261, P<0.01) and basal bone area (r = -0.225, P<0.05) were negatively correlated with the transverse diameter of the palatopharyngeal upper boundary. The minimum chin thickness (r = 0.245, P<0.05), chin angle (r = 0.249, P<0.05), and alveolar area (r = 0.213, P<0.05) were positively correlated with the sagittal diameter of the palatopharyngeal upper boundary. Gn-V (r = 0.217, P<0.05) and Po-NB distance (r = 0.208, P<0.05) were positively correlated with the transverse diameter of the glossopharynx upper boundary. Anterior chin thickness was negatively correlated with the sagittal diameter of the laryngopharynx upper boundary (r = -0.211, P<0.05). Chin depression was negatively correlated with the sagittal diameter of the laryngopharynx lower boundary (r = -0.237, P<0.05). Chin curvature was positively correlated with the transverse diameter of the laryngopharynx lower boundary (r = 0.231, P<0.05). Conclusion Patients with skeletal Class Ⅱ mandibular retraction exhibit thinner chins. The sagittal position of the chin is backward, and the vertical position is upward. Patients with skeletal Class Ⅱ mandibular retraction have a narrow glossopharyngeal airway. There is a correlation between the morphology and position of the chin and the morphology of the upper airway in patients with Class Ⅱ mandibular retraction.

MXenese is a type of two-dimensional inorganic compound in materials science that is composed of transition metal carbides, nitrides, or carbonitrides with several atomic layer thicknesses. Owing to the presence of hydroxyl groups or terminal oxygen groups on the surface of MXene materials, they exhibit metallic conductivity similar to that of transition metal carbides. Owing to their excellent optical, mechanical, electrothermal, and biocompatible properties, emerging 2D MXenes are widely used in biomedical fields such as tissue engineering, antimicrobial drugs, photothermal therapy, drug/gene delivery, sensing, and regenerative medicine. In this paper, we review the methods for synthesizing and modifying MXene-based composites, their research and application in stomatology, and their development prospects and challenges in the clinical application of tissue engineering. The biocompatibility and osteogenic properties of MXene and its nanocomposites have the potential to promote cell proliferation and bone regeneration. The anti-bacterial adhesion and biofilm formation properties can be applied to implant coating and prevent caries. The excellent photothermal, conductive, and mechanical sensitivity of this agent make it suitable for drug delivery, bio-photothermal therapy, immune signal sensing, and gene detection. On this basis, MXene has recently achieved outstanding results in the fields of stomatology, including bone tissue engineering, antimicrobial, drug delivery, physical and mechanical enhancement of dental biomaterials, oral cancer treatment, and periodontal disease monitoring. However, research on the prevention and treatment of refractory oral diseases has not yet been reported. At present, the properties and surface modification of MXene-based nanomaterials are relatively well understood. Future studies should focus on the dose-dependent biosafety, cellular and molecular mechanisms, and signaling pathways of MXene to fully exploit its unique advantages in oral clinical and tissue engineering fields.

Objective To investigate the changes of mitochondrial homeostasis of human gingival fibroblasts (HGFs) in periodontitis, and to provide a basis for exploring the mechanism of periodontitis. Methods This study has been reviewed and approved by the Ethics Committee. Gingival tissue was collected from patients who underwent periodontal surgery at the Department of Periodontology, School of Stomatology, the Fourth Military Medical University, from June 1, 2023 to December 31, 2023. All of the subjects signed informed consent forms prior to surgery. Gingival connective tissues were collected from patients with chronic periodontitis (CP group) and healthy individuals (control group) undergoing flap surgery and crown lengthening surgery, respectively. There were 6 cases in each group. The primary HGFs obtained from healthy periodontal subjects were cultured and divided into the control group (cultured in complete medium for 24 h) and the Pg.LPS group (cultured in medium with 5μg/mL Pg.LPS for 24 h). The number, morphology, and structure of mitochondria in gingival connective tissue and HGFs were observed by transmission electron microscopy. The number, circumference, and surface area of mitochondria were quantitatively analyzed. MitoSOX^TMRed, TMRM, and an ATP kit were used to determine the production levels of mitochondrial reactive oxygen species, mitochondrial membrane potential, and ATP in each group of HGFs. Results Transmission electron microscopy showed that the morphology and structure of mitochondria were abnormal in the gingival connective tissues of the periodontitis group and HGFs, which were stimulated by Pg.LPS. The mitochondrial ridges were broken or were not visible in these groups. The number of mitochondria decreased significantly, and the surface area and circumference of the mitochondria increased significantly (P < 0.05). In addition, after stimulation by Pg.LPS, the reactive oxygen species level in HGFs was significantly higher than that in the control group (P < 0.05). The mitochondrial membrane potential and the level of ATP production was significantly lower than that of the control group (P < 0.05). Conclusion The number, morphological structure, and function of mitochondria in HGFs changed significantly in periodontitis. The mitochondrial homeostasis is closely related to the occurrence and development of periodontitis.

Tooth wear is a common and complex oral problem, with a gradually increasing global incidence. Tooth wear not only affects the oral function and esthetics of patients but may also lead to tooth sensitivity, temporomandibular joint diseases, and other related complications. The continuous progress of digital technology has shown significant potential for the diagnosis and treatment of tooth wear. In recent years, researchers have extensively studied the application of digital technology in tooth wear research from the perspectives of digital support devices, cutting-edge deep learning applications, technology diagnosis, design and prediction, and current limitations. Such studies have provided a deep exploration of the micrometer-level resolution advantages of three-dimensional oral scanning technology in the early detection of tooth wear, which can assist in precise clinical and scientific research practices. Deep learning technology can also achieve image recognition and automated analysis to reduce human error and improve diagnostic efficiency, while quantitative analysis techniques guide clinical decision-making by more accurately calculating the tooth volume, surface area, and wear depth. Finally, simulation techniques can be employed to enhance understanding of the biomechanical and chemical mechanisms of tooth wear and predict its progression. These studies have also highlighted the current difficulties in data management, privacy protection, and obtaining high-quality big data, as well as technical barriers and insufficient evidence-based medical evidence in this field. Nevertheless, digital technology will undoubtedly improve and play an increasingly important role in future dental practice.

Oral submucous fibrosis (OSF) is an oral potentially malignant disorader that may be closely related to betel chewing and other factors. The pathogenic mechanism of OSF is still unclear, and there is no cure for OSF. Currently, there are many clinical treatments for OSF, such as medications, including steroids, pentoxifylline, lycopene, turmeric, salvia miltiorrhiza, and aloe vera, lasers, and surgery. In order to evaluate the safety and efficacy of these methods to improve the maximum mouth opening, alleviate the burning sensation, increase tongue flexibility, and other symptoms that accompany OSF, researchers have completed some evidence-based studies in recent years. We searched PubMed, Embase, Web of Science, The Cochrane Library, CNKI, Wanfang, and VIP databases for systematic reviews or meta-analyses of OSF research and treatment published over the last 10 years (July 2014-July 2024). Current evidence-based studies have shown that pentoxifylline, hyaluronidase combined with steroids, lycopene, curcumin, salvia miltiorrhiza combined with steroids, and aloe vera are effective in improving maximum mouth opening and alleviating the burning sensation in patients with OSF. The evidence levels of hyaluronidase combined with steroids, lycopene, curcumin, salvia miltiorrhiza combined with steroids, and aloe vera were all A, and pentoxifylline was B. Lycopene was more effective than other positive drugs in improving maximum mouth opening in patients, and aloe vera was more effective than positive drugs in improving the burning sensation in the early stage of treatment. In addition, antioxidants are good for improving OSF symptoms and have promising application. Lasers can improve maximum mouth opening and alleviate pain and other OSF symptoms, but laser treatment is costly and the level of evidence is C. Surgery is effective in improving maximum mouth opening, but it is traumatic and the level of evidence is C. However, the current evidence-based data are not of high quality, and additional well-designed multi-center, large-sample, randomized controlled clinical trials with long follow-up periods and standardized outcome indicators are needed in the future.

Objective To analyze the trends and hotspots in research related to microbiomes and microbes of dental caries; in addition, the study seeks to provide a reference for caries research. Methods We searched the Web of Science Core Collection (WOSCC) to extract relevant literature in the field of microbiomes and microbes of dental caries published from 2014 to 2023. We used bibliometric visualization evaluation methods such as CiteSpace to conduct visualized analysis of factors that include the number of publications, journals, countries, authors, institutions, co-cited references, and keywords. Results A total of 3 192 references were extracted, including 2 664 articles and 528 reviews. The number of annual publications is increasing. The United States and China lead the number of publications, with the United States demonstrating a greater capacity for international collaboration. The top 10 journals in percentage of literature are mainly in the field of dentistry followed by the field of microbiology. The author cooperation networks with the highest number of publications include the network led by Zhou Xuedong of Sichuan University, and the network led by Xu Hockin H.K and Weir Michael D of the University of Maryland, Baltimore. The research on microbiomes and microbes of dental caries focuses on the cariogenic toxicity and interaction of microorganisms, oral microbiomes, and the relationship between dental caries and systemic diseases. The articles with high citation frequency mainly involve topics such as dental caries, oral biofilm, oral microbiota, and Streptococcus mutans. Keyword research showed that “dental caries,” “Streptococcus mutans,” “bacteria,” “dental plaque,” and “antibacterial activity” have been the primary focus of research in the last decade. The number of keywords, such as “health” and “oral health,” is on the rise. The latest emergence of “gut microbiome/microbiota” suggests that the oral gut microbiome axis is at the forefront of research in this field, and researchers’ focus is gradually shifting toward the connection between dental caries and systemic diseases. Conclusion Over the last decade, the number of publications in the field microbiomes and microbes of dental caries has increased annually. This research trend will be the multi-omics of the overall oral microbiome, and new research methods and techniques will contribute to the field of cariology.

Objective To explore the expression and clinical significance of histone deacetylase 5 (HDAC5) in oral squamous cell carcinoma (OSCC) and provide a research basis for targeted therapy of HDAC5. Methods Screening sample data of OSCC patients in TCGA database, and receiver operating characteristic (ROC) curve analysis was used to evaluate the prognostic value of HDAC5 in OSCC. Kaplan-Meier analysis was also used to analyze the correlation between HDAC5 and the prognosis of OSCC patients. Further, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses were used to explore the potential role of HDAC5 in OSCC. Finally, the study was approved by the ethics committee and the expression level of HDAC5 in OSCC was detected by immunohistochemistry (IHC), while the relationship between HDAC5 and the clinical pathological characteristics of OSCC patients was analyzed. Results The expression of HDAC5 can be used to assess the prognosis of OSCC patients (AUC=0.743). High expression of HDAC5 was significantly correlated with low survival probability in OSCC patients (P < 0.05). OSCC patients with high HDAC5 expression in G3/G4 pathological grading (P=0.022), OSCC patients with high HDAC5 expression in the T3/T4 stage (P=0.028), and OSCC patients with high HDAC5 expression in lymph node metastasis (P=0.019) had lower survival probability. GO and KEGG enrichment analyses showed that genes differentially expressed with HDAC5 were mainly enriched in axon generation, neuronal cell body formation, collagen fiber synthesis, neuroactive ligand receptor interactions, gated channel activity, and extracellular matrix (ECM)-receptor interaction pathways (P < 0.05). The IHC results showed that HDAC5 was highly expressed in OSCC (P < 0.05). The high expression group of HDAC5 had higher T staging (P=0.041) and lymph node metastasis (P=0.010). Conclusion HDAC5 is highly expressed in OSCC and can predict the prognosis of OSCC, and HDAC5 could serve as a therapeutic target for OSCC.

Dysbiosis can cause microenvironmental dysregulation, which can further lead to local or systemic diseases, such as caries, inflammatory bowel disease, obesity, and diabetes. Dysbiosis is primarily manifested as the disturbance of metabolic processes and products. Arginine plays an important role in various metabolic processes and homeostasis of the microbial flora and the host. This study aims to explore the potential therapeutic value of arginine and its metabolism and homeostasis regulation in diseases associated with oral-intestinal dysbiosis. Host and microbial homeostasis can be restored by regulating the composition or function of host microbiota, and arginine has been found to exhibit significant clinical potential in restoring host microbiota composition and function. For example, arginine can reduce the risk of caries by regulating the relative abundance of Streptococcus mutans and Streptococcus sanguineus. Additionally, arginine metabolism may play a therapeutic role in inflammatory bowel disease and obesity by regulating the relative abundance of Firmicutes and Bacteroidetes. In addition, supplementation of arginine and its metabolite polyamine has clinical prospects in the treatment of diabetic patients with ketoacidosis. Although studies have demonstrated the therapeutic role of arginine in oral, intestinal, and metabolism-related diseases, the specific mechanism is yet to be explored. In addition, further research is required to determine the optimal clinical dosage of arginine that can maintain microbiota homeostasis without causing any side effects.

Objective To compare the effect of different scanning parameters of cone beam computed tomography (CBCT) on displaying trabecular microstructure in the anterior region of the mental foramen of the mandible, and to provide a basis for the rational selection of CBCT scanning parameters. Methods This study was approved by the Ethics Committee of the Affiliated Stomatological Hospital, Medical School of Nanjing University. An in vitro study was conducted using CBCT (ProMax 3D Mid) to scan eight dry human mandibular specimens with five scanning protocols: Group A: 90 kV/6.3 mA, Group B: 90 kV/8.0 mA, Group C: 90 kV/10.0 mA, Group D: 75 kV/8.0 mA, and Group E: 60 kV/8.0 mA, resulting in a total of 40 CBCT images. Entrance surface dose (ESD) and computed tomography dose index (CTDI) under different scanning conditions were recorded. The original CBCT images were imported into the image analysis software (Hiscan Analyzer) to measure four trabecular bone microstructural parameters in the region of interest of the mandible: trabecular thickness (Tb.Th), trabecular number (Tb.N), trabecular space (Tb.Sp), and bone volume/tissue volume (BV/TV). A total of 108 CBCT images were retrospectively collected from clinical implant patients using any of the 90 kV/6.3 mA, 90 kV/8.0 mA, or 90 kV/10.0 mA scanning conditions, and the above four parameters of the region of interest of the mandible were also measured. SPSS 26.0 software was used to compare the differences in the four trabecular bone microstructural parameters between the CBCT images of the mandibular specimens in vitro and clinical patients in vivo. Results The in vitro study results showed that reducing the tube voltage and tube current would lead to a decrease in the ESD and CTDI. When the tube voltage was maintained at 90 kV and the tube current was changed, BV/TV, Tb.N, and Tb.Th values increased with the increase of tube current; Tb.Sp values decreased with the increase of tube current, but there was no statistically significant difference in the four bone morphological parameters (P > 0.05). When the tube current was maintained at 8.0 mA and the tube voltage was altered, BV/TV and Tb.N decreased with the increase of tube voltage, Tb.Sp values increased with the increase of tube voltage, and BV/TV, Tb.N, and Tb.Sp showed statistically significant differences (P < 0.05). In clinical patients undergoing CBCT scanning, when the tube voltage was 90 kV and the tube current was different (6.3, 8.0, 10.0 mA), there was no statistically significant difference in the four bone morphological parameters (P > 0.05). Conclusions In this study, when the tube voltage was fixed at 90 kV, there was no difference in the trabecular microstructure of the anterior region of the mandible when the tube current was increased. When CBCT scanning of clinical patients needs to show the trabecular microstructure of the anterior region of the mandible, the tube current can be appropriately reduced to decrease the radiation dose received by the patient. Thus, it is recommended to use the parameters 90 kV and 6.3 mA for CBCT scanning.

The F-box protein (FBP) family is a large and diverse protein family that is present in all eukaryotes. Based on the secondary structure of the C-terminal, FBPs can be classified as FBXW, FBXL, and FBXO. FBPs can form the SCF complex by binding with S-phase kinase-associated protein 1 (SKP1), cullin 1 (CUL1), and ring-box 1 (Rbx1), functioning as E3 ubiquitin ligase. They specifically recognize substrate proteins via the ubiquitin-proteasome pathway and participate in various biological activities, such as cell cycle regulation, transcriptional regulation, apoptosis, and cell signaling transduction. Numerous studies have shown that FBPs play important roles in host-virus interactions. Being the substrate recognition component of the SCF complex, FBPs bind, ubiquitinate (at K-48), and transport substrates for proteasomal degradation. Based on the type of substrate, F-Box family proteins can either exert antiviral or proviral (immune evasive) effects. Some FBPs can specifically recognize and degrade interferon pathway-associated signal molecules via the ubiquitin-proteasome pathway, thereby upregulating or inhibiting interferon signals and regulating host-related immune responses. Additionally, some FBPs can recognize and degrade viral proteins via the ubiquitin-proteasome pathway, thereby inhibiting viral replication and transmission. However, viruses can hijack FBPs to promote the degradation of immunogenic host proteins, resulting in immune evasion. Although several FBP-targeting inhibitors have been developed, there are limited reports on the application of FBPs in antiviral drug research. Given the large number of FBP family members, further research is required on the functions and mechanisms of FBPs in virus-host interactions, to provide novel directions for the development of antiviral drugs.