Edentulous patients often present with severe alveolar bone resorption, restructured maxillofacial anatomy, and loss of occlusal relationships, making implant-supported rehabilitation technically more challenging—particularly in terms of guide stability, implant positioning accuracy, and prosthesis design. Traditional treatment workflows largely rely on clinician experience, which is inherently subjective and limits the ability to achieve precise, controlled implant placement and predictable restorative outcomes. In recent years, the widespread adoption of digital technologies has brought transformative progress to implantology for edentulous jaws. Innovations span from preoperative imaging and 3D reconstruction, intelligent surgical planning, personalized guide design, dynamic navigation, and robotic-assisted implant placement, to digital prosthesis design and immediate loading protocols. These advancements have markedly improved surgical precision, procedural efficiency, and patient satisfaction. This article systematically reviews the key applications and clinical value of digital technologies across the various stages of implant rehabilitation in edentulous cases. We also highlight current challenges, such as high costs and dependence on specialized equipment. Finally, we explore future directions toward more intelligent and integrated solutions that are driven by advances in artificial intelligence, multimodal image fusion, and robotics.

Objective To investigate the effect and mechanism of resveratrol-derived carbonized polymer dots (RSV-CPDs) on macrophage polarization and osteogenic differentiation of human periodontal ligament stem cells (hPDLSCs) under inflammatory conditions, and to provide an experimental basis for the treatment of periodontitis with RSV-CPDs. Methods RSV-CPDs were prepared by high-temperature pyrolysis of resveratrol (RSV) in the presence of ammonia as a catalyst, and RSV-CPDs were characterized by transmission electron microscope (TEM), Fourier transform infrared spectrometer (FTIR), X-ray diffraction (XRD), and X-ray photoelectron spectroscopy (XPS). CCK8 was used to detect the cytotoxicity of RSV-CPDs. The effects of RSV-CPDs on the apoptosis and cell polarization of macrophages stimulated by Porphyromonas gingivalis-lipopolysaccharide (P.g-LPS) were detected by flow cytometry: ① For the apoptosis detection experiment, the macrophages (RAW264.7) were divided into the control group (no treatment), P.g-LPS group [treated with P.g-LPS (2 μg/mL) for 24 h], RSV group [treated with P.g-LPS (2 μg/mL) + RSV (10 μg/mL) for 24 h], and RSV-CPDs group [treated with P.g-LPS (2 μg/mL) + RSV-CPDs (50 μg/mL) for 24 h]. ② For the cell polarization experiment, the macrophages (RAW264.7) were divided into four groups. They were the control group (no treatment), P.g-LPS + IFN-γ group [P.g-LPS (200 ng/mL) + IFN-γ (20 ng/mL) treated cells for 24 h], RSV group [P.g-LPS (200 ng/mL) + IFN-γ (20 ng/mL) + RSV (10 μg / mL) treated cells for 24 h], RSV-CPDs group [P.g-LPS (200 ng / mL) + IFN-γ (20 ng / mL) + RSV-CPD (50 μg / mL) treated cells for 24 h]. The supernatant of macrophages in the above four groups of cell polarization experiments was collected and mixed with osteogenic induction medium at a 1:1 ratio to culture hPDLSCs. The hPDLSCs were divided into the control group, P.g-LPS + IFN-γ group, RSV group, and RSV-CPDs group. The osteogenic trend of hPDLSCs was detected by alkaline phosphatase (ALP) staining and alizarin red staining (ARS). Real-time quantitative PCR (RT-qPCR) was used to detect the expression of osteogenesis-related genes. Western blot was used to detect the expression of osteogenesis-related proteins in hPDLSCs. Finally, transcriptome tests were used to explore the mechanism of the effect of RSV-CPDs on the phenotype of macrophages (THP-1) stimulated by inflammation. Results TEM results showed that RSV-CPDs exhibited a uniform spherical structure. FTIR results showed the O-C=O peak of RSV-CPDs. XRD results confirmed that the newly synthesized RSV-CPDs exhibited an amorphous structure. XPS results showed that RSV-CPDs formed a hydrophilic carboxyl group. CCK-8 results showed that RSV had specific toxicity to RAW264.7 when the concentration exceeded 10 μg/mL (P = 0.011), while RSV-CPDs still had good biosafety to cells when the concentration reached 50 μg/mL (P > 0.05). Therefore, the concentration of RSV was 10 μg/mL and RSV-CPDs was 50 μg/mL. The results of flow cytometry showed that RSV-CPDs inhibited the apoptosis of macrophages under inflammatory stimulation (P = 0.008), and the inhibitory effect was better than that of its precursor RSV (P = 0.009). Compared with the P.g-LPS + IFN-γ group, CD86⁺ cells in the RSV group and RSV-CPDs group decreased by varying degrees (P < 0.001, P = 0.004), while CD206⁺ cells increased by varying degrees (P = 0.006, P = 0.008), and the proportion of CD206⁺ cells in the RSV-CPDs group was higher than that in the RSV group (P = 0.010). Compared with the P.g-LPS + IFN-γ group, the supernatant of macrophages treated with RSV-CPDs significantly increased the ALP expression (P = 0.005) and ARS level (P = 0.006) of hPDLSCs. The mRNA expression of osteogenic-related genes RUNX-2, OCN, and COL-1 significantly increased (P < 0.05), and the level of RUNX-2 protein also significantly increased (P = 0.001). Transcriptome results showed that compared with the P.g-LPS + IFN-γ group, the nuclear factor kappa-B (NF-κB) signaling pathway and tumor necrosis factor (TNF) signaling pathway in the RSV-CPDs group showed downward trends. Conclusion RSV-CPDs can inhibit the apoptosis of macrophages in the inflammatory state, promote M2 polarization, and bolster the osteogenic differentiation of hPDLSCs. The mechanism involved may be related to the inhibition of NF-κB and TNF signaling pathways.

Objective This study investigated the effect of applying different torque values on the sagittal displacement tendency of mandibular incisors during intrusion using clear aligners, with the aim of providing a reference for achieving true vertical intrusion (intrusion without labiolingual movement) of mandibular incisors in clear aligner therapy. Methods This study was approved by the institutional ethics committee. A volunteer with an incisor mandibular plane angle of 94° was selected. Using cone-beam computed tomography and intraoral scan data, a high-precision three-dimensional finite element model was established. An intrusion amount of 0.2 mm was set for the mandibular incisors, and four simulation groups were defined by applying 0°, 1°, 2°, and 3° of root labial torque. The displacement tendency of the incisors and the stress distribution within the periodontal ligament were analyzed. Results When 0° of root labial torque was applied, the mandibular incisors exhibited intrusion accompanied by crown-labial, root-lingual inclination. When 1°-3° of root labial torque was applied, the mandibular incisors exhibited intrusion accompanied by the inclination gradually shifted from crown-labial, root-lingual towards crown-lingual, root-labial. Based on the line graph of sagittal displacement, the central incisors and lateral incisors approximated true vertical intrusion when 1.8° and 2.5° of root labial torque was applied, respectively. The mandibular canines consistently exhibited extrusion accompanied by labial crown inclination. Stress within the periodontal ligament of the incisors and canines was primarily concentrated at the root apex and cervical region. After applying root labial torque, the area of stress concentration in the incisors cervical periodontal ligament shifted from the labial side to the lingual side. The stress in the periodontal ligament at the cervical region of the canines is predominantly concentrated on the labial side. Conclusion Applying appropriate torque control during mandibular incisor intrusion with clear aligners facilitates true vertical intrusion, thereby enhancing the efficiency of the intrusion.

Objective To investigate the differences in three-dimensional maxillary and palatal parameters as well as midpalatal suture maturation stages between Skeletal Class I malocclusion patients with maxillary transverse deficiency (MTD) and normal maxillary transverse development, in order to provide clinical guidance for orthodontic diagnosis and treatment. Methods This study was approved by the institutional ethics committee and informed consent was obtained. Cone-bean CT data from 66 Skeletal Class I malocclusion patients [22 males, 44 females; age (14.39 ± 1.68) years] were analyzed. Based on Yonsei University width analysis, participants were divided into two groups: the maxillary transverse deficiency group [n = 33, age (14.34 ± 1.99) years] and the maxillary transverse normal group [n = 33, age (14.43 ± 1.33) years]. Parameters compared included midpalatal suture maturation stages (A-E), maxillary skeletal width on nasal floor (NF) and maxillary skeletal width on hard palate (HP), maxillary arch width on buccal alveolar crest (BAC) and maxillary arch width on lingual alveolar crest (LAC), palatal vault height, palatal bone thickness, palatal length, surface area, and volume. Results The proportion of patients with palatal suture maturity at stages D+E in the maxillary transverse deficiency group (33%, 11/33) was lower than that in the normal maxillary transverse development group (45%, 15/33), showing no statistically significant difference between the two groups. Compared to the maxillary transverse normal group, significant reductions were observed in the maxillary transverse deficiency group for maxillary widths [NF: (67.63 ± 3.74) mm vs. (71.49 ± 5.11) mm; HP: (64.60 ± 3.53) mm vs. (68.40 ± 4.64) mm], dental arch widths [BAC: (56.88 ± 2.25) mm vs. (59.81 ± 2.71) mm; LAC: (33.90 ± 1.89) mm vs. (36.91 ± 2.20) mm], and palatal surface area [(1 170.80 ± 126.48) mm² vs. (1 264.76 ± 140.10) mm²]. No significant differences were noted in palatal height, bone thickness, length, or volume. Conclusion Skeletal Class I malocclusion patients with MTD have narrowed maxillary and dental arch widths, reduced palatal surface area, and delayed midpalatal suture maturation. Early maxillary expansion is recommended to harmonize jaw relationship.

Objective To investigate the predictive value of EZH2 expression for malignant transformation in oral leukoplakia (OLK) and to provide a reference for clinical practice. Methods This study was approved by the institutional ethics committee, and informed consent was obtained from all participants. A total of 114 patients diagnosed with OLK by pathological examination and treated at our hospital between November 2020 and July 2022 were initially enrolled. After excluding those with incomplete data or follow-up, 105 participants were included in the final analysis, comprising 14 in the high EZH2 expression group and 91 in the low EZH2 expression group. Histopathological examination of oral mucosa and immunohistochemical detection of EZH2 protein expression were performed. The follow-up period was 30 months; participants were followed until malignant transformation occurred or until the end of follow-up, at which point they were withdrawn from the study. The exposure factor was the level of EZH2 protein expression, and the outcome was the malignant transformation rate of OLK. Differences in EZH2 expression levels and transformation outcomes were analyzed. Results There were no statistically significant differences between the high and low EZH2 expression groups in terms of age, sex, history of systemic disease, lifestyle habits, psychological status, diet, and sleep conditions (P > 0.05). Lesions in the high EZH2 expression group were mainly located on the ventral tongue, while in the low EZH2 expression group, they were more commonly found on the dorsal tongue and buccal mucosa. The malignant transformation rate was 28.6% (4/14) in the high expression group and 8.8% (8/91) in the low expression group; these differences were not statistically significant (P=0.053). In univariate Cox regression analysis, the risk of malignant transformation in the high EZH2 expression group was 3.647 times that of the low EZH2 expression group (HR = 3.647, 95% CI: 1.097-12.120, P<0.05). Kaplan-Meier survival analysis showed that over the 30-month follow-up period, the cancer-free survival rate in the high EZH2 expression group was 19.8% lower than in the low expression group, and the difference was statistically significant (P<0.05). In multivariate Cox regression analysis, only moderate and severe epithelial dysplasia were identified as independent risk factors for malignant transformation. The risk of malignant transformation in the moderate and severe dysplasia groups was 10.695 and 13.623 times higher, respectively, than in the mild dysplasia group (HR = 10.695, 95% CI: 2.270-50.396, P<0.05; HR=13.623, 95% CI: 1.918-96.774, P<0.05). EZH2 high expression was not an independent risk factor in the multivariate model (HR= 2.528, 95% CI: 0.752-8.500, P = 0.134). Conclusion High EZH2 protein expression is a risk factor for the malignant transformation of OLK but does not have independent predictive value.

Objective To investigate the reciprocal causal relationships between periodontitis and hepatobiliary diseases through Mendelian randomization (MR) analyses, to provide evidence for joint prevention and clinical decision-making in patients with concurrent periodontitis and hepatobiliary diseases. Methods Single nucleotide polymorphisms (SNPs) were extracted from the largest genome-wide association study on periodontitis (17 353 cases, 28 210 controls) and hepatobiliary diseases within the European ancestry and used as instrumental variables (IVs). The strength of the associations was examined by calculating the F-statistic. The SNPs significantly associated with the outcome were removed by scanning on Phenoscanner platform. Bidirectional causal associations between periodontitis and hepatobiliary diseases were estimated using inverse variance weighted (IVW), MR-Egger, and Weighted Median methods. The robustness of the findings was further verified through additional sensitive MR approaches, including Cochran’s Q statistic （IVW）, Rucker’s Q statistic （MR-Egger）, MR-PRESSO and Leave-one-out analysis. Further MR analyses, utilizing other available genome-wide association studies (GWAS) on hepatobiliary diseases, were conducted to validate the results. Results The IVW method found that periodontitis had a causal impact on acalculous cholecystitis (odds ratio = 1.277, 95% CI 1.097-1.485, P=0.002), implying an increased risk of acalculous cholecystitis associated with periodontitis, while the MR-Egger regression and Weighted Median failed to observe significant causal effects of periodontitis on acalculous cholecystitis. However, no bidirectional causal associations between periodontitis and nonalcoholic fatty liver disease, cirrhosis or liver cancer were observed using IVW, MR-Egger regression and Weighted Median. The bidirectional causal relationships were deemed unlikely to be influenced by horizontal pleiotropy. Further, the validation analysis based on alternative GWAS data suggested parallel results. Conclusions The MR analyses suggest that periodontitis may elevate the risk of acalculous cholecystitis. Further investigations, including clinical studies and mechanistic explorations, are warranted to validate these findings. However, the MR analyses do not support bidirectional causal associations between periodontitis and nonalcoholic fatty liver disease, cirrhosis or liver cancer.

Periodontitis is a chronic inflammatory disease that affects the tooth-supporting tissues, and it constitutes a major global public health concern. Methylation modifications, including DNA methylation, histone methylation, and RNA m⁶A modification, represent reversible processes coordinately regulated by methyltransferases, demethylases, and binding proteins. In periodontitis, aberrant methylation modifications suppress Toll-like receptor 2 expression, leading to oral microbial dysbiosis. These modifications further disrupt normal immune regulatory functions through C-C motif chemokine ligands, Fc-γ receptor-mediated phagocytosis, and NF-κB signaling pathways, resulting in localized immune-inflammatory imbalance in periodontal tissues. In addition, various methylation modifications regulate the expression of Runt-related transcription factor 2 (RUNX2), osteoblast-specific transcription factor Osterix (OSX), and receptor activator of nuclear factor-κB ligand (RANKL), thereby interfering with osteoclast and osteoblast differentiation, disrupting bone homeostasis, and ultimately driving alveolar bone resorption. Methylation-related biomarkers demonstrate promising potential for periodontitis screening and prognostic evaluation. While numerous abnormally methylated sites have been identified in periodontitis, the precise signaling pathways and comprehensive epigenetic regulatory networks remain to be fully elucidated. This review systematically summarizes the functional roles of DNA methylation modifications in the pathogenesis of periodontitis and explores their potential value in etiological studies, diagnostic biomarker discovery, and targeted therapeutic interventions, with the aim of providing novel perspectives for periodontitis prevention and treatment strategies.

During tumor progression, the mechanical properties of the tumor microenvironment play a pivotal regulatory role. As core mechanical indicators, cellular stiffness and extracellular matrix stiffness profoundly influence tumor development through multiple pathways, including cytoskeletal remodeling, activation of signaling pathways, and metabolic regulation. Studies have demonstrated that the tissue stiffness of various solid tumors is significantly higher than that of corresponding normal tissues, while their cellular stiffness exhibits the opposite trend. This mechanical characteristic is also observed in oral squamous cell carcinoma and exerts crucial regulatory effects during tumor progression. This review systematically summarizes the molecular composition and regulatory mechanisms underlying the stiffness of tumor cells and extracellular matrix (ECM). Mainstream stiffness detection technologies such as atomic force microscopy, microfluidic deformation, and real-time deformability cytometry are outlined, with particular emphasis on their applications and limitations in oncology research. This review comprehensively analyzes how mechanical properties regulate key processes in tumor progression, including growth, proliferation, invasion, metastasis, angiogenesis, lymphangiogenesis, drug resistance, and immune escape. This review synthesizes biomechanics-based therapeutic strategies, including: ① targeting the regulation of tumor cell stiffness through cytoskeletal modulators and cholesterol-depleting agents to enhance immune responses; ② reducing ECM stiffness by matrix remodeling enzyme inhibitors, ECM component modulators, or receptor antagonists to improve drug delivery efficiency, and combining with immunotherapy or photothermal therapy for enhanced therapeutic effects; ③ enhancing the mechanical adaptability and anti-tumor activity of immune cells through pharmacological or genetic approaches. This review establishes a robust conceptual framework for developing novel anti-tumor therapeutic strategies and provides insights for future clinical management of oral squamous cell carcinoma.

Cleft lip and palate (CLP) are common congenital craniofacial developmental disorders with a high incidence rate among newborns. Due to the influence of the cleft, an increased frequency of anomalies occurs in cleft-adjacent teeth. This review summarizes the abnormality of tooth development and malposition characteristics of the central incisors, lateral incisors, and canines adjacent to the alveolar cleft in CLP patients and treatment progress in order to provide information for related clinical treatment and research. The literature reveals that central incisors, lateral incisors, and canines adjacent to the alveolar cleft exhibit various types and degrees of abnormalities. The alveolar cleft-adjacent central incisors show significantly smaller mesiodistal diameters, root lengths, and root volumes compared to the non-alveolar cleft side, while the crown-to-root ratio is larger. Further, they are inclined distally and lingually compared to the non-alveolar cleft side. The alveolar cleft-adjacent lateral incisor is the most common missing or impacted tooth and is often affected by microdontia. The total length and root length of the alveolar cleft-adjacent canines are significantly smaller, while the crown-to-root ratio is larger on the alveolar cleft side. In addition, they are inclined mesially and buccally compared to the non-alveolar cleft side. Further, they are higher positioned and located closer to the midline. For developmental anomalies, impacted central incisors can be addressed by orthodontic space preparation to facilitate eruption or surgical crown exposure and orthodontic traction. Treatment of missing lateral incisors can involve orthodontic closure of the gap or preservation of the space for subsequent prosthetic restoration. When lateral incisors present with developmental defects, such as microdontia, peg-shaped teeth, or invaginated teeth, a comprehensive decision is necessary to determine whether to retain and restore or extract the malformed lateral incisors. Treatment of impacted canines after bone grafting involves either extraction or traction to facilitate the eruption of the impacted tooth. For malposition, presurgical orthodontic treatment can correct teeth with excessive inclination or rotation on the cleft side to improve the effectiveness of bone grafting surgery. Postsurgical orthodontic treatment can enhance the stability of bone grafting surgery. Although numerous studies have explored the dental characteristics of patients with CLP, the lack of applicability and specificity still need to be elucidated, thus indicating the need for further research.