中华口腔医学杂志最新文献

Objective: To compare the three-dimensional positional deviations of immediate and delayed implant placement by using autonomous dental implant robotic system, and to evaluate the clinical applicability and operational stability of the robotic system under different conditions. Methods: This retrospective study included 44 patients (25 males and 19 females, aged 22-45 years) who underwent autonomous oral implant robotic surgery at the Department of Oral Implantology, The Affiliated Hospital of Qingdao University, between April 2022 and August 2025. A total of 60 implants were placed, with 20 patients (30 implants) in the immediate implant group and 24 patients (30 implants) in the delayed implant group. Preoperative cone-beam CT and intraoral scans were performed on all patients, and preoperative three-dimensional implant planning was conducted based on the imaging data. The autonomous oral implant robotic system autonomously completed osteotomy and implant placement according to the preoperative plan. Postoperatively, cone-beam CT was taken and superimposed with the preoperative plan, and the deviations in the implant site, apex point, and angular deviation were calculated as precision evaluation indicators. The normality of the data was assessed using the Shapiro-Wilk test. Differences between the two groups were evaluated using the Student's t-test, Welch's t-test, or Mann-Whitney U test. Results: The median (interquartile range, IQR) of the implant site deviation, apex point deviation, and angular deviation in the immediate implant group were 0.325 (0.190), 0.375 (0.380) mm, and 0.645° (0.170°), respectively. In the delayed implant group, the corresponding values were 0.365 (0.200), 0.350 (0.100) mm, and 0.665° (0.160°). Statistical analysis showed no significant differences in the three-dimensional positional accuracy between the two groups (all P>0.05). Conclusions: The autonomous dental implant robotic system provides excellent three-dimensional positioning accuracy in both immediate and delayed implant placements, effectively compensating for complex extraction socket anatomy and operator variability.

Objective: To develop an automatic oral lesion segmentation model (TopoFormer) that integrates topological data analysis (TDA) with a Transformer architecture, thereby improving the accuracy and robustness of lesion segmentation for oral potentially malignant disorders (OPMD) and oral squamous cell carcinoma (OSCC). Methods: Experiments were conducted on a public comprehensive oral cavity image dataset released by Piyarathne et al., containing 2 271 oral white-light photographs from 623 patients and covering three categories: At the patient level, the data were stratified and randomly split into training, validation, and test sets with a ratio of 0.8/0.1/0.1. SegFormer was used as the backbone network, and a self-designed topological attention module (TAM) was embedded in the deep feature space. TAM leveraged persistent homology to extract robust topological structures from feature maps and dynamically suppressed low-persistence noise. Performance was evaluated using the Dice similarity coefficient (DSC), mean intersection over union (mIoU), mean pixel accuracy (mPA), 95% Hausdorff distance (HD95), and Betti number error (BNE), and was compared with mainstream segmentation networks (U-Net, DeepLabV3+, and SegFormer). Results: On the test set, TopoFormer achieved a DSC of 0.801, an mIoU of 71.1%, an mPA of 82.31%, reduced HD95 to 9.62 pixels, and obtained a BNE of 1.28. Compared with the baseline model, the proposed model effectively reduced false positives caused by specular reflections and produced smoother and more continuous lesion boundaries. Conclusions: TopoFormer demonstrates higher accuracy and robustness in segmenting OPMD and OSCC lesions. Topological priors can enhance segmentation performance in complex oral environments, indicating use potential in computer-aided diagnosis.

Bone defects resulting from trauma, tumors or other etiologies are common, but their repair remains a major clinical challenge. Autologous bone grafting, the current gold standard, faces limitations including donor site morbidity and limited graft availability. In recent years, with the rapid development of bone tissue engineering and regenerative medicine, the focus of research has gradually shifted from single-factor optimization to integrated multi-factor strategies. This review highlights three cutting-edge directions in regenerative medicine for jawbone defects: the evolution from stem cell therapy to cell-free strategies, precision delivery of bioactive factors, and the coupling mechanisms of immune-bone repair. It emphasizes the necessity of integrated approaches, discusses the persistent challenges in clinical translation and outlines future research priorities. This review aims to provide a theoretical foundation for advancing multidisciplinary integration and develop personalized, standardized regenerative treatment strategies.

Ameloblastoma is a locally invasive benign tumor of odontogenic epithelial origin. Research into its molecular mechanisms is hindered by the lack of unified norms for normal control tissue selection, which undermines data comparability. Current studies employ highly heterogeneous control tissues, including tooth germs, pericoronal tissue, normal oral mucosa and even commercial samples, thereby complicating data integration and potentially affecting the accurate interpretation of disease mechanisms. Based on principles of tooth development and the concept of "developmental arrest" in ameloblastoma, we propose a three-tier reference framework for normal control tissue selection: Tier 1 controls (preferred) include normal tooth germs (bell stage prioritized), reduced enamel epithelium and dental lamina remnants among other odontogenic epithelial components, which provide optimal consistency in developmental origin and stage; Tier 2 controls (alternative) consist of site-matched oral mucosa or specific odontogenic cysts linings and may be served as supplements but require explicit limitation disclosure; Tier 3 controls (not recommended), such as tissues of unknown origin or xenogeneic sources, should be avoided due to limited biological comparability. We also propose complementary quality control and normalized reporting recommendations encompassing tissue source verification, histopathological validation, and ethical compliance documentation. This reference framework establishes a reproducible and comparable strategy for controlling tissue selection in ameloblastoma research, thereby contributing to enhanced data reliability and cross-study comparability, while providing methodological reference for other odontogenic tumors and developmental disorders.

Degenerative temporomandibular joint disease (TMJ-DJD), a common condition in middle-aged and elderly populations, has seen a continuous rise in incidence with global population aging. Aging synergistically promotes TMJ degeneration through multilevel mechanisms. At the cellular level, aging manifests as epigenetic alterations, formation of the senescence-associated secretory phenotype, mitochondrial dysfunction, exacerbated oxidative stress, and declined stem cell repair capacity, collectively accelerating degradation of the chondrocyte extracellular matrix and apoptosis. At the systemic level, immunosenescence leads to a chronic low-grade inflammatory state; various endocrine changes (e.g. in sex hormones, the growth hormone/insulin-like growth factor-1 axis, and thyroid hormones) impair tissue anabolic and repair capacity. Meanwhile, declined tissue mechanosensation and hardening of the extracellular matrix further reduce the joint's adaptability to external load. Additionally, aging acts as an endogenous factor that disrupts central and peripheral circadian rhythms, indirectly promoting TMJ degeneration by impairing cartilage metabolism and inflammatory responses. In summary, aging drives the pathogenesis and progression of TMJ-DJD via multiple pathways, including cellular dysfunction, systemic homeostasis imbalance, and disruption of biological rhythms. Targeting the above mechanisms may provide novel therapeutic strategies for future clinical interventions in TMJ degenerative joint diseases.

Periodontitis is a chronic inflammatory disease triggered by plaque biofilm and impacts patients' quality of life and overall health. In recent years, fibrin (ogen), serving as a crucial molecular bridge connecting inflammation and coagulation, has been drawing increasing attention for its role in periodontitis. This review explores the association between fibrin (ogen) and periodontitis and its underlying mechanisms, with a focus on how it regulates neutrophil and macrophage functions, interacts with periodontal pathogens, and activates signaling pathways such as nuclear factor κB, thereby synergistically driving periodontal inflammation and bone resorption. The aim is to provide a theoretical basis for intervention strategies targeting fibrin (ogen) in the management of periodontitis.