A portion of patients undergoing implant restoration require bone augmentation procedures to ensure that there is sufficient bone volume around the implant. For the patients with horizontal bone ridge defects at edentulous sites, with or without mild to moderate vertical bone defects, the shell technique serves as a reliable and minimally invasive bone augmentation method with effective space maintenance. The shell technique involves fixating 1 mm cortical bone blocks to the recipient site, using retention screws and filling the gap between the bone block and recipient bed with particulate bone substitute materials, and covering the barrier membrane to achieve bone augmentation. The overlying tension-free soft tissue closure seals the surgical site while local peripheral blood releases osteoclasts and cytokines that gradually degrade the bone block. The rigid fixation of the bone block ensures a stable internal environment for osteogenesis and a new bone regeneration cycle. Although this technique demonstrates favorable bone augmentation outcomes, it is highly technique-sensitive. There are certain differences in the application scenarios and osteogenic processes for autologous and allogeneic bone shells. The selection of bone blocks and particulate bone substitute materials significantly influences the osteogenic biological process and the predictability of bone augmentation results. Complications associated with the shell technique possess distinct characteristics, such as the immunogenicity of allogeneic bone fragments, soft tissue cracking, and bone fragment loosening. Their prevention and subsequent management substantially impact the success rate of osteogenesis. This article delves into the biological mechanisms of osteogenesis in the bone block technique, summarizing the indications, clinical outcomes, classification of bone blocks, and surgical workflow management, as well as complication prevention and management, aiming to provide a reference for the future application and development of the bone shell technique.

Objective To investigate the effect of different surface treatment protocols on the surface properties and immediate shear bond strength (SBS) between 3D-printed zirconia and resin cement to provide a reference for clinical practice. Methods Disc-shaped zirconia specimens (Ø 14 mm× 1.2 mm) with two different surface designs were fabricated using 3D printing technology: a smooth surface (Group S) and microporous surface (Group M), with 40 specimens in each group. Each group was further randomly divided into four subgroups according to surface treatment: untreated (Subgroup U), alumina sandblasting (Subgroup ST), alumina sandblasting + Z-Prime ceramic primer (Subgroup ZP), and alumina sandblasting + Monobond N ceramic primer (Subgroup MN). The surface morphology was examined, roughness was measured, and wettability was evaluated via contact-angle testing. Composite resin cylinders (Ø 3.5 mm× 2.0 mm) were bonded to the zirconia surfaces with resin cement. Immediate SBS was determined by shear testing, and failure modes were analyzed. Results Scanning electron microscopy revealed clear micro-grooves (2-5 μm wide) in Subgroup S-U and micropores (approximately 400 μm in diameter) in Subgroup M-U. After sandblasting, the micro-grooves in Subgroup S-ST were partially destroyed with some micro-cracks, while the microporous structure in Subgroup M-ST remained clear. Compared with Subgroups S-U and M-U, sandblasted zirconia specimens (Subgroups S-ST, S-ZP, S-MN, M-ST, M-ZP, M-MN) showed significantly increased roughness and decreased contact angles. Different surface treatments significantly affected SBS between 3D-printed zirconia and resin. Sandblasted groups (Subgroups S-ST and M-ST) had significantly higher SBS than untreated groups (Subgroups S-U and M-U). The application of ceramic primers after sandblasting (Subgroups S-ZP, S-MN, M-ZP, M-MN) further increased SBS; however, there was no statistically significant difference in SBS between the two primers used after sandblasting (Subgroup S-ZP vs. S-MN, Subgroup M-ZP vs. M-MN). Under the same surface treatment, microporous surface groups (Subgroups M-U, M-ST, M-MN, M-ZP) all exhibited significantly higher SBS than smooth surface groups (Subgroups S-U, S-ST, S-MN, S-ZP). Conclusion Fabricating a microporous surface using 3D printing technology can improve resin bonding effectiveness. Sandblasting combined with a ceramic primer yields the highest immediate SBS.

Objective To investigate the causal relationship between neutrophil extracellular traps (NETs) and head and neck squamous cell carcinoma (HNSCC) using Mendelian randomization (MR) methods, and to explore the clinical significance of NETs in the occurrence and development of HNSCC. Methods Data related to NET biomarker myeloperoxidase-DNA complex (MPO-DNA) complex and HNSCC were obtained from the pooled statistical data of the Genome-Wide Association Study database (GWAS). This study was reviewed and approved by the Medical Ethics Committee, and informed consent was obtained from patients. Patients with HNSCC admitted to Department of Oral Maxillofacial, the First Affiliated Hospital of Harbin Medical University were included as the research group, and volunteers matched for age and gender were randomly selected from the Clinical Examination Center as the control group. The levels of MPO-DNA and citrullinated histone H3 (CitH3), two markers of NETs, as well as the levels of soluble adhesion factor CD44 variant 6 (CD44v6) and leukocyte differentiation antigen CD109, markers of lymph node metastasis, were measured in all subjects. Blood coagulation indicators, including plasma prothrombin time (PT), activated partial thromboplastin time (APTT), thrombin time (TT), D-dimer (DD), and fibrinogen levels (FIB), were recorded to analyze the relationship and potential mechanisms between NETs and HNSCC. Results MR results indicated a possible causal relationship between NETs and HNSCC. The inverse variance weighted P values for the four datasets were P1 = 0.037, P2 = 0.017, P3 = 0.004, and P4 = 0.023. Ultimately, 52 patients with head and neck squamous cell carcinoma and 20 healthy individuals were included. Compared with the control group, the expression levels of NETs markers MPO-DNA, CitH3, lymph node metastasis markers CD44v6 and CD109, and coagulation indicators FIB and DD were significantly elevated in the group with head and neck squamous cell carcinoma, with statistically significant differences (all P<0.001). In correlation studies between NETs markers and lymph node metastasis markers, as well as coagulation indicators, the Pearson correlation coefficient was 0.686, 0.531, 0.7, and 0.5 for MPO-DNA and DD, FIB, CD44v6, and CD109, respectively, and the Pearson correlation coefficient was 0.456, 0.503, 0.525, and 0.603 for CitH3 and DD, FIB, CD44v6, and CD109, respectively (P<0.05). In terms of diagnostic efficacy, the area under the curve (AUC) for MPO-DNA, CitH3, and MPO-DNA + CitH3 in patients with head and neck squamous cell carcinoma was 0.863, 0.892, and 0.905, respectively, with an increasing AUC of the receiver operating characteristic curve (ROC) in the order mentioned. Levels of MPO-DNA and CitH3 in patients with early-stage head and neck squamous cell carcinoma were (132.4 ± 16.4) ng/mL and (21.3 ± 2.9) ng/mL, respectively, which were lower than those in patients with advanced head and neck squamous cell carcinoma, who had MPO-DNA and CitH3 levels of (199.3 ± 33.1) ng/mL and (26.6 ± 3.7) ng/mL, respectively. The serum concentrations of FIB, DD, CD44v6, and CD109 in patients with high MPO-DNA expression were significantly higher than those in patients with low MPO-DNA expression (all P<0.05). The serum concentrations of FIB, CD44v6, and CD109 in patients with high CitH3 expression were significantly higher than those in patients with low CitH3 expression (all P<0.05). Conclusion The study indicates a potential causal relationship between NETs and HNSCC. NETs-related markers may serve as potential biomarkers for HNSCC, as they correlate with the hypercoagulable state of the cancer. NETs-related markers have potential diagnostic utility for HNSCC and are associated with tumor progression.

Objective To investigate the prognostic significance and biological functions of neutrophil extracellular traps (NETs) related genes in oral squamous cell carcinoma (OSCC). Methods A total of 333 transcriptome datasets and 6 single-cell sequencing datasets of OSCC were retrieved from the Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases. Based on 69 NETs related gene sets, univariate Cox and Lasso-Cox regression were used to construct a prognostic risk model for OSCC. The model's efficacy was evaluated through Kaplan-Meier analysis and receiver operating characteristic (ROC) curves, and risk scoring and nomogram analysis were conducted. Further, the relationship between NETs risk scores and angiogenesis, epithelial-mesenchymal transition (EMT), and cell cycle was explored. Enrichment analysis was performed to annotate the functional characteristics of relevant pathways. Kaplan-Meier analysis was employed to screen for prognostic key genes. Candidate targets were validated through drug prediction and molecular docking assays. Single-cell RNA sequencing was utilized to characterize the expression profile of the key gene cathepsin G (CTSG) within the tumor microenvironment (TME). Using pan-cancer and OSCC related data retrieved from the TCGA database, we analyzed the differences in CTSG expression between tumor tissues and normal tissues. Subsequently, immunohistochemical staining experiments were performed on tissue microarrays to validate its expression at the protein level. Results A prognostic risk model based on six NETs related genes (F3, AKT1, CTSG, VNN3, MPO, and IL17A) was successfully established. Patients in the high-risk group exhibited significantly shorter overall survival (OS) (P < 0.000 1). The area under the ROC curve (AUC) of the established model for predicting 1-, 3-, and 5-year overall survival (OS) rates was 0.718, 0.820, and 0.805, respectively. The NETs related risk score was identified as an independent prognostic factor (P < 0.001), with the constructed nomogram demonstrating good calibration. The NETs related risk score correlated with angiogenesis (r = ˗0.20,, P < 0.001), EMT (r = 0.17, P < 0.01), G1/S phase transition (r = 0.11, P < 0.05), and G2/M phase transition (r = 0.17, P < 0.01). GSEA（gene set enrichment analysis）revealed that the high-risk group was significantly enriched in pathways including basal cell carcinoma, whereas the low-risk group exhibited significant enrichment in pathways such as alpha-linolenic acid metabolism (P < 0.05). Kaplan-Meier analysis revealed that patients with low expression of CTSG had a poorer prognosis (P < 0.001). Molecular docking assays demonstrated a stable binding interaction between CTSG and glutathione (binding energy: -7.4 kcal/mol). Single-cell RNA sequencing analysis further showed that CTSG was highly expressed in mast cell subsets but weakly expressed in malignant cells (P < 0.001). TCGA pan-cancer analysis revealed that CTSG is underexpressed in multiple cancer tissues, including OSCC (P < 0.05). Immunohistochemical staining confirmed that CTSG protein expression was lower in tumor tissues than in paracancerous tissues (P < 0.01). Conclusion The NETs related prognostic model established in this study exhibits robust predictive performance. CTSG was identified as a key prognostic gene, thereby providing a novel biomarker and potential therapeutic target for prognostic evaluation and targeted therapy of OSCC.

Objective To explore the prevalence of bone defect and alveolar bone thickness changes in the mandibular incisors of untreated adults and post-orthodontic treatment adults, with the aim of providing strategies for preventing and managing alveolar bone defects during orthodontic treatment. Methods This study was reviewed and approved by the Medical Ethics Committee. Clinical records, panoramic radiographs, cephalometric radiographs, and cone beam computed tomography (CBCT) images and informed consent were obtained for 150 untreated adults and 150 post-orthodontic adults. The untreated adults and post-orthodontic adults were respectively divided into three subgroups: skeletal ClassⅠ, Class Ⅱ and Class Ⅲ, with 50 cases per subgroup. Meanwhile, 60 cases with completeness of pre- and post-orthodontic data were enrolled from 150 post-orthodontic adults, including 20 cases each of skeletal ClassⅠ, Class Ⅱ, and Class Ⅲ. Cephalometric radiographs were imported into Dolphin software to measure skeletal parameters. CBCT images were imported into Mimics software to assess alveolar bone defects and to measure alveolar bone thickness of mandibular incisors among three groups: 150 untreated adult groups, 150 post-orthodontic groups and the pre- and post-treatment status of 60 patients selected from the latter group. Results Untreated adult patients: the prevalence of labial dehiscence and fenestration in the mandibular incisors was higher than that on the lingual side among skeletal ClassⅠ, Ⅱ, and Ⅲ malocclusion patients, and there was a statistically significant difference in the alveolar bone thickness of the mandibular incisors among the three classes. Post-orthodontic treatment adults: for skeletal ClassⅠ and Ⅱ patients, the prevalence of lingual bone dehiscence in the mandibular incisors was significantly higher in the extraction groups than in the non-extraction groups; correspondingly, the lingual alveolar bone was also thinner in the extraction groups; Class Ⅱ non-extraction patients showed a higher prevalence of labial bone fenestration but a lower prevalence of lingual bone fenestration in mandibular incisors compared to Class Ⅱ extraction patients; the orthodontic-orthognathic combined treatment group showed significantly higher prevalence of labial/lingual bone dehiscence and thinner alveolar bone at multiple sites in the mandibular incisors compared to the camouflage group in skeletal Class Ⅲ patients. Comparison of mandibular incisor bone defects and thickness before and after orthodontic treatment in adult patients: in skeletal ClassⅠ and Ⅱ patients treated with premolar extraction and Class Ⅲ patients treated with orthodontic-orthognathic combined treatment, the lingual alveolar bone of mandibular incisors exhibited significant resorption and thinned after treatment, and this was accompanied by an increased prevalence of dehiscence; in non-extraction patients, ClassⅠ non-extraction patients showed thinning of the crestal-labial bone and apical-lingual bone, Class Ⅱ patients showed thinning of the crestal-labial bone and middle-labial bone of the mandibular incisors, along with an increased prevalence of dehiscence. Conclusion In malocclusion adults, alveolar bone defects were already present in the mandibular incisors before orthodontic treatment. The alveolar bone defects and thickness in mandibular incisors among post-orthodontic adults were influenced by the treatment plan and Class of skeletal malocclusion.

Objective To explore the application method and clinical efficacy of endoscopic and computerized navigation technology in maxillofacial foreign body removal surgery, and to provide a reference for the clinical application of this technology. Methods This study, which was approved by the Medical Ethics Committee of the hospital, retrospectively analyzed the data of five patients with maxillofacial foreign bodies who were admitted to Sun Yat-sen Memorial Hospital, Sun Yat-sen University from January 2018 to December 2024. All patients underwent preoperative CT scanning. Intraoperatively, endoscopic and computer navigation techniques were used in combination or separately according to the location, size, and adjacency of the foreign body to important neurovascular vessels. The foreign body was precisely localized by endoscopic magnification and direct visualization, and the optimal surgical path was designed and verified under the real-time guidance of computerized navigation to accurately remove the foreign body. The type of foreign body, location, length and diameter, duration of surgery, length of incision, success rate of foreign body removal, postoperative complications, and follow-up were recorded and analyzed. Results The foreign body was successfully removed in all five patients with a success rate of 100%. The intraoperative computerized navigation system was accurate in positioning, and the alignment stability was not significantly affected by mandibular movement; the endoscope provided good illumination and exposure of the operative field. All surgical incisions were small, and no serious complications, such as foreign body residue, important neurovascular injury, or infection, occurred after surgery. One month after the operation, the patients were followed up and recovered well. Conclusion The combination of endoscopy and computer navigation or separately assisted technology can provide a clear field and real-time positioning for maxillofacial foreign body removal, effectively avoiding important anatomical structures, thus realizing safe and complete foreign body removal with minimized trauma. This assistive technology significantly improves the accuracy and safety of the operation and has clinical promotion value.

Radiotherapy is a crucial treatment modality for head and neck tumors. However, while effectively killing tumor cells, it significantly disrupts the homeostasis of the oral microecology, which is closely associated with various complications such as radiation-induced oral mucositis. Literature review indicates that as radiotherapy doses accumulate and treatment durations extend, the richness and diversity of the oral microbiota show a declining trend, with the genus Streptococcus decreasing most markedly. In contrast, radiotherapy selectively promotes the proliferation of bacterial phyla such as Proteobacteria and Bacteroidetes, which are rich in opportunistic pathogens. Mechanistically, radiotherapy activates the nuclear factor-kappa B pathway, triggering chronic inflammation and oxidative stress, damaging the epithelial barrier, suppressing local immunity, and causing damage to organs such as the salivary glands. It can also induce systemic diseases via the oral-gut axis, forming a multi-level, interconnected pathogenic network. In terms of interventions, treatment strategies including probiotics and prebiotics have shown promising efficacy against side effects such as radiation-induced oral mucositis. Saliva-based oral microbiota transplantation is an emerging strategy that is expected to become widely utilized for restoring oral microecological balance. Existing interventions provide preliminary pathways for clinical practice, but this field still faces several key scientific questions. The association between oral microecology and systemic diseases remains largely correlative, lacking causal evidence. Furthermore, critical parameters for oral microbiota transplantation, such as donor screening criteria, transplantation protocols, and long-term safety, are not yet well-defined. Therefore, future research should focus on conducting large-scale clinical trials to establish standardized protocols and safety evaluation systems for oral microecological interventions, and explore combined treatment therapies such as probiotics, prebiotics, and microbiota transplantation to advance the development of personalized precision modulation. These will enable more effective management of radiotherapy-induced oral microecological dysbiosis and improve treatment outcomes and quality of life for patients with head and neck tumors.

Periodontitis is a chronic inflammatory disease triggered by periodontal pathogens and mediated by immune responses. Traditionally, gingival fibroblasts (GFs) were considered to be primarily responsible for maintaining periodontal matrix homeostasis. However, recent studies reveal that GFs play a significant immunoregulatory role in periodontitis. Through signaling pathways, such as the Toll-like receptor 4 (TLR4) pathway, GFs recognize virulence factors from pathogens, such as Porphyromonas gingivalis, and secrete various inflammatory mediators, thus driving extracellular matrix degradation and osteoclast differentiation. Simultaneously, GFs modulate immune cells, including neutrophils and macrophages, amplifying inflammatory responses and fostering a chronic inflammatory microenvironment. Risk factors, such as hyperglycemia and smoking, exacerbate GFs dysfunction via oxidative stress-mediated activation of the nuclear factor kappa B (NF-κB) pathway and other mechanisms, while inflammation and cellular senescence form a vicious cycle. Senescent GFs further aggravate alveolar bone destruction by activating the mechanistic target of the rapamycin (mTOR) pathway. Therapeutic strategies targeting GFs, such as suppressing NF-κB signaling or modulating mTOR-mediated senescence, may disrupt the link between inflammation and tissue destruction, showing promising therapeutic potential. Future studies should employ advanced technologies such as spatial multi-omics and single-cell proteomics to elucidate the spatial distribution, functional interactomes, and heterogeneity of GFs subsets, in order to deepen our understanding of their roles in periodontitis progression. This review summarizes the multifaceted mechanisms of GFs in periodontitis and explores potential therapeutic strategies targeting GFs, offering novel insights for periodontitis prevention and treatment.

Dental pulp stem cells (DPSCs) are a type of adult stem cell with abundant sources, easy accessibility, multipotent differentiation potential, and low immunogenicity. In recent years, they have attracted considerable attention due to their promising applications in repairing neural tissue injuries. Under specific induction conditions, DPSCs can directly differentiate into neuron-like cells and exert neuroprotective, immunomodulatory, anti-inflammatory, and anti-apoptotic effects through the paracrine secretion of neurotrophic and immunomodulatory factors. DPSCs can also be combined with biomaterial scaffolds such as hydrogels, chitosan, and polylactic acid, thereby enhancing neural differentiation efficiency and regenerative outcomes. However, their clinical application in neural repair still faces challenges, including poor microenvironmental adaptability, low differentiation efficiency and controllability, immune rejection, difficulties in large-scale production and quality control, and a lack of standardized operational protocols. Future research should focus on optimizing the adaptability of DPSCs to the injury microenvironment, improving their neural differentiation efficiency, strengthening immune regulation to ensure the safety of allogeneic transplantation, establishing GMP-compliant cell preparation and quality control systems, and developing standardized clinical procedures combined with multicenter trials to validate efficacy, thereby promoting the efficient, safe, and reproducible clinical translation of DPSCs in neural regeneration. This review summarizes the research progress on the neural differentiation of DPSCs, with an emphasis on strategies and molecular mechanisms for promoting neural regeneration, the challenges in clinical translation, and future development directions, aiming to provide a theoretical basis for research on the neural differentiation of DPSCs.