In the field of oral medicine, 3D-printed individualized titanium mesh technology is gradually becoming an important means for the treatment of severe alveolar bone defect augmentation. This article provides a comprehensive analysis of the advantages of this technology, the evaluation of osteogenic effects, and the progress of research in clinical applications. In response to the current issue of variability in bone augmentation outcomes, this paper delves into multiple factors affecting bone augmentation effects, including individualized titanium mesh design (involving the thickness, pore size, pore shape, porosity, contour shape, selection of titanium alloy materials, and 3D printing technology), intraoperative procedures (the accuracy of placement during 3D-printed individualized titanium mesh surgery), and postoperative care (including the prevention of complications, formation of pseudoperiosteum, and stability of the titanium mesh). By integrating the clinical experience and research findings of our team, we propose a series of targeted optimization strategies, including designing, manufacturing, and clinically applying self-positioning individualized titanium meshs (positioning wings + individualized titanium meshs) to improve the positioning accuracy of the titanium mesh; propose individualized treatment processes and titanium mesh design schemes based on specific conditions of alveolar bone defects and soft tissue status; and emphasize the importance of long-term stable fixation of the titanium mesh to reduce the risk of postoperative mesh loosening and displacement. In addition, we appropriately summarize the evaluation methods for the bone augmentation effects of 3D-printed individualized titanium meshes, covering the following key indicators: (1) vertical bone augmentation and horizontal bone augmentation; (2) changes in bone contour morphology; (3) bone volume increase; (4) clinical indicators (surgical success rate, titanium mesh exposure, infection rate, and postoperative recovery); (5) aesthetic effect evaluation; (6) long-term stability; (7) radiological assessment; (8) patient satisfaction; and (9) precision of surgical operation, aiming to assist doctors in comprehensively assessing and in-depth analyzing the surgical outcomes to achieve the best therapeutic effects. The purpose of this article is to provide a reference for the optimization and clinical application of 3D-printed individualized titanium mesh technology and to lay a theoretical foundation for achieving the best osteogenic effects.

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.

The management of antibiotic-resistant, bacterial biofilm infections in skin wounds poses an increasingly challenging clinical scenario. Pseudomonas aeruginosa infection is difficult to eradicate because of biofilm formation and antibiotic resistance. In this study, we identified a new benzothiazole derivative compound, SN12 (IC₅₀ = 43.3 nmol/L), demonstrating remarkable biofilm inhibition at nanomolar concentrations in vitro. In further activity assays and mechanistic studies, we formulated an unconventional strategy for combating P. aeruginosa-derived infections by targeting the two-component (Gac/Rsm) system. Furthermore, SN12 slowed the development of ciprofloxacin and tobramycin resistance. By using murine skin wound infection models, we observed that SN12 significantly augmented the antibacterial effects of three widely used antibiotics-tobramycin (100-fold), vancomycin (200-fold), and ciprofloxacin (1000-fold)-compared with single-dose antibiotic treatments for P. aeruginosa infection in vivo. The findings of this study suggest the potential of SN12 as a promising antibacterial synergist, highlighting the effectiveness of targeting the two-component system in treating challenging bacterial biofilm infections in humans.

Selective tooth agenesis (STA) is an abnormal number of teeth due to genetic factors or the environment and is most commonly observed for permanent teeth. LRP6 is one of the common causative genes of STA and is inherited by an autosomal dominant mechanism, leading to non-syndrome tooth agenesis (NSTA) or syndrome tooth agenesis (STA). NSTA is only involved in tooth number and appearance abnormalities, whereas STA caused by LRP6 gene mutation results abnormal ear development, oral-facial clefting, sparse hair and hypohidrosis. In this paper, we review the phenotype and gene mutation traits of selective STA caused by LRP6 gene mutation identified in recent years and describe 38 patients with tooth agenesis from 24 mutation sites of LRP6 gene. We analyzed the percentage of missing teeth and found that the lateral incisor in the maxilla and the second premolar in the maxilla and mandible were most commonly lost, whereas all central incisors in the maxilla remained. LRP6 gene plays a major role in tooth development via the WNT/β-catenin signaling pathway, and LRP6 gene mutation can lead to a series of abnormal manifestations due to the disruption of the signaling pathway. The literature showed that LRP6 gene mutations occurred mostly at the E1 or E2 subdomain, meaning that STA due to the mutants extracellularly disturbed the WNT/β-catenin signaling pathway. However, mature treatments for selective congenital tooth loss are lacking.

Objective: To explore the pathogenic genes in a Chinese family affected by nonsyndromic tooth agenesis so as to study the pathogenesis of oligodontia. Methods : Hospital ethical approval and informed consent of the patients and family members were obtained. Clinical data of the proband and close family members were collected, peripheral venous blood was collected, and DNA was extracted. Gene sequencing was performed through whole-exome sequencing, and then the screened pathogenic genes were verified by Sanger sequencing. The three-dimensional structure of the mutant proteins was analyzed and compared with the wild-type using bioinformatics tools. Results: The two patients with congenital majority tooth loss in this family were cousins, and there were no other patients with congenital majority tooth loss in the family. Besides congenital multiple tooth loss, the two patients had no obvious hair abnormalities, finger/toe abnormalities, sweating abnormalities or other abnormal manifestations of ectodermal tissue. We found a mutant gene that in this family by carrying out gene sequencing of the patients and their close family members. A novel EDA (ectodysplasin A) missense mutation c.983C>T (p. Pro328Leu) was identified, which changed the encoded amino acid from proline (Pro) to leucine (Leu). Analysis of the mutation site showed that the site was highly conserved, and three-dimensional structure modeling also found that it changed the structure of EDA. Conclusion A novel EDA missense variant (c.983C>T, p.Pro328Leu) was first identified in a Chinese family with nonsyndromic tooth agenesis, extending the mutation spectrum of the EDA gene.

Objective: To detect WNT10A gene mutations in patients with oligodontia or anodontia (≥6 teeth missing) and analyze their dental phenotype. Methods: Patients with oligodontia or anodontia were enrolled from the clinic for oral examination, genetic history collection and whole exon sequencing, and patients with WNT10A gene mutations were included. Sanger sequencing was utilized to validate the WNT10A gene variations in probands and family members compared with the normal sequence. The pathogenicity of WNT10A mutations was evaluated by functional prediction, conservation analysis and structure prediction of protein mutants. Implant rehabilitation was applied to restore the patients' oral function. Results: Five WNT10A gene mutations were detected in six unrelated patients, and c.26G>A (p. Trp9X) and c.1036delT (p. Cys346fs) were novel mutations with pathogenic potential. The mean number of missing teeth was (15.33±8.64) per case. The most frequently missing permanent teeth were maxillary canines (100%), and the least frequently missing teeth were mandibular first molars (25%). Implant rehabilitation was applied in five patients, and patients were found to have ideal implant osseointegration and functional restoration. Conclusion This study identified novel WNT10A gene pathogenic variants, enriching the WNT10A gene spectrum and providing new evidence for genetic diagnosis and prenatal consultation. Implant rehabilitation was also proven to be a treatment option for these patients.

Oligodontia is the congenital absence of six or more teeth and comprises the more severe forms of tooth agenesis. Many genes have been implicated in the etiology of tooth agenesis, which is highly variable in its clinical presentation. The purpose of this study was to identify associations between genetic mutations and clinical features of oligodontia patients. An online systematic search of papers published from January 1992 to June 2021 identified 381 oligodontia cases meeting the eligibility criteria of causative gene mutation, phenotype description, and radiographic records. Additionally, ten families with oligodontia were recruited and their genetic etiologies were determined by whole-exome sequence analyses. We identified a novel mutation in WNT10A (c.99_105dup) and eight previously reported mutations in WNT10A (c.433 G > A; c.682 T > A; c.318 C > G; c.511.C > T; c.321 C > A), EDAR (c.581 C > T), and LRP6 (c.1003 C > T, c.2747 G > T). Collectively, 20 different causative genes were implicated among those 393 cases with oligodontia. For each causative gene, the mean number of missing teeth per case and the frequency of teeth missing at each position were calculated. Genotype-phenotype correlation analysis indicated that molars agenesis is more likely linked to PAX9 mutations, mandibular first premolar agenesis is least associated with PAX9 mutations. Mandibular incisors and maxillary lateral incisor agenesis are most closely linked to EDA mutations.
Humans ; Phenotype ; Wnt Proteins

Objective: The aim of the present study was to evaluate the clinical outcomes of implant-supported prostheses for oral function rehabilitation in patients with ectodermal dysplasia. Methods : Thirteen patients were included in the present study. After bone augmentation, zygomatic implants (ZIs) or regular implants (RIs) were placed, fabrication of dental prostheses were applied, and psychological and oral education was carried out. Implant survival rates, patient satisfaction and other related evaluation indicators were assessed. Results: The ilium was chosen for autogenic bone grafts in two patients. The fibula was used in two other patients and the mandibular ramus in one other patient. One patient was treated through alveolar distraction osteogenesis of the mandible. Guided bone regeneration was applied in seven other patients. Bone graft resorption in the maxilla was observed in one patient; bone augmentation of the mandible was successful in all patients, and no obvious bone resorption was observed. One hundred and eighteen implants were placed, among which 22 were ZIs, and 96 were RIs. Five RIs failed and were removed. The survival rate for ZIs was 100%, and the survival rate for RIs was 94.79%, in a follow up after 3 years. All patients were satisfied with the restoration of their oral function. More than 50% of the patients exhibited self-confidence. Conclusion Oral function can be restored in edentulous ectodermal dysplasia patients using bone augmentation and implant-supported prostheses, and patient self-confidence can be enhanced. However, the resorption of grafted bone in the anterior region of the maxilla cannot be ignored.

Objective To explore the interaction between polymorphisms of rs17222919 which located in the 5-1ipoxygenase-activating protein(ALOX5AP) gene promoter and environmental risk factors in ischemic stroke(IS).Methods We conducted a case-control study involving a total of 622 cases and 631 unrelated healthy controls which were selected from Henan Han populations,and the environment risk factors were recorded.Genotyping aimed at detecting both genetic and environmental factors in relation to IS was performed by TaqMan-polymerase chain reaction technology while interaction indexes (Υ) were calculated to determine interactions and their role models.Results The rs17222919 TG (189/622,30.4％),GG (18/622,2.9％)genotype frequencies and G (225/1244,18.1％)allele frequencies in IS subjects were significantly lower than those in controls (221/631,35.0％ ; 31/631,4.9％ ; 283/1262,22.4％ ; x2 =4.117,P =0.042 ; x2 =4.457,P =0.035 ; x2 =7.294,P =0.007).Negative interactions between TG + GG genotype and hypertension,diabetes or cigarette smoking in the occurrence of IS (Υ =0.943,0.922,0.830) were observed,whose role models were all super-multiplicative models.Conclusions According to our study,ischemic stroke is the result of the interaction of genetic and environmental factors and G allele of rs17222919 may have weakened the role of environmental factors for hypertension,diabetes and cigarette smoking in IS incidence.