Objective: To study the therapeutic mechanism of adenovirus mediated cytosine deaminase /5-fluorocytosine (AdCMVCD/ 5-FC) suicide gene system in the treatment of oral squamous carcinoma cells in vitro. Methods: 3H-thymidine ( 3H-TdR) incorporation assay, flow cytometry (FCM), transmission electron microscope and TUNEL (TdT-mediated dUTP Nick End Labeling)assay were used to detected the changes of Tca8113 cells after the treatment with AdCMVCD/5-FC system. Results: After treatment with CD/5-FC system, 3H-TdR incorporation rate of the cells decreased and significantly decreased between different MOI (multiple of infection) at 5-FC 10 -3 mol/L (P0.05); many apoptotic cells were found under transmission electron microscope and the positive rate of apoptotic cells increased from (4.40?0.87)% (before treatment) to (15.80?1.55)% (P

BACKGROUND:During the restoration of residual molar crown, a little part of tooth is still remained commonly. After the restoration, with various forces, stress distribution affects directly the results after restoration. Finite element method is gradually applied in stress analysis on artificial tooth.OBJECTIVE: To establish the three-dimensional (3-D) finite element model of post-inlay restoration of the first residual mandibular molar crown so as to provide experimental data for improving model establishment of complicated teeth and analysis on the property of stress distribution of restoring methods.DESIGN: Repeated observation and measurement were given.SETTING: Department of Stomatology and Department of Radiology of First Hospital affiliated to Sun Yat-sen University;Department of Solid Mechanics,College of Traffics and Communications, South China University of Technology; Department of Restoration of Guanghua College of Stomatology.MATERIALS: The experiment was performed in Department of Solid Mechanics, College of Traffics and Communications of South China University of Technology from November 2003 to December 2004. Six first mandibular molars on the right side with normal morphology in vitro were collected, and Toshiba Xpress/SX spiral CT machine, image photo synthesis software and finite element analysis software ANSYS were applied in the experiment.METHODS: 1 of the 6 first mandibular molars on the right side with normal morphology in vitro was selected for pulpectomy, which was the best in density and near to clinical requirement in morphology. With pulpectomy, the prosthesis of braking-lock post-inlay restoration was prepared. Spiral CT-cross scanning was performed in premolar crown before the restoration, the residual crown with post-inlay in main root canal after restoration and the residual crown with braking-lock second post-inlay restoration. With image photosynthesis software, 3-D digital model of residual tooth and metal part was established and the entire tooth model was prepared after adhesion of two parts. In order to provide better boundary conditions of simulated natural tooth in practice, alveolar bone was considered. Under Mesh order in ANSYS software, automatic mesh generation was performed in the model directly.MAIN OUTCOME MEASURES: Establishment of 3-D finite element models of residual tooth before restoration, post inlay, and alveolar bone and tooth after restoration and the results of mesh generation.RESULTS: By establishing 3-D finite element models of residual tooth before restoration, post inlay, alveolar bone and tooth after restoration and automatic mesh generation, there were altogether 117720 units and 20988nodes. Good geometric similarity presents between the construction model of 3-D finite element model and solid tissue.CONCLUSION: Combination of 3-D finite-element model with spiral Ctcross technology establishes complex dental models, simulates practical conditions authentically and is good in operation.

In recent decades, although great progress has been made on the diagnosis and treatment of oral squamous cell carcinoma (OSCC), its 5-year survival rate has not been significantly improved. The basic reason is the unclear pathogenesis, lack of effective molecular markers for assessing invasion, metastasis, and recurrence as well as therapeutic targets. The present view is that genetic and epigenetic abnormalities are related to the occurrence and development of OSCC. Epigenetic inheritance is a biological behavior that can be regulated and reversed, and it plays an important role in the occurrence and development of malignant tumors. First, this review will describe the role of epigenetic modifications in the development of OSCC in combination with our research and the latest research progress of epigenetics, including DNA methylation, RNA methylation, short noncoding RNAs (miRNAs, etc.), long noncoding RNAs, circular RNAs, histone modifications (acetylation and methylation), chromatin remodeling and genomic imprinting. Then, we will analyze the value of epigenetic studies in the prevention, diagnosis, and targeted therapy of OSCC.

The evaluation of immune function plays an important role in the diagnosis, treatment and prognosis of many diseases. To date, immune function detection includes cellular immunity, humoral immunity, and inflammatory markers. In this paper, the application of immune function detection in the diagnosis, differential diagnosis and treatment monitoring of various diseases was discussed; then, the application value of immune function detection in the diagnosis and treatment of three common oral mucosa-related diseases, including recurrent aphthous ulcer (RAU), oral lichen planus (OLP), and oral squamous cell carcinoma (OSCC), were reviewed combined with the literature and our research. Our research found that RAU patients present abnormal humoral immune function and obvious inflammatory reactions, whereas OLP and OSCC patients present mild inflammatory reactions and more serious abnormal cellular and humoral immune function, so the combined detection of immune function has a certain guiding value for the diagnosis and treatment of these diseases. Moreover, in the future, it is necessary to carry out a study on large sample, multicenter and multiindex joint detection to better clarify the role of immune dysfunction in the pathogenesis of various diseases and its mechanism, to establish the corresponding diagnostic model and prognostic prediction model, to find more effective treatment methods.

Benign condylar hyperplasia is one of the causes of mandibular lateral deformity, it is easily to be misdiagnosed clinically and leads to the treatment failure. This article will elaborate the etiology and clinical features of benign condylar hyperplasia, as well as the diagnostic points and treatment progress, based on the literature and the clinical experience of our research group, to provide evidence-based medical evidence for the standardized clinical treatment of benign condylar hyperplasia. The etiology of benign condylar hypertrophy includes neurotrophic disorders, local circulatory disorders, traumatic injuries (especially condylar injuries that occur in childhood), unilateral mastication, temporomandibular arthritis, endocrine disorders, condylar osteoma, and heredity. Benign condylar hypertrophy is insidious, and occurs most frequently in individuals 10-30 years old, and the course of disease can last for many years. Its clinical characteristics are slow progressive facial asymmetry. Radionuclide bone scans have become the basis for the diagnosis and differential diagnosis of and treatment planning for benign condylar hypertrophy. Different treatment plans for active and inactive periods need to be developed, including close observation, proportional condylar resection and orthognathic surgery.

Epidemiological studies have shown that abnormal glucose and lipid metabolism is associated with a variety of malignant tumors, including oral squamous cell carcinoma. In this paper, the role of abnormal glucose and lipid metabolism, especially diabetes mellitus and obesity, in the occurrence and development of oral squamous cell carcinoma and its pathogenesis are reviewed based on the research results of our group and the literature. Hyperglycemia and insulinemia in diabetes mellitus are the main mechanisms that increase the risk of cancer. Our research shows that hyperglycemia can promote the proliferation, invasion and metastasis of tongue squamous cell carcinoma through the glycolytic enzyme M2 pyruvate kinase (PKM2) and hexokinase 2 (HK2). Hyperinsulinemia can promote the proliferation, invasion and metastasis of tongue squamous cell carcinoma by activating the insulin-like growth factor signal transduction system. Obese patients are often accompanied by increased serum adipokine Chemerin (Chem). Our study shows that serum Chem concentrations in obese patients with tongue cancer are significantly higher compared with nonobese patients. Chem can regulate the proliferation, invasion and migration of tongue squamous cell carcinoma cells through the SOD2-H2O2 signaling pathway. These results provide a basis for the prevention of oral squamous cell carcinoma, provide a new iqdea for the precise treatment of oral squamous cell carcinoma, and suggest that the treatment of oral squamous cell carcinoma should also actively treat patients with diabetes and obesity.

OBJECTIVETo investigate the therapeutic effect and metabolism of 5-fluorocytosine (5-FC) in human tongue squamous carcinoma cells after treatment with adenovirus-mediated cytosine deaminase (AdCMVCD)/5-FC system.

METHODSHuman tongue squamous carcinoma cells (Tca8113 cell line) and its xenografts in BALB/c nude mice were treated with AdCMVCD/5-FC system. The killing effect in vitro and bystander effect were detected by microculture tetrazolium (MTT) assay. Tumor inhibition effect and histopathological changes were observed in vivo. High-performance liquid chromatography (HPLC) was performed to determine the metabolism of 5-FC in vitro and in vivo.

RESULTSAdCMVCD/5-FC system had strong killing effect and bystander effect on Tca8113 cells. Both condition media and cell extracts showed two peaks identified as 5-FC and 5-fluorouracil (5-FU) by HPLC and a time-dependent generation of 5-FU and concomitant time-dependent decreases of 5-FC. Compared to the control groups, mice treated with AdCMVCD/5-FC system demonstrated significant tumor regression (P < 0.001); the tumor doubling time prolonged and inhibition rate was 92.62%. There were substantial tumor necrotic areas and infiltrative lymphocytes around necrotic areas in the AdCMVCD/5-FC treated group under light microscope. There was a significantly low concentration of 5-FC and high concentration of 5-FU in tumor tissue, but only 5-FC was found in blood.

CONCLUSIONAdCMVCD/5-FC suicide gene system had significant in vitro and in vivo anti-tumor effect on human tongue squamous cell carcinoma due to convert 5-FC into 5-FU.

Adenoviridae ; genetics ; Animals ; Carcinoma, Squamous Cell ; pathology ; therapy ; Cytosine Deaminase ; Female ; Flucytosine ; metabolism ; therapeutic use ; Genetic Therapy ; Humans ; Mice ; Mice, Inbred BALB C ; Neoplasm Transplantation ; Nucleoside Deaminases ; genetics ; Tongue Neoplasms ; pathology ; therapy ; Transplantation, Heterologous ; Tumor Cells, Cultured

PURPOSE: Several signaling pathways have been shown to regulate the lineage commitment and terminal differentiation of bone marrow stromal cells (BMSCs). Bone morphogenetic protein (BMP) signaling has important effects on the process of skeletogenesis. In the present study, we tested the role of bone morphogenetic protein receptor (BMPR) in the osteogenic differentiation of rat bone marrow stromal cells in osteogenic medium (OM) with or without BMP-2. MATERIALS AND METHODS: BMSCs were harvested from rats and cultured in OM containing dexamethasone, beta-glycerophosphate, and ascorbic acid, with or without BMP-2 in order to induce osteogenic differentiation. The alkaline phosphatase (ALP) activity assay and von kossa staining were used to assess the osteogenic differentiation of the BMSCs. BMPR mRNA expression was assessed using reverse transcription-polymerase chain reaction (RT-PCR). RESULTS: The BMSCs that underwent osteogenic differentiation in OM showed a higher level of ALP activity and matrix mineralization. BMP-2 alone induced a low level of ALP activity and matrix mineralization in BMSCs, but enhanced the osteogenic differentiation of BMSCs when combined with OM. The OM significantly induced the expression of type IA receptor of BMPR (BMPRIA) and type II receptor of BMPR (BMPRII) in BMSCs after three days of stimulation, while BMP-2 significantly induced BMPRIA and BMPRII in BMSCs after nine or six days of stimulation, respectively. CONCLUSION: BMSCs commit to osteoblastic differentiation in OM, which is enhanced by BMP-2. In addition, BMP signaling through BMPRIA and BMPRII regulates the osteogenic differentiation of rat BMSCs in OM with or without BMP-2.
Alkaline Phosphatase/metabolism ; Animals ; Bone Marrow Cells/*cytology/drug effects/*metabolism ; Bone Morphogenetic Protein 2/pharmacology ; Bone Morphogenetic Protein Receptors/genetics/*metabolism ; *Cell Differentiation/drug effects ; Cell Proliferation/drug effects ; Cells, Cultured ; Culture Media/pharmacology ; Male ; Osteogenesis/drug effects/genetics ; Rats ; Rats, Wistar ; Reverse Transcriptase Polymerase Chain Reaction ; Stromal Cells/*cytology/drug effects/*metabolism

Free tissue flap transplantation is the preferred option for repairing and reconstructing postoperative defects in oral and maxillofacial-head malignant tumors. However, challenges remain for oral and maxillofacial-head and neck oncology surgeons in terms of ischemia-reperfusion (I/R) injury, airway management, quality of life and prognosis. I/R injury is an inevitable complication of free-flap transplantation surgery. In addition to shortening the vascular anastomosis time as much as possible during the surgical process, many studies have attempted to further prevent and treat free-flap I/R injury using physical intervention therapy, antioxidant and reactive oxygen species (ROS) scavenger therapy, hyperbaric oxygen therapy, etc. However, there is a lack of large-scale clinical randomized controlled trial evidence to further support these methods. Postoperative tracheal management of patients receiving free tissue flap transplantation is very important. In recent years, delayed extubation has been proposed as an alternative to traditional tracheostomy. This method can facilitate wound care for patients, reduce infections, speed up patient recovery, and reduce the incidence of vascular crises. In the future, such management is expected to improve the practicality and safety of delayed extubation by formulating more appropriate patient selection criteria and intensive care plans. Preoperative selection of suitable free tissue flaps according to the defect for repair and reconstruction is beneficial for improving the quality of life and survival rate of patients. At the same time, for patients who require postoperative radiotherapy, reducing the complications of postoperative radiotherapy and improving the quality of life of patients can be achieved through intraoperative nerve anastomosis, preradiation oral hygiene maintenance, early speech training, and other methods.

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.