Traumatic temporomandibular joint ankylosis refers to fibrous or bony fusion between the condyle and the glenoid fossa. It can cause problems with mouth-opening limitations, mastication difficulties, obstructive sleep apnea and hypopnea syndrome. When traumatic temporomandibular joint ankylosis occurs during childhood, it can cause facial asymmetry, micrognathia, and malocclusion, which significantly affect the physical and mental health. Once temporomandibular joint ankylosis occurs, it will be refractory and recurrent. The pathogenesis of temporomandibular joint ankylosis has not been completely elucidated and has always been a research hotspot in the oral and maxillofacial fields. In this paper, worldwide research was conducted, and the pathogenesis of traumatic temporomandibular joint ankylosis was clarified, such as “damage of condyle”,“disc displacement or rupture”,“damage to the glenoid fossa” and “lateral pterygoid muscle distraction”. The relative pathogenesis hypotheses were summarized, such as “hematoma organization” and “lateral pterygoid muscle distraction osteogenesis”. The related pathogenesis of traumatic temporomandibular joint ankylosis was discussed based on the latest cytology and molecular biology research.
Objective To construct a hit-deficient mutant strain of S. mutans ATCC25175 and verify its cell cycle regulatory function. Method Genomic DNA was extracted from S. mutans ATCC25175 strains, and then the upstream and downstream DNA fragments of the hit gene were cloned into the pFW5 vector (spectinomycin resistant) to construct recombinant plasmids using PCR amplification. Third, employed by natural genetic transformation in S. mutans ATCC25175 strains, the linearized recombinant plasmids were transformed into their genetic competence, induced by the synthesized competence-stimulating peptide (CSP), and then, homologous recombination was utilized to produce crossover and noncrossover products. Fourth, the hit-deficient mutant strains of S. mutans ATCC25175 were screened through the spectinomycin-resistance marker and identified by the electrophoresis of PCR products and PCR Sanger sequencing. Finally, its growth rate in vegetative BHI medium was also investigated. Results The upstream (856 bp) and downstream (519 bp) DNA fragments of the hit gene from the genomic DNA materials of S. mutans ATCC25175 were cloned into two multiple cloning sites (MCS-I and MCS-II) of the pFW5 vector, respectively, and the recombinant plasmid pFW5_hit_Up_Down was constructed and identified by double-emzyme digestion and PCR Sanger sequencing. The linearized recombinant plasmids were transformed into their genetic competence, induced by the synthetic CSP, and then, homologous recombination was utilized to produce various products. The hit-deficient mutant strains of S. mutans ATCC25175 were screened through the spectinomycin resistance marker and identified by the electrophoresis of PCR products and Sanger sequencing. The growth rate of the hit-deficient mutant strains versus their parental S. mutans ATCC25175 strains was increased greatly (P<0.001). Conclusion The hit-deficient mutant strains of S. mutans ATCC25175, having heritable traits, were successfully constructed, and the encoding Hit protein is growth-phase regulated in the cell cycle.
Objective To explore the potential mechanism of the main active component Tripterygium wilfordii in the treatment of oral lichen planus based on network pharmacology. Methods The components of Tripterygium wilfordii and targets were searched through the Traditional Chinese Medicine system pharmacology database and analysis platform (TCMSP) and the Traditional Chinese Medicine integrated database (TCMID) databases. The related targets of oral lichen planus (OLP) were obtained through databases such as Gene Cards. The OLP targets were mapped by Venn analysis to the targets of Tripterygium wilfordii to screen out the common targets as the treatment of OLP targets of Tripterygium wilfordii. The Cytoscape software and STRING were used to construct a chemical component-target network and protein-protein interaction network, a network analyzer was used to compute the network topology properties, a cluster profiler software was used to analyze the GO classification enrichment analysis and KEGG signal path analysis, and a Tripterygium wilfordii chemical components-targets-pathway network diagram was constructed. Results Twenty-three components and 44 OLP treatmenttargets of Tripterygium wilfordii were obtained. The key active ingredients of Tripterygium wilfordii in the treatment of OLP are triptolide, kaempferol, and tangerine peel. The key targets include TNF and AKT1. The GO classification enrichment analysis obtained 63 GO terms, which are mainly involved in the leukocyte differentiation and reaction to lipopolysaccharides. The KEGG analysis identified 111 signaling pathways, which are mainly related to the TNF signaling pathway and IL17 signaling pathway. Conclusion Based on the network pharmacology, this study preliminarily revealed themain components, targets and pathways of Tripterygium wilfordii in the treatment of OLP. This study can provide a theoretical basis for further research to explore drugs with high activity and low toxicity to treat OLP from Tripterygium wilfordii.
Objective Systematic evaluation of the correlation of HLA-DQB1 and HLA-DRB1 allele polymorphisms with caries, to provide reference for caries prevention and treatment. Methods Relevant literature published before December 2020 was searched in the Cochrane Library, PubMed, Embase, Web of Science, Scopus, CNKI, Wanfang, VIP, and CBM databases. Meta-analysis was performed using the R4.0.2 software to test for heterogeneity and evaluate the publication bias. Results In total,10 case-control studies were included with 564 people in the case group and 676 people in the control group. The results of the Meta-analysis show that: ① HLA-DQB1*02 (OR=0.52, 95%CI=0.29-0.93, P < 0.05) and HLA-DRB1*09 (OR=0.34, 95%CI=0.21-0.58, P < 0.05) are protective factors of dental caries; ② HLA-DRB1*13 (OR=2.96, 95%CI=2.03-4.33, P < 0.05) and HLA-DRB1*14 (OR=1.95, 95%CI=1.26-3.02, P < 0.05) alleles are risk factors for the development of dental caries. The results of the subgroup analysis are: HLA-DRB1*07 is a caries susceptibility factor in the Chinese population (OR=0.48, 95% CI=0.24-0.97, P < 0.05), while it is not statistically significant in the Brazilian and Turkish populations; HLA-DRB1*11 is a caries protective factor in the saliva group (OR=2.26, 95% CI=1.46-3.52, P < 0.05). 3.52, P < 0.001), while it is a caries susceptibility factor in the blood group (OR=0.09, 95% CI=0.12-0.34, P < 0.001). Conclusion HLA-DRB1*13 and HLA-DRB1*14 alleles are caries susceptibility genes, and HLA-DQB1*02 and HLA-DRB1*09 have protective effects on the caries development. HLA-DRB1*07 is a caries susceptibility gene in the Chinese population; HLA-DRB1*11 is a caries protective gene in the saliva group. Due to the limited sample size and quality of the included studies, more high-quality studies will be included later for verification.
Objective To study the changes in levels of interleukin (IL)-6, IL-10, tumor necrosis factor-alpha (TNF-α), and alkaline phosphatase (ALP) in the gingival crevicular fluid (GCF) of patients with severe chronic periodontitis before and after nonsurgical periodontal therapy and to explore the relationship among the levels of these four biomarkers in GCF, their periodontal status and their clinical significance to evaluate the effect of nonsurgical periodontal therapy and periodontitis activity. Methods In total, 30 patients with severe chronic periodontitis were enrolled in a 1-year longitudinal pilot study (Chinese Clinical Trial Registry: ChiCTR-OCH-13004679). At baseline and 1, 3, 6, and 12 months after nonsurgical therapy, the periodontal clinical indicators plaque index (PLI), probing depth (PD), clinical attachment loss (CAL), sulcus bleeding index (SBI) were recorded. Filter paper strips were used to collect two deep-pocket (probing depth ≥ 6 mm) and two shallow-pocket (probing depth ≤ 4 mm) periodontal sites for each patient and weighed. The levels of interleukin IL-6, IL-10, TNF-α, and ALP in GCF were assessed using enzyme-linked immunosorbent assay. Meanwhile, 30 healthy sites of 15 subjects with healthy periodontium were used as the baseline controls for patients with severe chronic periodontitis. Results At the baseline, the TNF-α, ALP and IL-6 levels in GCF of the disease sites of patients with periodontitis were significantly higher than those in healthy periodontal sites of the control group (P < 0.001), and the levels of IL-10 were significantly lower than those in the control group (P < 0.001). In patients with severe chronic periodontitis, the levels of TNF-α, ALP and IL-6 in GCF at deep-pocket sites were significantly higher than those at shallow-pocket sites (P <0.001), and the IL-10 levels were significantly lower than those at shallow-pocket sites (P < 0.001). 1, 3, 6, and 12 months after nonsurgical treatment, the levels of TNF-α and ALP in GCF at the shallow- and deep-pocket sites in patients with chronic periodontitis significantly decreased, the level of IL-10 significantly increased (P < 0.005), and the level of IL-6 in GCF at the deep-pocket sites significantly decreased (P < 0.005). However, there was no significant difference in IL-6 level at shallow-pocket sites (P > 0.05). 1, 3, 6, and 12 months after nonsurgical treatment, the periodontal clinical indicators were improved compared with the baseline. In addition, there was a significant correlation between the levels of these four biomarkers and the periodontal clinical parameters (P < 0.05). During the two follow-up visits after nonsurgical periodontal therapy, the sites with more than 2-mm increase in attachment loss had significant differences in the levels of the four biomarkers in the GCF compared with the previous visit time (P < 0.005). Conclusion The detection of the levels of these four biomarkers in GCF has strong clinical significance for assessing the severity of periodontitis and the efficacy of nonsurgical periodontal therapy. Increased levels of TNF-α, ALP, and IL-6 and decreased IL-10 levels in GCF may indicate periodontitis progression at this site.
Objective To observe the root and root canal morphology of mandibular second molars in Western Guangxi by CBCT, to provide a reference for clinical diagnosis and treatment. Methods In total, 564 patients′ 1 128 mandibular second molars that satisfy the inclusion criteria were analyzed with a planmecaromexis CBCT machine and its own image analysis software. The patients′ gender, age and ethnic differences in the root and canal morphology and the symmetry of the bilateral root and canal were statistically analyzed. Results Among the 1 128 mandibular second molars, 662 were the Zhuang ethnic group and 384 were the Han ethnic group, and 82 were other ethnic groups; the double root type and C-shaped root type accounted for a relatively high proportion: 73.94% and 24.47%, respectively. The detection rates of the double root type were higher in males than in females (P < 0.05); the detection rates of the C-shaped root type were higher in females than in males (P <0.05); the root type of the teeth was mainly double-rooted in the Zhuang ethnic group (P<0.01). The incidence of type IV in the mesial root of the double root type mandibular second molar was the highest (P < 0.01), and the incidence of type I in the distal root was the highest (P < 0.01). The C-shaped root canal is more continuous at the mouth of the root canal, more downward corresponds to a worse continuity: in three different levels of root canal orifice, root middle and root apex, the root canal orifice is dominated by the C1 type, and both root middle and root apex are mainly C3-type (P < 0.01). The difference in symmetry of bilateral roots and root canals was statistically significant among different gender groups, age groups, and ethnic groups (P < 0.05): there were more males than females, the results in the 18-35-year-old group and the Zhuang ethnic group were higher. Conclusion The root and root canal morphology of mandibular second molars in western Guangxi people are complex and changeable. The roots are mainly double root type in the Han ethnic group and the Zhuang ethnic group. C-shaped roots are also common. The detection rate of C-shaped roots in the Zhuang ethnic group was higher, and the symmetry rate of bilateral roots and that of bilateral root canals was higher in the Zhuang ethnic group than in the Han ethnic group.
Objective To investigate the clinicopathological features, treatment and prognosis of oralmucosal malignant melanoma to provide a reference for clinical practice. Methods Data from 19 patients with oralmucosal malignant melanoma were collected, and their clinical manifestations, treatment methods and follow-up results were retrospectively analyzed. Results Among the 19 patients, 11 cases (58%) had lesions in the gingiva, 7 cases (37%) had lesions in the palate, and 1 case (5%) had lesions in the tongue, the difference was statistically significant (P<0.05). Eight patients had regional lymph node metastasis with a metastasis rate of 42%, of which 4 cases had multiple site metastasis, and the total number of regional lymph node metastasis sites was 15. Among the 19 patients, 3 cases received only surgery, 4 cases received cryotherapy, and 12 cases received combined surgery, cryotherapy and biological immunotherapy. Pathological examination showed malignant melanoma. The positive rates of S-100, HMB-45 and Melan-A were 95%, 89% and 84%, respectively. Kaplan-Meier survival analysis showed that patients with lesions less than 5 cm2 had a higher survival rate (P < 0.05). Conclusions Oral malignant melanomas usually present as black lesions in the oral mucosa, which are prone to metastasis in early stage. The area of lesions may affect the prognosis of the disease. Therefore, the large range of black lesions or masses should be the alert for the clinicians. Oral malignant melanoma patients are usually treated with combined treatment with surgery, cryotherapy and biological immunotherapy.
Objective To investigate the multi-disciplinary team (MDT) management in the treatment of giant neurofibroma in maxillofacial and neck region, to provide reference for clinical practice. Methods Retrospective analysis was conducted on the perioperative whole-process management process of 2 cases of giant neurofibroma in maxillofacial and neck region jointly formulated treatment plan by oral and maxillofacial surgery department with the assistance of the department of anesthesiology, ICU, vascular surgery, thoracic surgery, etc. Results MDT treatment process (anesthesia-embolization-collaborative surgery-ICU-post-operative management) of the two patients was smoothly conducted according to the pre-operative plan. There were no adverse events or accidents that were not predicted by the risk assessment from multiple teams during the operation, and no serious complications occurred after the operation. The post-operative pathological report of both cases was "neurofibroma". Wounds in both patients healed in stage I. The course of treatment was smooth, and the surgical treatment was completed without serious complications. Conclusion MDT management can play a positive role in the diagnosis and treatment of giant maxillofacial and neck neurofibroma so that patients can obtain safer and more effective diagnosis and treatment.
Mesenchymal stem cells (MSCs) are capable of self-replication and multi-directional differentiation, which are very important for the development and reconstruction of mesenchymal tissue. Bone tissue damage repair involves the participation of various cells and molecules. The recovery of bone mass requires sufficiently many MSCs to migrate to the damaged site to perform the reconstruction function. The local inflammatory response at the injury site can recruit MSCs and promote new bone formation. Simultaneously, niche changes during the migration of MSCs will affect their biological performance and initiate the phase of directed differentiation. This article explores the relevant mechanisms that mediate the migration of MSCs in the process of bone injury repair, including the regulation of immune cells and chemotactic signaling molecules in the inflammatory response in the bone repair stage through signaling pathways such as BMP/Smads. Then, it summarizes the mechanism by which the high matrix stiffness upregulates the expression of the integrin and focal adhesions to promote the MSCs migration and osteogenic differentiation. Simultaneously, the migration ability of MSCs can be regulated through drugs or genetic modification to promote the bone injury repair. The improvement of MSCs migration ability can shorten the time of bone tissue damage repair and improve the bone quality. This article reviews the role of the MSCs migration ability in bone tissue injury repair to provide a reference for the application of MSCs with high migration ability in the fields of stem cell therapy for bone related diseases and bone tissue engineering.
Periodontitis is the inflammation of periodontal tissue caused by dental plaque, which absorbs the alveolar bone and cementum. The immune response triggered by CD4+T cells is the key factor for the aggravation of periodontitis. The activation of dendritic cells and the receptor activator of the NF-κB ligand (RANKL) pathway is an important link in the alveolar bone resorption of periodontal tissue. Pro-inflammatory factors such as interferon-γ (IFN-γ), tumor necrosis factor (TNF-α) and interleukin-1β (IL-1β) also play important roles in the development of periodontitis. Interleukin-37(IL-37), which is a newly discovered cytokine in the IL-1 family, has five shear variants from a to e, among which the clover β-structure encoded by exon 4 plays an important role in the binding of cytokines and the corresponding receptors. IL-37 has strong anti-inflammatory and inhibition of autoimmunity, can enter the nucleus with the help of caspase-1 and bind with Smad proteins to regulate the transcription of pro-inflammatory genes. Extracellular IL-37 can bind to IL-18 binding protein and inhibit the production of pro-inflammatory factors. IL-37 can inhibit the progression of periodontitis by inhibiting the RANKL signaling pathway, inhibiting the proliferation and differentiation of dendritic cells and CD4+T cells, binding to Smad proteins, and releasing pro-inflammatory factors such as IFN-γ and TNF-α. The IL-37 concentration in periodontal tissue can indicate the progression of periodontitis. Few studies have described the interaction between the anti-inflammatory factor IL-37 and periodontitis. Thus, in this paper, the structure and function of IL-37 and the related factors between IL-37 and periodontitis will be reviewed.