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Objective: This article focus on patients with moderate-to-severe periodontitis and periodontitis patients with cardiovascular disease. After they received periodontal initial therapy or antimicrobial drug treatment, was there any improvement in endothelial function during short- and long-term followups? Method: Relevant randomized controlled trials and clinical trials up to 30th June 2024 were identified and retrieved from electronic databases including PubMed, Cochrane Library, Web of Science and CNKI databases, with periodontitis therapy, periodontal disease and endothelial function as the keywords. The weighted (WMD) or standardized mean difference (SMD) was calculated using a fixed- or random-effect model and assessed heterogeneous results. Result: Generally, 14 studies published between 2004 and 2022 were eligible for the meta-analysis, which are all randomised clinical trials. A total of 491 periodontitis patients were screened. All participants received whole-mouth supragingival and subgingival scaling and root planing of the teeth, some trials combined with antimicrobial drug treatment as well as extracting teeth that could not be saved. The outcome indicators were measured by flow-mediated dilatation(FMD) levels. The results of the short term (≤3 months) periodontitis initial therapy group showed positive results (WMD = -3.78,95%CI = [-5.49,-2.07], P<0.0001), while the results of the long term (6 months) periodontitis therapy group exhibited significant difference (WMD = -0.96,95%CI = [-2.06,0.14],P = 0.09). Furthermore, study population were categorized according to the severity of periodontitis, the presence of comorbidities, endothelial dysfunction, and the inclusion of extractions and antimicrobial therapy in the treatment process. The effects of each of these factors on FMD were explored and the results of these subgroups all support periodontitis therapy. Conclusion: The results showed that periodontal treatment enhances endothelial function. Additionally, after subgroup analysis of long-term and short-term follow-up, patients with severe periodontitis, and different periodontal treatments, periodontal therapy was shown to increase FMD levels. [ABSTRACT FROM AUTHOR]

Background: Periodontal ligament cells (PDLCs) are a major component of the periodontal ligament and have an important role in the regeneration of periodontal tissue and maintenance of homeostasis. High glucose can affect the activity and function of PDLCs in a variety of ways; therefore, it is particularly important to find ways to alleviate the effects of high glucose on PDLCs. Annexin A2 (ANXA2) is a calcium- and phospholipid-binding protein involved in a variety of cellular functions and processes, including cellular cytokinesis, cytophagy, migration, and proliferation. Aim: The aim of this study was to exploring whether ANXA2 attenuates the deleterious effects of high glucose on PDLCs and promotes osteogenic differentiation capacity. Methods and results: Osteogenic differentiation potential, cellular senescence, oxidative stress, and cellular autophagy were detected. Culturing PDLCs with medium containing different glucose concentrations (CTRL, 8 mM, 10 mM, 25 mM, and 40 mM) revealed that high glucose decreased the protein expression of ANXA2 (p < 0.0001). In addition, high glucose decreased the osteogenic differentiation potential of PDLCs as evidenced by decreased calcium deposition (p = 0.0003), lowered ALP activity (p = 0.0010), and a decline in the expression of osteogenesis-related genes (p = 0.0008). Moreover, β-Galactosidase staining and expression of p16, p21 and p53 genes showed that it increased cellular senescence in PDLCs (p < 0.0001). Meanwhile high glucose increased oxidative stress in PDLCs as shown by ROS (p < 0.0001). However, these damages caused by high glucose were inhibited after the addition of 1 µM recombinant ANXA2 (rANXA2), and we found that rANXA2 enhanced autophagy in PDLCs under high glucose conditions. Conclusions and discussion: Therefore, our present study demonstrates that alterations in ANXA2 under high glucose conditions may be a factor in the decreased osteogenic differentiation potential of PDLCs. Meanwhile, ANXA2 is associated with autophagy, oxidative stress, and cellular senescence under high glucose conditions. [ABSTRACT FROM AUTHOR]

Orthodontic patients often suffer from mucosal discomfort due to the friction stimulation of orthodontic components on the oral mucosa, and semiconductor laser can treat the oral mucosal discomfort caused by orthodontic treatment, such as redness, swelling, ulcers, etc. This study innovatively created a persistent traumatic environment in the mouth of rats to simulate the intraoral conditions of orthodontic patients, with the aim of using animal models to broaden the understanding of semiconductor laser repair mechanisms of orthodontic traumatic ulcers. 32 male Wistar rats were randomly divided into 6 groups: 1) blank control group; 2) control group; 3) chlorhexidine group; 4) laser group 1; 5) laser group 2; 6) laser group 3. The research contents included ulcer healing degree score, enzyme-linked immunosorbent assay, histological observation of stained sections of ulcer tissue, and analysis of microbial attachment on ulcer surface. The results showed that the continuous traumatic environment significantly prolonged the healing time of ulcer (P<0.05). During the ulcer duration, the proinflammatory factor level was lower, the anti-inflammatory factor level was higher and the healing score was better in the laser group (P<0.05). The antibacterial effect of semiconductor laser is less than 0.12% chlorhexidine solution; Hematoxylin-eosin tissue sections showed lower inflammatory cell infiltration and better epithelial healing in the laser group. This study shows that continuous traumatic environment can delay ulcer healing, and semiconductor laser with appropriate irradiation time is superior to traditional 0.12% chlorhexidine solution in reducing inflammation, relieving pain and promoting ulcer tissue healing. Compared with previous studies, the animal model in this study has made some progress and is closer to the real oral conditions of orthodontic patients. The results further demonstrated the potential of semiconductor laser in the treatment of oral traumatic ulcers during orthodontics. [ABSTRACT FROM AUTHOR]

The purpose of this work is to explore the properties of the lignin-derived amine-free photoinitiating systems (PISs) during the curing process. Four novel hydrogen donors (HD1, HD2, HD3, and HD4) derived from lignin α-O-4 structural were designed and synthesized by simple methods, and their low C–H bond dissociation energies on methylene were determined by molecular orbitals theory. Four experimental groups using CQ (camphorquinone)/HD PIs formulated with Bis-GMA/TEGDMA (70 w%/30 w%) were compared to CQ/EDB (ethyl 4-dimethylamino benzoate) system. The photopolymerization profiles and double bond conversion rate was tracked by FTIR experiments; the color bleaching ability of the samples and color aging test assay were performed using color indexes measurements; The cytotoxicity of the samples was also compared to EDB related systems. All of the experimental groups with new HDs were compared to the control group with EDB by statistical analysis. Compared to CQ/EDB system, new lignin-derived hydrogen donors combined with CQ showed comparable or even better performances in polymerization initiation to form resin samples, under a blue dental LED in air. Excellent color bleaching property was observed with the new HDs. Aging tests and cytotoxicity examination of the resin were performed, indicating the new lignin compounds to be efficient hydrogen donors for amine-free CQ-based photo-initiating system. Novel lignin α-O-4 derived hydrogen donors are promising for further usage in light-curing materials. [ABSTRACT FROM AUTHOR]

Electrospinning technology has recently attracted increased attention in the biomedical field, and preparing various cellulose nanofibril membranes for periodontal tissue regeneration has unique advantages. However, the characteristics of using a single material tend to make it challenging to satisfy the requirements for a periodontal barrier film, and the production of composite fibrous membranes frequently impacts the quality of the final fiber membrane due to the influence of miscibility between different materials. In this study, nanofibrous membranes composed of polylactic acid (PLA) and polycaprolactone (PCL) fibers were fabricated using side-by-side electrospinning. Different concentrations of gelatin were added to the fiber membranes to improve their hydrophilic properties. The morphological structure of the different films as well as their composition, wettability and mechanical characteristics were examined. The results show that PCL/PLA dual-fibrous composite membranes with an appropriate amount of gelatin ensures sufficient mechanical strength while obtaining improved hydrophilic properties. The viability of L929 fibroblasts was evaluated using CCK-8 assays, and cell adhesion on the scaffolds was confirmed by scanning electron microscopy and by immunofluorescence assays. The results demonstrated that none of the fibrous membranes were toxic to cells and the addition of gelatin improved cell adhesion to those membranes. Based on our findings, adding 30% gelatin to the membrane may be the most appropriate content for periodontal tissue regeneration, considering the scaffold's mechanical qualities, hydrophilic properties and biocompatibility. In addition, the PCL-gelatin/PLA-gelatin dual-fibrous membranes prepared using side-by-side electrospinning technology have potential applications for tissue engineering. [ABSTRACT FROM AUTHOR]

Objectives: In order to predict the patients' prognosis with tongue squamous cell carcinoma (SCC), this study set out to develop a clinically useful and trustworthy prognostic nomogram. Subjects and Methods: The Surveillance, Epidemiology, and End Results (SEER) Program was used to compile clinical information on patients with tongue SCC between 2010 and 2015. The likelihood of Cancer‐Specific Survival (CSS) and Overall Survival (OS) for specific patients was predicted using a prognostic nomogram created with the help of the RStudio software. The nomogram's predictive ability was evaluated using the consistency index (C‐index) and decision curve analysis, and the nomogram was calibrated for 1‐, 2‐, 3‐, 5‐, and 10‐year CSS and OS. Results: Patients numbering 6453were enrolled in this study. The primary cohort (3895) and validation cohort (2558) were each randomly assigned. Sex, age, tumor‐node‐metastasis (TNM) stage, surgery, chemotherapy, and radiation were significant risk factors for OS, whereas age, TNM stage, surgery, chemotherapy, and radiotherapy were significant risk factors for CSS. Additionally, C‐index and calibration curves indicated that the prognostic nomogram prediction and the actual observation in both cohorts would be very coherent. Conclusions: The predictive nomogram created in this study can offer patients with tongue SCC customized treatment and survival risk assessment. [ABSTRACT FROM AUTHOR]

The association between the anatomical features of teeth and the pathogenesis of periodontitis is well-documented. This study aimed to evaluate the influence of the mesial concavity of the maxillary first premolar on periodontal clinical indices and alveolar bone resorption rates. Employing a cross-sectional design, in 226 patients with periodontitis, we used cone beam computed tomography(CBCT) to examine the mesial concavity and alveolar bone resorption of 343 maxillary first premolar. Periodontal clinical indicators recorded by periodontal probing in the mesial of the maxillary first premolar in patients with periodontitis. Our findings indicate that the presence of mesial concavity at the cemento-enamel junction of the maxillary first premolar was not significantly influenced by either tooth position or patient sex (p > 0.05). Nonetheless, the mesial concavity at the cemento-enamel junction of the maxillary first premolar was found to exacerbate alveolar bone resorption and the inflammatory condition (p < 0.05). We infer that the mesial concavity at the cemento-enamel junction of the maxillary first premolar may contribute to localized alveolar bone loss and accelerate the progression of periodontal disease. [ABSTRACT FROM AUTHOR]

Periodontitis has a known association with pathological calcification in the cardiovascular system. Considering the close anatomic and circulatory association between dental pulp and the periodontium, this study aimed to evaluate the prevalence of pulp calcification (PC) under different periodontal conditions, as well as the associations of PC with the degree of periodontal damage, via cone beam computed tomography (CBCT) examination. In this study, 55 patients were categorized into three groups according to periodontal condition: group 1 (healthy controls), group 2 (periodontitis stage I–II), and group 3 (periodontitis stage III–IV). PC and radiographic bone loss (RBL) was assessed by CBCT in sagittal, axial, and coronal views, and statistical analyses were conducted. PC was identified in 378 of 1170 teeth (32.3%). The prevalence significantly differed among the three groups (P < 0.001). Group 2 had a 2.43-fold (P < 0.001, 95% confidence interval [CI] 1.64–3.61) higher risk of PC than group 1; and the risk of PC was 3.04-fold (P < 0.001, 95% CI 2.06–4.48) higher in group 3 than group 1. Teeth with more severe RBL exhibited a higher prevalence of PC (P < 0.001). Molar teeth had a higher risk of PC than incisors and premolars. In conclusion, the occurrence of PC is related to the periodontal state, and the prevalence of PC is higher in teeth with periodontitis; tooth type and periodontitis status are important risk factors for PC. [ABSTRACT FROM AUTHOR]

BACKGROUND: The effectiveness and availability of conservative therapies for osteonecrosis of the femoral head (ONFH) are limited. Transplantation of bone marrow mesenchymal stem cells (BMSCs) combined with Bio-Oss, which is a good bone scaffold biomaterial for cell proliferation and differentiation, is a new potential therapy. Of note, the expression of miRNAs was significantly modified in cells cultured with Bio-Oss, and MiR-214 was correlated positively with osteonecrosis. Furthermore, miR-214 was upregulated in cells exposed to Bio-Oss. OBJECTIVE: To investigate whether targeting miR-214 further improves the transplantation effect. METHODS: We treated BMSCs with agomiR-214 (a miR-214 agonist), antagomiR-214 (a miR-214 inhibitor), or vehicle, followed by their transplantation into ONFH model rats. RESULTS: Histological and histomorphometric data showed that bone formation was significantly increased in the experimental groups (Bio-Oss and BMSCs treated with antagomiR-214) compared with other groups. CONCLUSIONS: miR-214 participates in the inhibition of osteoblastic bone formation, and the inhibition of miR-214 to bone formation during transplantation therapy with Bio-Oss combined with BMSCs for ONFH. [ABSTRACT FROM AUTHOR]

Background: Pulmonary metastasis is the most frequent cause of death in osteosarcoma (OS) patients. Recently, several bioinformatics studies specific to pulmonary metastatic osteosarcoma (PMOS) have been applied to identify genetic alterations. However, the interpretation and reliability of the results obtained were limited for the independent database analysis.Objective: The expression profiles and key pathways specific to PMOS remain to be comprehensively explored. Therefore, in our study, three original datasets of GEO database were selected.Methods: Initially, three microarray datasets (GSE14359, GSE14827, and GSE85537) were downloaded from the GEO database. Differentially expressed genes (DEGs) between PMOS and nonmetastatic osteosarcoma (NMOS) were identified and mined using DAVID. Subsequently, GO and KEGG pathway analyses were carried out for DEGs. Corresponding PPI network of DEGs was constructed based on the data collected from STRING datasets. The network was visualized with Cytoscape software, and ten hub genes were selected from the network. Finally, survival analysis of these hub genes also used the TARGET database.Results: In total, 569 upregulated and 1238 downregulated genes were filtered as DEGs between PMOS and NMOS. Based on the GO analysis result, these DEGs were significantly enriched in the anatomical structure development, extracellular matrix, biological adhesion, and cell adhesion terms. Based on the KEGG pathway analysis result, these DEGs were mainly enriched in the pathways in cancer, PI3K-Akt signaling, MAPK signaling, focal adhesion, cytokine-cytokine receptor interaction, and IL-17 signaling. Hub genes (ANXA1 and CXCL12) were significantly associated with overall survival time in OS patient.Conclusion: Our results may provide new insight into pulmonary metastasis of OS. However, experimental studies remain necessary to elucidate the biological function and mechanism underlying PMOS. [ABSTRACT FROM AUTHOR]

Background: An increasing number of studies have shown that dysregulated miR-589-3p is associated with multiple diseases. However, the role of miR-589-3p in osteogenic differentiation of periodontal ligament stem cells (PDLSCs) remains unknown. This study aimed to explore the biological function and potential molecular mechanism of miR-589-3p in osteogenic differentiation of PDLSCs. Methods: GSE159508 was downloaded from Gene Expression Omibus (GEO, http://www.ncbi.nlm.nih.gov/geo/). Differentially expressed miRNAs between osteogenic induction PDLSCs versus non-induction PDLSCs were obtained by R software. miR-589-3p mimic and miR-589-3p inhibitor and corresponding negative control were obtained and to identify the role of miR-589-3p in osteogenic differentiation of PDLSCs. ALP staining and ARS were used to evaluate ALP activity and mineralization, respectively. The targeted binding relationship between miR-589-3p and ATF1 was predicted and verified by target prediction analysis and dual-luciferase assay. Furthermore, the functional mechanism based on miR-589-3p and ATF1 in osteogenic differentiation of PDLSCs was further investigated through rescue experiments. Results: According to the cut-off criteria with log 2 FC > 1.0 and P < 0.05, 514 differentially expressed miRNAs were identified between osteogenic induction and non-induction PDLSCs, including 309 upregulated miRNAs and 205 downregulated miRNAs. Compared with control PDLSCs, miR-589-3p expression level was notably increased in PDLSCs that underwent osteogenic induction. The overexpression of miR-589-3p promoted the cell viability of PDLSCs, while the low expression of miR-589-3p had the opposite effect. The dual luciferase reporter assay verified that ATF1 was proved to be a direct target of miR-589-3p in PDLSCs. And overexpressed miR-589-3p reduced the expression of ATF1. Overexpression of miR-589-3p enhanced the osteogenic capacity of PDLSCs, as demonstrated by increases in ALP activity, matrix mineralization, and RUNX2, OCN and OSX expression. In addition, the rescue experiments confirmed that overexpressed ATF1 restored the effects of overexpressed miR-589-3p on cell proliferation and osteogenic differentiation of PDLSCs. Conclusion: miR-589-3p could down-regulate the expression of ATF1, thereby promote the proliferation and osteogenic differentiation of PDLSCs. This finding may provide a new therapeutic target for molecular therapy of periodontitis. [ABSTRACT FROM AUTHOR]

Human periodontal ligament cells (hPDLCs) and human alveolar osteoblasts (hAOBs) play pivotal roles in periodontium. The regulatory effects of epigallocatechin gallate (EGCG) on hPDLCs and hAOBs remained unclear. This study probed into the functions of EGCG treating periodontal diseases. Cultured hAOBs and hPDLCs were passaged and observed by microscopic examination, and alkaline phosphatase (ALP) and immumohistochemical staining were performed for verification. hAOBs and hPDLCs were treated with EGCG and LY294002 + EGCG, then the proliferation of the two cells was assayed by MTT. Mineralization of the treated hAOBs and hPDLCs was detected by ALP activity experiment and Alizarin Red S staining kit. Quantitative real-time polymerase chain reaction (qRT-PCR) and Western blotting were performed for the detection of the expressions of differentiation-related mRNAs and PI3K/Akt signaling pathway-related proteins in the two cells. The third passage of hAOBs mainly showed triangle shape and were positive by ALP staining. hPDLCs in passage 3 adhered to the wall in spiral or radial pattern with positively stained vimentin and negatively stained keratin. Cell proliferation and ALP activity of the hAOBs and hPDLCs were increased by EGCG treatment. The mineralized nodules and expressions of differentiation-related mRNAs, the phosphorylation of PI3K and Akt of the hAOBs and hPDLCs were promoted by EGCG treatment, while the effects of LY294002 treatment were opposite to EGCG treatment. Epigallocatechin gallate affected the proliferation and differentiation of hAOBs and hPDLCs through regulating PI3K/Akt signaling pathway. [ABSTRACT FROM AUTHOR]

Background and Objectives: Periodontal pathogens initiate various diseases and induce inflammatory host responses. The activation of inflammasomes triggers caspase‐1 and interleukin (IL)‐1β‐mediated pyroptosis via gasdermin D (GSDMD). Differentiated embryo chondrocyte 2 (Dec2) is a transcription repressor that controls the expression of genes involved in innate immune and inflammatory responses. However, the effects of Dec2 on inflammasome‐induced pyroptosis in periodontal tissues remain elusive. This study aimed to characterize the activation of Dec2 inflammasomes that contribute to P. gingivalis lipopolysaccharide (LPS)‐induced pyroptosis and its functional and regulatory importance in periodontal inflammation. Materials and Methods: Human gingival fibroblasts (HGFs) and human periodontal ligament fibroblasts (HPDLFs) were stimulated with P. gingivalis LPS in vitro. An experimental periodontitis mouse model (wild‐type (WT) and Dec2KO) was established to profile periodontal pyroptosis. Results: The results demonstrate that P. gingivalis LPS activates caspase‐1, caspase‐11, and NF‐κB in HGFs and in HPDLFs. siRNA knockdown of Dec2 stimulated the induction and further upregulated LPS‐induced pyroptosis in HGFs and HPDLFs, resulting in the release of IL‐1β. Further, a deficiency of Dec2 alleviated periodontal pyroptosis via the transcriptional induction of GSDMD. In addition, P. gingivalis‐induced IL‐1β expression and Dec2‐deficient mice subsequently increased the inflammatory effect of P. gingivalis in HGFs and in HPDLFs, confirming the importance of Dec2 in the activation of inflammasomes and the regulation of pyroptosis. Conclusion: Our results demonstrate that Dec2 alleviates periodontal pyroptosis by regulating the expression of NF‐κB, caspase‐1 and GSDMD, suggesting that Dec2 is a crucial component of inflammasome activation and subsequent pyroptosis. [ABSTRACT FROM AUTHOR]

Introduction: Transcriptional regulation of autophagy depends on the transcription factors coordinated inflammatory feedback mechanism. Here, we provide a comprehensive functional characterization of periodontal ligament fibroblasts (PDLFs) treated with Porphyromonas gingivalis lipopolysaccharide (LPS), aiming to reveal previously unappreciated biological changes and to investigate how a transcription factor differentiated embryonic chondrocytes 2 (Dec2)‐deficient environment influences the function of autophagy in nflamed human PDLFs. Methods: A Dec2‐deficient (Dec2KO) experimental periodontal inflammation mouse model and treatment with P. gingivalis LPS were employed to examine the role of autophagy in PDLFs using hematoxylin and eosin staining and immunohistochemistry in vivo. A Dec2 small interfering RNA (siRNA) was used to modulate autophagy, and the effect of autophagy on the Dec2 pathway was explored using real‐time polymerase chain reaction and western blot analysis in vitro. Results: LPS‐treated human PDLFs (HPDLFs) induced autophagy, as demonstrated by the enhanced levels of microtubule‐associated protein 1 light chain 3‐II (LC3‐II) and the induction of ATG5, Beclin1, and Dec2. Compared with a scrambled siRNA, a Dec2 siRNA triggered the detrimental influences of LPS and markedly enhanced autophagy expression in inflamed HPDLFs. The expression of phosphorylated ERK was increased and levels of phosphorylated mammalian target of rapamycin (mTOR) were decreased after exposure to LPS in Dec2 siRNA transfected HPDLFs. The Dec2KO model exhibited that P. gingivalis in Dec2 deficient conditions increases the inflammation of PDLFs by regulating autophagy. Conclusions: These results demonstrate that a Dec2 deficiency can alleviate LPS‐induced inflammation via the ERK/mTOR signaling pathway by regulating autophagy, conceivably delivering a novel approach for the detection of periodontal treatments. [ABSTRACT FROM AUTHOR]

Periodontal ligament fibroblasts (PDLFs) are integral to the homeostasis of periodontal tissue. The transcription factor Dec1 functions to modulate Porphyromonas gingivalis-induced periodontal inflammation. Here, we aimed to characterize the Dec1-mediated autophagy in PDLFs under inflammatory conditions. Human PDLFs were subjected to an inflammatory environment using P. gingivalis Lipopolysaccaride (LPS) along with Dec1 siRNA in vitro. Quantitative real-time polymerase chain reaction and Western blot analyses were used to evaluate the expression levels of autophagy-related genes and their upstream AKT/mTOR signaling pathways. An experimental P. gingivalis-treated Dec1 knockout (Dec1KO) mouse model was used to confirm the expression of autophagy in PDLFs in vivo. Treatment with P. gingivalis LPS induced the expression of ATG5, Beclin1 and microtubule-associated protein 1 light chain 3 (LC3) and elevated the expression of pro-inflammatory cytokine IL-1β and Dec1 in human PDLFs. Knockdown of Dec1 partly reversed the detrimental influences of LPS on these autophagy markers in human PDLFs. The inhibition of autophagy with Dec1 siRNA suppressed the inflammatory effect of AKT/mTOR signaling pathways following treatment with P. gingivalis LPS. P. gingivalis-treated Dec1KO mice partly reduced autophagy expression. These findings suggest that a Dec1 deficiency can modulate the interaction between autophagy and inflammation in PDLFs. [ABSTRACT FROM AUTHOR]

Cerebral stroke is an acute cerebrovascular disease that is a leading cause of death and disability worldwide. Stroke includes ischemic stroke and hemorrhagic strokes, of which the incidence of ischemic stroke accounts for 60–70% of the total number of strokes. Existing preclinical evidence suggests that inhibitors of histone deacetylases (HDACs) are a promising therapeutic intervention for stroke. In this study, the purpose was to investigate the possible effect of HDAC9 on ischemic brain injury, with the underlying mechanism related to microRNA-20a (miR-20a)/neurogenic differentiation 1 (NeuroD1) explored. The expression of HDAC9 was first detected in the constructed middle cerebral artery occlusion (MCAO)-provoked mouse model and oxygen-glucose deprivation (OGD)-induced cell model. Next, primary neuronal apoptosis, expression of apoptosis-related factors (Bax, cleaved caspase3 and bcl-2), LDH leakage rate, as well as the release of inflammatory factors (TNF-α, IL-1β, and IL-6) were evaluated by assays of TUNEL, Western blot, and ELISA. The relationships among HDAC9, miR-20a, and NeuroD1 were validated by in silico analysis and ChIP assay. HDAC9 was highly-expressed in MCAO mice and OGD-stimulated cells. Silencing of HDAC9 inhibited neuronal apoptosis and inflammatory factor release in vitro. HDAC9 downregulated miR-20a by enriching in its promoter region, while silencing of HDCA9 promoted miR-20a expression. miR-20a targeted Neurod1 and down-regulated its expression. Silencing of HDAC9 diminished OGD-induced neuronal apoptosis and inflammatory factor release in vitro as well as ischemic brain injury in vivo by regulating the miR-20a/NeuroD1 signaling. Overall, our study revealed that HDAC9 silencing could retard ischemic brain injury through the miR-20a/Neurod1 signaling. [ABSTRACT FROM AUTHOR]

Intracellular signaling complexes of the innate immune system orchestrate the development of inflammation. Porphyromonas gingivalis is a commensal bacterium that induces periodontal pyroptosis. The transcription factor Dec1 can regulate the expression of inflammatory molecules. In this study, we investigated whether a deficiency of Dec1 activates/represses Caspase-1 and/or Gasdermin-D in periodontal pyroptosis, resulting in the release of the proinflammatory mediator interleukin-1β. Dec1 expression in human periodontal ligament fibroblasts (HPDLFs) treated with P. gingivalis lipopolysaccharide (LPS) was assessed and pyroptosis activation was determined by microscopy, qRT-PCR and Western blot analysis. Moreover, a siRNA targeting Dec1 was introduced into HPDLFs to determine the function of Dec1 in periodontal pyroptosis and a Dec1-deficient experimental mouse model of periodontitis was used. Treatment of HPDLFs with P. gingivalis LPS-stimulated levels of cleaved-Caspase-1 and cleaved-GSDMD and increased levels of phosphorylated NF-κB and interleukin-1β. In contrast, Dec1 knockdown maintained cellular homeostasis with low levels of pyroptosis. Treatment with P. gingivalis alleviated periodontal pyroptosis in PDLFs of wild-type mice and a Dec1 deficiency subsequently repressed the inflammatory effect of P. gingivalis. These results reveal for the first time the novel function of Dec1 in periodontal pyroptosis, suggesting that Dec1 is a crucial target to prevent periodontal inflammation. [ABSTRACT FROM AUTHOR]

Objective: Nail biting leads to a variety of health issues. Habit reversal treatment is a major approach to cease nail biting, but is often ineffective since patients continue to suffer from anxiety, a major trigger. This study investigated whether the potential anxiety relief provided by auricular acupressure could improve the efficacy of habit reversal treatment, as evidenced by improved stomatological and other outcomes. Methods: In a pragmatic, randomized, crossover, pilot clinical trial, 83 nail biters (8–12 years old) received habit reversal treatment in combination with either auricular acupressure intended to reduce anxiety (Method A) or placebo auricular acupressure (Method B). The alternative protocol was employed after a two-month washout period. The primary outcome measured was the 41-item child self-reported version of the Screen for Child Anxiety Related Emotional Disorders, while the secondary outcomes were the nail growth status (NS), which represented the fingernail growth of each finger during habit reversal treatment, simplified plaque index (SPI), and the simplified gingival index (SGI) as measures of oral health. A paired sample t-test was used to assess the differences between Methods A and B, and the differences in the anxiety scores, NS, SGI, and SPI between the baseline and each time point. Results: Forty-one children successfully completed both arms of the treatments and attended all appointments. There were significant differences in the efficacy of habit reversal treatment, the anxiety score, the nail status, and the SGI in favor of Method A (p < 0.001). Conclusion: Auricular acupressure appears to improve the efficacy of habit reversal treatment, likely by reducing anxiety. [ABSTRACT FROM AUTHOR]

Background: This review assesses the associations of interleukin-8 gene (IL -8 ) -251 A/T (rs4073) and -845T/C (rs2227532) polymorphisms with susceptibility to periodontitis. Methods: Several electronic databases were searched for eligible articles. Twelve studies involving 2,233 cases and 2,655 controls were retrieved and analyzed. Odds ratios (ORs) along with 95% confidence intervals (Cls) were calculated to assess the strength of relationship between the IL-8 polymorphisms and periodontitis risk. Results: No significant association was found for IL-8 -251A/T polymorphism with periodontitis in the overall analysis and stratification by periodontitis type and smoking status. Subgroup analysis by ethnicity revealed that -251 A/T T allele and TT genotype were associated with decreased risk of periodontitis in a Brazilian mixed population (T allele versus A allele: OR 0.80, 95% Cl 0.68 to 0.94, Pheterogeneity = 0.30; TT versus AA: OR 0.65, 95% Cl 0.46 to 0.93, Pheterogeneity = 0.39; TT versus AA/AT: OR 0.58, 95% Cl 0.35 to 0.98, Pheterogeneity = 0.01). In addition, -251A/T T allele was associated with increased periodontitis risk in Asians. Pooled estimates showed that the -8 4 5T /C polymorphism was associated with periodontitis susceptibility in overall analysis and the chronic periodontitis subgroup. In addition, marginal associations were observed between -845T/C polymorphism and periodontitis in a Brazilian mixed population. Moreover, this association was also confirmed to be significant in Brazilian non-smokers. Conclusion: This meta-analysis indicated that both IL-8 -251 A/T and -845T/C polymorphisms may be involved in the development of periodontitis in a Brazilian mixed population, whereas the -251 A/T allele T appeared to be a risk factor for periodontitis in Asians. [ABSTRACT FROM AUTHOR]

Aim Tumour necrosis factor-alpha ( TNF- α) plays a critical role in the pathogenesis of periodontal disease. TNF-α gene polymorphisms can influence the TNF- α production. Many studies have focused the association between TNF-α gene promoter polymorphisms and periodontitis risk, but these results are still controversial. Materials and Methods A meta-analysis was performed to assess the effect of TNF-α −308G/A (rs1800629), −238G/A (rs361525) and −863C/A (rs1800630) polymorphisms on either chronic ( CP) or aggressive periodontitis (AgP) risk. Odds ratios ( ORs) along with their 95% confidence intervals ( CIs) were calculated to assess the strength of the association. Forty-six studies involving 5186 cases and 6683 controls were retrieved and analyzed. Results The TNF-α −308G/A AA genotype was associated with increased CP risk in Asians, non-smoking Asians and Caucasians, and this polymorphism was significantly associated with elevated risk of AgP in Asians and Caucasians. Asian individuals carrying AA genotype had a significantly increased risk for −863C/A. No significant association was identified between TNF −238G/A polymorphism and CP. Conclusions These findings supported that TNF-α −308G/A and −863C/A polymorphisms may contribute to the susceptibility of periodontitis. [ABSTRACT FROM AUTHOR]

Aim Tumour necrosis factor-alpha ( TNF- α) plays a critical role in the pathogenesis of periodontal disease. TNF-α gene polymorphisms can influence the TNF- α production. Many studies have focused the association between TNF-α gene promoter polymorphisms and periodontitis risk, but these results are still controversial. Materials and Methods A meta-analysis was performed to assess the effect of TNF-α −308G/A (rs1800629), −238G/A (rs361525) and −863C/A (rs1800630) polymorphisms on either chronic ( CP) or aggressive periodontitis (AgP) risk. Odds ratios ( ORs) along with their 95% confidence intervals ( CIs) were calculated to assess the strength of the association. Forty-six studies involving 5186 cases and 6683 controls were retrieved and analyzed. Results The TNF-α −308G/A AA genotype was associated with increased CP risk in Asians, non-smoking Asians and Caucasians, and this polymorphism was significantly associated with elevated risk of AgP in Asians and Caucasians. Asian individuals carrying AA genotype had a significantly increased risk for −863C/A. No significant association was identified between TNF −238G/A polymorphism and CP. Conclusions These findings supported that TNF-α −308G/A and −863C/A polymorphisms may contribute to the susceptibility of periodontitis. [ABSTRACT FROM AUTHOR]

Bone marrow-derived mesenchymal stem cells have become an attractive cell source for periodontal ligament regeneration treatment because of their potential to engraft to several tissue types after injury. Most researchers have focused on the transplantation process, but few have paid attention to cell safety concerns and rapid proliferation before transplantation. Using serum-free medium to culture stem cells may be an effective method to avoid problems associated with exogenous serum and the addition of growth factors to promote cell proliferation. Here, we randomly divided our serum-free cultures and treated them with different levels of epidermal growth factor (EGF). We then evaluated changes in rates of cell adhesion, proliferation, apoptosis, and cell cycle ratio as well as their differentiation potential. The data showed that all of these parameters were significantly different when comparing serum-free cultures with and without 10 nM/L EGF ( p < 0.05/0.01); however, cells with 10 nM/L EGF did not respond differently than cells grown in standard serum-containing media without EGF ( p > 0.05). In summary, our results demonstrate that 10 nM/L EGF was the optimal dose for serum-free culture, which can replace traditional standard serum medium for in vitro expansion of miniature pig bone marrow-derived mesenchymal stem cells. [ABSTRACT FROM AUTHOR]

Objective This study aims to investigate the feasibility of tongue reconstruction by a rectus abdominis musculoperitoneal flap with neurovascular pedicled in a canine model. Methods Twelve Beagle dogs were enrolled to the experiment. The animals were randomly divided into three groups, two of which (group A and B) had nerve anastomosis. The left sides were experimental sides, whereas the right sides were control sides. Twelve weeks after operation, electrophysiological test was performed to detect hypoglossal nerve latency amplitude and conduction velocity as well as to evaluate the reinner-vation of the rectus abdominis musculoperitoneal flap. Results Among the 12 Beagle dogs, nine animal tongue reconstruction models by rectus abdominis musculoperitoneal flap with neurovascular pedicled were successful, whereas one male Beagle dog died from ventral hernia 3 d after the operation, two female rectus peritoneal flaps were abandoned because their arterial anatomy differed from the male, which was not ideal. Hypoglossal nerve conduction velocity of group A and B were restored to the normal side of the 40%, 30%. Conclusion Animal models of tongue reconstruction can be established by a rectus abdominis musculoperitoneal flap with neurovascular pedicled in Beagle dogs. Denervated rectus abdominis musculoperitoneal flap can regain hypoglossal nerve innervation. Hypoglossal nerve functions partly recover. [ABSTRACT FROM AUTHOR]