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Oral lichen planus (OLP) is a chronic inflammatory disorder featured with T lymphocytes infiltration and epithelial basement membrane breakdown. Although matrix metalloproteinase-12 (MMP12) is reported to be involved in the pathogenesis of oral diseases such as oral squamous cell carcinoma and periodontitis, the roles of MMP12 in the context of OLP remain poorly understood. Here, we demonstrate that MMP12 in macrophages derived from mucosal diseased tissues compromises the epithelial barrier integrity in OLP. The increased MMP12 facilitates fibronectin degradation in keratinocytes, leading to oral epithelial barrier disruption. Overexpression of fibronectin in oral keratinocytes prevents epithelial barrier from MMP12-induced damage. In addition, pharmacological inhibition of MMP12 reverses keratinocyte barrier disruption in a cell model. Altogether, our study reveals that MMP12 mediates oral epithelial barrier integrity in the setting of OLP.

Bone defects pose significant challenges in healthcare, with over 2 million bone repair surgeries performed globally each year. As a burgeoning force in the field of bone tissue engineering, 3D printing offers novel solutions to traditional bone transplantation procedures. However, current 3D-printed bone scaffolds still face three critical challenges in material selection, printing methods, cellular self-organization and co-culture, significantly impeding their clinical application. In this comprehensive review, we delve into the performance criteria that ideal bone scaffolds should possess, with a particular focus on the three core challenges faced by 3D printing technology during clinical translation. We summarize the latest advancements in non-traditional materials and advanced printing techniques, emphasizing the importance of integrating organ-like technologies with bioprinting. This combined approach enables more precise simulation of natural tissue structure and function. Our aim in writing this review is to propose effective strategies to address these challenges and promote the clinical translation of 3D-printed scaffolds for bone defect treatment. Graphical abstract

Periodontal disease (PD) refers to a chronic inflammatory disorder affecting the supporting tissues of the teeth triggered by bacterial infection and is recognized to promote systemic inflammation, leading to dysfunction in specific organs. Adverse pregnancy outcomes (APOs), including preterm birth, small for gestational age infants, gestational diabetes and preeclampsia, are linked to pregnancy complications. Recently, the correlation between periodontal disease and adverse pregnancy outcomes has garnered global attention. However, bibliometric studies in this area remain limited. This study aimed to visualize knowledge framework and research trends concerning the relationship between periodontal disease and adverse pregnancy outcomes from 2000 to 2023 through bibliometric approaches. On September 22, 2024, articles and reviews on the connection between periodontal disease and adverse pregnancy outcomes were retrieved from the Web of Science Core Collection (WOSCC). CiteSpace [6.3.R1 (64-bit) Advanced] was used to perform knowledge mapping and bibliometric studies. Over the past 23 years, 932 articles from 73 countries were collected, with the U.S. contributing over one-third (355), followed by Brazil (85) and India (59). The literature in this field has experienced multiple growth phases since 2000, with particularly rapid growth observed after 2019. The University of North Carolina ( = 34, 3.65%) is the leading institution in terms of publication output, primarily representing the U.S. Notably, the and the are the most frequently cited journals in the fields of periodontology and obstetrics, respectively. These publications are authored by 94 researchers, with Steven Offenbacher being both the most productive and most highly cited author, making significant contributions to the field. A visual analysis of keywords identifies \"oral microbiota,\" \"oral health,\" \"adverse pregnancy outcomes,\" and \"global burden\" as emerging research hotspots in exploring the correlation between periodontal disease and adverse pregnancy outcomes. This first bibliometric and visual analysis of periodontal disease and adverse pregnancy outcomes offers a concise overview of the field and suggests future research should focus on risk factors, high-risk populations, oral microbiota, mechanisms, interventions, and international collaboration.

Background Although obstructive sleep apnea (OSA) and periodontitis are associated, whether this association is causative is uncertain. Methods We conducted a bidirectional Mendelian randomization (MR) analysis using data from publically accessible genome-wide association studies. The single-nucleotide polymorphisms (SNPs) for OSA were derived from 16,761 cases and 201,194 controls. The pooled data of periodontitis association involved up to 17,353 individuals. Disease-associated single-nucleotide polymorphisms were selected as an instrumental variable at the genome-wide significance level ( p  < 5.0 × 10 − 6 ). Subsequently, the causal effects were estimated using three different methods: inverse variance weighting (IVW), MR-Egger, and weighted median. Then, these causal estimates were expressed as dominance ratios [odds ratio (OR)]. Results The MR analysis revealed that genetically determined OSA promotes the development of periodontitis [ IVW OR = 1.117, 95% confidence interval (CI) = 1.001–1.246, p  = 0.048). Furthermore, no causal effect of genetically predicted periodontitis on OSA was noted in the reverse MR analysis (IVW OR = 1, 95% CI: 0.95–1.06, p  = 0.87). The trend in results from the MR-Egger regression and weighted median (WM) was consistent with that in results from the IVW method. The robustness of the results was confirmed by the sensitivity analysis. Conclusions In summary, the results of our MR investigation suggest an association between OSA and periodontitis, proposing that early screening and treatment of OSA is beneficial for the prevention and prognosis of periodontitis.

Background: Peripheral artery disease (PAD) is a high-risk vascular condition, and vascular remodeling has become a promising therapeutic approach. Paeoniflorin (PF) is the main bioactive compound in the roots of Paeonia lactiflora Pall, which is commonly used to treat a range of cardiovascular disorders. However, the mechanisms underlying the ameliorating effects of PF on PAD remain unclear. Therefore, the purpose of this study was to explore the therapeutic efficiency of PF on PAD and determine its mechanisms. Methods: The blood flow of mice was detected with a laser Doppler dot scanning imaging system. HE staining was used to observe the morphological changes of ischemic muscle. The changes in the serologic indexes were detected with an automatic biochemical assay, and the capillary density of ischemic gastrocnemius was detected with a Lectin immunofluorescence assay. The expression of angiogenesis-related proteins in ischemic gastrocnemius was detected with Western blotting, and the proportion of macrophages and neutrophils in total cells was detected with flow cytometry. Results: PF significantly increased blood flow, capillary density and protein expressions of vascular endothelial growth factor A (VEGFA), matrix metalloproteinase 2 (MMP2), matrix metalloproteinase 2 (MMP9), and estrogen receptor α (ERα) in mouse ischemic tissue in a PAD model. PF enhances the migration of endothelial cells and promotes the formation of tubular structures, involving the ERα/ROCK2 signaling pathway. Furthermore, PF was found to promote the phenotypic transformation of macrophages and alleviated grave inflammatory responses during vascular remodeling. Conclusions: We determined that PF as a potent compound in promoting angiogenesis and mitigating inflammatory responses during revascularization.

Aim The study aimed to identify the underlying differentially expressed genes (DEGs) and mechanism of unstable atherosclerotic plaque using bioinformatics methods. Methods GSE120521, which includes four unstable samples and four stable atherosclerotic samples, was downloaded from the GEO database. DEGs were identified using LIMMA. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses of DEGs were performed using the Database for metascape Visualization online tool. Based on the STRING database, protein–protein interactions (PPIs) network among DEGs were constructed. Regulatory networks were visualized using Cytoscape. We use the xCell to analyze the different immune cell subtypes. Results A total of 1626 DEGs (1034 up-regulated and 592 down-regulated DEGs) were identified between unstable and stable samples. I pulled 62 transcription factors (34 up-regulated TFs and 28 down-regulated TFs) from the Trust database. The up-regulated TFs were mainly enrichment in positive regulation of myeloid leukocyte differentiation, and the down-regulated TFs were mainly enrichment in connective tissue development. In the PPI network, RB1, CEBPA, PPARG, BATF was the most significantly up-regulated gene in ruptured atherosclerotic samples. The immune cell composition enriched in CD cells and macrophages in the unstable carotid plaque. Conclusions Upregulated RB1, CEBPA, PPARG, BATF and down-regulated SRF, MYOCD, HEY2, GATA6 might perform critical promotional roles in atherosclerotic plaque rupture, furthermore, number and polarization of macrophages may play an important role in vulnerable plaques.

Periodontal disease is a chronic inflammatory condition affecting the supporting structures of the teeth, involving complex interactions between systemic and local immune responses. Autophagy is a tightly regulated cellular process that is responsible for degrading and recycling cellular components, playing a pivotal role in maintaining cellular homeostasis and modulating inflammation in periodontal disease. In recent years, the relationship between these two factors has attracted attention from scholars globally. However, bibliometric analyses in this field are still limited. To analyze the bibliometric trends and research hotspots related to the role of autophagy in periodontal disease. Articles and reviews examining the association between periodontal disease and autophagy were retrieved from the Web of Science Core Collection (WOSCC) on 20 June 2024. Bibliometric and knowledge mapping analyses were performed using CiteSpace [6.3. R1 (64-bit) Advanced]. Through a bibliometric analysis of literature published between 2006 and 2023 on the role of autophagy in periodontal disease, 341 relevant studies were identified. The results indicate a steady annual increase in studies on this topic, with a significant upward trend observed post-2015. Keyword analysis identifies \"apoptosis,\" \"Porphyromonas gingivalis,\" \"oxidative stress,\" \"inflammation,\" \"periodontitis,\" \"osteogenic differentiation,\" \"cell death,\" and \"orthodontic tooth movement\" as key research hotspots. Collaboration network analysis identifies China as the leading contributor to research in this field. Document co-citation analysis highlights several influential studies examining the \"double-edged sword\" role of autophagy in periodontal disease, illustrating how autophagy alleviates oxidative stress and inflammation in periodontitis by removing damaged organelles, inhibiting pro-inflammatory mediators, and promoting periodontal tissue repair through the secretion of pro-angiogenic cytokines. However, excessive autophagy may lead to apoptosis when cellular stress surpasses the repair capacity. This study identifies key trends and research hotspots in autophagy and periodontal disease, underscoring the importance of international collaboration and high-impact journals for advancing the field and guiding future research. Recent studies indicate that autophagy has emerged as a critical mediator with dual roles in periodontal disease. Therefore, early control of periodontal inflammation, along with the exploration of how to harness the protective functions of autophagy, may provide future research directions for managing periodontal disease.

Background In March 2021, the supervision group of our hospital inspected the daily work of the outpatient department in the branch and found many problems in the process, such as an excessive number of daily check-up forms, nurses’ confusion regarding the daily check-up process, and the omission of daily check-up items. Therefore, focusing on these problem, our hospital established a quality improvement team to conduct a status survey and perform this study. This study evaluated the feasibility, availability and sustainability of using a daily goals sheet in the routine work of a stomatological outpatient department and investigated the satisfaction of the nursing staff with the sheet. Methods After determining the theme of this study through the status survey, 60 nurses were randomly selected and divided into an experimental group and a control group by a random grouping method. Then, the study was divided into two stages: Applying the PDCA cycle method and following the MECE (Mad Exclusive, Collectively Exhaustive) principle to design, manufacture and apply the daily goals sheet. After the expert group performed Stage one, an analysis of work efficiency and routine omissions and a staff satisfaction survey were carried out. The results of the groups either using the daily goals sheet ( n  = 30) or not ( n  = 30) were analysed and compared. Results The average work time of the daily goals sheet group was 15.20 ± 1.70 min, and that of the nondaily goals sheet group was 25.30 ± 2.70 min ( P  < 0.001). The omission rate was 0% in the daily goals sheet group and 16.67% in the nondaily goals sheet group. Staff satisfaction with the use of the daily goals sheet was high. Conclusion The daily goals sheet can make routine work more efficient and convenient in a stomatological outpatient department. It is recommended for use in stomatological outpatient departments or hospitals.

Background Common chronic infections induced low-grade inflammation has been correlated with atherosclerosis as supported by strong evidence. The balance between pro-and anti-inflammatory factors was exploited to elucidate the effects of chronic periodontitis on diabetes-associated atherosclerosis. Methods Study subjects encompassed 30 SPF male rats randomly divided into four groups: A group (NC), B group (T2DM), C group (CP), D group (DM + CP). After developing the model, blood samples were collected from the angular vein analyze serum APN, hs-CRP, and blood lipid. the carotid artery was isolated for HE staining. Result Compared with group A, the serum APN in group B, C and D decreased gradually with the progression of the disease. Serum hs-CRP in group B, C and D was significantly increased. At T3, T4 and T5 in group B, C and D, APN/hs-CRP significantly decreased. TC, LDL and TG significantly increased in group B, D; HDL significantly decreased in group C. Carotid artery HE staining showed: compared with group A, different degrees of endothelial defect, destruction of elastic fibers in the middle membrane, disorder of smooth muscle arrangement, and partial dissolution 、 fragmentation and Calcium salt deposition necrosis occurred in group B, C and D. Conclusion Enhanced systemic inflammation, decreased adiponectin level, and disorganized lipid metabolism with or without type 2 diabetes attributed to local inflammation of periodontitis can result in an imbalance of pro-inflammatory and anti-inflammatory effects. Therefore, it’s more meaningful to predict the progression of DAA with anti-inflammatory/pro-inflammatory variation.