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Abstract Objective: To investigate the involvement of IL-6/STAT3 signaling pathway activation in macrophage polarization and bone destruction related to apical periodontitis (AP) stimulated by Porphyromonas gingivalis. Methodology: Macrophage polarization, IL-6/STAT3 expression, and the presence of P. gingivalis were detected in human AP tissues via RT-qPCR, western blotting, and immunohistochemistry staining. Murine bone marrow derived macrophages were isolated and cultured with P. gingivalis W83 in vitro, and levels of macrophage IL-6 expression, STAT3 phosphorylation, and macrophage polarization with or without the selective STAT3 phosphorylation inhibitor Stattic (5 μM) were detected via ELISA, western blotting, RT-qPCR, and flow cytometry, respectively. P. gingivalis-induced murine AP models were constructed, and bone destruction and macrophage polarization in the apical region were evaluated. Transwell co-culture systems were used to investigate the effects of macrophages infected with P. gingivalis on osteogenesis and osteoclastogenesis. Results: P. gingivalis was detected in human AP tissues that highly expressed IL-6/STAT3, and the M1 subtype of macrophages was more abundant in these tissues. P. gingivalis infection induced IL-6 expression, STAT3 phosphorylation, and M1 polarization of macrophages, while 5 μM of Stattic partially abolished these activation effects. Systemic STAT3 blockade via oral administration of Stattic at a dose of 25 mg kg-1 alleviated murine periapical bone resorption and apical infiltration of M1 macrophages induced by P. gingivalis infection in vivo. Furthermore, macrophages infected with P. gingivalis promoted bone destruction via secretion of IL-6, TNF-α, and RANKL, which hinder pre-osteoblast expression of Runx2 and accelerate pre-osteoclast expression of NFAT2. Conclusions: The activation of IL-6/STAT3 signaling pathway is involved in mediating macrophages M1 polarization in the P. gingivalis induced apical inflammatory context and may also be intimately involved in the bone loss caused by P. gingivalis infection, directing the M1 macrophage infiltration during the progression of AP.
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Objective@#To investigate the effects of srtA on the oxidation tolerance of the Streptococcus mutans UA159 strain and to explore the potential mechanism.@*Methods@#The oxidation tolerance in the planktonic state and biofilm state were compared among UA159, the srtA-deleted strain and the complementary strain through oxidative tolerance experiments. The RNA-sequencing data from both the exponential and stationary phases of UA159 and the srtA-deleted strain were obtained by using the Illumina HiSeq 4 000 sequencing platform to determine the impact of srtA knockout on S. mutans genomic transcription. We compared the differences in the transcriptional expression of oxidative tolerance-related genes between the UA159 strain and the srtA gene deletion strain and further explored the intrinsic relationship between the changes in oxidative tolerance and the genetic transcriptome. qPCR was used to verify the changes in the expression level of oxidation tolerance-related genes.@*Results @#The oxidation tolerance of the srtA-deleted strain decreased significantly in both the planktonic state and the biofilm state compared to that of UA159 (P < 0.05). A total of 33 oxidation tolerance-related genes were differentially expressed according to transcriptome sequencing. There was no significant change in the expression of peroxide synthesis- and metabolic-related enzyme genes, but in the stationary phase samples, the two-component signal transcription systems lrgA, lrgB, and lytT were significantly downregulated (2.2- to 2.4-fold) in the srtA-deleted strain. qPCR further confirmed that in both the exponential and stationary phases, lrgB and lytT expression in the planktonic state was reduced 11.01-53.51-fold, while the expression of the other two-component system-encoding gene vicK was reduced by 6.57-10.88-fold (P < 0.001).@*Conclusion@#SrtA gene deletion did not change the expression level of peroxide synthesis-related and metabolic enzyme-encoding genes but downregulated the expression of the associated transcription regulation factors to reduce the oxidation tolerance of S. mutans.
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@#Dentin hypersensitivity is mainly associated with abrasion, wear, acid etching, cracking, wedge-shaped defects, enamel hypoplasia, caries, a lack of neck enamel, and cementum coverage accompanied by gingival recession, resulting in direct exposure of dentin tubules to the oral environment. Dentin hypersensitivity is mainly treated by sealing the exposed dentin tubules and reducing the excitability of the pulpal nerves. Laser therapy, as a safe, fast and convenient treatment measure, has achieved good results both alone and in combination with other medicines and has attracted increasing attention. This paper reviews the research progress in the treatment of dentin hypersensitivity using several common laser therapy mechanisms with parameter selections in various scopes of application. A review of the literature shows that the Nd:YAG laser has a strong penetrating power and a large thermal effect and can denature and coagulate proteins in dentin tubules in a very short time; while the CO2 laser causes little damage to the dental pulp and has an obvious immediate curative effect by high absorption of water molecules in hydroxyapatite and the dentin surface is melted and recrystallized; the Er:YAG laser has high water absorption and a large thermal effect and can block the tubules by evaporating the fluid in the tubules and depositing salts; Er, Cr:YSGG laser energy can be fully absorbed by hydroxyapatite and water and result in desensitization by cutting hard tissues and melting periodontal dentin of the tube simultaneously; The Ga-Al-As semiconductor laser and He:Ne laser are low energy. The laser dosage mainly changes the permeability of nerve fibers to potassium and sodium ions and depolarizes the nerve fibers, producing an analgesic effect. The combination of a laser with a desensitizer can improve the clinical efficacy of treating dentin hypersensitivity.
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@#Conventional root canal therapy can not completely treat all periradicular lesions, especially combined endodontic-periodontic diseases, large periapical lesions and bone defect lesions. Guided tissue regeneration greatly improves the success rate of endodontic surgery in treating these lesions. This article focuses on the application of various grafting materials, guided bone regeneration membranes and regulatory factors in endodontic surgery.
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@#The aim of vital pulp therapy is to preserve vital, healthy pulp tissue through pulp capping or pulpotomy. Pulp-capping materials are applied to isolate infection, promote odontoblast differentiation and reparative dentine formation during the progress. Calcium silicon-based materials play significant roles in vital pulp therapy with their favorable mechanical properties, bioactivity and biocompatibility. The present paper will review current progress for these novel calcium silicon-based materials used in vital pulp therapy.
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<p><b>OBJECTIVE</b>To evaluate the effectiveness and toxicity of sorafenib for advanced hepatocellular carcinoma.</p><p><b>METHODS</b>According to the Cochrane handbook for systematic review, two reviewers independently completed the whole process of literature search, study selection, data collection, and quality assessment. Seven electric databases(PubMed, Cochrane Library, Embase, Chinese Journal Full-text Database, Chinese Biomedical Literature Database, Chinese Scientific and Technical Journal Database, Chinese Medical Association Digital Periodicals Database) were searched and randomized controlled trials (RCT) of sorafenib in the treatment of advanced hepatocellular carcinoma were collected and analyzed.</p><p><b>RESULTS</b>Two RCT involving 828 patients were finally included. Compared with placebo, sorafenib significantly extended the overall survival and time to radiologic progression and improved the disease control rate. The main adverse effects were systemic, gastrointestinal, and dermatologic symptoms (grade 1 or 2 in severity), although the incidences were significantly higher in sorafenib groups than in control groups.</p><p><b>CONCLUSION</b>Sorafenib is effective and safe for the treatment of advanced hepatocellular carcinoma.</p>