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BACKGROUND: LncRNA-TNFRSF13C, an important factor in B cell development and function, is expressed in periodontal tissues of patients with periodontitis, but the specific mechanism is still unclear. OBJECTIVE: To investigate the mechanism of lncRNA-TNFRSF13C regulating miR-1246 on hypoxia-inducible factor 1α in periodontal cells. METHODS: Human periodontal ligament cells (hPDLCs) were treated with lipopolysaccharide and divided into group A (hPDLCs cell lines without transfection), group B (hPDLCs cell lines transfected with TNFRSF13C NC-siRNA), group C (hPDLCs cell lines transfected with TNFRSF13C-siRNA), group D (hPDLCs cell line transfected with miR-1246 mimics), group E (hPDLCs cell line transfected with miR-1246 siRNA), group F (hPDLCs cell line transfected with TNFRSF13C- siRNA+miR-1246 mimics), and group G (hPDLCs cell line transfected with TNFRSF13C-siRNA+miR-1246 siRNA). The relative expression of lncRNA-TNFRSF13C and miR-1246 in each group was detected by qRT-PCR. Cell counting kit-8 assay was used to detect cell viability. Apoptosis was detected by flow cytometry. Expression of hypoxia-inducible factor 1α and vascular endothelial growth factor proteins was detected by western blot. The correlation between lncRNA- TNFRSF13C and miR-1246 was analyzed by Pearson, and the targeting relationship was analyzed by dual-luciferase reporter assay. RESULTS AND CONCLUSION: There was no significant difference in human periodontal ligament cell activity, apoptosis rate and protein indexes between groups A and B (P >0.05). Compared with group B, hPDLCS cell activity in group C was increased, and apoptosis rate and the expression of hypoxia-inducible factor 1α and vascular endothelial growth factor proteins were decreased (P < 0.05). Compared with group C, hPDLCS cell activity in group D was decreased, and apoptosis rate and the expression of hypoxia-inducible factor 1α and vascular endothelial growth factor proteins were increased (P < 0.05). Compared with group D, the cell activity of group E was increased (P < 0.05). The cell activity in group F was lower than that in group E, and the apoptosis rate was reduced in both groups E and F (P < 0.05). Compared with group F, the cell activity of group G was increased, and the apoptosis rate and the expression of hypoxia- inducible factor 1α and vascular endothelial growth factor were decreased (P < 0.05). LncRNA-TNFRSF13C was positively correlated with miR-1246 (P < 0.05). Compared with the TNFRSF13C-siRNA group, the fluorescence activity of miR-1246-wt in the TNFRSF13C-NC group was reduced (P > 0.05); compared with the miR-1246-NC group, the fluorescence activities of hypoxia-inducible factor 1α-wt and vascular endothelial growth factor-wt in the miR-1246 mimics group were increased (P < 0.05). To conclude, down-regulation of lncRNA-TNFRSF13C can promote the activity of periodontal cells treated with lipopolysaccharide, reduce apoptosis, and inhibit hypoxia-inducible factor 1α and vascular endothelial growth factor. The mechanism is related to the regulation of miR-1246 activity. [ABSTRACT FROM AUTHOR]

BACKGROUND: Leonurine has many biological activities such as improving microcirculation, anti-oxidation, anti-apoptosis, scavenging free radicals, anti- inflammation, and anti-fibrosis, and can promote osteogenic differentiation of bone marrow mesenchymal stem cells, which has the potential to be applied in the treatment of periodontitis. OBJECTIVE: To explore the anti-inflammatory and osteogenic effects of leonurine loading into chitosan/sodium glycerophosphate/sodium alginate hydrogel. METHODS: (1) Chitosan/sodium glycerophosphate/sodium alginate hydrogel (blank hydrogel) and chitosan/sodium glycerophosphate/sodium alginate/leonurus alkali hydrogel were prepared respectively. RAW 264.7 and MC3T3-E1 cells were inoculated with the two kinds of hydrogel. The cytotoxicity of hydrogels was detected by CCK-8 assay and live/dead cell staining. (2) RAW 264.7 cells were cultured in five groups. The blank group was cultured for 24 hours routinely. The lipopolysaccharide group was treated with lipopolysaccharide. The simple hydrogel group was treated with lipopolysaccharide and blank hydrogel. The drug- loaded hydrogel group was treated with lipopolysaccharide and drug-loaded hydrogel. The inhibitor group was treated with lippolysaccharide, drug-loaded hydrogel, and PI3K inhibitor LY294002. 24 hours later, mRNA expression of inflammation-related factors was detected by qRT-PCR. Western blot assay was utilized to detect the protein expression of inflammation-related factors and PI3K/AKT signaling pathway. (3) MC3T3-E1 cells were inoculated in four groups. The blank group was cultured without any material. The simple hydrogel group was treated with blank hydrogel. The drug-loaded hydrogel group was treated with drug-loaded hydrogel. The inhibitor group was treated with drug-loaded hydrogel and PI3K inhibitor LY294002 for 7 days. Alkaline phosphatase staining was performed. mRNA expression levels of osteogenic factors were detected by qRT-PCR. The protein expression levels of the PI3K/AKT signaling pathway were detected by western blot assay. RESULTS AND CONCLUSION: (1) The results of CCK-8 assay and live/dead cell staining showed that the two kinds of hydrogels had no cytotoxic effect and had good cytocompatibility. (2) Compared with the blank group, the mRNA and protein expression levels of interleukin 6, tumor necrosis factor α, and interleukin 1β were significantly increased (P < 0.05), and the protein expression levels of p-AKT, p-PI3K, p-p65, and p-IκBα were significantly increased in the lipopolysaccharide group (P < 0.05). Compared with lipopolysaccharide group, mRNA and protein expression levels of the above indexes were decreased in drug-loaded hydrogel group (P < 0.05). Compared with the drug-loaded hydrogel group, the mRNA and protein expression levels of the above indexes were decreased in the inhibitor group (P < 0.05). (3) The activity of alkaline phosphatase in drug-loaded hydrogel group was higher than that in the blank group, simple hydrogel group, and inhibitor group (P < 0.05). Compared with blank group, the mRNA expression levels of alkaline phosphatase, Runx2, osteocalcin, and type I collagen were increased (P < 0.05), and the protein expression levels of p-AKT and p-PI3K were increased in the simple hydrogel group (P < 0.05). Compared with the simple hydrogel group, the mRNA and protein expression levels of the above indexes were increased in the drug-loaded hydrogel group (P < 0.05). Compared with the drug-loaded hydrogel group, the mRNA and protein expression levels of the above indexes were decreased in the inhibitor group (P < 0.05). (4) These findings conclude that chitosan/sodium glycerophosphate/sodium alginate/leonurine hydrogel has anti-inflammatory and osteogenic effects, which may be related to the regulation of PI3K/AKT signaling pathway. [ABSTRACT FROM AUTHOR]

Matrix metalloproteinase-8 (MMP-8), as an important member of MMPs family, undergoes activation through cysteine transformation mechanism in the presence of inflammation and reactive oxygen species, and finally changes from inactive form to active form to play a pathogenic role. Numerous studies have shown that the overexpression and release of MMP-8 can cause common oral diseases, such as dental caries, periodontal tissue damage and peri-implantitis. This article aimed to review the effect of MMP-8 in oral diseases, understand the mechanism of MMP-8,and provided potential targets and therapeutic ideas for the clinical treatment of oral diseases. [ABSTRACT FROM AUTHOR]

BACKGROUND: Inflammation affects the osteogenic differentiation of periodontal ligament stem cells, and the osteogenic ability and autophagy level of periodontal ligament stem cells are closely related. However, there are no relevant reports on whether inflammation affects the osteogenic ability and autophagy level of periodontal ligament stem cells at different stages of osteogenic differentiation. OBJECTIVE: To explore alkaline phosphatase expression and autophagy periodontal ligament stem cells levels in periodontitis and normal conditions. METHODS: Periodontal ligament stem cells from normal and periodontitis patients were isolated and cultured, and underwent Vimentin, pan-CK, and Stro1 fluorescence staining. At 3, 7, and 14 days of osteogenic differentiation, western blot assay was used to detect the protein expression levels of alkaline phosphatase, LC3B, Beclin1, and ATG5 in normal and inflammatory periodontal ligament stem cells. The mRNA expression levels of alkaline phosphatase, bone sialoprotein, osteocalcin, Runx2, LC3B, Beclin1, and ATG5 were detected by real-time PCR. RESULTS AND CONCLUSION: (1) Stro-1 was positive, Vimentin was positive, and pan CK was negative in periodontal ligament stem cells. (2) At 3, 7, and 14 days after osteogenic differentiation, compared with normal periodontal ligament stem cells, the mineralization nodules formed by periodontal ligament stem cells from inflammatory sources were significantly reduced (P < 0.01); the expression of alkaline phosphatase protein and mRNA was significantly lower (P < 0.05); the mRNA expression levels of bone sialoprotein, osteocalcin, and Runx2 were significantly decreased (P < 0.05). (3) At 7 and 14 days after osteogenic differentiation, compared with normal periodontal ligament stem cells, the expression levels of ATG5, LC3B, and Beclin1 proteins and mRNA of periodontal ligament stem cells were downregulated (P < 0.05). These findings suggest that inflammation reduces the activity of periodontal ligament stem cells in mineralizing nodule formation and the expression of alkaline phosphatase and weakens the autophagy potential of periodontal ligament stem cells at 7 and 14 days after osteogenic differentiation. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Prevention & Treatment For Stomatological Diseases is the property of Journal of Prevention & Treatment For Stomatological Diseases Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Prevention & Treatment For Stomatological Diseases is the property of Journal of Prevention & Treatment For Stomatological Diseases Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Prevention & Treatment For Stomatological Diseases is the property of Journal of Prevention & Treatment For Stomatological Diseases Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

BACKGROUND: Previous studies have shown that puerarin can inhibit the differentiation of osteoclasts, and the expression of Notch signaling pathway-related proteins such as Notch1, HES1, and Jagged1 is decreased. However, the specific mechanism of the Notch1 signaling pathway for the inhibition of osteoclast differentiation by puerarin is not clear. OBJECTIVE: To explore the effect of Notch signaling pathway on puerarin inhibiting the differentiation of mouse macrophage Raw264.7 into osteoclasts. METHODS: Raw264.7 cells were divided into seven groups for intervention culture. Blank control group was cultured in high-sugar DMEM medium; the osteoclast induction group was cultured in osteoclast induction medium; the puerarin intervention group was cultured with 50 μmol/L puerarin at the same time of osteoclast induction; Notch1 siRNA control group, Notch1 siRNA group, Notch1 overexpression control group and Notch1 overexpression group were transfected with Notch1 siRNA control sequence, Notch1 siRNA, Notch1 overexpression control plasmid and Notch1 overexpression plasmid, respectively, and then cultured with osteoclast induction medium and puerarin. The number and size of osteoclasts were observed by tartrate-resistant acid phosphatase staining, the skeleton formation of osteoclasts was observed by F-actin staining, and the gene expression level of osteoclast formation markers was detected by RT-PCR. RESULTS AND CONCLUSION: Tartrate-resistant acid phosphatase staining results showed that puerarin intervention could inhibit the generation of osteoclasts, Notch1 silencing could further reduce the number of osteoclasts, while the number of osteoclasts in the osteoclast-induced group increased significantly after Notch1 overexpression. The results of F-actin showed that Raw264.7 cells could form a well-defined F-actin ring after osteoclast induction. Puerarin intervention would inhibit the formation of cytoskeleton, and Notch1 silencing could aggravate the inhibitory effect of cytoskeleton formation, while Notch1 overexpression could alleviate this inhibitory effect of puerarin. RT-PCR results showed that puerarin could inhibit the mRNA expression levels of tartrateresistant acid phosphatase, Cathepsin K and c-Fos, the expression of the above-mentioned three factors decreased significantly after Notch1 gene silencing, and Notch1 overexpression could upregulate the expression of these factors. These finding indicate that puerarin inhibits the differentiation of Raw264.7 cells into osteoclasts through the Notch signaling pathway. [ABSTRACT FROM AUTHOR]

To investigate the effects of luteic acid on inflammation and apoptosis of human periodontal stem cells induced by lipopolysaccharide and the regulation of Wnt/β-catenin signaling pathway, hPDLSCs were cultured in vitro, which was divided into two steps: pre-experiment and formal experiment. The pre-experiment was divided into control group (no intervention), lipopolysaccharide group (10 μg/mL lipopolysaccharide), low/medium/high concentration luboflavic acid group (10 μg/mL lipopolysaccharide +0.5, 1.0, 2.0 μmol/L luboflavic acid). The formal experiment was divided into control group, lipopolypaccharide group, luteic acid group (10 μg/mL lipopolypaccharide +2.0 μmol/L luteic acid), inhibitor group (10 μg/mL lipopolypaccharide +2 μmol/L Wnt/β-catenin signaling pathway inhibitor XAV939), luteic acid + inhibitor group (10 μg/mL lipopolysaccharide +2.0 μmol/L luteic acid +2 μmol/L XAV939) and luteic acid + activator group (10 μg/mL lipopolysaccharide +2.0 μmol/L luteic acid +20 μmol/L Wnt/β-catenin signaling pathway activator SKL2001), they were treated for 24 h. Cell viability was measured by CCK-8. The expression levels of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and interleukin-6 (IL-6) were detected by enzyme-linked immunosorbent assay (ELISA). The apoptosis rate was detected by Hoechst 33258 staining. The expression levels of B lymphoblastoma-2 (Bcl-2), cysteine aspartate protease-3 (Caspase-3) and Wnt/β-catenin signaling pathway were detected by Western blot (Wb). In the preliminary experiment, the cell viability of LPS group decreased compared with control group (P<0.05), and the expression levels of inflammatory factors TNF-α, IL-1β and IL-6 increased (P<0.05). Compared with LPS group, the cell viability of high-concentration luteic acid group increased (P<0.05), and the levels of inflammatory factors TNF-α, IL-1β and IL-6 decreased (P<0.05). Therefore, the high-concentration luteic acid group was selected as the optimal concentration for formal experiment. In the formal experiment, the cell viability and anti-apoptotic Bcl-2 protein expression levels in LPS group decreased compared with those in control group (P<0.05), while the expression levels of inflammatory factors TNF-α, IL-1β and IL-6, apoptosis rate and the expression levels of Caspase-3, Wnt and β-catenin proteins increased (P<0.05). Compared with LPS group, the cell viability and anti-apoptotic Bcl-2 protein expression levels in luteic acid group and inhibitor group increased (P<0.05), while the expression levels of inflammatory factors TNF-α, IL-1β, IL-6, cell apoptosis rate and the expression levels of Caspase-3, Wnt and β-catenin proteins decreased (P<0.05). Compared with the luteic acid group, the change trend of the above indexes in the luteic acid + inhibitor group was more significant (P<0.05), and the change trend of these indexes in the luteic acid + activator group was significantly reversed (P<0.05). Luteic acid may promote the cellular activity of human hPDLSCs induced by lipopolysaccharide and inhibit their apoptosis and inflammation by inhibiting the signal transduction of Wnt/β-catenin signaling pathway. This study can provide a new theoretical reference for the treatment of periodontitis. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Prevention & Treatment For Stomatological Diseases is the property of Journal of Prevention & Treatment For Stomatological Diseases Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Prevention & Treatment For Stomatological Diseases is the property of Journal of Prevention & Treatment For Stomatological Diseases Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Prevention & Treatment For Stomatological Diseases is the property of Journal of Prevention & Treatment For Stomatological Diseases Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

BACKGROUND: In recent years, the application of exosomes of periodontal ligament stem cells in periodontal tissue regeneration engineering has been widely studied, but the effect of exosomes on periodontal ligament stem cells derived from inflammatory environment is still unclear. OBJECTIVE: To investigate the effects of exosomes secreted by periodontal ligament stem cells from healthy and inflammatory environments on the proliferation and differentiation of periodontal ligament stem cells from inflammatory environments. METHODS: Human periodontal ligament stem cells from healthy and inflammatory tissues were isolated and cultured by enzyme digestion method. Exosomes were extracted from two kinds of periodontal ligament stem cells using ultracentrifugation. Passage 3 periodontal ligament stem cells derived from inflammatory tissue were selected and cultured in three groups. Cells in the blank group were cultured routinely. The healthy exosome group was added with exosomes secreted by peripheral ligament stem cells derived from healthy tissue. The inflammatory exosome group was added with exosomes secreted by human periodontal ligament stem cells derived from inflammatory tissue. Cell proliferation and cloning were detected. The expression of alkaline phosphatase, the formation of mineralized nodules, and the expression of mRNA and protein of genes related to osteogenesis were detected under osteogenic differentiation. RESULTS AND CONCLUSION: (1) CCK-8 assay and clonal formation test showed that compared with the blank group, two kinds of exosomes could promote the proliferation and colony formation of periodontal ligament stem cells from inflammatory tissue (P < 0.05), and the effect of the healthy exosome group was stronger than that of the inflammatory exosome group (P < 0.05). (2) Alkaline phosphatase and alizarin red staining showed that compared with the blank group, the two kinds of exosomes could promote the expression of alkaline phosphatase and the formation of mineralized nodules in periodontal ligament stem cells from inflammatory tissue, and the promoting effect of the healthy exosome group was stronger than that of the inflammatory exosome group. RTPCR and western blot assay showed that compared with the blank group, the two kinds of exosomes could promote the expression of alkaline phosphatase, RUNX2, and type I collagen mRNA and protein in periodontal ligament stem cells from inflammatory tissue (P < 0.05). The promoting effect of the healthy exosome group was stronger than that of the inflammatory exosome group (P < 0.05). (3) The results showed that exosomes secreted by human periodontal ligament stem cells could promote the proliferation and osteogenic differentiation of periodontal ligament stem cells derived from inflammatory environments, and the promoting effect of exosomes secreted by human periodontal ligament stem cells derived from healthy tissues was better than that from human periodontal ligament stem cells derived from inflammatory tissues. [ABSTRACT FROM AUTHOR]

BACKGROUND: In recent years, with the deepening of cell death research, necroptosis has gradually become a hot and difficult topic in academic research. Its various signaling pathways and proteins play an important role in the occurrence and development of periodontitis. People try to delay the process of periodontal tissue inflammation by preventing the occurrence of necroptosis. OBJECTIVE: To provide a review on the molecular mechanism of necroptosis and its correlation with periodontitis in the hope of providing new ideas and directions for the prevention, diagnosis, treatment and evaluation of periodontitis. METHODS: The first author searched PubMed, CNKI, and other databases in October 2023 for relevant literature published up to April 2024 with the search terms of “necroptosis, programmed cell death, periodontitis, periodontal, immunity, inflammation, receptor interacting protein kinase 1, receptor interacting protein kinase 3, mixed lineage kinase domain-like” in Chinese and “necroptosis, programmed cell death, periodontitis, periodontal, immunity, inflammation, RIP1, RIP3, MLKL” in English, respectively. The titles and abstracts of each document were read for preliminary screening, and 56 documents were finally selected for generalization and analysis. RESULTS AND CONCLUSION: (1) The main pathogenesis of periodontitis is that periodontal pathogenic bacteria stimulate the organism, leading to changes in the periodontal microenvironment, breaking the original immune balance and releasing a variety of inflammatory factors, triggering an inflammatory response resulting in destruction of periodontal tissues. Necroptosis can modulate the immuno-inflammation in periodontal tissues, thus affecting the development of periodontitis. (2) The occurrence of necroptosis is related to a variety of proteins, signaling pathways, and signaling molecules. Animal experiments have confirmed that the expression of phosphorylated mixed lineage kinase domain-like protein (pMLKL) is related to the degree of inflammation, and RIP3 and pMLKL are highly expressed in the periodontal tissues of mice suffering from periodontitis. Blocking the RIP3/MLKL pathway is conducive to the reduction of inflammation in periodontal tissues and the control of periodontitis progression. (3) To explore whether pMLKL can be used as a diagnostic indicator of periodontitis is of great value in the prevention, diagnosis and treatment of periodontitis. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Prevention & Treatment For Stomatological Diseases is the property of Journal of Prevention & Treatment For Stomatological Diseases Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Prevention & Treatment For Stomatological Diseases is the property of Journal of Prevention & Treatment For Stomatological Diseases Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Prevention & Treatment For Stomatological Diseases is the property of Journal of Prevention & Treatment For Stomatological Diseases Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

白细胞介素 -1 (IL-1) 家族主要包括IL-1α, IL-1β, IL-18及IL-1Ra 等, 参与调控细胞免疫和炎症反应。牙周 炎是-种由免疫, 遗传和环境等多因素共同影响的慢性疾病。IL-1家族的基因多态性与牙周炎疾病进展密切相关。 IL-1 家族常见的基因多态性包括 IL-1A -889C/T 多态性, IL-1B -511C/T 和+3954/3953C/T 多态性, IL-18 -137G/C 和-607C/A多态性, IL-1RN VNTR和IL-1RN +2018等。IL-1A基因-889C/T多态性可通过促进 IL-1α 表达, 增强炎症 反应, 促进牙周炎的发生。IL-1B基因-511C/T和 +3954/3953C/T 多态性可促进骨吸收；IL-18基因 -137G/C 和 -607C/A 多态性则通过破坏调控位点和改变启动子结合, 增加牙周炎的发病风险。然而, IL-1RN +2018基因多态性表现出对 牙周炎的保护效应。此外, IL-33基因多态性通过调节NF-κB通路和上调关键炎症因子参与牙周炎的发生发展, 以 及 IL-37 基因多态性可能通过调控 IL-1β 的表达来影响牙周炎的严重程度. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Hainan Medical University is the property of Journal of Hainan Medical College Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of West China Journal of Stomatology is the property of Sichuan University, West China College of Stomatology and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Prevention & Treatment For Stomatological Diseases is the property of Journal of Prevention & Treatment For Stomatological Diseases Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Prevention & Treatment For Stomatological Diseases is the property of Journal of Prevention & Treatment For Stomatological Diseases Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Periodontitis is a chronic inflammatory disease caused by plaque biofilm, and the homeostasis of the periodontal microenvironment is crucial for periodontal health. The epigenetics explores how the environmental and other non-genetic factors regulate the gene expression without changing the DNA nucleotide sequence, thereby affecting the occurrence and development of this disease. The histone acetylation modification is one of the common epigenetic modifications, primarily regulated by the histone acetyltransferases and histone deacetylases. Imbalance in this regulation can lead to the gene regulatory disorders, causing the chronic inflammation, autoimmune diseases and cancer. Recent studies have shown there is a clear correlation between histone acetylation modifications and the development of periodontitis. This paper discusses the changes in histone acetylation modifications in the gingival epithelial cells, immune cells, and periodontal ligament stem cells during periodontitis, elucidating the role and molecular mechanisms of histone acetylation modifications in the development of periodontitis and providing the basis for the epigenetic treatment of periodontitis. [ABSTRACT FROM AUTHOR]

Objective: To discuss the anti-inflammatory and antioxidant effect of mesalazine (MSZ) in the RAW264. 7 cell model, and to elucidate its therapeutic effect on periodontitis in the rats. Methods: The proliferation rates of RAW264. 7 cells stimulated by different concentrations (0, 62. 5, 125. 0, 250. 0, 500. 0, 1 000. 0, and 2 000. 0 mg·L-1 )of MSZ were detected by CCK-8 method to determine the optimal concentration of MSZ for cell treatment. Porphyromonas gingivalis lipopolysaccharide (P. g-LPS) and MSZ were used to treat the RAW264. 7 cells, and the cells were divided into control group, P. g-LPS group, and MSZ+P. g-LPS group. The levels of reactive oxygen species (ROS) in the cells in various groups were detected by the DCFH-DA fluorescent probe assay; the malondialdehyde (MDA) levels, glutathione (GSH) levels and superoxide dismutase (SOD) activities in the cells in various groups were detected by ELISA method; the expression levels of inflammatory factors interleukin-8 (IL-8) and interleukin-1β (IL-1β) mRNA in the cells in various groups were detected by real-time fluorescence quantitative PCR (RT-qPCR) method. The periodontitis rat model was established by the ligation method combined with the injection of P. g bacterial fluid. A total of 18 rats were randomly divided into control group (without treatment), model group (making periodontits model), and drug administration group (making periodontits model and given MSZ), and there were 6 rats in each group. Micro-CT was used to assess the alveolar bone destruction of the rats in various groups; HE staining was used to observe the morphology of periodontal tissue of the rats in various groups. Results: Compared with control group, the proliferation rate of the cells in 500. 0 mg·L-1 MSZ group was significantly increased (P<0. 01), so 500. 0 mg·L-1 MSZ was subsequently selected to treat the cells. Compared with control group, the levels of ROS and MDA in the cells in P. g-LPS group were significantly increased (P<0. 01), and the level of GSH and activity of SOD were significantly decreased (P<0. 01), and the expression levels of IL-1β and IL-8 mRNA were significantly increased (P<0. 01); compared with P. g-LPS group, the levels of ROS and MDA in the cells in MSZ+P. g-LPS group were significantly decreased (P<0. 01), the level of GSH and activity of SOD were significantly increased (P<0. 01), and the expression levels of IL-1β and IL-8 mRNA were significantly decreased (P<0. 01). The micro-CT assay results showed that compared with control group, the distance from the cemento-enamel junction to alveolar bone crest (CEJ-ABC) of the rats in model group was significantly increased (P<0. 01), and the bone volume fraction (BV/TV) was significantly decreaced (P<0. 05); compared with model group; the CEJ-ABC of the rats in drug administration group was decreased (P<0. 01), and the BV/TV was increased (P<0. 05). The HE staining results showed that the inflammatory cell infiltration in periodontal tissue of the rats in drug administration group was reduced, and epithelial attachment was restored. Conclusion: MSZ effectively inhibits the production of pro-inflammatory factors and peroxides in the P. g-LPS-induced RAW264. 7 cells, improves the cellular anti-inflammatory and antioxidant capacity, inhibits the alveolar bone resorption, and alleviates the inflammation of periodontal tissues in the periodontitis rats. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Prevention & Treatment For Stomatological Diseases is the property of Journal of Prevention & Treatment For Stomatological Diseases Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Prevention & Treatment For Stomatological Diseases is the property of Journal of Prevention & Treatment For Stomatological Diseases Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Prevention & Treatment For Stomatological Diseases is the property of Journal of Prevention & Treatment For Stomatological Diseases Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of West China Journal of Stomatology is the property of Sichuan University, West China College of Stomatology and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

BACKGROUND: Host immune response triggered by plaque biofilm is an initiator of periodontitis progression and destruction. Macrophages are an important component of the innate immune response, which play an important role in inflammation occurrence and development. OBJECTIVE: To review the relationship between macrophage polarization and periodontitis and the related progress in the treatment of periodontitis by regulating macrophage polarization. METHODS: PubMed and CNKI databases were searched for relevant literature published from 1990 to 2023, with “macrophage polarization, M1/M2 macrophage, periodontitis, periodontitis treatment, macrophage polarization and periodontitis, osteoimmunology, ferroptosis, macrophage polarization and ferroptosis, periodontitis and ferroptosis” as the English and Chinese search terms. After the initial screening, 96 articles were selected for review. RESULTS AND CONCLUSION: The switch between different phenotypes of macrophages is closely related to the tissue destruction caused by periodontitis, and various cytokines and inflammatory mediators secreted from macrophages are involved in the destruction and repair of periodontal tissue. Therefore,regulation of macrophage polarization and cytokine secretion in inflammatory state helps to alleviate periodontitis inflammation and improve the periodontal microenvironment, thereby reducing tissue destruction or promoting periodontal tissue regeneration. Many studies have been conducted to develop drugs or biomaterials to modulate macrophage function for the purpose of immunomodulatory treatment of periodontitis. However, macrophages act throughout the development of periodontitis and play an important role in the process of anti-infection, bone destruction and bone repair, and polarization is a complex and dynamic process influenced by many factors. Therefore, further exploration on possible mechanisms is still needed to clarify the interaction between materials or drugs and macrophages. [ABSTRACT FROM AUTHOR]

BACKGROUND: Previous studies have shown that human beta-defensin 3 has significant antifungal, antibacterial, and antiviral activities and plays an important bridging role in linking innate and acquired immune responses. OBJECTIVE: To observe the effect of human beta-defensin 3 hydrogel on treatment of periodontitis in rats. METHODS: Using Poloxamer 188 and 407 as the matrix, a blank hydrogel was constructed by cold solution. Human beta-defensin 3 hydrogel was prepared by mixing human beta-defensin 3 with the hydrogel. Twenty-five SD rats were randomly divided into five groups with five rats in each group: No treatment was given in the healthy group. The periodontitis model was constructed by the orthodontic ligature wire method in the periodontitis group, blank hydrogel group, minocycline hydrochloride group, and human beta-defensin 3 hydrogel group. 8 weeks after modeling, blank hydrogel, minocycline hydrochloride, and human β-defensin 3 hydrogel were injected into the buccal and palatal periodontal bags, once a week, and relevant tests were carried out after continuous administration for 4 weeks. RESULTS AND CONCLUSION: (1) Compared with the healthy group, periodontal plaque index, gingival bleeding index, and periodontal probing depth were increased in the periodontitis group (P < 0.01). Compared with the periodontitis group, the periodontal plaque index, gingival bleeding index, and periodontal probing depth of rats were decreased in the minocycline hydrochloride group and the human beta-defensin 3 hydrogel group (P < 0.05). (2) Hematoxylin-eosin staining proved that the hydrogel was not toxic to the rat organism. (3) Stereomicroscopy and Micro CT showed that compared with the healthy group, the root exposure and the distance between enamel cementum boundary and alveolar crest of the periodontitis group were increased (P < 0.05). Compared with the periodontitis group, the root exposure and the distance between enamel cementum boundary and alveolar crest of rats were reduced in the minocycline hydrochloride group and human beta-defensin 3 hydrogel group (P < 0.05). (4) Hematoxylin-eosin, Masson, and tartrate-resistant acid phosphatase staining showed that periodontal inflammation was obvious, fiber structure was disordered and osteoclasts were active in the periodontitis group and blank hydrogel group, while periodontal inflammation was decreased, fiber arrangement was more regular, and osteoclasts were reduced in the minocycline hydrochloride group and human beta-defensin 3 hydrogel group. (5) qRT-PCR showed that compared with the healthy group, the mRNA expressions of interleukin 1β, tumor necrosis factor α, interleukin 6, and inducible nitric oxide synthase were increased in the periodontitis group (P < 0.05). Compared with the periodontitis group, the mRNA expressions of interleukin 1β, tumor necrosis factor α, interleukin 6, and inducible nitric oxide synthase in gingival tissue of rats were decreased in the minocycline hydrochloride group and human beta-defensin 3 hydrogel group (P < 0.05). (6) The results showed that human beta-defensin 3 hydrogel was able to attenuate inflammation in rat periodontal tissues by decreasing the relative expression of inflammatory factors and inhibiting osteoblasts. [ABSTRACT FROM AUTHOR]

BACKGROUND: Shikonin contributes to the promotion of bone defect repair and the treatment of osteoporosis. OBJECTIVE: To summarize the application potential of shikonin and its derivatives in oral soft and hard tissue regeneration. METHODS: A literature review was conducted in databases such as PubMed, Web of Science, Wanfang, China National Knowledge Infrastructure (CNKI), and VIP, spanning articles from 2002 to 2023. The search terms were “shikonin, oral cavity, periodontitis, antibacterial, bone formation, osteoclast, osteoporosis, toxicology” in Chinese and English. RESULTS AND CONCLUSION: Shikonin and its derivatives possess anti-inflammatory effects, inhibit periodontal pathogens such as Porphyromonas gingivalis, promote periodontal wound healing, and regenerate alveolar bone tissue. Shikonin formulations can be used to treat oral diseases such as aphthous ulcers and oral candidiasis. These findings suggest a promising future for shikonin and its derivatives in treating periodontal diseases, preventing oral ailments, and promoting the regeneration of both soft and hard periodontal tissues. Further research is needed to explore how to combine shikonin with tissue engineering to achieve quicker healing of oral soft and hard tissues. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Prevention & Treatment For Stomatological Diseases is the property of Journal of Prevention & Treatment For Stomatological Diseases Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objective To investigate the effects of pachymic acid (PA) on alveolar bone resorption and inflamma tion in periodontitis rats and the mechanism. Methods A total of 108 rats were randomly divided into the control group, model group, 1 mg/kg PA (PA-L group), 5 mg/kg PA (PA-M group), 10 mg/kg PA (PA-H group), 10 mg/kg PA + 10 mg/kg CXCL12（PA-H + CXCL12 group), with 18 rats in each. Periodontitis models were established in all groups except the Control group. After modeling, rats in the PA-L group, PA-M group and PA-H group were intraperitone ally injected with 1, 5 and 10 mg/kg PA, rats in the PA-H + CXCL12 group were intraperitoneally injected with 10 mg/kg PA + 10 mg/kg CXCL12, and rats in the Control group and Model group were intraperitoneally injected with the same amount of normal saline. The drug was administered once a day for 4 weeks. Periodontal index ［plaque index (PLI) score, bleeding index (SBI) score］ were detected. Serum TNF-α, IL-6, and IL-1β were detected by ELISA. The distance between alveolar crest and enamel cementum boundary (CEJ-AC) was measured by micro-CT to observe the resorption of alveolar bone. The pathological changes of periodontal tissues were observed by routine HE staining. The expression levels of IL-1β and OPG protein in periodontal tissues were detected by immunohistochemistry. The expression of CXC chemo kine 12（CXCL12) and CXC chemokine receptor 4（CXCR4) protein in periodontal tissues was detected by Western blot ting. Results Compared with the Control group, the gingival epithelium in the Model group showed erosion, a large number of inflammatory cell infiltration, tissue edema, structural damage, disarranged arrangement, significantly reduced alveolar bone height, a large number of bone resorption lacunae, high PLI score, SBI score, CEJ-AC, TNF-α, IL-6, IL-1β, CXCL12, and CXCR4 protein expression, and low OPG protein expression (all P<0. 05) . Compared with the Model group, periodontal tissue inflammation in the PA-L group, PA-M group and PA-H group gradually decreased, struc tural damage was alleviated, alveolar bone height became shallow, PLI score, SBI score, CEJ-AC, TNF-α, IL-6, IL-1β and CXCL12 and CXCR4 protein expression decreased successively, and the expression of OPG protein increased succes sively (all P<0. 05) . Compared with the PA-H group, PA-H+CXCL12 group had increased periodontal tissue inflamma tion, obvious edema, disordered structure and serious injury, and increased protein expression levels of PLI score, SBI score, CEJ-AC, TNF-α, IL-6, IL-1β, CXCL12 and CXCR4, and decreased expression of OPG protein (all P<0. 05) . Conclusion PA can inhibit alveolar bone absorption and reduce inflammatory response in rats with periodontitis by regulating CXCL12/CXCR4 signaling pathway. [ABSTRACT FROM AUTHOR]

Objective: To investigate impacts of soy isoflavones (SIF) on alveolar bone resorption and inflammatory response in periodontitis rats based on Slit homologue 2 (Slit2)/P38 mitogen-activated protein kinase (MAPK) signaling pathway. Methods: Rats were separated into Control group, Model group, SIF low-dose group (L-SIF, 25 mg/kg) and SIF high-dose group (H-SIF, 75 mg/kg), with 10 rats per group, and periodontitis model was established by ligating necks of maxillary first molars of rats with silk thread except for control group. Rats in L-SIF group and H-SIF group were given corresponding doses of SIF by gavage, Control group and Model group were given same amount of normal saline by gavage, once a day, for 4 consecutive weeks. After administration, serum Slit2, TNF-α, IL-6 and IL-1β levels were detected by ELISA; Micro-CT scan was performed to detect distance between cementumenamel junction and alveolar ridge crest (CEJ-ABC), bone mineral density( BMD), bone volume fraction( BV/TV), and alveolar bone loss was evaluated; HE staining and tartrate-resistant acid phosphatase( TRAP) staining were performed to evaluate tissue inflammation, bone resorption and osteoclast activity; expressions of osteoprotegerin (OPG) and receptor activator of nuclear factor κB ligand (RANKL) in periodontal tissues were detected by immunohistochemistry (IHC); Western blot was performed to detect protein expressions of Slit2, P38 MAPK and p-P38 MAPK in periodontal tissues. Results: Compared with Control group, serum levels of Slit2, TNF-α, IL-1β, IL-6, CEJ-ABC distance, periodontal histopathological damage score, osteoclast number, positive expression of RANKL, protein level of Slit2 and p-P38 MAPK/P38 MAPK were greatly increased in Model group, BMD, BV/TV and positive expression of periodontal tissues OPG were greatly decreased (all P<0.05); compared with Model group, serum levels of Slit2, TNF-α, IL-1β, IL-6, CEJ-ABC distance, periodontal histopathological damage score, osteoclast number, positive expression of RANKL, protein levels of Slit2 and p-P38 MAPK/P38 MAPK were greatly decreased, BMD, BV/TV and OPG positive expression of periodontal tissues were greatly increased in L-SIF group and H-SIF group (P<0.05), the above indicators in H-SIF group changed greatly better than L-SIF group (P<0.05). Conclusion: SIF can inhibit alveolar bone resorption and inflammatory response in periodontitis rats and improve periodontitis, whose mechanism may be related to inhibition of Slit2/P38 MAPK signaling pathway. [ABSTRACT FROM AUTHOR]

Copyright of West China Journal of Stomatology is the property of Sichuan University, West China College of Stomatology and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of West China Journal of Stomatology is the property of Sichuan University, West China College of Stomatology and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

牙周炎患者种植治疗面临多重风险, 包括炎症复发、骨量不足、咬合关系紊乱及患者依从性差等。这些 风险因素可能影响种植体稳定性与长期效果。通过术前全面评估、牙周基础治疗、多学科联合治疗及术后细致维护, 可有效防控风险, 提升治疗成功率。 [ABSTRACT FROM AUTHOR]

本研究旨在探讨综合护理干预在牙周炎患者治疗中的应用效果, 通过对比分析实验组与对照组患者在治 疗依从性、临床指标改善情况及生活质量等方面的差异, 评估综合护理干预的实际效果。研究结果显示, 综合护理干 预能够显著提高患者的治疗依从性, 有效改善牙周组织健康状况, 提升患者的生活质量。本研究为优化牙周炎治疗方 案、提升护理服务质量提供了科学依据。 [ABSTRACT FROM AUTHOR]

BACKGROUND: In recent years, numerous studies have shown that long non-coding RNAs (lncRNAs) have an important role in the pathogenesis of periodontitis, including the immune response process and the biological activity and function of cells (periodontal stem cells and osteoblasts). Researchers attempt to regulate periodontal inflammation and periodontal regeneration by regulating lncRNA expression levels. OBJECTIVE: To review the progress of research on lncRNAs in periodontitis, thereby advancing the research of lncRNAs in periodontitis. METHODS: The first author searched PubMed, China National Knowledge Infrastructure (CNKI), Web of Science database, and WanFang Database for relevant literature published up to March 2023. “Long non-coding RNA, lncRNA, periodontitis, periodontium, immunity, inflammation, periodontal ligament stem cells, osteoclasts, osteogenic differentiation, bone resorption, bone formation, recurrence, hypoxia, oxidative stress, static mechanical strain”were used as the Chinese search terms. “lncRNA, periodontitis, periodontal, immunity, inflammation, periodontal membrane stem cells, osteoclasts, osteogenic differentiation, bone resorption, bone formation, recurrence, hypoxia, oxidative stress, static mechanical strain” were used as the English search terms. The title and abstract of each paper were read for initial screening, and 87 papers were finally selected for inductive analysis. RESULTS AND CONCLUSION: Periodontal pathogens stimulate the body, leading to immune imbalance that triggers inflammatory response and destroy periodontal tissue, and lncRNAs are involved in its regulatory mechanism. LncRNAs are involved in the pro-inflammatory regulation of periodontal ligament cells in an inflammatory environment, and their effects on osteoclast differentiation are regulated through ceRNA mechanism, which provides new clues for exploring the pathogenesis of periodontitis. For B cells and macrophages, lncRNAs can regulate the infiltration, cell activity and function of their subsets in periodontitis. LncRNAs participate in the immune response related to periodontitis mainly through two pattern recognition receptors, Toll-like receptors and NOD-like receptors, and nuclear factor-κB signaling pathway. To investigate whether lncRNAs can be used as a biomarker of periodontitis has great value in the diagnosis and prognosis of periodontitis. Animal experiments have demonstrated that the role of lncRNAs in periodontitis can be reversed by modulating the expression level of lncRNAs and thus lncRNAs act as an anti-inflammatory agent, which is of great value for the study of immunotherapy in periodontitis. The regulation of lncRNAs on periodontal ligament stem cells is mainly realized through endogenous competition mechanism and various signaling pathways, and its effects are influenced by various factors, such as inflammatory environment, mechanical strain, hypoxia and oxidative stress. Research on related mechanisms through these related factors provides new ideas for the treatment of periodontitis. [ABSTRACT FROM AUTHOR]

BACKGROUND: Reactive oxygen species is a double-edged sword in the development of periodontitis and the regeneration of periodontal tissue. Low concentration of reactive oxygen species induces the differentiation of periodontal fibroblasts, and excessive reactive oxygen species will cause damage to periodontal tissue. In the process of inflammation, the accumulation of reactive oxygen species in periodontal tissue induces damage to cells and tissues through a variety of signaling pathways or through redox reactions. OBJECTIVE: To review the double-edged sword effect of reactive oxygen species in periodontitis and periodontal tissue regeneration, thereby providing potential targets and treatment ideas for the clinical treatment of periodontitis and periodontal tissue regeneration. METHODS: Databases of CNKI and PubMed were searched for relevant articles published from April 1990 to April 2023 with the key words of “periodontal tissue engineering, periodontal defect, regeneration of periodontal tissue, chronic periodontitis, reactive oxygen species, oxidative stress, antioxidative stress, oxidative injuries, free radicals, reactive nitrogen species” in Chinese and English, respectively. By reading the titles and abstracts, repetitive studies or irrelevant literatures were excluded. Finally, 77 articles were included for review. RESULTS AND CONCLUSION: Reactive oxygen species are a kind of free radicals with high reactivity. When bacteria invade, reactive oxygen species are released in large quantities by the respiratory explosion of neutrophils and play a double-edged sword role in the body through their redox reactions or as pleiotropic physiological signal transmitters. In periodontitis, low concentrations of reactive oxygen species can kill invading pathogenic bacteria, but high concentrations of reactive oxygen species promote the secretion of inflammatory factors through JNK, RANK, Wnt/β-Catenin and other pathways, promote immune damage or directly damage tissues through oxidative reactions or through other ways to aggravate periodontitis. In the process of periodontal tissue regeneration, low concentrations of reactive oxygen species can promote the proliferation and differentiation of periodontal ligament stem cells through Nrf2 and other pathways and can promote the secretion of vascular endothelial growth factor to promote vascular regeneration. This provides seeds and a nutrient environment for periodontal tissue regeneration, which is extremely important for promoting periodontal tissue regeneration. However, high concentrations of reactive oxygen species will reduce the activity of periodontal ligament stem cells and damage endothelial cells, which are not conducive to vascular regeneration. This will inhibit wound healing and periodontal tissue regeneration. Therefore, it is important to explore the role of reactive oxygen species in the development of periodontitis and periodontal tissue regeneration and to discover the potential mechanism of its action and to explore the appropriate concentration for its role in reducing periodontal inflammation and promoting periodontal tissue regeneration for the future treatment of periodontitis and periodontal tissue regeneration in clinical practice. Using reactive oxygen species as a target to explore ways to reduce periodontal inflammation and promote periodontal ligament stem cell activity and vascular regeneration may become a clinically effective method for treating periodontitis and promoting periodontal tissue regeneration. [ABSTRACT FROM AUTHOR]

The macrophages, as a crucial component of the body’s immune system, can be polarized into M1 and M2 types by different cellular molecules in various environments, and contribute to the progression of various diseases. In inflammatory responses, the M1 macrophages are primarily regarded as the pro-inflammatory cells, facilitate the inflammation progression, tissue destruction, and bone resorption, while M2 macrophages, as inflammatory cells, participate in tissue healing and bone repairment. In the tumor microenvironment, the roles of M1 and M2 macrophages are reversed. The periodontitis, pulpitis, and oral squamous cell carcinoma (OSCC) are the most prevalent inflammation and tumor in the oral cavity. Therefore, this article summarizes the relevant researches from home and abroad on the polarization of macrophages in oral inflammatory responses such as periodontitis, peri-implantitis, and pulpitis, bone remodeling during orthodontic treatment, and OSCC, and elucidate the metabolic activities of macrophages in inflammation, tumor, and bone remodeling and the mechanism of regulating the onset and development of diseases by the macrophage polarization, and provides new perspectives for the clinical treatment. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Prevention & Treatment For Stomatological Diseases is the property of Journal of Prevention & Treatment For Stomatological Diseases Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

BACKGROUND: Periodontitis is an inflammatory and destructive disease with plaque biofilm as the main pathogenic material, which occurs in the gingiva, periodontal ligament, alveolar bone and cementum. The antigen of bacterial complex and its secreted toxin and enzyme directly lead to the destruction of periodontal tissue and trigger the host’s immune response, causing indirect damage to the body tissue. Silence information regulatory factors (Sirtuins, SIRTs) play an important role in anti-aging, anti-oxidative stress, regulating inflammation, and mediating autophagy, and are closely related to the occurrence and development of periodontitis. OBJECTIVE: To review the research status of Sirtuins in periodontitis. METHODS: The first author used the computer to search the relevant research regarding the role of Sirtuins in periodontitis in PubMed, Web of Scene, CNKI and WanFang databases. The key words were “Sirtuins, Sirtuin1-7, periodontitis” in English and Chinese. After literature screening, 57 articles were included for review and analysis. RESULTS AND CONCLUSION: SIRT1, SIRT2, SIRT3, and SIRT6 participate in regulating the occurrence and development of periodontitis. Inhibition of SIRT1 expression may be the target of periodontitis treatment, while overexpression of SIRT1 can inhibit periodontitis and protect periodontal tissue. The activator of SIRT1 can reduce the inflammation of periodontal tissue and improve the systemic pathological changes caused by periodontitis. SIRT2 is involved in nicotinamide phosphoribosyltransferase-mediated periodontal inflammation and plays a role in the treatment and prognosis of periodontal diseases. SIRT3 can improve age-related periodontal disease. Gastrodin promotes the osteogenic differentiation of periodontal ligament stem cells through the up-regulation of SIRT3. The activator of SIRT3 reduces the damage of periodontitis to periodontal and renal tissues by regulating the level of autophagy in the cells. SIRT6 can inhibit the inflammatory reaction of periodontal tissue and inhibit the differentiation and mineralization of cementoblasts. SIRT6 is beneficial to the prognosis of periapical periodontitis. The relationship between SIRT4, SIRT5, SIRT7 and periodontitis is rarely reported. [ABSTRACT FROM AUTHOR]

Copyright of West China Journal of Stomatology is the property of Sichuan University, West China College of Stomatology and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of West China Journal of Stomatology is the property of Sichuan University, West China College of Stomatology and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Prevention & Treatment For Stomatological Diseases is the property of Journal of Prevention & Treatment For Stomatological Diseases Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)