Oral submucous fibrosis patients exhibited a significantly higher risk of malignant transformation than those without OSF. OL could enhance malignant transformation in patients with OSF.

This large-scale government-centered survey demonstrates that the prevalence of OSF in Taiwan significantly increased from 1996 to 2013. The prevalence was higher among men than among women.

Periodontitis is one of the most prevalent oral diseases. In this study, we probed the nationwide registered database to assess the time trends of prevalence of periodontitis in Taiwan.A retrospective study was conducted to analyze the registered database compiled by the National Health Insurance provided by the Department of Health, Taiwan, from 1997 to December 2013.We found that the prevalence of periodontitis significantly increased from 11.5% in 1997 to 19.59% in 2013 (P for trend < .0001). The mean age ± standard deviation with periodontitis from 1997 to 2013 was 54.46 ± 14.47 and 45.51 ± 16.58 years old, respectively. The proportion of individuals with periodontitis in age group >65 years old decreased markedly. The proportion of individuals with periodontitis in age groups <25 and 26 to 35 years old demonstrated an increased pattern. Compared to the reference cohort of 1953 to 1957, the recent birth cohort of 1993 to 1997 revealed the highest relative risk (RR) of periodontitis (male: RR, 67.42, 95% confidence interval [CI], 17.04–266.76; female: RR, 65.85, 95% CI, 16.70–259.70). Both male and female groups showed the similar age-effect pattern in the cross-sectional age curve from age–period–cohort model. There was an upturn with advancing age up to 40 to 50 years old and then a downward trend in both genders. Population dwelling in suburban area (RR, 0.95; 95% CI, 0.94–0.97) and rural area (RR, 0.97; 95% CI, 0.95–0.99) had the lower risk of periodontitis than those who lived in urban area. The higher income group revealed the higher risk of periodontitis compared with lower income group (RR, 1.20; 95% CI, 1.18–1.23).The prevalence of periodontitis significantly increased in Taiwan over past 17 years. The mean age with periodontitis was shown in a decreased pattern. The use of a nationwide population-based database could provide sufficient sample size, generalizability, and statistical power to assess the periodontal status in Taiwan.

No abstract

Rutin, also called quercetin-3-rhamnosyl glucoside, is a natural flavonol glycoside present in many plants. Rutin is used to treat various diseases, such as inflammation, diabetes, and cancer. For polymeric biomaterials, triethylene glycol dimethacrylate (TEGDMA) is the most commonly used monomer and serves as a restorative resin, a dentin bonding agent and sealant, and a bone cement component. Overall, TEGDMA induces various toxic effects in macrophages, including cytotoxicity, apoptosis, and genotoxicity. The aim of this study was to investigate the protective mechanism of rutin in alleviating TEGDMA-induced toxicity in RAW264.7 macrophages. After treatment with rutin, we assessed the cell viability and apoptosis of TEGDMA-induced RAW264.7 macrophages using an methylthiazol tetrazolium (MTT) assay and Annexin V-FITC/propidium iodide assay, respectively. Subsequently, we assessed the level of genotoxicity using comet and micronucleus assays, assessed the cysteinyla aspartate specific proteinases (caspases) and antioxidant enzyme (AOE) activity using commercial kits, and evaluated the generation of reactive oxygen species (ROS) using a dichlorodihydrofluorescein diacetate (DCFH-DA) assay. We evaluated the expression of heme oxygenase (HO)-1, the expression of nuclear factor erythroid 2 related factor (Nrf-2), and phosphorylation of AMP activated protein kinase (AMPK) using the Western blot assay. The results indicated that rutin substantially reduced the level of cytotoxicity, apoptosis, and genotoxicity of TEGDMA-induced RAW264.7 macrophages. Rutin also blocked the activity of caspase-3, caspase-8, and caspase-9 in TEGDMA-stimulated RAW264.7 macrophages. In addition, it decreased TEGDMA-induced ROS generation and AOE deactivation in macrophages. Finally, we found that TEGDMA-inhibited slightly the HO-1 expression, Nrf-2 expression, and AMPK phosphorylation would be revered by rutin. In addition, the HO-1 expression, Nrf-2 expression, and AMPK phosphorylation was enhanced by rutin. These findings indicate that rutin suppresses TEGDMA-induced caspase-mediated toxic effects through ROS generation and antioxidative system deactivation through the Nrf-2/AMPK pathway. Therefore, rutin has the potential to serve as a novel antitoxicity agent for TEGDMA in RAW264.7 macrophages.

Bisphenol A-glycidyl methacrylate (BisGMA) is a methacrylate monomer that is mainly used in three-dimensional structures to reconstruct dental and bony defects.BisGMA has toxic and proinflammatory effects on macrophages. Rutin is a natural flavonol glycoside that is present in various plants and has useful biological effects, such as anti-inflammatory, anticancer, and antioxidative effects. The aim of this study was to investigate the anti-inflammation of rutin in macrophages after exposure to BisGMA. Pretreatment of the RAW264.7 macrophage with rutin at 0, 10, 30, and 100 μM for 30 min before being incubated with BisGMA at 0 or 3 μM. Proinflammatory cytokines and prostaglandin (PG) E2 were detected by enzyme-linked immunosorbent assay (ELISA). Nitric oxide (NO) was detected by the Griess assay. Expression and phosphorylation of proteins were measured by Western blot assay. Pretreatment with rutin inhibited the BisGMA-induced generation of proinflammatory cytokines, including tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, and PGE2, in macrophages. Rutin also suppressed the BisGMA-induced secretion of NO and expression of inducible nitric oxide synthase (iNOS) in a concentration-dependent manner. Furthermore, rutin suppressed the mitogen-activated protein kinase (MAPK) phosphorylation in a concentration-dependent manner. Finally, rutin suppressed the BisGMAinduced phosphorylation of nuclear factor (NF)-κB p65 and degradation of inhibitor of κB (IκB). These results indicate that the concentration of rutin has an inhibitory effect on proinflammatory mediator generation, MAPK phosphorylation, NF-κB p65 phosphorylation, and IκB degradation. In conclusion, rutin is a potential antiinflammatory agent for BisGMA-stimulated macrophages through NF-κB p65 phosphorylation and IκB degradation resulting from MAPK phosphorylation.

Composites, resins, and sealants that are commonly used in orthopedics and dentistry are based on 2,2‐bis[p‐(2′‐hydroxy‐3′‐methacryloxypropoxy)phenylene]propane (BisGMA), which induces proinflammatory responses in macrophages. The present study aimed to explore the anti‐inflammatory responses of wogonin, which is a natural dihydroxyl flavonoid compound, in BisGMA‐treated macrophages. According to the findings, wogonin exhibits anti‐inflammatory, antiallergic, anticancer, and antioxidative properties. The generation of nitric oxide (NO) and the expression of inducible nitric oxide synthase (iNOS) were noted to be inhibited by wogonin in BisGMA‐treated macrophages. Furthermore, the production of proinflammatory cytokines including tumor necrosis factor (TNF)‐α, interleukin (IL)‐1β, and IL‐6 was reduced. In addition, BisGMA‐induced nuclear factor (NF)‐κB p65 phosphorylation and inhibitor of κB (IκB) degradation were inhibited. Finally, the BisGMA‐induced phosphorylation of mitogen‐activated protein kinases (MAPKs), including p38 MAPK, extracellular signal‐regulated kinase (ERK), c‐Jun N‐terminal kinase (JNK) was inhibited. All these effects were induced by wogonin in the macrophages in a concentration‐dependent manner. Similar inhibitory effects of wogonin were observed on the production of NO and proinflammatory cytokines, expression of iNOS, phosphorylation of NF‐κB p65 and MAPK, and degradation of IκB. These results indicated that rutin is a potential anti‐inflammatory agent for BisGMA‐treated macrophages that undergo NFκB p65 phosphorylation and IκB degradation through upstream MAPK phosphorylation. Therefore, wogonin inhibits BisGMA‐induced proinflammatory responses in macrophages through the regulation of the NFκB pathway and its upstream factor, MAPK.

Background/purpose Temporomandibular disorder (TMD) is defined as various clinical signs and symptoms involving the masticatory muscles, the temporomandibular joint and associated structures. The aim of this study was to investigate the prevalence of diagnosed TMD in Taiwan using a National Health Insurance Research Database from 2004 to 2013. Materials and methods A retrospective study was conducted to analyze the registered database compiled by the National Health Insurance from 2004 to 2013. The diagnosis of TMDs was identified in accordance with the International Classification of Disease, Ninth revision (ICD-9-CM 524.6). The relative risk of TMD from 2004 to 2013 after adjusting for year, age, and gender was evaluated by logistic regression analysis. Results The prevalence of TMD increased significantly from 14 (per 10 4 ) to 26 (per 10 4 ) over the past 10 year period [odds ratio (OR), 1.07; 95% confidence interval (CI), 1.04–1.09]. The mean age with TMD from 2004 to 2013 was 52.31 ± 17.15 years and 45.12 ± 17.32 years, respectively. The female group had a higher risk of TMD than the male group (OR, 1.70; 95% CI, 1.49–1.94). Conclusion Taken together, the estimated prevalence of TMD significantly increased from 2004 to 2013 in Taiwan. In addition, the risk for TMD was higher among women than among men.