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Malnutrition-inflammation-atherosclerosis (MIA) syndrome is a significant risk factor for mortality in patients undergoing hemodialysis. This study aimed to investigate the association between MIA syndrome and oral health status in hemodialysis patients. A cross-sectional study was conducted on 254 hemodialysis patients. Comprehensive medical and dental examinations were performed. Three components were included to define MIA syndrome: Geriatric Nutritional Risk Index, serum high-sensitivity C-reactive protein, and history of cardiovascular events as indicators of malnutrition, inflammation, and atherosclerosis, respectively. The association of MIA syndrome components with periodontitis and occlusal support was examined by multiple-ordered logistic regression analysis. Of 254 participants, 188 (74.0%) had at least one component of MIA syndrome. After adjusting for possible confounding factors, severe periodontitis was significantly associated with presence of more components of MIA syndrome (odds ratio [OR]: 2.64, 95% confidence interval [CI], 1.44-4.84, p = 0.002) and inflammation and malnutrition components (OR: 2.47 and 3.46, 95% CI 1.16-5.28 and 1.70-7.05, p = 0.020 and 0.001). On the other hand, occlusal support, evaluated by Eichner index, was not significantly associated with MIA syndrome or any of its components. In conclusion, periodontitis is associated with MIA syndrome, particularly with inflammation and malnutrition in hemodialysis patients, independent of occlusal support.

Background: This study aimed to investigate the effects of low‐level erbium‐doped: yttrium, aluminum, and garnet (Er:YAG) laser irradiation on periodontal tissue healing and regeneration through angiogenesis in vivo and in vitro studies. Methods: Intrabony defects were surgically created in the bilateral maxilla molar of rats. The defects were treated by open flap debridement (OFD) with Er:YAG laser, including low‐level laser irradiation (LLLI) to bone and blood clot surfaces, or conventional procedures. The mRNA expression of vascular endothelial growth factor (VEGF) in the surgical sites was quantified using real‐time polymerase chain reaction. The decalcified specimens were prepared for histometric analysis. Also, LLLI was performed on human umbilical vein endothelial cells to evaluate the effects on angiogenesis. Cell proliferation, VEGF expression, and tube formation were assessed. In addition, capsazepine (CPZ), a selective inhibitor of transient receptor potential vanilloid 1 (TRPV1), treatment was performed before LLLI for the same assays. Results: OFD using Er:YAG laser did not generate thermal damage on bone or root surfaces. LLLI accelerated hemostasis by coagulation of the superficial layers of blood clots in the laser‐treated group. Postoperative healing was sound in all animals in both groups. VEGF expression and bone formation were significantly increased in the laser‐treated group compared to those in the conventional treatment group. In vitro, cell proliferation and VEGF expression were significantly increased in the LLLI group compared to the control group. Tube‐formation assays showed that LLLI significantly promoted angiogenesis. CPZ treatment significantly suppressed VEGF expression and tube formation following LLLI. Conclusions: This study suggests that Er:YAG laser irradiation may promote periodontal tissue healing by enhancing angiogenetic effect of endothelial cells via TRPV1. [ABSTRACT FROM AUTHOR]

Objective: This study aims to investigate the mechanisms underlying the impaired healing response by diabetes after periodontal therapy. Background: Outcomes of periodontal therapy in patients with diabetes are impaired compared with those in patients without diabetes. However, the mechanisms underlying impaired healing response to periodontal therapy have not been sufficiently investigated. Materials and Methods: Zucker diabetic fatty (ZDF) and lean (ZL) rats underwent experimental periodontitis by ligating the mandibular molars for one week. The gingiva at the ligated sites was harvested one day after ligature removal, and gene expression was comprehensively analyzed using RNA‐Seq. In patients with and without type 2 diabetes (T2D), the corresponding gene expression was quantified in the gingiva of the shallow sulcus and residual periodontal pocket after non‐surgical periodontal therapy. Results: Ligation‐induced bone resorption and its recovery after ligature removal were significantly impaired in the ZDF group than in the ZL group. The RNA‐Seq analysis revealed 252 differentially expressed genes. Pathway analysis demonstrated the enrichment of downregulated genes involved in the peroxisome proliferator‐activated receptor (PPAR) signaling pathway. PPARα and PPARγ were decreased in mRNA level and immunohistochemistry in the ZDF group than in the ZL group. In clinical, probing depth reduction was significantly less in the T2D group than control. Significantly downregulated expression of PPARα and PPARγ were detected in the residual periodontal pocket of the T2D group compared with those of the control group, but not in the shallow sulcus between the groups. Conclusions: Downregulated PPAR subtypes expression may involve the impaired healing of periodontal tissues by diabetes. [ABSTRACT FROM AUTHOR]

The gastrointestinal (GI) tract harbors trillions of microorganisms known to influence human health and disease, and next-generation sequencing (NGS) now enables the in-depth analysis of their diversity and functions. Although a significant amount of research has been conducted on the GI microbiome, comprehensive metagenomic datasets covering the entire tract are scarce due to cost and technical challenges. Despite the widespread use of fecal samples, integrated datasets encompassing the entire digestive process, beginning at the mouth and ending with feces, are lacking. With this study, we aimed to fill this gap by analyzing the complete metagenome of the GI tract, providing insights into the dynamics of the microbiota and potential therapeutic avenues. In this study, we delved into the complex world of the GI microbiota, which we examined in five healthy Japanese subjects. While samples from the whole GI flora and fecal samples provided sufficient bacteria, samples obtained from the stomach and duodenum posed a challenge. Using a principal coordinate analysis (PCoA), clear clustering patterns were identified; these revealed significant diversity in the duodenum. Although this study was limited by its small sample size, the flora in the overall GI tract showed unwavering consistency, while the duodenum exhibited unprecedented phylogenetic diversity. A visual heat map illustrates the discrepancy in abundance, with Fusobacteria and Bacilli dominating the upper GI tract and Clostridia and Bacteroidia dominating the fecal samples. Negativicutes and Actinobacteria were found throughout the digestive tract. This study demonstrates that it is possible to continuously collect microbiome samples throughout the human digestive tract. These findings not only shed light on the complexity of GI microbiota but also provide a basis for future research. [ABSTRACT FROM AUTHOR]

Aim: This study aimed to investigate the effects of diabetes care on periodontal inflammation. Materials and Methods: This prospective cohort study included 51 Japanese patients with type 2 diabetes who underwent intensive diabetes care including educational hospitalization and regular outpatient treatment for 6 months. Dental prophylaxis without subgingival scaling was provided three times during the observational period. Associations between changes in periodontal parameters and glycaemic control levels were evaluated using multiple regression analysis. Results: Overall, 33 participants (mean age: 58.7 ± 12.9) were followed up for 6 months. At baseline examination, 82% were diagnosed with Stage III or IV periodontitis. Haemoglobin A1c (HbA1c) level changed from 9.6 ± 1.8% at baseline to 7.4 ± 1.3% at 6 months. The ratio of probing pocket depth (PPD) ≥4 mm, bleeding on probing (BOP), full‐mouth plaque control record (PCR), periodontal epithelial surface area (PESA) and periodontal inflamed surface area (PISA) also significantly improved. The reduction in PPD and PESA was significantly associated with changes in both HbA1c and fasting plasma glucose (FPG) levels, and the reduction in PISA was significantly associated with an improvement in FPG after adjusting for smoking, change in body mass index and full‐mouth PCR. Conclusions: This is the first study to report a significant improvement in PPD and BOP after intensive diabetes care and dental prophylaxis without subgingival scaling. Clinical trial registration number: UMIN000040218. [ABSTRACT FROM AUTHOR]

Background: The origin of hangekobokuto (HKT) is from Jin Gui Yao Lue (Kinkiyōryaku in Japanese), and it has been indicated for treating throat discomfort in women. Key Findings: HKT consists of five crude drugs. Clinical studies have shown that HKT can improve the swallowing reflex by increasing the substance P level in saliva; improve the cough reflex; reduce pneumonia in patients with dementia, cerebrovascular disease, Alzheimer's disease, or Parkinson's disease; reduce postoperative aspiration pneumonia in patients who undergo cardiovascular surgery; and improve depression and anxiety scores in patients with globus hystericus. Furthermore, HKT has been reported to increase serotonin (5‐HT) and noradrenaline levels in the hypothalamus, and dopamine (DA) levels in the striatum in a healthy rodent model; improve 5‐HT levels in the striatum and hippocampus, and ameliorate 5‐HT and DA reductions in the whole brain in an acute stress model; improve 5‐HT levels in the striatum, and ameliorate 5‐HT and DA reductions in the prefrontal cortex in a chronic stress model; and decrease corticosterone and corticotropin‐releasing factor levels in a chronic stress model. Reported adverse events of HKT include interstitial pneumonia (0.38 per 100 000 cases) and liver damage (0.89 per 100 000 cases), which are rare. Conclusion: HKT is widely used and shows a low rate of adverse events. Several clinical studies have reported its effects in reducing aspiration pneumonia and improving depression and anxiety, some of which may be explained by the regulation of monoamines and stress hormones in the brain and substance P levels in the oral cavity. [ABSTRACT FROM AUTHOR]

Background: "Long COVID" or "post‐COVID conditions" describes prolonged symptoms after the acute phase of coronavirus disease 2019 (COVID‐19). However, there is a paucity of published reports on its treatment. Method: This retrospective cohort study included adult, non‐hospitalized patients with COVID‐19 symptoms at least one month after the onset who had been examined at the isolation facility in Miyagi prefecture between October 2020 and September 2021. Results: In total, 70 patients with a median age of 46 (21–69) years were included, and 37 were women (52.9%). The median time from onset to the end of treatment was 46 (28–396) days. Thirty‐eight patients (53.5%) showed improvement in all symptoms, while four (5.7%) did not recover within the study period. The symptoms at six months with high residual rates were dizziness (33.3%), fatigue (14.3%), myalgia (14.3%), abdominal discomfort (14.3%), and taste dysfunction (11.8%). For treatment of prolonged symptoms, formulae of Kampo medicine (Japanese traditional medicine) were used alone or in combination with Western medications in 76%, 66%, 53%, and 66% of patients at 1–2 months, 2–3 months, 3–6 months, and over 6 months respectively. Kampo formulae with anti‐inflammatory effects were used in the early period; however, tonifying formulae and blood stasis‐resolving formulae were used in the late period. Conclusion: Non‐hospitalized patients with COVID‐19 may suffer from persistent symptoms after the acute phase of infection. For the management of long COVID, a comprehensive and holistic approach is needed. Kampo medicine should be considered as a treatment option for long COVID. [ABSTRACT FROM AUTHOR]

Background: Diabetes involves metabolic disorders in various tissues via hyperglycemia-induced oxidative stress. This study aimed to investigate the antioxidative effect of enamel matrix derivative (EMD) on periodontal regeneration in diabetes.Methods: Twenty-two rats were equally divided into streptozotocin (STZ)-induced diabetes or control group. Two months after induction of hyperglycemia, systemic oxidative stress was measured using urinary 8-hydroxy-2'-deoxyguanosine. EMD or saline was applied into the intrabony defects created in the bilateral maxillary molar. mRNA expressions of inflammatory and oxidative stress markers were quantified (n = 6). Histometric analyses and immunohistochemistry of superoxide dismutase-1 (SOD-1) were performed 7 days postoperatively (n = 5). For in vitro experiments, the bone marrow-derived mesenchymal stem cells were isolated from rat femur and cultured in a high glucose (HG) or control medium. Reactive oxygen species (ROS) measurement and alizarin red staining were performed with/without EMD.Results: Systemic oxidative stress was significantly higher in the diabetic group. The connective tissue attachment and cementum formation were significantly increased at EMD-treated sites in both diabetic and non-diabetic groups. The expression of nicotinamide adenine dinucleotide phosphate oxidase two and four was significantly lower at EMD-treated sites than at EMD-untreated sites in both diabetic and non-diabetic rats. Immunohistochemistry showed significantly higher SOD-1 expression at the EMD-treated site. In vitro, HG culture had significantly higher ROS production compared with control, which was downregulated by EMD. EMD treatment significantly recovered the impaired calcification in HG.Conclusion: EMD promoted early-phase wound healing and periodontal tissue regeneration in the surgically created bony defect of STZ-induced diabetic rat by suppressing hyperglycemia-induced oxidative stress. [ABSTRACT FROM AUTHOR]

Disruption of eshA, which encodes a 52-kDa protein that is produced late during the growth of Streptomyces coelicolor A3(2), resulted in elimination of actinorhodin production. In contrast, disruption of eshB, a close homologue of eshA, had no effect on antibiotic production. The eshA disruptant accumulated lower levels of ppGpp than the wild-type strain accumulated. The loss of actinorhodin production in the eshA disruptant was restored by expression of a truncated relA gene, which increased the ppGpp level to the level in the wild-type strain, indicating that the reduced ppGpp accumulation in the eshA mutant was solely responsible for the loss of antibiotic production. Antibiotic production was also restored in the eshA mutant by introducing mutations into rpoB (encoding the RNA polymerase [3 subunit) that bypassed the requirement for ppGpp, which is consistent with a role for EshA in modulating ppGpp levels. EshA contains a cyclic nucleotide-binding domain that is essential for its role in triggering actinorhodin production. EshA may provide new insights and opportunities to unravel the molecular signaling events that occur during physiological differentiation in streptomycetes.