Search

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.

Many studies on the cholinergic pathway have indicated that cholinergic receptors, which are widely expressed in various cells, play an important role in all body organs. In this review, we present the concept that cholinergic responses are regulated through a neuronal or non-neuronal mechanism. The neuronal mechanism is a system in which acetylcholine binds to cholinergic receptors on target cells through the nerves. In the non-neuronal mechanism, acetylcholine, produced by neighboring cells in an autocrine/paracrine manner, binds to cholinergic receptors on target cells. Both mechanisms subsequently lead to physiological and pathophysiological responses. We also investigated the subunits/subtypes of cholinergic receptors on target cells, physiological and pathophysiological responses of the organs via cholinergic receptors, and extracellular factors that alter the subtypes/subunits of cholinergic receptors. Collectively, this concept will elucidate how cholinergic responses occur and will help us conduct further experiments to develop new therapeutic agents.

ObjectiveThis study aimed to histologically compare periodontal regeneration of one-wall intrabony defects treated with open flap debridement, β-tricalcium phosphate (β-TCP), and carbonate apatite (CO3Ap) in dogs.MethodsThe mandibular third premolars of four beagle dogs were extracted. Twelve weeks after the extraction, a one-wall bone defect of 4 mm × 5 mm (mesio-distal width × depth) was created on the distal side of the mandibular second premolar and mesial side of the fourth premolar. Each defect was randomly allocated to open flap debridement (control group), periodontal regeneration utilizing β-TCP, or CO3Ap. Eight weeks after the surgery, histologic and histometric analyses were performed.ResultsNo ankylosis, infection, or acute inflammation was observed at any of the experimental sites. Newly formed bone and cementum were observed in all experimental groups. The mineral apposition rate of the alveolar bone crest was higher in the CO3Ap group than in the control and β-TCP groups. The ratio of the new bone area was significantly higher in the CO3Ap group than in the control group (P

IntroductionFibroblast growth factor-2 (FGF-2) has been reported to promote periodontal tissue regeneration. However, no study has investigated the long-term prognosis of periodontal regenerative therapy using FGF-2 to date. The aim of this study was to observe the long-term outcomes as well as to investigate the factors affecting the prognosis of periodontal regenerative therapy using FGF-2.MethodsSixty intrabony defects were prospectively investigated for three years after periodontal regenerative therapy with recombinant human FGF-2 (rhFGF-2) by evaluating probing pocket depth (PPD) and radiographic bone defect depth (RBD). The factors influencing RBD were assessed by conducting a multivariate linear regression analysis after adjusting for confounders.ResultsThe mean age of the participants was 62.4 ± 13.4 years, and baseline PPD and RBD were 6.1 ± 1.9 mm and 4.5 ± 1.8 mm, respectively. At six months, one year, and three years after surgery, PPD and RBD had significantly improved to 4.2 ± 1.7, 3.7 ± 1.4, 4.0 ± 1.9 mm and to 3.08 ± 2.05, 2.73 ± 1.90, 2.51 ± 2.15 mm, respectively. At the three-year examination, a significant positive association was deteced between RBD reduction and RBD at baseline, while the association was not significant between RBD reduction and the radiographic bony angle, number of bony walls of the defect, or the furcation involvement at baseline.ConclusionsrhFGF-2 was effective for alveolar bone regeneration in patients with periodontitis and maintained the improved parameters over the three-year observation period. The radiographic bone defect depth at baseline was found to be the factor affecting the periodontal regenerative therapy using rhFGF-2 in the intrabony defects.Trial registration numberUMIN000027979.

PURPOSE: We aimed to histologically evaluate the influence of bone materials used during guided bone regeneration (GBR) on subsequent peri-implantitis in an experimental ligature-induced peri-implantitis model in beagle dogs. METHODS: Bilateral mandibular premolars (PM2-4) were extracted from six beagle dogs. After 3 months, standardized bone defects (3 mm [mesio-distal width] × 2 mm [bucco-lingual width] × 3 mm [depth]) were created in the experimental group, with simultaneous dental implant placement at the center of the defects. The defects were randomly filled with either autograft (AG) or deproteinized bovine bone mineral (DBBM) and covered with a collagen membrane. In the control group, implant fixtures were placed without creating an intrabony defect. After 3 months, a healing abutment was placed. Four weeks later, a 3-0 silk thread was ligated around the implants to induce peri-implantitis. After 4 weeks, the specimens were dissected and histologically examined. RESULTS: There were no clinical findings of inflammation until silk thread ligation. Four weeks after the onset of peri-implantitis, gingival redness and swelling were seen with mild resorption of the peri-implant bone on dental radiographs. There were no significant differences between the AG, DBBM, and control groups for the following parameters: bone-to-implant contact, distance from the implant shoulder to the base of the bone defect, area of bone defect, and area of new bone. CONCLUSIONS: Within the limitations of this study, it can be concluded that peri-implant tissues after GBR using AG and DBBM underwent the same degree of bone resorption by peri-implantitis as the no defect group.

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]

Background: There have been limited studies with statistically sufficient sample sizes for assessment of suitable bone defect morphology for combination therapy with enamel matrix derivative (EMD) and bone grafting. The aim of this study was to investigate the appropriate feature of intrabony defects, such as bone defect angle (DA) and the containment by bony wall, for yielding the additional benefit of bone grafting in combination with periodontal regenerative therapy using EMD. Methods: Following periodontal regenerative therapy using EMD with or without autologous bone grafting, 282 intrabony defects of 177 participants were maintained for 3 years. Multilevel linear regression analysis was performed to evaluate the radiographic bony defect depth (RBD) reduction after adjusting for confounders. Results: The baseline parameters, except for the proportion of contained bony defects and tooth mobility, did not differ significantly between the groups with and without bone grafts. There was no significant difference in the improvement of clinical parameters between the groups. The 1‐ and 3‐year reduction of RBD showed significant inverse correlations with preoperative DA only in the group without bone graft. Furthermore, multivariate analysis showed a significant interaction between DA at baseline ≥40° and adjunctive bone grafting in the reduction of RBD, regardless of the number of bony walls. Conclusion: Adjunctive autologous bone grafting with enamel matrix derivative might be significantly beneficial for defect depth improvement in the case of DA at baseline ≥40°. [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]

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]

Objective: This study aimed to evaluate the in vitro antibacterial effects of lysozyme‐chitosan oligosaccharide conjugates (LYZOX) against Streptococcus gordonii and Porphyromonas gingivalis. Materials and Methods: Planktonic S. gordonii and P. gingivalis were treated with various concentrations of LYZOX for 10 min. The treated bacteria were incubated on trypticase soy agar plates, and colony‐forming unit (CFU) was calculated. The antibacterial effect of LYZOX was compared with that of lysozyme, chitosan, physiological saline, and benzalkonium chloride solution. Cell morphology before and after LYZOX treatment was observed using a scanning electron microscope (SEM). The antibacterial effect of LYZOX with decanoic acid against the biofilm‐like bacteria was also examined via crystal violet staining. The Kruskal–Wallis test and post hoc Dunn tests were performed to compare the difference in antibacterial activity of each treatment. Results: Bacterial CFU numbers were reduced after LYZOX treatment in a concentration‐dependent manner. The reduction in CFUs was smaller for corresponding concentrations of chitosan or lysozyme alone. SEM analyses revealed bacterial cells shrank following LYZOX treatment. The combined use of LYZOX and decanoic acid yielded an even higher antibacterial effect against bacterial biofilms. Conclusion: LYZOX exhibits antibacterial activity against two periodontal bacteria and may be a promising plaque control agent. [ABSTRACT FROM AUTHOR]

We investigated the effects of low‐level Er:YAG laser irradiation on proliferation and alternations in early gene expression of gingival fibroblasts. Mice primary gingival fibroblasts were irradiated with an Er:YAG laser (1.8, 3.9, and 5.8 J/cm2). Irradiation at 3.9 J/cm2 promoted cell proliferation without significant changes in lactate dehydrogenase or Hspa1a expression. Three hours after irradiation at 3.9 J/cm2, the Fn1 expression level was significantly increased. RNA‐seq identified 15 differentially expressed genes between irradiated and non‐irradiated cells, some of which belonged to immediate early genes (IEGs). Kyoto Encyclopedia of Genes and Genomes pathway analysis indicated MAPK pathway enhancement, and gene set enrichment analysis showed enrichment in the TGF‐β signaling gene set. Enhanced proliferation via laser irradiation disappeared upon inhibition of Dusp4, Dusp5, and Tgfr1 expression. Low‐level Er:YAG laser irradiation, especially at 3.9 J/cm2 without a major temperature elevation, enhanced fibroblast proliferation, via TGF‐β and the MAPK signaling pathway following IEG expression. [ABSTRACT FROM AUTHOR]