epiglucan and Periodontal-Diseases

This study was aimed to verify the hypothesis that periodontal disease contributes to endothelial dysfunction in the coronary arteries of middle-aged rats. Besides we evaluated the effects of a prebiotic (β-glucan isolated from Saccharomyces cerevisiae) in preventing vascular dysfunction. The sample comprised young (sham and induced to periodontal disease) and middle-aged rats (sham, periodontal disease, sham-treated and periodontal disease-treated), at 12 and 57 weeks, respectively. The treated-groups received daily doses of β-glucan (50 mg/kg) orally (gavage) for 4 weeks, and periodontal disease was induced in the last 2 weeks by ligature. A myograph system assessed vascular reactivity. The expression of endothelial nitric oxide synthase (eNOS), cyclooxygenase 1 (COX-1), COX-2, p47phox, gp91phox, NF-KB p65, p53, p21, and p16 was quantified by western blotting. Serum hydroperoxide production was measured by the ferrous oxidation-xylenol orange (FOX-2) assay method. Interleukin-1 beta (IL-1β), IL-10, and tumor necrosis factor-alpha (TNF-α) levels were evaluated by spectroscopic ultraviolet-visible analysis. Periodontal disease in middle-aged rats was associated with reduced acetylcholine-induced relaxations of coronary artery rings affecting the endothelium-dependent hyperpolarization- and the nitric oxide-mediated relaxations. The endothelial dysfunction was related to eNOS downregulation, pronounced impairment of the EDH-mediated relaxation, increased IL-1β and TNF-α proinflammatory cytokines, and also upregulation of NADPH oxidase and COXs, starting accumulate aging markers such as p53/p21 and the p16. Treatment with β-glucan effectively reduced bone loss in periodontal disease and delayed endothelial dysfunction in the coronary artery. Our data show that yeast β-glucan ingestion prevented oxidative stress and synthesis of proinflammatory marker and prevented eNOS reduction induced by periodontal disease in middle-aged rats. These results suggest that β-glucan has a beneficial effect on the coronary vascular bed.

Topics: Animals; beta-Glucans; Coronary Vessels; Dietary Fiber; Disease Models, Animal; Endothelium, Vascular; NADPH Oxidases; Nitric Oxide Synthase Type III; Oxidative Stress; Periodontal Diseases; Prebiotics; Protective Agents; Rats; Reactive Oxygen Species; Treatment Outcome; Vascular Diseases; Vasodilation

The aim of this study was to evaluate the effects of β-glucan on the expression of inflammatory mediators and metabolomic profile of oral cells [keratinocytes (OBA-9) and fibroblasts (HGF-1) in a dual-chamber model] infected by Aggregatibacter actinomycetemcomitans. The periodontopathogen was applied and allowed to cross the top layer of cells (OBA-9) to reach the bottom layer of cells (HGF-1) and induce the synthesis of immune factors and cytokines in the host cells. β-glucan (10 μg/mL or 20 μg/mL) were added, and the transcriptional factors and metabolites produced were quantified in the remaining cell layers and supernatant.. The relative expression of interleukin (IL)-1-α and IL-18 genes in HGF-1 decreased with 10 μg/mL or 20 μg/mL of β-glucan, where as the expression of PTGS-2 decreased only with 10 μg/mL. The expression of IL-1-α increased with 20 μg/mL and that of IL-18 increased with 10 μg/mL in OBA-9; the expression of BCL 2, EP 300, and PTGS-2 decreased with the higher dose of β-glucan. The production of the metabolite 4-aminobutyric acid presented lower concentrations under 20 μg/mL, whereas the concentrations of 2-deoxytetronic acid NIST and oxalic acid decreased at both concentrations used. Acetophenone, benzoic acid, and pinitol presented reduced concentrations only when treated with 10 μg/mL of β-glucan.. Treatment with β-glucans positively modulated the immune response and production of metabolites.

Topics: Acetophenones; Aggregatibacter actinomycetemcomitans; Anti-Infective Agents; Benzoic Acid; beta-Glucans; Cell Culture Techniques; Cell Line; Coculture Techniques; Cyclooxygenase 2; Cytokines; E1A-Associated p300 Protein; Fibroblasts; gamma-Aminobutyric Acid; Gene Expression; Host-Pathogen Interactions; Humans; Hydroxybutyrates; Immunomodulation; Inositol; Interleukin-18; Interleukin-1alpha; Keratinocytes; Lymphoma, B-Cell; Metabolome; Mouth; Oxalic Acid; Periodontal Diseases; Proto-Oncogene Proteins c-bcl-2; Real-Time Polymerase Chain Reaction

The objective of this study was to assess the effects of oral ingestion of β-glucans isolated from Saccharomyces cereviseae on the metabolic profile, expression of gingival inflammatory markers and amount of alveolar bone loss in diabetic rats with periodontal disease. Diabetes mellitus was induced in 48 Wistar rats by intraperitoneal injection of streptozotocin (80 mg/kg). After confirming the diabetes diagnosis, the animals were treated with β-glucans (by gavage) for 28 days. On the 14th day of this period, periodontal disease was induced using a ligature protocol. β-glucans reduced the amount of alveolar bone loss in animals with periodontal disease in both the diabetic and non-diabetic groups (p < 0.05). β-glucans reduced blood glucose, cholesterol and triacylglycerol levels in diabetic animals, both with and without periodontal disease (p < 0.05). Furthermore, treatment with β-glucans reduced the expression of cyclooxygenase-2 and receptor activator of nuclear factor kappa-B ligand and increased osteoprotegerin expression in animals with diabetes and periodontal disease (p < 0.05). It was concluded that treatment with β-glucans has beneficial metabolic and periodontal effects in diabetic rats with periodontal disease.

Topics: Alveolar Bone Loss; Animals; beta-Glucans; Blood Glucose; Cholesterol; Cyclooxygenase 2; Diabetes Mellitus, Experimental; Disease Models, Animal; Gingiva; Male; Osteoprotegerin; Periodontal Diseases; RANK Ligand; Rats; Rats, Wistar; Saccharomyces cerevisiae; Streptozocin; Triglycerides

We have investigated whether a purified immunomodulatory water soluble beta-1,3/1,6-glucan isolated from the cell wall of Bakers yeast, Saccharomyces cerevisiae, would influence the progression of ligature-induced periodontal disease, and to modulate accompanying cytokine and hypothalamic-pituitary-adrenal (HPA) axis responses to a lipopolysaccharide (LPS) challenge.. beta-1,3/1,6-glucan (10 mg/kg/day) was given in the drinking water to Wistar rats during the entire experiment, starting 14 days before disease induction, while control rats were given tap water only. Periodontal disease was assessed when the ligatures had been in place for 35 days.. Orally administered soluble beta-1,3/1,6-glucan significantly reduced periodontal bone loss as measured on digital X-rays (p=0,026). Glucan-treated rats also showed a significantly enhanced plasma level of the HPA axis-driven hormone corticosterone (p=0.047), and of the cytokine transforming growth factor-1beta (p=0.032), as well as a tendency to enhanced IL-10 (p=0.106), induced by intra-peritoneally administered LPS.. Soluble beta-1,3/1,6-glucan administered by the oral route diminishes ligature-induced periodontal bone loss in this model. This effect may be attributable to the well documented ability of beta-1,3/1,6-glucan to stimulate macrophage phagocytosis and to skew the T helper (Th)1/Th2 balance towards Th1 and T regulatory responses. The HPA axis may play a significant role in beta-1,3/1,6-glucan induced immune modulation.

Topics: Alveolar Bone Loss; Animals; beta-Glucans; Corticosterone; Glucans; Hypothalamo-Hypophyseal System; Interleukin-10; Ligation; Lipopolysaccharides; Male; Periodontal Diseases; Pituitary-Adrenal System; Rats; Rats, Wistar; Saccharomyces cerevisiae; Transforming Growth Factor beta; Transforming Growth Factor beta1; Tumor Necrosis Factor-alpha