Abstract
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.
Highlights
Periodontal disease is characterized by chronic inflammation that affects tooth support tissues and may lead to tooth loss [1,2]
Diabetes mellitus is a disease in which carbohydrate, protein and lipid metabolism homeostasis is inadequately regulated by the pancreatic hormone insulin, resulting in an increase in blood glucose levels [5]
It was observed that the metabolic parameters criteria, namely analyzed: final blood glucose, total cholesterol and triacylglycerols, were higher in diabetic animal groups compared to nondiabetic groups (Table 1—p < 0.05)
Summary
Periodontal disease is characterized by chronic inflammation that affects tooth support tissues and may lead to tooth loss [1,2]. Diabetes mellitus is a disease in which carbohydrate, protein and lipid metabolism homeostasis is inadequately regulated by the pancreatic hormone insulin, resulting in an increase in blood glucose levels [5]. Periodontal disease is the sixth most common co-morbid condition in patients with diabetes mellitus [6,7] and evidence indicates a bidirectional relationship between these two pathologies [8,9]. In non-compensated diabetic patients, hyperglycemia promotes vascular alterations (microangiopathies) as well as inefficacious phagocytosis by neutrophils and macrophages. It causes retardation of collagen synthesis, which delays tissue repair [10]. The chronic release of pro-inflammatory cytokines in active periodontal disease reduces insulin action and aggravates these metabolic alterations [11]
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