Abstract
BackgroundPeriodontal disease is one of the most frequent comorbidities in diabetic patients and can contribute to poor blood glucose control.ObjectiveTo evaluate the effects of ingesting different doses of beta-glucans (BG) isolated from Saccharomyces cerevisiae on alveolar bone loss (ABL) and inflammatory/metabolic parameters in normal and diabetic rats with ligature-induced periodontal disease (PD).DesignSixty male rats were assigned into two groups: non-diabetic or diabetic (i.p. 70 mg/kg streptozotocin) with PD. Then, groups were subdivided into five subgroups according BG doses: 0 mg/Kg; 10 mg/Kg; 20 mg/Kg; 40 mg/Kg or 80 mg/Kg. Animals received BG for 28 days and ligatures were placed on lower first molars during the last 14 days.ResultsABL of diabetic and non-diabetic animals receiving BG 40 mg/kg (1.33 ± 0.03 mm and 0.77 ± 0.07 mm, respectively) and 80 mg/kg (1.26 ± 0.07 mm and 0.78 ± 0.05 mm, respectively) doses was lower (p < 0.05) in comparison to respective controls (1.59 ± 0.11 mm and 0.90 mm ±0.08). COX-2 (Control: 1.66 ± 0.12; 40 mg/kg: 1.13 ± 0.07; 80 mg/kg: 0.92 ± 0.18) and RANKL expressions (Control: 1.74 ± 0.34; 40 mg/kg: 1.03 ± 0.29 ;80 mg/kg: 0.75 ± 0.21), together with the RANKL/OPG ratio (Control: 1.17 ± 0.08; 40 mg/kg: 0.67 ± 0.09; 80 mg/kg: 0.63 ± 0.28) were attenuated above the same dose (p < 0.05). BG did not influence (p > 0.05) metabolic parameters in non-diabetic rats. In diabetic animals, doses above 40 mg/kg reduced IL-1β (Control: 387 ± 66; 40 mg/kg: 309 ± 27; 80 mg/kg: 300 ± 14) and TNF-α (Control: 229 ± 19; 40 mg/kg: 128 ± 53; 80 mg/kg: 71 ± 25), blood glucose levels (Control: 402 ± 49; 40 mg/kg: 334 ± 32; 80 mg/kg: 287 ± 56), total cholesterol (Control: 124 ± 8; 40 mg/kg: 120 ± 10; 80 mg/kg: 108 ± 9), LDL-c + VLDL-c (Control: 106 ± 8; 40 mg/kg: 103 ± 10; 80 mg/kg: 87 ± 10) and triacylglycerols (Control: 508 ± 90; 40 mg/kg: 301 ± 40; 80 mg/kg: 208 ± 61), whereas increased HDL-c (Control: 18 ± 0.5; 40 mg/kg: 19 ± 1; 80 mg/kg: 21 ± 1) (p < 0.05). Optimal dose needed to reduce ABL was higher in diabetic animals with PD.ConclusionsBG ingestion reduced ABL and improved inflammatory profile in a dose-dependent manner. Best effects were achieved with doses above 40 mg/kg.
Highlights
Periodontal disease (PD) is a group of inflammatory conditions initiated by the presence of disbiotic biofilm associated to teeth supporting tissues [1, 2]
Optimal dose needed to reduce alveolar bone loss (ABL) was higher in diabetic animals with PD
Specific components of bacteria stimulate periodontal cells to secrete several pro-inflammatory cytokines, including prostaglandins, IL-1, IL-6, TNF-α and endothelin [3], and promote bone loss through osteoclast activation. This process involves the expression of the receptor activator of nuclear factor kappa-Β ligand (RANKL) and reduced expression of osteoprotegerin (OPG) [4, 5]
Summary
Periodontal disease (PD) is a group of inflammatory conditions initiated by the presence of disbiotic biofilm associated to teeth supporting tissues [1, 2]. Specific components of bacteria (e.g., lipopolysaccharide-LPS) stimulate periodontal cells to secrete several pro-inflammatory cytokines, including prostaglandins, IL-1, IL-6, TNF-α and endothelin [3], and promote bone loss through osteoclast activation. This process involves the expression of the receptor activator of nuclear factor kappa-Β ligand (RANKL) and reduced expression of osteoprotegerin (OPG) [4, 5]. Blood glucose control in diabetic patients is hampered in the presence of PD [7]. Periodontal disease is one of the most frequent comorbidities in diabetic patients and can contribute to poor blood glucose control
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