astaxanthine and Periodontitis

This study evaluated the effects of astaxanthin (ASX) on alveolar bone loss, receptor activator of nuclear factor-κB ligand (RANKL), and osteoprotegerin (OPG) activity in ligature-induced periodontitis in diabetic rats. Diabetes mellitus (DM) was induced with 50 mg/kg intraperitoneal streptozotocin in 40 male Wistar rats. The Wistar rats were divided into six experimental groups: non-ligated (NL; n = 6); ligature only (L; n = 6); DM only (D; n = 6); DM + ligature (DP; n = 6); DM + ligature + 1 mg/kg/day ASX (ASX 1 group; n = 8); and DM + ligature + astaxanthin 5 mg/kg/day ASX (ASX 5 group; n = 8). Silk ligatures were placed along the gingival margin of the left mandibular first molar tooth. The study duration was 11 days, after which the animals were euthanised. Changes in alveolar bone levels were clinically measured, and RANKL and OPG activities were immunohistochemically examined. Alveolar bone loss was the most significant in the DP group (p < 0.05). Decreased alveolar bone loss was observed in the ASX 5 group (p < 0.05). Although RANKL activity was highest in the DP group, it was observed at lower levels in the groups to which ASX was administered. OPG activity did not differ between groups (p > 0.05). The results of this study suggested that 1 and 5 mg/kg ASX administration reduced RANKL activity and alveolar bone loss in rats with experimentally induced periodontitis.

Topics: Alveolar Bone Loss; Animals; Diabetes Mellitus, Experimental; Male; Models, Theoretical; Periodontitis; Rats; Rats, Wistar; Rodent Diseases; Xanthophylls

Numerous studies highlight that astaxanthin (ASTX) ameliorates hyperglycemic condition and hyperglycemia-associated chronic complications. While periodontitis and periodontic tissue degradation are also triggered under chronic hyperglycemia, the roles of ASTX on diabetes-associated periodontal destruction and the related mechanisms therein are not yet fully understood. Here, we explored the impacts of supplemental ASTX on periodontal destruction and systemic complications in type I diabetic mice. To induce diabetes, C57BL/6 mice received a single intraperitoneal injection of streptozotocin (STZ; 150 mg/kg), and the hyperglycemic mice were orally administered with ASTX (12.5 mg/kg) (STZ+ASTX group) or vehicle only (STZ group) daily for 60 days. Supplemental ASTX did not improve hyperglycemic condition, but ameliorated excessive water and feed consumptions and lethality in STZ-induced diabetic mice. Compared with the non-diabetic and STZ+ASTX groups, the STZ group exhibited severe periodontal destruction. Oral gavage with ASTX inhibited osteoclastic formation and the expression of receptor activator of nuclear factor (NF)-κB ligand, 8-OHdG, γ-H2AX, cyclooxygenase 2, and interleukin-1β in the periodontium of STZ-injected mice. Supplemental ASTX not only increased the levels of nuclear factor erythroid 2-related factor 2 (Nrf2) and osteogenic transcription factors in the periodontium, but also recovered circulating lymphocytes and endogenous antioxidant enzyme activity in the blood of STZ-injected mice. Furthermore, the addition of ASTX blocked advanced glycation end products-induced oxidative stress and growth inhibition in human-derived periodontal ligament cells by upregulating the Nrf2 pathway. Together, our results suggest that ASTX does not directly improve hyperglycemia, but ameliorates hyperglycemia-triggered periodontal destruction and oxidative systemic complications in type I diabetes.

Topics: Adolescent; Alveolar Process; Animals; Antioxidants; Blood Glucose; Catalase; Cell Proliferation; Cytokines; Diabetes Mellitus, Experimental; Dietary Supplements; DNA Damage; Feeding Behavior; Glycation End Products, Advanced; Humans; Hyperglycemia; Inflammation Mediators; Injections; Lymphocytes; Male; Mice, Inbred C57BL; NF-E2-Related Factor 2; Osteoclasts; Oxidative Stress; Periodontal Ligament; Periodontitis; Reactive Oxygen Species; Streptozocin; Superoxide Dismutase; Up-Regulation; Xanthophylls; Young Adult

Astaxanthin is a keto-carotenoid that has a strong antioxidant effect. The purpose of this study was to evaluate the effects of astaxanthin on alveolar bone loss and histopathological changes in ligature-induced periodontitis in rats.. Wistar rats were divided into four experimental groups: non-ligated (C, n = 6); ligature only (L, n = 6); ligature and astaxanthin (1 mg/kg/day astaxanthin, AS1 group, n = 8); ligature and astaxanthin (5 mg/kg/day astaxanthin, AS5 group, n = 8). Silk ligatures were placed at the gingival margin of lower first molars of the mandibular quadrant. The study duration was 11 days and the animals were killed at the end of this period. Changes in alveolar bone levels were clinically measured and tissues were immunohistochemically examined, osteocalcin, bone morphogenic protein-2, inducible nitric oxide synthase, Bax and bcl-2 levels in alveolar bone and tartrate-resistant acid phosphatase-positive osteoclast cells, osteoblast and inflammatory cell counts were determined.. Alveolar bone loss was highest in the L group and the differences among the L, AS1 and AS5 groups were also significant (P < .05). Both doses of astaxanthin decreased tartrate-resistant acid phosphatase-positive+ osteoclast cell and increased osteoblast cell counts (P < .05). The inflammation in the L group was also higher than those of the C and AS1 groups were (P < .05) indicating the anti-inflammatory effect of astaxanthin. Although inducible nitric oxide synthase, osteocalcin, bone morphogenic protein-2 and bax staining percentages were all highest in the AS5 group and bcl-2 staining percentage was highest in the AS1 group, values were close to each other (P > .05).. Within the limits of this study, it can be suggested that astaxanthin administration may reduce alveolar bone loss by increasing osteoblastic activity and decrease osteoclastic activity in experimental periodontitis model.

Topics: Alveolar Bone Loss; Animals; Antioxidants; bcl-2-Associated X Protein; Bone Morphogenetic Protein 2; Cell Count; Disease Models, Animal; Nitric Oxide Synthase; Osteoblasts; Osteocalcin; Periodontitis; Rats, Wistar; Xanthophylls