The effect of boron on alveolar bone loss in osteoporotic rats

Background/purpose: The aim of this study is to investigate the effects of systemically administered boric acid on osteoporosis-related bone alterations, alveolar bone loss, receptor activator of nuclear factor kappa-b ligand (RANKL) expressions, and mandibular bone density in experimental periodontitis model in osteoporotic rats. Materials and methods: Thirty-six male Wistar rats were separated into five study groups: non-ligated control (C, n = 6) group; periodontitis (P, n = 6) group; osteoporosis (0, n = 8) group; osteoporosis + periodontitis n = 8) group, and osteoporosis + periodontitis with 50 mg/kg/d boric acid (BA50, n = 8) group for 15 days. Osteoporosis was created with intraperitoneal injection of 80 mg/kg retinoic acid for 15 days. Silk ligatures (4/0) were placed around the mandibular right first molar teeth to induce experimental periodontitis. After induction of osteoporosis and periodontitis, rats were sacrificed at Day 15. Alveolar bone loss was evaluated with a stereomicroscope by measuring the distance from the cement-enamel junction to the alveolar crest. Density measurements were performed on radiographs. RANKL and tartrate resistant acid phosphatase (TRAP) staining were performed on histological slides. Results: Alveolar bone loss was significantly higher in the O+P group than those of the other groups (P < 0.05). Boric acid decreased bone loss (P < 0.05). TRAP + osteoclast numbers were highest in the P group and lowest in the control group. The differences in TRAP + osteoclast numbers among control, P, O+P, and BA50 groups were significant (P < 0.05). There were no significant differences in RANKL expression and mandibular bone density (P > 0.05). Conclusion: Within limitations of this study, we conclude that boric acid may decrease alveolar bone loss in a rat model with periodontitis and osteoporosis. Copyright (C) 2016, Association for Dental Sciences of the Republic of China. Published by Elsevier Taiwan LLC. This is an open access article under the CC BY-NC-ND license.