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    Boric acid inhibits alveolar bone loss in rats by affecting RANKL and osteoprotegerin expression
    (Wiley, 2014) Saglam, M.; Hatipoglu, M.; Koseoglu, S.; Esen, H. H.; Kelebek, S.
    Background and Objective: The goal of the present study was to evaluate the effects of systemic boric acid on the levels of expression of RANKL and osteoprotegerin (OPG) and on histopathologic and histometric changes in a rat periodontitis model. Material and Methods: Twenty-four Wistar rats were divided into three groups of eight animals each: nonligated (NL); ligature only (LO); and ligature plus treatment with boric acid (BA) (3 mg/kg per day for 11 d). A 4/0 silk suture was placed in a subgingival position around the mandibular right first molars; after 11 d the rats were killed, and alveolar bone loss in the first molars was histometrically determined. Periodontal tissues were examined histopathologically to assess the differences among the study groups. RANKL and OPG were detected immunohistochemically. Results: Alveolar bone loss was significantly higher in the LO group than in the BA and NL groups (p < 0.05). The number of inflammatory infiltrate and osteoclasts in the LO group was significantly higher than that in the NL and BA groups (p < 0.05). The numbers of osteoblasts in LO and BA groups were significantly higher compared with NL group (p < 0.05). There were significantly more RANKL-positive cells in the LO group than in the BA and NL groups (p < 0.05). There was a higher number of OPG-positive cells in the BA group than in the LO and NL groups (p < 0.05). Conclusion: The present study shows that systemic administration of boric acid may reduce alveolar bone loss by affecting the RANKL/OPG balance in periodontal disease in rats.
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    Interleukin-33 could play an important role in the pathogenesis of periodontitis
    (Wiley, 2015) Koseoglu, S.; Hatipoglu, M.; Saglam, M.; Enhos, S.; Esen, H. H.
    Background and ObjectiveInterleukin-33 (IL-33) controls T-helper type 2 (Th2) cytokines and the development of mast cells. This study aimed to investigate the expression of IL-33 and its association with RANKL and osteoprotegerin (OPG) in periodontal health and experimental periodontitis. Material and MethodsEighteen Wistar rats were assigned to two study groups of nine animals each: ligature only (LO) and nonligated (NL). Silk sutures were placed subgingivally, surrounding the right lower first molars. The animals were killed on day 11 after ligature placement, and the alveolar bone loss at the first molars was determined histometrically. Periodontal tissues were examined histopathologically to evaluate the differences between the groups. The expression of IL-33, RANKL and OPG was detected immunohistochemically. ResultsThe LO group showed significantly greater alveolar bone loss compared with the NL group (p<0.05). The numbers of osteoclasts, osteoblasts and inflammatory cells were significantly higher in the LO group compared with the NL group (p<0.05). Osteoblastic activity was significantly lower in the LO group than in the NL group (p<0.05). There was significantly higher expression of IL-33 and RANKL and a greater number of OPG-positive cells in the LO group (p<0.05). IL-33 expression showed a positive correlation with RANKL expression and with the number of mast cells (p<0.05). ConclusionThe experimental periodontitis group exhibited increased expression of IL-33 and RANKL compared with the healthy group. Additionally, there was a positive correlation between these expressions. According to these results, IL-33 could be associated with the pathogenesis of periodontal disease.