Toker Hulya, Ozdemir Hakan, Balci Yuce Hatice, Goze Fahrettin
Department of Periodontology, Faculty of Dentistry, Cumhuriyet University, Sivas, Turkey.
Department of Periodontology, Faculty of Dentistry, Gaziosmanpaşa University, Tokat, Turkey.
J Dent Sci. 2016 Sep;11(3):331-337. doi: 10.1016/j.jds.2016.03.011. Epub 2016 May 4.
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.
Thirty-six male Wistar rats were separated into five study groups: nonligated control (C, = 6) group; periodontitis (P, = 6) group; osteoporosis (O, = 8) group; osteoporosis + periodontitis (O+P, = 8) group, and osteoporosis + periodontitis with 50 mg/kg/d boric acid (BA50, = 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.
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).
Within limitations of this study, we conclude that boric acid may decrease alveolar bone loss in a rat model with periodontitis and osteoporosis.
背景/目的:本研究旨在探讨全身应用硼酸对骨质疏松大鼠实验性牙周炎模型中与骨质疏松相关的骨改变、牙槽骨吸收、核因子κB受体活化因子配体(RANKL)表达及下颌骨密度的影响。
将36只雄性Wistar大鼠分为5个研究组:未结扎对照组(C,n = 6);牙周炎组(P,n = 6);骨质疏松组(O,n = 8);骨质疏松+牙周炎组(O+P,n = 8);骨质疏松+牙周炎+50 mg/kg/d硼酸组(BA50,n = 8),持续15天。通过腹腔注射80 mg/kg维甲酸15天诱导骨质疏松。用4/0丝线结扎下颌右侧第一磨牙周围以诱导实验性牙周炎。诱导骨质疏松和牙周炎后,在第15天处死大鼠。用体视显微镜通过测量从牙骨质-釉质界到牙槽嵴的距离评估牙槽骨吸收。在X线片上进行密度测量。在组织学切片上进行RANKL和抗酒石酸酸性磷酸酶(TRAP)染色。
O+P组的牙槽骨吸收明显高于其他组(P < 0.05)。硼酸减少了骨吸收(P < 0.05)。TRAP+破骨细胞数量在P组最高,在对照组最低。对照组、P组、O+P组和BA50组之间TRAP+破骨细胞数量的差异有统计学意义(P < 0.05)。RANKL表达和下颌骨密度无显著差异(P > 0.05)。
在本研究的局限性内,我们得出结论,硼酸可能减少患有牙周炎和骨质疏松的大鼠模型中的牙槽骨吸收。