High-salt and glucose diet attenuates alveolar bone recovery in a ligature-induced rat model of experimental periodontitis

Wan-Ruoh Lee, Seoung Hoon Lee, Min-Seuk Kim, E. Choi
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Abstract

Excessive intake of sodium caused by high salt diet promotes the expression of inflammatory cytokines and differentiation of helper T cells resulting in inflammatory responses. High-glucose diet also contributes to the pathogenesis of periodontitis by inducing changes in the oral microbiome and reducing salivation. However, the effect of a high-salt and glucose diet (HSGD) on the prognosis of periodontitis remains unclear. In this study, a rat model of experimental periodontitis was established by periodic insertion of absorbable sutures containing Porphyromonas gingivalis and Fusobacterium nucleatum strains into the right gingival sulcus to analyze the effect of HSGD on the incidence and progression of periodontitis. The alveolar bone heights (ABH) was measured with microcomputed tomography imaging of the HSGD- and general diet (GD)-treated groups. The right ABH was significantly decreased compared to the left in both groups at 4 weeks after induction of inflammation; however, no significant difference was noted between the groups. Notably, the ABH in the HSGD-treated group was significantly decreased at 8 weeks after induction of inflammation, whereas in the GD-treated group, an increase in the ABH was observed; a significant difference of the ABH was noted between the two groups (p < 0.05). At 12 weeks, recovery of the alveolar bone was observed in both groups, with no significant differences in ABH between the two groups. These findings indicate that the intake of excessive sodium attenuates the recovery rate of the alveolar bone even after the local infectant is removed. In addition, this study demonstrates the use of HSGD in establishing a new animal model of periodontitis.
在结扎诱导的实验性牙周炎大鼠模型中,高盐和高糖饮食减缓了牙槽骨的恢复
高盐饮食引起的钠摄入过多,可促进炎症细胞因子的表达和辅助性T细胞的分化,引起炎症反应。高糖饮食也有助于牙周炎的发病机制,通过诱导口腔微生物组的变化和减少唾液分泌。然而,高盐高糖饮食(HSGD)对牙周炎预后的影响尚不清楚。本研究通过将含有牙龈卟啉单胞菌和核梭杆菌菌株的可吸收缝合线定期插入右侧牙龈沟,建立实验性牙周炎大鼠模型,分析HSGD对牙周炎发生和发展的影响。用微计算机断层成像测量HSGD组和普通饮食组的牙槽骨高度(ABH)。诱导炎症后4周,两组小鼠右侧ABH均明显低于左侧;然而,两组之间没有显著差异。值得注意的是,炎症诱导后8周,hsgd治疗组的ABH明显降低,而gd治疗组的ABH则升高;两组间ABH差异有统计学意义(p < 0.05)。12周时,两组牙槽骨均恢复正常,两组间ABH无显著差异。这些结果表明,过量钠的摄入会降低牙槽骨的恢复速度,即使在局部感染被清除后也是如此。此外,本研究还验证了HSGD在牙周炎动物模型中的应用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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