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

서지정보

ㆍ발행기관 : 대한구강생물학회 ㆍ수록지정보 : International Journal of Oral Biology / 45권 / 4호
ㆍ저자명 : Wan Lee, Seoung Hoon Lee, Min-Seuk Kim, Eun Joo Choi

목차

Introduction
Materials and Methods
1. 실험동물 및 치주질환 동물모델 확립
2. μCT 촬영
3. 통계분석
Results
1. 식이 조건에 따른 체중 변화량 및 사료/물 섭취량 분석
2. 식이 조건에 따른 치조골 높이의 변화
Discussion
Acknowledgements
Conflicts of Interest
References

영어 초록

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.

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