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非手术牙周治疗和二甲双胍通过调节肠道微生物群改善肥胖牙周炎小鼠的骨质流失。

Non-Surgical Periodontal Therapy and Metformin Improve Bone Loss in Obese Mice With Periodontitis by Modulating the Gut Microbiota.

作者信息

Chen Rixin, Wei Wei, Li Lili, Zhang Miaomiao, Wang Nannan, Ge Ruiyang, Shen Yue, Zhang Wen, Lu Daiyv, Liao Wenzheng, Li Yanfen, Yan Fuhua

机构信息

Nanjing Stomatological Hospital, Affiliated Hospital of Medical School, Institute of Stomatology, Nanjing University, Nanjing, China.

Stomatology Center, Shenzhen Hospital of Southern Medical University, Shenzhen, China.

出版信息

FASEB J. 2025 Jul 15;39(13):e70814. doi: 10.1096/fj.202501689R.

Abstract

Periodontitis and obesity are chronic inflammatory diseases associated with osteoporosis. Controlling inflammation is crucial for managing periodontitis in individuals with obesity. Metformin has shown potent anti-inflammatory effects under inflammatory conditions. However, the effects of adjunctive systemic administration of metformin alongside non-surgical periodontal therapy (NSPT) on periodontal and systemic bone health in obesity remain unknown. In this study, a high-fat diet (HFD)-induced obese murine model was created with periodontitis through ligation. Periodontal treatment consisted of standard mechanical debridement via NSPT, with or without metformin treatment through oral gavage. Outcomes were evaluated based on changes in periodontal status, systemic bone resorption and inflammation, as well as the gut microbiota community and metabolism. Our results indicated that periodontitis significantly increased osteoclastic activity and resulted in alveolar and femoral bone loss in HFD-fed mice. Compared to NSPT alone, NSPT and metformin significantly improved periodontitis, reduced systemic inflammation, and alleviated femoral bone absorption in HFD-fed mice. Mechanistically, periodontitis promoted gut microbiota dysbiosis and disrupted microbial linoleic acid metabolism. NSPT and metformin normalized the gut microbiota, enhanced the growth of species with anti-inflammatory properties, including Faecalibacterium prausnitzii, Akkermansia muciniphila, Lactobacillus reuteri, and Butyricicoccus pullicaecorum, and restored the balance of linoleic acid metabolism in the gut and serum. This research presents novel evidence that metformin may serve as a promising adjunct to enhance the response of obese subjects to NSPT by regulating the gut microbiota and linoleic acid metabolism, indicating that the gut microbiota could be a potential therapeutic target for multidisciplinary intervention in periodontitis and obesity.

摘要

牙周炎和肥胖是与骨质疏松症相关的慢性炎症性疾病。控制炎症对于管理肥胖个体的牙周炎至关重要。二甲双胍在炎症条件下已显示出强大的抗炎作用。然而,在肥胖患者中,非手术牙周治疗(NSPT)联合全身应用二甲双胍对牙周和全身骨骼健康的影响尚不清楚。在本研究中,通过结扎建立了高脂饮食(HFD)诱导的肥胖小鼠牙周炎模型。牙周治疗包括通过NSPT进行标准机械清创,同时或不通过灌胃给予二甲双胍治疗。根据牙周状况、全身骨吸收和炎症、肠道微生物群群落及代谢的变化评估结果。我们的结果表明,牙周炎显著增加了破骨细胞活性,并导致高脂饮食喂养小鼠的牙槽骨和股骨骨丢失。与单独的NSPT相比,NSPT和二甲双胍显著改善了牙周炎,减轻了全身炎症,并缓解了高脂饮食喂养小鼠的股骨骨吸收。从机制上讲,牙周炎促进了肠道微生物群失调,并扰乱了微生物亚油酸代谢。NSPT和二甲双胍使肠道微生物群正常化,增强了具有抗炎特性的物种的生长,包括普拉梭菌、嗜黏蛋白阿克曼氏菌、罗伊氏乳杆菌和普氏粪丁酸球菌,并恢复了肠道和血清中亚油酸代谢的平衡。这项研究提供了新的证据,表明二甲双胍可能作为一种有前景的辅助药物,通过调节肠道微生物群和亚油酸代谢来增强肥胖受试者对NSPT的反应,这表明肠道微生物群可能是牙周炎和肥胖多学科干预的潜在治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7957/12239949/1234fb8e719a/FSB2-39-e70814-g007.jpg

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