Periodontal therapy favorably modulates the oral-gut-hepatic axis in cirrhosis
Periodontal therapy favorably modulates the oral-gut-hepatic axis in cirrhosis
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DOI：
10.1152/ajpgi.00230.2018
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发表时间：
2018-11-01
影响因子：
4.5
通讯作者：
Sahingur, Sinem E.
中科院分区：
文献类型：
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作者：
Bajaj, Jasmohan S.;Matin, Payam;Sahingur, Sinem E.
肝硬变与全身性促炎环境、内毒素血症和肠道生物失调有关。口腔可能是炎症的另一个来源。我们的目的是通过评估内毒素血症、炎症、认知和生活质量(QOL)来确定牙周治疗在肝硬变中的效果。年龄匹配的肝硬变和非肝硬变受试者表现为慢性牙周炎和/或轻度或中度牙周炎，接受牙周治疗，并在30天内进行随访。分别于基线和第30天收集唾液/粪便微生物组成和血清终末期肝病模型(MELD)评分、内毒素和脂多糖结合蛋白(LBP)和免疫炎症标志物(IL-1β、IL-6、组抑素1、3、5和溶菌酶)。认知功能和生活质量也进行了类似的评估。另一组肝硬变患者在没有牙周治疗的情况下进行了相同的持续时间的随访。肝硬变患者，尤其是肝性脑病患者，在牙周治疗后，大便和唾液的生物失调得到改善，内毒素、LBP、唾液和血清炎症介质得到改善。这些参数在基线时在HE中较高，在治疗后在统计学上变得相似。口服干预后，HE患者治疗前和治疗后的生活质量和认知能力也得到了改善。从另一方面来说。在没有接受治疗的肝硬变患者中，LBP和内毒素随着时间的推移而增加，但在没有接受治疗的组中，其余的参数，包括微生物区系，随着时间的推移保持相似。这项概念验证研究表明，牙周治疗对肝硬变患者，特别是对肝硬变患者.与改善口腔和肠道菌群失调、全身炎症、MELD评分和认知功能有关，这在同期没有接受治疗的患者中没有观察到。新的和值得注意的系统性牙周治疗改善了肝硬变门诊患者的内毒素血症。以及全身和局部炎症，以及30天内调节的唾液和粪便微生物失调。这与既往有肝性脑病患者的生活质量和认知能力的改善有关。在没有接受牙周治疗的肝硬化组中，内毒素和脂多糖结合蛋白在相同的时间段内增加。口腔可能是肝硬变中一个重要的未明确的炎症来源。
Cirrhosis is associated with a systemic proinflammatory milieu, endotoxemia, and gut dysbiosis. The oral cavity could be an additional source of inflammation. We aimed to determine the effect of periodontal therapy in cirrhosis through evaluating endotoxemia, inflammation, cognition, and quality of life (QOL). Age-matched cirrhotic and noncirrhotic subjects exhibiting chronic gingivitis and/or mild or moderate periodontitis underwent periodontal therapy with follow-up at 30 days. Saliva/stool for microbial composition and serum for Model for End-stage Liver Disease (MELD) score, endotoxin and lipopolysaccharide binding protein (LBP) and immune-inflammatory markers (IL-1 beta; IL-6; histatins 1, 3, 5; and lysozyme) were collected at baseline and day 30. The cognitive function and QOL were also evaluated similarly. A separate group of cirrhotic patients were followed for the same duration without periodontal therapy. Cirrhotics, especially those with hepatic encephalopathy (HE), demonstrated improved dysbiosis in stool and saliva, and improved endotoxin, LBP, and salivary and serum inflammatory mediators following periodontal therapy. These parameters, which were higher in HE at baseline, became statistically similar posttherapy. Pretherapy vs. posttherapy QOL and cognition also improved in HE patients following oral interventions. On the other hand. LBP and endotoxin increased over time in cirrhotic patients not receiving therapy, but the rest of the parameters, including microbiota remained similar over time in the no-therapy group. This proof-of-concept study demonstrates that periodontal therapy in cirrhosis, especially in those with HE. is associated with improved oral and gut dysbiosis, systemic inflammation, MELD score, and cognitive function, which was not observed in those who did not receive therapy over the same time period.NEW & NOTEWORTHY Systematic periodontal therapy in cirrhotic outpatients improved endotoxemia. as well as systemic and local inflammation, and modulated salivary and stool microbial dysbiosis over 30 days. This was associated with improved quality of life and cognition in patients with prior hepatic encephalopathy. In a cirrhotic group that was not provided periodontal therapy, there was an increase in endotoxin and lipopolysaccharide binding protein in the same duration. The oral cavity could be an important underdefined source of inflammation in cirrhosis.