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不对称二甲基精氨酸作为牙周炎与心血管疾病关联中的潜在介质:当前证据的系统评价

Asymmetric Dimethylarginine as a Potential Mediator in the Association between Periodontitis and Cardiovascular Disease: A Systematic Review of Current Evidence.

作者信息

Rapone Biagio, Inchingolo Francesco, Tartaglia Giulia Margherita, De Francesco Maurizio, Ferrara Elisabetta

机构信息

Interdisciplinary Department of Medicine, University of Bari, 70121 Bari, Italy.

School of Medicine, European University of Madrid, 28670 Madrid, Spain.

出版信息

Dent J (Basel). 2024 Sep 21;12(9):297. doi: 10.3390/dj12090297.

DOI:10.3390/dj12090297
PMID:39329863
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11431043/
Abstract

Periodontitis, a chronic inflammatory disease, has been associated with an elevated risk of cardiovascular disease (CVD). Asymmetric dimethylarginine (ADMA), an endogenous inhibitor of nitric oxide synthase, has emerged as a potential biomarker linking periodontitis, endothelial dysfunction, and CVD. This systematic review aimed to synthesize the existing evidence on the relationship between ADMA, periodontitis, and CVD, and to evaluate ADMA's potential as a biomarker for periodontal disease progression and its correlation with endothelial dysfunction. A comprehensive literature search was conducted in PubMed, Scopus, and Web of Science databases from their inception to March 2023. Observational and interventional studies assessing ADMA levels in patients with periodontitis and/or CVD were included. The methodological quality of the included studies was evaluated using the NIH Quality Assessment Tools. Due to the heterogeneity of the included studies, a qualitative synthesis was performed. Cross-sectional studies consistently demonstrated significantly elevated ADMA levels in patients with periodontitis and CVD compared to healthy controls. The prospective cohort study indicated that successful periodontal treatment was associated with a significant reduction in ADMA levels and concomitant improvement in endothelial function. The pilot cohort study reported a significant decrease in ADMA levels following periodontal therapy in patients with chronic kidney disease. However, the randomized controlled trials did not demonstrate significant alterations in ADMA levels or endothelial function subsequent to periodontal treatment in patients with periodontitis alone. : Periodontal treatment may effectively reduce ADMA levels and improve endothelial function, particularly in patients with comorbidities. These findings suggest that ADMA is a promising biomarker linking periodontitis, endothelial dysfunction, and CVD. However, the limitations of this study include the small number of studies, heterogeneity in the study designs, and a lack of long-term follow-up data. Further high-quality, longitudinal studies are required to confirm its clinical utility and elucidate the underlying mechanisms of these relationships. The integration of periodontal care into CVD prevention and management strategies warrants consideration, as it may contribute to mitigating the cardiovascular risk associated with periodontitis.

摘要

牙周炎是一种慢性炎症性疾病,与心血管疾病(CVD)风险升高有关。不对称二甲基精氨酸(ADMA)是一氧化氮合酶的内源性抑制剂,已成为连接牙周炎、内皮功能障碍和心血管疾病的潜在生物标志物。本系统评价旨在综合现有关于ADMA、牙周炎和心血管疾病之间关系的证据,并评估ADMA作为牙周疾病进展生物标志物的潜力及其与内皮功能障碍的相关性。从创刊至2023年3月,在PubMed、Scopus和Web of Science数据库中进行了全面的文献检索。纳入评估牙周炎和/或心血管疾病患者ADMA水平的观察性和干预性研究。使用美国国立卫生研究院质量评估工具评估纳入研究的方法学质量。由于纳入研究的异质性,进行了定性综合分析。横断面研究一致表明,与健康对照相比,牙周炎和心血管疾病患者的ADMA水平显著升高。前瞻性队列研究表明,成功的牙周治疗与ADMA水平显著降低及内皮功能随之改善有关。试点队列研究报告称,慢性肾病患者牙周治疗后ADMA水平显著下降。然而,随机对照试验并未证明单纯牙周炎患者牙周治疗后ADMA水平或内皮功能有显著变化。牙周治疗可能有效降低ADMA水平并改善内皮功能,尤其是在合并症患者中。这些发现表明,ADMA是连接牙周炎、内皮功能障碍和心血管疾病的有前景的生物标志物。然而,本研究的局限性包括研究数量少、研究设计异质性以及缺乏长期随访数据。需要进一步的高质量纵向研究来证实其临床效用并阐明这些关系的潜在机制。将牙周护理纳入心血管疾病预防和管理策略值得考虑,因为这可能有助于减轻与牙周炎相关的心血管风险。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bdad/11431043/7bd3562adacc/dentistry-12-00297-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bdad/11431043/7bd3562adacc/dentistry-12-00297-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bdad/11431043/7bd3562adacc/dentistry-12-00297-g001.jpg

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Int Endod J. 2023 Dec;56(12):1499-1516. doi: 10.1111/iej.13979. Epub 2023 Oct 3.
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