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本文引用的文献

1
Tobacco and gingivitis.
J Dent Res. 1947 Jun;26(3):261: passim.
2
Do periodontopathogens disappear after full-mouth tooth extraction?牙周致病菌在全口拔牙后会消失吗?
J Clin Periodontol. 2009 Dec;36(12):1043-7. doi: 10.1111/j.1600-051X.2009.01477.x.
3
The influence of tobacco smoking on the onset of periodontitis in young persons.吸烟对年轻人牙周炎发病的影响。
Tob Induc Dis. 2004 Jun 15;2(2):53-65. doi: 10.1186/1617-9625-2-2-53.
4
Role of pathogenic oral flora in postoperative pneumonia following brain surgery.致病性口腔菌群在脑外科手术后肺炎中的作用。
BMC Infect Dis. 2009 Jun 29;9:104. doi: 10.1186/1471-2334-9-104.
5
The structurally similar, penta-acylated lipopolysaccharides of Porphyromonas gingivalis and Bacteroides elicit strikingly different innate immune responses.牙龈卟啉单胞菌和拟杆菌结构相似的五酰化脂多糖引发截然不同的天然免疫反应。
Microb Pathog. 2009 Aug;47(2):68-77. doi: 10.1016/j.micpath.2009.04.015. Epub 2009 May 19.
6
The effect of a supragingival plaque-control regimen on the subgingival microbiota in smokers and never-smokers: evaluation by real-time polymerase chain reaction.龈上菌斑控制方案对吸烟者和非吸烟者龈下微生物群的影响:通过实时聚合酶链反应进行评估。
J Periodontol. 2008 Dec;79(12):2297-304. doi: 10.1902/jop.2008.070558.
7
Progression of periodontal disease in a maintenance population of smokers and non-smokers: a 3-year longitudinal study.吸烟者和非吸烟者维持期人群牙周疾病的进展:一项为期3年的纵向研究。
J Periodontol. 2008 Mar;79(3):461-8. doi: 10.1902/jop.2008.070296.
8
Detection of Treponema denticola in saliva obtained from patients with various periodontal conditions.在患有各种牙周疾病的患者的唾液中检测具核梭杆菌。
Clin Oral Investig. 2008 Mar;12(1):73-81. doi: 10.1007/s00784-007-0147-7. Epub 2007 Sep 7.
9
Chemical structure and immunobiological activity of Porphyromonas gingivalis lipid A.牙龈卟啉单胞菌脂多糖的化学结构与免疫生物学活性
Front Biosci. 2007 May 1;12:3795-812. doi: 10.2741/2353.
10
The impact of cigarette smoking on periodontal disease and treatment.吸烟对牙周疾病及治疗的影响。
Periodontol 2000. 2007;44:178-94. doi: 10.1111/j.1600-0757.2007.00212.x.

慢性牙周炎吸烟者的脂肪酸谱。

Fatty acid profiles in smokers with chronic periodontitis.

机构信息

Department of Periodontology, School of Dentistry, Ege University, İzmir, Turkey.

出版信息

J Dent Res. 2011 Jan;90(1):47-52. doi: 10.1177/0022034510380695. Epub 2010 Nov 1.

DOI:10.1177/0022034510380695
PMID:21041552
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3144094/
Abstract

We hypothesized that tobacco smoke induces alterations to the 3-OH fatty acids present in lipid A in a manner consistent with a microflora of reduced inflammatory potential. Whole saliva samples and full-mouth clinical periodontal recordings were obtained from persons with (22 smokers; 15 non-smokers) and without (14 smokers; 15 non-smokers) chronic periodontitis. Clear differences in the contributions of multiple saturated 3-OH fatty acid species were noted in the group with disease compared with healthy individuals. Increases in the long-chain fatty acids associated with anaerobic bacterial periodontopathogens, particularly 3-OH-C(i17.0) (146.7%, relative to controls), were apparent. Significant reductions in the 3-OH fatty acids associated with the consensus (high potency) enteric LPS structure (3-OH-C(12.0) and 3-OH-C(14.0); 33.3% and 15.8% reduction, respectively) were noted in smokers compared with non-smokers with chronic periodontitis. Thus, smoking is associated with specific structural alterations to the lipid-A-derived 3-OH fatty acid profile in saliva that are consistent with an oral microflora of reduced inflammatory potential. These findings provide much-needed mechanistic insight into the established clinical conundrum of increased infection with periodontal pathogens but reduced clinical inflammation in smokers.

摘要

我们假设烟草烟雾以一种与炎症潜能降低的微生物群一致的方式诱导脂质 A 中 3-OH 脂肪酸的改变。从患有(22 名吸烟者;15 名非吸烟者)和不患有(14 名吸烟者;15 名非吸烟者)慢性牙周炎的人获得全唾液样本和全口临床牙周记录。与健康个体相比,在患有疾病的组中注意到多种饱和 3-OH 脂肪酸种类的贡献存在明显差异。与厌氧细菌牙周病原体相关的长链脂肪酸增加,特别是 3-OH-C(i17.0)(相对于对照组增加 146.7%)。与共识(高效力)肠内 LPS 结构相关的 3-OH 脂肪酸(3-OH-C(12.0)和 3-OH-C(14.0);分别减少 33.3%和 15.8%)在患有慢性牙周炎的吸烟者中与非吸烟者相比显著减少。因此,吸烟与唾液中脂质 A 衍生的 3-OH 脂肪酸谱的特定结构改变有关,这些改变与炎症潜能降低的口腔微生物群一致。这些发现为吸烟者牙周病病原体感染增加但临床炎症减少的既定临床难题提供了急需的机制见解。