L. Lakio, M. Lehto, Anita M. Tuomainen, M. Jauhiainen, E. Malle, S. Asikainen, P. Pussinen
{"title":"Pro-atherogenic properties of lipopolysaccharide from the periodontal pathogen Actinobacillus actinomycetemcomitans","authors":"L. Lakio, M. Lehto, Anita M. Tuomainen, M. Jauhiainen, E. Malle, S. Asikainen, P. Pussinen","doi":"10.1177/09680519060120010601","DOIUrl":null,"url":null,"abstract":"Periodontitis is a common bacterial infection that affects tooth-supporting tissues and may eventually lead to tooth loss. The number and proportion of Gram-negative bacteria are extensively elevated in the pathologically deepened inflamed periodontal pockets.1 Chronic infections (e.g. periodontitis) have been linked to an increased risk for atherosclerosis,2 a progressive disease characterized by the accumulation of lipids and fibrous elements in the large arteries. The mechanisms behind the association between periodontitis and atherosclerosis are largely unknown, but may include bacteria-derived activation of inflammatory reactions systemically and in the arterial wall, enhanced cytokine production, low-density lipoprotein (LDL) modifications, lipoprotein-derived cholesterol/cholesteryl ester (CE) enrichment of macrophages,3 and adverse alterations in the lipoprotein profile resulting in decreased levels of anti-atherogenic, high-density lipoprotein (HDL).4 Periodontitis further causes changes in the activities of HDL conversion factors, which is paralleled by alterations in HDL composition and subclass distribution leading to an","PeriodicalId":80292,"journal":{"name":"Journal of endotoxin research","volume":"12 1","pages":"57 - 64"},"PeriodicalIF":0.0000,"publicationDate":"2006-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/09680519060120010601","citationCount":"9","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of endotoxin research","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1177/09680519060120010601","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 9
Abstract
Periodontitis is a common bacterial infection that affects tooth-supporting tissues and may eventually lead to tooth loss. The number and proportion of Gram-negative bacteria are extensively elevated in the pathologically deepened inflamed periodontal pockets.1 Chronic infections (e.g. periodontitis) have been linked to an increased risk for atherosclerosis,2 a progressive disease characterized by the accumulation of lipids and fibrous elements in the large arteries. The mechanisms behind the association between periodontitis and atherosclerosis are largely unknown, but may include bacteria-derived activation of inflammatory reactions systemically and in the arterial wall, enhanced cytokine production, low-density lipoprotein (LDL) modifications, lipoprotein-derived cholesterol/cholesteryl ester (CE) enrichment of macrophages,3 and adverse alterations in the lipoprotein profile resulting in decreased levels of anti-atherogenic, high-density lipoprotein (HDL).4 Periodontitis further causes changes in the activities of HDL conversion factors, which is paralleled by alterations in HDL composition and subclass distribution leading to an