Periodontitis and cardiovascular diseases: The link and relevant mechanisms

被引:8
作者
Izumi, Yuichi [1 ,2 ]
Nagasawa, Toshiyuki [3 ]
Umeda, Makoto [1 ]
Kobayashi, Hiroaki [1 ]
Takeuchi, Yasuo [1 ]
Yashiro, Reiko [1 ]
Hormdee, Doosadee [4 ]
Suda, Tomonari [1 ]
Ushida, Yuka [1 ]
Wara-aswapati, Nawarat [4 ]
机构
[1] Tokyo Med & Dent Univ, Grad Sch, Dept Hard Tissue Engn, Sect Periodontol,Bunkyo Ku, 1-5-45 Yushima, Tokyo 1138549, Japan
[2] Tokyo Med & Dent Univ, Int Res Ctr Mol Sci Tooth & Bone Dis, GCOE Program, Tokyo, Japan
[3] Hlth Sci Univ Hokkaido, Dept Periodontol & Endodontol, Div Oral Maxiollofacial Rehabil, Tobetsu, Hokkaido, Japan
[4] Khon Kaen Univ, Fac Dent, Dept Periodontol, Khon Kaen, Thailand
基金
日本学术振兴会;
关键词
Periodontitis; Cardiovascular diseases; Atherosclerosis; Buerger's disease; Periodontal treatment;
D O I
10.1016/j.jdsr.2009.06.001
中图分类号
R78 [口腔科学];
学科分类号
1003 ;
摘要
This paper reviews the association between periodontitis and CVD. In addition, the potential mechanisms of any association between periodontitis and CVD as well as the effects of periodontal treatment on CVD are herein discussed. Among the studies carried out by this group and others on coronary artery diseases, peripheral arterial diseases, abdominal aortic aneurysm, and Buerger's disease, periodontopathic bacteria were frequently detected in the diseased blood vessels, thus suggesting an association between periodontitis and CVD. The potential mechanisms of the association between periodontitis and CVD are not fully elucidated. However, inflammation and some autoimmune mechanisms, including molecular mimicry between the periodontopathic bacteria and host molecules, are suggested. The effects of periodontal treatment on CVD might thus vary among the different treatment modalities, and full-mouth mechanical debridement might induce strong transient systemic inflammatory responses in comparison to the quadrant-wise mechanical debridement. (C) 2009 Japanese Association for Dental Science. Published by Elsevier Ireland. All rights reserved.
引用
收藏
页码:98 / 108
页数:11
相关论文
共 92 条
[1]   CELLULAR-SENSITIVITY TO COLLAGEN IN THROMBOANGIITIS OBLITERANS [J].
ADAR, R ;
PAPA, MZ ;
HALPERN, Z ;
MOZES, M ;
SHOSHAN, S ;
SOFER, B ;
ZINGER, H ;
DAYAN, M ;
MOZES, E .
NEW ENGLAND JOURNAL OF MEDICINE, 1983, 308 (19) :1113-1116
[2]   Thrombo-angiitis obliterans: A clinical study of 200 cases I Etiology, pathology, symptoms, diagnosis [J].
Allen, EV .
ANNALS OF INTERNAL MEDICINE, 1928, 1 (08) :535-549
[3]   The effect of novel cardiovascular risk factors on the ethnic-specific odds for peripheral arterial disease in the Multi-ethnic Study of Atherosclerosis (MESA) [J].
Allison, Matthew A. ;
Criqui, Michael H. ;
McClelland, Robyn L. ;
Scott, JoAnn M. ;
McDermott, Mary M. ;
Liu, Kiang ;
Folsom, Aaron R. ;
Bertoni, Alain G. ;
Sharrett, A. Richey ;
Homma, Shunichi ;
Kori, Sujata .
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 2006, 48 (06) :1190-1197
[4]   Chronic infections and atherosclerosis [J].
Ayada, Kiyoshi ;
Yokata, Kenji ;
Kobayashi, Kazuko ;
Shoenfeld, Yehuda ;
Matsuura, Eiji ;
Oguma, Keiji .
AUTOIMMUNITY, PT D: AUTOIMMUNE DISEASE, ANNUS MIRABILIS, 2007, 1108 :594-602
[5]   The prevalence and incidence of coronary heart disease is significantly increased in periodontitis: A meta-analysis [J].
Bahekar, Amol Ashok ;
Singh, Sarabjeet ;
Saha, Sandeep ;
Molnar, Janos ;
Arora, Rohit .
AMERICAN HEART JOURNAL, 2007, 154 (05) :830-837
[6]   STAPHYLOCOCCUS-AUREUS INDUCES PLATELET-AGGREGATION VIA A FIBRINOGEN-DEPENDENT MECHANISM WHICH IS INDEPENDENT OF PRINCIPAL PLATELET GLYCOPROTEIN IIB/IIIA FIBRINOGEN-BINDING DOMAINS [J].
BAYER, AS ;
SULLAM, PM ;
RAMOS, M ;
LI, C ;
CHEUNG, AL ;
YEAMAN, MR .
INFECTION AND IMMUNITY, 1995, 63 (09) :3634-3641
[7]   Periodontal disease and cardiovascular disease [J].
Beck, J ;
Garcia, R ;
Heiss, G ;
Vokonas, PS ;
Offenbacher, S .
JOURNAL OF PERIODONTOLOGY, 1996, 67 (10) :1123-1137
[8]  
Beck J D, 1998, J Dent Educ, V62, P859
[9]   Bacterial induction of autoantibodies to β2-glycoprotein-I accounts for the infectious etiology of antiphospholipid syndrome [J].
Blank, M ;
Krause, I ;
Fridkin, M ;
Keller, N ;
Kopolovic, J ;
Goldberg, I ;
Tobar, A ;
Shoenfeld, Y .
JOURNAL OF CLINICAL INVESTIGATION, 2002, 109 (06) :797-804
[10]  
Blank M, 2007, CLIN REV ALLERG IMMU, V32, P111