| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
1 Institute of Dentistry, University of Helsinki, and Department of Oral and Maxillofacial Diseases, Helsinki University Central Hospital, PB 41, FIN-00014 Helsinki, Finland; 2 Faculty of Odontology, Complutense University, Ciudad Universitaria, E-28040 Madrid, Spain; and 3 Boston University Goldman School of Dental Medicine and 4 Harvard School of Public Health, Boston, MA 02215-1204, USA;
* corresponding author, jukka.meurman{at}helsinki.fi
During the last two decades, there has been an increasing interest in the impact of oral health on atherosclerosis and subsequent cardiovascular disease (CVD). The advent of the inflammation paradigm in coronary pathogenesis stimulated research in chronic infections caused by a variety of micro-organisms—such as Chlamydia pneumoniae, Helicobacter pylori, and cytomegalovirus—as well as dental pathogens, since these chronic infections are thought to be involved in the etiopathogenesis of CVD by releasing cytokines and other pro-inflammatory mediators (e.g., C-reactive protein [CRP], tumor necrosis factor [TNF-
]) that may initiate a cascade of biochemical reactions and cause endothelial damage and facilitate cholesterol plaque attachment. Yet, due to the multi-factorial nature of dental infection and CVD, confirming a causal association is difficult, and the published results are conflicting. The main deficit in the majority of these studies has been the inadequate control of numerous confounding factors, leading to an overestimation and the imprecise measurement of the predictor or overadjustment of the confounding variables, resulting in underestimation of the risks. A meta-analysis of prospective and retrospective follow-up studies has shown that periodontal disease may increase the risk of CVD by approximately 20% (95% confidence interval [CI], 1.08–1.32). Similarly, the reported risk ratio between periodontal disease and stroke is even stronger, varying from 2.85 (CI 1.78–4.56) to 1.74 (CI 1.08–2.81). The association between peripheral vascular disease and oral health parameters has been explored in only two studies, and the resultant relative risks among individuals with periodontitis were 1.41 (CI 1.12–1.77) and 2.27 (CI 1.32–3.90), respectively. Overall, it appears that periodontal disease may indeed contribute to the pathogenesis of cardiovascular disease, although the statistical effect size is small.
Key words. Oral health, periodontitis, atherosclerosis, coronary heart disease, stroke, peripheral vascular disease
This article has been cited by other articles:
|
|
 |
|
  F. Ghannad, D. Nica, M. I. Garcia Fulle, D. Grenier, E. E. Putnins, S. Johnston, A. Eslami, L. Koivisto, G. Jiang, M. D. McKee, et al. Absence of {alpha}v{beta}6 Integrin Is Linked to Initiation and Progression of Periodontal Disease Am. J. Pathol., May 1, 2008; 172(5): 1271 - 1286. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. T. Demmer and M. Desvarieux Periodontal infections and cardiovascular disease: The heart of the matter J Am Dent Assoc, October 1, 2006; 137(suppl_2): 14S - 20S. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 E. Harokopakis, M. H. Albzreh, M. H. Martin, and G. Hajishengallis TLR2 Transmodulates Monocyte Adhesion and Transmigration via Rac1- and PI3K-Mediated Inside-Out Signaling in Response to Porphyromonas gingivalis Fimbriae. J. Immunol., June 15, 2006; 176(12): 7645 - 7656. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. Aduse-Opoku, J. M. Slaney, A. Hashim, A. Gallagher, R. P. Gallagher, M. Rangarajan, K. Boutaga, M. L. Laine, A. J. Van Winkelhoff, and M. A. Curtis Identification and Characterization of the Capsular Polysaccharide (K-Antigen) Locus of Porphyromonas gingivalis Infect. Immun., January 1, 2006; 74(1): 449 - 460. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| IADR Journals | Advances in Dental Research ® | Journal of Dental Research ® | Critical Reviews (1990-2004) |
