Department of Cardiology, University of Marseille, Hôpital Nord, Marseille, France. nicolas.amabile@mail.ap-hm.fr

BACKGROUND: Periodontal disease (PD) has been recognized as a risk factor for systemic diseases, but its involvement in the pathogenesis of coronary artery disease (CAD) remains debated. OBJECTIVES: We sought to evaluate the potential relations between severity of the PD, inflammatory response and angiographic lesions extent in patients with stable CAD. DESIGN: A total of 131 subjects referred to our centre for coronary angiography were evaluated for presence and extension of CAD, then divided into two groups, one with presence of lesions (cases, n = 85) and other one with absence of lesions (controls, n = 46). Mean periodontal pocket depth (PPkD), high sensitivity C reactive protein (hs-CRP), serum amyloid A protein (SAA) and fibrinogen levels were measured in all patients. RESULTS: Cases and controls did not differ according to their baseline characteristics and prevalence of traditional cardiovascular risk factors. PPkD was greater in patients with CAD than in controls (2.24 +/- 1.28 mm vs 1.50 +/- 0.93 mm, P < 0.001 by Student's t-test). Systemic inflammatory response was more pronounced in cases than in controls, with higher values of hs-CRP, SAA and fibrinogen. Furthermore, PPkD values correlated with hs-CRP (r = 0.80, P < 0.001), SAA (r = 0.71, P < 0.001), fibrinogen levels (r = 0.72, P < 0.001) and the American College of Cardiology/American Heart Association angiographic score (r = 0.68, P < 0.001) in cases. Multivariate analysis indicated a persistent independent correlation between PPkD and angiographic score after adjustment for inflammatory markers levels. CONCLUSION: In the present study, PD lesions predicted presence of CAD stenosis in patients with cardiovascular risk factors. PD severity was correlated to angiographic extent of coronary lesions, independent of systemic inflammatory status. Those results suggest that these patients might benefit from an intensive periodontal therapy to prevent CAD progression.

J Intern Med. 2008 Jun;263(6):644-52. Epub 2008 Jan 16.

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Dipartimento di Scienze Stomatologiche G. Messina, Università, Palermo.

The present paper reviews relationship between chronic periodontitis and cardiovascular diseases. Original papers on this subject, published in English in the period between 2001 and the first semester 2006, were located in the MEDLINE/PubMed database. Additional studies were obtained by searching reference lists of previously published papers. Periodontal infection provides a chronic reservoir of inflammatory mediators and cytokines, lipopolysaccharide, which contribute to the formation of atheroma. Moreover, periodontal pathogens can penetrate the epithelial barrier of the periodontal tissues and reach the blood stream, carrying out a local atherogenic activity. Some studies indicated that periodontal treatment could result in reduction of cardiovascular events. If these results are confirmed in further intervention studies, the prevention and the treatment of periodontitis should be considered as factors able to avoid or reduced the onset and/or evolution of cardiovascular diseases.

Recenti Prog Med. 2007 Jul-Aug;98(7-8):426-32.

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Department of Dental Ecology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA. james_beck@unc.edu

BACKGROUND: During the last 15 years, a substantial number of population-based, clinical, laboratory, and animal studies have been published that reported findings on the relationship between periodontal disease and cardiovascular disease. The Periodontitis and Vascular Events (PAVE) pilot study was conducted to investigate the feasibility of a randomized secondary prevention trial to test whether treatment of periodontal disease reduces the risk for cardiovascular disease. This article describes the occurrence of adverse events during the pilot study. METHODS: The PAVE pilot study was a multicenter, randomized trial comparing periodontal therapy to community dental care. Baseline and follow-up clinic visits included a periodontal examination; blood, subgingival plaque, and crevicular fluid specimen collection; and medical and dental histories. Telephone follow-up contacts were scheduled to occur 3 months after randomization and every 6 months thereafter to assess adverse events or endpoints. RESULTS: Cardiovascular adverse events occurred with similar frequency (23 versus 24 [P = 0.85] in the community control and the treatment groups, respectively). There were 15 serious adverse events (SAEs) with a non-significantly higher percentage occurring in the community care group (6.6% versus 3.3%; P = 0.19). A time-to-event analysis of patterns of SAEs indicated that subjects in the periodontal therapy group tended to be less likely to experience an SAE over the entire 25 months of the study. CONCLUSION: For those individuals who remained in the study, it appears that provision of periodontal scaling and root planing treatment to individuals with heart disease resulted in a similar pattern of adverse events as seen in the community care group, which also received some treatment.

J Periodontol. 2008 Jan;79(1):90-6.

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Department of Stomatology, First Affiliated Hospital, Xinjiang Medical University, Urümqi 830054, China.

OBJECTIVE: To explore the possible correlation between coronary heart disease and periodontitis. METHODS: Subgingival plaque samples and coronary atherosclerotic plaques were harvested from a total of 31 patients with periodontitis who scheduled for coronary artery bypass surgery. The bacteria DNA was obtained from subgingival plaque samples and coronary atherosclerotic plaques using the chelex-100 method. The extracted DNA was examined using the polymerase chain reaction (PCR) technique. RESULTS: In coronary atherosclerotic plaques samples from the 31 patients, Porphyromonas gingivalis (Pg, 38.7%), Actinobacillus actinomycetemcomitans (Aa, 0%), Fusobacterium nucleatum (Fn, 22.6%), Prevotella intermedia (Pi, 12.9%), Bacteroides forsythus (Bf, 38.7%) were detected. The concordant presence of the same periodontal bacteria DNA in subgingival plaques and in coronary atherosclerotic plaques in the same patient was Pg 5 (16.1%), Aa 0 (0%), Pi 2 (6.5%), Fn 4 (12.9%) and Bf 8 (25.8%). CONCLUSIONS: The presence of periodontal bacteria DNA in coronary atherosclerotic plaques could indicate that periodontal pathogenic bacteria may play a role in the coronary heart disease process.

Zhonghua Kou Qiang Yi Xue Za Zhi. 2008 Jan;43(1):4-7.

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Department of Medicine, Helsinki University Central Hospital, Helsinki, Finland.

Periodontitis and coronary artery disease (CAD) are inflammatory diseases and associated with each other. The major histocompatibility complex (MHC) region carries genes involved in immune response and inflammation. We investigated whether the MHC genes correlate with the presence of periodontitis or with the occurrence of periodontal pathogens in patients with CAD. Blood and saliva samples from CAD patients (n = 106) were collected at the time of hospitalization. Nine MHC genetic markers [human leukocyte antigen (HLA)-A, HLA-B, HLA-DRB1, lymphotoxin alpha (LTA) +253(a/g), +496(C/T), +633(c/g), +724(C/A), C4A and C4] were typed. Based on panoramic tomography, patients were categorized into nonperiodontitis and periodontitis groups. Two major periodontal pathogens, Aggregatibacter (Actinobacillus) actinomycetemcomitans and Porphyromonas gingivalis, were cultivated and polymerase chain reaction-amplified from salivary samples.

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Clin Microbiol Rev. 2000 October; 13(4): 547–558.
 PMCID: PMC88948
 
Systemic Diseases Caused by Oral Infection

Xiaojing Li,1* Kristin M. Kolltveit,1 Leif Tronstad,2 and Ingar Olsen1

Recently, it has been recognized that oral infection, especially periodontitis, may affect the course and pathogenesis of a number of systemic diseases, such as cardiovascular disease, bacterial pneumonia, diabetes mellitus, and low birth weight. The purpose of this review is to evaluate the current status of oral infections, especially periodontitis, as a causal factor for systemic diseases. Three mechanisms or pathways linking oral infections to secondary systemic effects have been proposed: (i) metastatic spread of infection from the oral cavity as a result of transient bacteremia, (ii) metastatic injury from the effects of circulating oral microbial toxins, and (iii) metastatic inflammation caused by immunological injury induced by oral microorganisms. Periodontitis as a major oral infection may affect the host's susceptibility to systemic disease in three ways: by shared risk factors; subgingival biofilms acting as reservoirs of gram-negative bacteria; and the periodontium acting as a reservoir of inflammatory mediators. Proposed evidence and mechanisms of the above odontogenic systemic diseases are given.

Paraskevas S, Huizinga JD, Loos BG. A systematic review and meta-analyses on C-reactive protein in relation to periodontitis. J Clin Periodontol 2008; 35: 277–290. doi: 10.1111/j.1600-051X.2007.01173.x.

Abstract

Aim: Elevated plasma C-reactive protein (CRP) is regarded as a risk predictor for cardiovascular diseases. This systematic review explored the robustness of observations that CRP is elevated in periodontitis. Similarly, the effect of periodontal therapy on CRP levels was investigated.

Material and Methods: Selection of publications was based on: (1) cross-sectional (case–control) studies; (2) longitudinal (treatment) studies; (3) high-sensitivity CRP measurement; (4) median and/or mean (±SD) values presented; and (5) subjects with no systemic disorders.

Results: Screening of the initially 448 identified studies and reference checking resulted in 18 suitable papers. The majority of the studies showed that CRP levels are higher in patients than in controls. Often, studies showed that patients had CRP levels >2.1 mg/l. A meta-analysis of 10 cross-sectional studies showed that the weighted mean difference (WMD) of CRP between patients and controls was 1.56 mg/l (p<0.00001). Evidence from available treatment studies (n=6) showed lower levels of CRP after periodontal therapy. Eligible treatment studies in a meta-analysis demonstrated a WMD of reductions of CRP after therapy of 0.50 mg/L (95% CI 0.08–0.93) (p=0.02).

Conclusions: There is strong evidence from cross-sectional studies that plasma CRP in periodontitis is elevated compared with controls. There is modest evidence on the effect of periodontal therapy in lowering the levels of CRP.

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