Correlation between Detection Rates of Periodontopathic Bacterial DNA in Coronary Stenotic Artery Plaque and in Dental Plaque Samples

Ishihara, Kazuyuki; Nabuchi, Akihiro; Ito, Rieko; Miyachi, Kouji; Kuramitsu, Howard K.; Okuda, K

doi:10.1128/jcm.42.11.5437.2004

Cited by 26 publications

(40 citation statements)

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“…The link found in this study supports the concept that there may be a true inflammatory link between atherogenesis and periodontitis. The data of this study were consistent with those reported by Haraszthy et al 12 (PCR-amplified 16S rDNA and DNA species-specific probes, 30% positive for T. forsythia, 26% for P.gingivalis, 14% for P. intermedia), Ishiara et al 13 (PCR-amplified 16S rRNA, 21.6% positive for P. gingivalis, 5.9% for T. forsythia) and ZHANG Y M et al 14 Periodontal patients harboring Porphyromonas gingivalis have shown higher levels of lipids, low-density lipoprotein and total cholesterol in the bloodstream, which seem to be associated with the development of atheromatous plaques. On the other hand, the high prevalence of Gram-negative oral bacteria in atherosclerotic tissues may induce the secretion of several cytokines associated with the development of cardiovascular diseases by their LPS.…”

Section: Discussionsupporting

confidence: 92%

Porphyromonas Gingivalis in Coronary Atheroma and Subgingival Plaque – A Clinical and Microbiological Study

Rath¹,

Sen²,

Gupta³

et al. 2014

jemds

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: BACKGROUND:There has been increasing attention paid in recent years to the possibility that oral bacterial infection, particularly periodontal disease may influence the initiation and or progression of systemic diseases. These studies confirm the observation that heart disease is the most commonly found systemic condition in patients with periodontal disease. Moreover, the literature has also highlighted substantial evidence indicating the presence of gram negative periodontal pathogens in atheromatous plaques. AIMS : The present study intends to investigate the possible association between periodontal health and coronary artery disease by evaluating periodontal status, association between the periodontal plaque and coronary atheromatous plaques for presence of P.gingivalis. SETTINGS AND DESIGN: A case control study was designed with 07 patients who had underwent coronary endarterectomy for CVD and 28 controls . The periodontal examination for cases was performed one day before vascular surgery and the controls were clinically examined. METHODS AND MATERIAL : The atheromatous plaque sample collected during endarterectomy and the Intraoral plaque samples were subjected to PCR for identification of P.gingivalis. The presence of periodontal bacteria DNA in coronary atheromatous plaques and subgingival plaque samples of the same patients was confirmed by this study. STATISTICAL ANALYSIS USED : Means and proportions for personal characters, major risk factors and clinical parameters were calculated for both the groups. The significance of any difference in means was tested by using "Students t test", and the significance of any difference in proportions was tested by using Dunn-Sidak Adjusted p Value. RESULTS : During the microbial analysis of plaque samples by PCR in group A it was seen that Porphyromonas gingivalis in 100 % of the samples.

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Section: Discussionsupporting

confidence: 92%

Porphyromonas Gingivalis in Coronary Atheroma and Subgingival Plaque – A Clinical and Microbiological Study

Rath¹,

Sen²,

Gupta³

et al. 2014

jemds

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“…Similarly to the gut, the oral cavity is colonized by a wide variety and number of microorganisms, including commensal, opportunistic, and pathogenic species (about 1 ϫ 10 8 to 1 ϫ 10 9 bacteria/mg of plaque) (66). Growing evidence suggests that periodontal pathogens, including F. nucleatum and P. gingivalis, or their products can not only cause local inflammation at the oral cavity but also appear to emerge systemically and enhance inflammatory responses associated with conditions such as atherosclerosis, preterm birth, and diabetes (13,21,37,47,52). A high prevalence of oral opportunistic infections, including severe forms of periodontal disease in HIV-1 ϩ patients, has been demonstrated widely (18,48).…”

Section: Discussionmentioning

confidence: 99%

HIV-1 Reactivation Induced by the Periodontal Pathogens Fusobacterium nucleatum and Porphyromonas gingivalis Involves Toll-Like Receptor 4 and 9 Activation in Monocytes/Macrophages

González

Ebersole

et al. 2010

Clin Vaccine Immunol

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Although oral coinfections (e.g., periodontal disease) are highly prevalent in human immunodeficiency virus type 1-positive (HIV-1 ؉ ) patients and appear to positively correlate with viral load levels, the potential for oral bacteria to induce HIV-1 reactivation in latently infected cells has received little attention. We showed that HIV-1 long terminal repeat (LTR) promoter activation can be induced by periodontopathogens in monocytes/ macrophages; nevertheless, the mechanisms involved in this response remain undetermined. Since Toll-like receptor 2 (TLR2), TLR4, and TLR9 activation have been involved in HIV-1 recrudescence, we sought to determine the role of these TLRs in HIV-1 reactivation induced by the periodontal pathogens Fusobacterium nucleatum and Porphyromonas gingivalis using BF24 monocytes/macrophages stably transfected with the HIV-1 promoter driving chloramphenicol acetyltransferase (CAT) expression and THP89GFP cells, a model of HIV-1 latency. We demonstrated that TLR9 activation by F. nucleatum and TLR2 activation by both bacteria appear to be involved in HIV-1 reactivation; however, TLR4 activation had no effect. Moreover, the autocrine activity of tumor necrosis factor alpha (TNF-␣) but not interleukin-1␤ (IL-1␤) produced in response to bacteria could impact viral reactivation. The transcription factors NF-B and Sp1 appear to be positively regulating HIV-1 reactivation induced by these oral pathogens. These results suggest that oral Gram-negative bacteria (F. nucleatum and P. gingivalis) associated with oral and systemic chronic inflammatory disorders enhance HIV-1 reactivation in monocytes/macrophages through TLR2 and TLR9 activation in a mechanism that appears to be transcriptionally regulated. Increased bacterial growth and emergence of these bacteria or their products accompanying chronic oral inflammatory diseases could be risk modifiers for viral replication, systemic immune activation, and AIDS progression in HIV-1 ؉ patients.

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“…The accumulation of clinical and experimental evidence also suggests that periodontal infection may be a contributing risk factor for heart disease (27,31,34,50,51). For example, the occurrence of P. gingivalis in subgingival sites correlates with the detection of P. gingivalis in coronary artery plaque samples (25). A correlation between high levels of antibody to P. gingivalis and prevalence of coronary heart disease has also been observed (50,51).…”

mentioning

confidence: 87%

Hemagglutinin B Is Involved in the Adherence of Porphyromonas gingivalis to Human Coronary Artery Endothelial Cells

et al. 2005

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Porphyromonas gingivalis is a periodontopathogen that may play a role in cardiovascular diseases. Hemagglutinins may function as adhesins and are required for virulence of several bacterial pathogens. The aim of this study was to determine the role of hemagglutinin B (HagB) in adherence of P. gingivalis to human coronary artery endothelial (HCAE) cells. P. gingivalis strain 381, a P. gingivalis 381 HagB mutant, Escherichia coli JM109 expressing HagB (E. coli-HagB), and E. coli JM109 containing pUC9 (E. coli-pUC9) were tested for their ability to attach to HCAE cells. Inhibition assays were performed to determine the ability of purified recombinant HagB (rHagB) as well as antibodies to HagB, including the polyclonal antibody (PAb) A7985 and the monoclonal antibody (MAb) HL1858, to inhibit the attachment of P. gingivalis to HCAE cells. As expected, when the attachment of P. gingivalis and the HagB mutant were compared, no statistical significance was observed between the two groups (P ‫؍‬ 0.331), likely due to the expression of the hagB homolog hagC. However, E. coli-HagB adhered significantly better to HCAE cells than did E. coli-pUC9, the control strain. In a competition assay, the presence of purified rHagB decreased bacterial adhesion of P. gingivalis or E. coli-HagB to HCAE cells. The presence of PAb A7985 or MAb HL1858 also significantly decreased attachment of P. gingivalis and E. coli-HagB to host cells. These results indicate that HagB is involved in the adherence of P. gingivalis to human primary endothelial cells.

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Correlation between Detection Rates of Periodontopathic Bacterial DNA in Coronary Stenotic Artery Plaque and in Dental Plaque Samples

Cited by 26 publications

References 0 publications

Porphyromonas Gingivalis in Coronary Atheroma and Subgingival Plaque – A Clinical and Microbiological Study

Porphyromonas Gingivalis in Coronary Atheroma and Subgingival Plaque – A Clinical and Microbiological Study

HIV-1 Reactivation Induced by the Periodontal Pathogens Fusobacterium nucleatum and Porphyromonas gingivalis Involves Toll-Like Receptor 4 and 9 Activation in Monocytes/Macrophages

Hemagglutinin B Is Involved in the Adherence of Porphyromonas gingivalis to Human Coronary Artery Endothelial Cells

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