Locally Produced Anti‐Phosphorylcholine and Anti‐Oxidized Low‐Density Lipoprotein Antibodies in Gingival Crevicular Fluid from Aggressive Periodontitis Patients

Schenkein, Harvey A.; Berry, Collin R.; Burmeister, J. A.; Brooks, Carol N.; Best, Al M.; Tew, John G.

doi:10.1902/jop.2004.75.1.146

Cited by 27 publications

(31 citation statements)

References 29 publications

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“…For this reason, increases in the plasma level of small LDLs, such as those seen in our group of GAgP subjects, may be particularly atherogenic. This notion is consistent with increased plasma titers of antioxidized LDL antibodies found in subjects with periodontitis (66)(67)(68)(69).…”

Section: Discussionsupporting

confidence: 84%

Altered lipoprotein subclass distribution and PAF-AH activity in subjects with generalized aggressive periodontitis

Rufail

Schenkein

Barbour

et al. 2005

Journal of Lipid Research

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In this study, we examined whether the documented increase of plasma triglycerides in patients with generalized aggressive periodontitis (GAgP) is associated with changes in lipoprotein subclass distribution and/or LDL-associated platelet-activating factor acetylhydrolase (PAF-AH) activity. Lipoprotein subclasses were analyzed in whole plasma samples using nuclear magnetic resonance methods. Compared with subjects without periodontitis (NP subjects; n ‫؍‬ 12), GAgP subjects (n ‫؍‬ 12) had higher plasma levels of large, medium, and small VLDL (

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Section: Discussionsupporting

confidence: 84%

Altered lipoprotein subclass distribution and PAF-AH activity in subjects with generalized aggressive periodontitis

Rufail

Schenkein

Barbour

et al. 2005

Journal of Lipid Research

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“…Elevated anti-PC antibodies have been demonstrated in periodontitis patients compared to those with no attachment loss [30] and to those with less suppuration [52]. Studies also demonstrate recognition of PC moieties on oxidized LDL by serum and gingival crevicular fluid anti-PC antibodies [50], [53]. The other oxidized epitope displaying molecular mimicry with bacterial epitopes is cardiolipin, a phospholipid located in the inner leaflet of mitochondria and present also in OxLDL and bacteria.…”

Section: Discussionmentioning

confidence: 99%

Recognition of Porphyromonas gingivalis Gingipain Epitopes by Natural IgM Binding to Malondialdehyde Modified Low-Density Lipoprotein

et al. 2012

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Objective Increased risk for atherosclerosis is associated with infectious diseases including periodontitis. Natural IgM antibodies recognize pathogen-associated molecular patterns on bacteria, and oxidized lipid and protein epitopes on low-density lipoprotein (LDL) and apoptotic cells. We aimed to identify epitopes on periodontal pathogen Porphyromonas gingivalis recognized by natural IgM binding to malondialdehyde (MDA) modified LDL. Methods and Results Mouse monoclonal IgM (MDmAb) specific for MDA-LDL recognized epitopes on P. gingivalis on flow cytometry and chemiluminescence immunoassays. Immunization of C57BL/6 mice with P. gingivalis induced IgM, but not IgG, immune response to MDA-LDL and apoptotic cells. Immunization of LDLR −/− mice with P. gingivalis induced IgM, but not IgG, immune response to MDA-LDL and diminished aortic lipid deposition. On Western blot MDmAb bound to P. gingivalis fragments identified as arginine-specific gingipain (Rgp) by mass spectrometry. Recombinant domains of Rgp produced in E. coli were devoid of phosphocholine epitopes but contained epitopes recognized by MDmAb and human serum IgM. Serum IgM levels to P. gingivalis were associated with anti-MDA-LDL levels in humans. Conclusion Gingipain of P. gingivalis is recognized by natural IgM and shares molecular identity with epitopes on MDA-LDL. These findings suggest a role for natural antibodies in the pathogenesis of two related inflammatory diseases, atherosclerosis and periodontitis.

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“…Treatment effects were dependent on baseline LPS levels, with increases in HDL and LDL particle size following therapy. Using Periodontal pathogens express HSPs such as HSP-60 (GroEL) Lu & McBride 1994, Maeda et al 1994, Vayssier et al 1994, Anti-Porphyromonas gingivalis GroEL and anti-Fusobacterium nucleatum GroEL, elevated in periodontitis patients, stimulates inflammatory cytokine production as well as monocyte and endothelial cell activation Ueki et al 2002, Lee et al 2012 Elevated levels in periodontitis patients, cross-reacts with oxidized low-density lipoproteins (oxLDL) and oral bacteria Schenkein et al 1999Schenkein et al , 2001Schenkein et al , 2004 Anti-oxLDL Locally produced in gingiva, found in GCF Schenkein et al 2004, Cross-react with P. gingivalis Rgp protease Turunen et al 2012, Higher in serum of periodontitis patients, and in periodontitis patients with CVD Montebugnoli et al 2004, Monteiro et al 2009 similar methodologies, they found that HDL promoted the enhanced efflux of cholesterol from macrophages following therapy, especially in patients in which CRP levels were also reduced by periodontal treatment (Pussinen et al 2004a). Kallio (Kallio et al 2008) observed that in periodontitis patients, elevated serum LPS levels persisted following therapy and that LPS was associated with highly atherogenic lipids, including vLDL and intermediate density lipoproteins (IDL).…”

Section: Dyslipidemia Lipid Peroxidation and Inflammationmentioning

confidence: 99%

Inflammatory mechanisms linking periodontal diseases to cardiovascular diseases

Schenkein

Loos

2013

Journal of Periodontology

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Inflammatory mechanisms linking periodontal diseases to cardiovascular diseasesSchenkein HA, Loos BG. Inflammatory mechanisms linking periodontal diseases to cardiovascular diseases. AbstractAims: In this article, inflammatory mechanisms that link periodontal diseases to cardiovascular diseases are reviewed. Methods: This article is a literature review. Results: Studies in the literature implicate a number of possible mechanisms that could be responsible for increased inflammatory responses in atheromatous lesions due to periodontal infections. These include increased systemic levels of inflammatory mediators stimulated by bacteria and their products at sites distant from the oral cavity, elevated thrombotic and hemostatic markers that promote a prothrombotic state and inflammation, cross-reactive systemic antibodies that promote inflammation and interact with the atheroma, promotion of dyslipidemia with consequent increases in pro-inflammatory lipid classes and subclasses, and common genetic susceptibility factors present in both disease leading to increased inflammatory responses. Conclusions: Such mechanisms may be thought to act in concert to increase systemic inflammation in periodontal disease and to promote or exacerbate atherogenesis. However, proof that the increase in systemic inflammation attributable to periodontitis impacts inflammatory responses during atheroma development, thrombotic events or myocardial infarction or stroke is lacking.

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Locally Produced Anti‐Phosphorylcholine and Anti‐Oxidized Low‐Density Lipoprotein Antibodies in Gingival Crevicular Fluid from Aggressive Periodontitis Patients

Abstract: The local production of anti-PC and anti-oxLDL further implicates the oral flora as a source of antigen that may mediate immune reactions of relevance to cardiovascular and other systemic diseases.

Cited by 27 publications

References 29 publications

Altered lipoprotein subclass distribution and PAF-AH activity in subjects with generalized aggressive periodontitis

Altered lipoprotein subclass distribution and PAF-AH activity in subjects with generalized aggressive periodontitis

Recognition of Porphyromonas gingivalis Gingipain Epitopes by Natural IgM Binding to Malondialdehyde Modified Low-Density Lipoprotein

Inflammatory mechanisms linking periodontal diseases to cardiovascular diseases

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