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

Rufail, Miguel; Schenkein, Harvey A.; Barbour, Suzanne E.; Tew, John G.; Antwerpen, Rik van

doi:10.1194/jlr.m500389-jlr200

Cited by 23 publications

(29 citation statements)

References 67 publications

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“…Studies have shown that advanced HIV infection and severe periodontitis are associated with a high prevalence of sdLDL particles [5,6]. We have previously shown that patients with acute brucellosis and EBV infection have decreased mean LDL particle size [4,7].…”

Section: Discussionmentioning

confidence: 97%

Leptospirosis is Associated with Markedly Increased Triglycerides and Small Dense Low‐Density Lipoprotein and Decreased High‐Density Lipoprotein

Gazi¹,

Apostolou²,

Liberopoulos³

et al. 2011

Lipids

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The objective of the present study was to evaluate the effects of acute infection with Leptospira interrogans on lipids, lipoproteins and associated enzymes. Fasting serum levels of total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), triglycerides (TG), apolipoproteins (apo) A-Ι, B, E, C-II, C-III and lipoprotein (a) [Lp(a)] were determined in patients with Leptospirosis on diagnosis and 4 months after recovery as well as in age- and sex-matched controls. Activities of cholesteryl-ester transfer protein (CETP) and lipoprotein-associated phospholipase A(2) (Lp-PLA(2)) as well as paraoxonase 1 (PON1) hydrolysing activity and levels of cytokines were determined. LDL subclass analysis was performed with Lipoprint LDL System. Eleven patients (10 men, mean age 49.5 ± 8.4 years) and 11 controls were included. TC, HDL-C, LDL-C, apoA-I, apoB and Lp(a) levels were lower at baseline, whereas TG and apoE levels were elevated compared with 4 months later. At baseline, higher levels of cytokines and cholesterol concentration of small dense LDL particles (sdLDL-C) were noticed, whereas LDL particle size was lower compared with follow-up. Activities of plasma Lp-PLA(2) and HDL-associated Lp-PLA(2) were lower at baseline compared with post treatment values, whereas PON1 activity was similar at baseline and 4 months later. 4 months after recovery, the levels of all lipid parameters evaluated did not differ compared with controls, except for HDL-C which remained lower. PON1 activity both at baseline and 4 months later was lower in patients compared with controls. Leptospirosis is associated with atherogenic changes of lipids, lipoproteins and associated enzymes.

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Section: Discussionmentioning

confidence: 97%

Leptospirosis is Associated with Markedly Increased Triglycerides and Small Dense Low‐Density Lipoprotein and Decreased High‐Density Lipoprotein

Gazi¹,

Apostolou²,

Liberopoulos³

et al. 2011

Lipids

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“…Advanced stages of human immunodefi ciency virus infection are associated with an atherogenic lipid profi le, including a high prevalence of sdLDL particles ( 32 ). Moreover, severe periodontitis is associated with an increase in sdLDL-C levels ( 2 ). But which could be the reasons for the increased sdLDL-C and consequently decreased LDL size during acute infection in the absence of increased TGs?…”

Section: Discussionmentioning

confidence: 99%

“…The effects of infl ammation on the distribution of LDL subclasses have been investigated ( 9,31 ). An increase in sdLDL particles in response to infection has been reported in some studies ( 2,32 ).…”

Section: Biochemical Measurementsmentioning

confidence: 99%

Persistence of an atherogenic lipid profile after treatment of acute infection with brucella

Apostolou

Gazi

Kostoula

et al. 2009

Journal of Lipid Research

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This article is available online at http://www.jlr.org herpes simplex virus, helicobacter pylori, as well as periodontitis have been studied ( 2-4 ). On the contrary, other studies have disputed the causal role of infectious agents in atherogenesis ( 5-7 ).Current evidence suggests that atherosclerosis develops as a response to infl ammatory stimulus. Therefore, common or uncommon infections could represent a risk factor. Mechanisms that may be implicated in the atherogenesis caused by infectious agents include local increase of proinfl ammatory cells, local effusion of endotoxins, autoimmune reaction, systemic cytokine release, and changes in lipid metabolism ( 8 ).Infection and infl ammation cause similar cytokineinduced changes in lipid and lipoprotein metabolism ( 9 ). These include reductions in serum levels of total cholesterol (TC), HDL-cholesterol (HDL-C), LDL-cholesterol (LDL-C), apolipoproteins (Apo) AI and B, and lipoprotein (a) [Lp(a)] and increases in triglyceride (TG) and ApoE concentrations ( 9-14 ).Current evidence suggests that the host response to infection and infl ammation increases oxidized lipids in serum and induces LDL oxidation in vivo. Oxidative modifi cation of LDL is an important event in the development of atherosclerosis ( 15 ). In addition, the cholesterol ester transfer protein (CETP) plays a central role in HDL metabolism and the regulation of HDL-C levels in serum. High levels of CETP activity lead to a reduction in HDL-C levels and an atherogenic lipoprotein profi le ( 16 ).Platelet-activating factor (PAF) is a potent pro-infl ammatory phospholipid produced by activated platelets, -C), ApoB, ApoAI, and ApoCIII and higher LDL-C/HDL-C and ApoB/ApoAI ratios; 2 ) higher levels of IL-1b, IL-6, and TNFa; 3 ) similar ApoCII and oxLDL levels and Lp-PLA 2 activity, lower PON1, and higher CETP activity; and 4 ) higher small dense LDL-C concentration. Four months later, increases in TC, HDL-C, LDL-C, ApoB, ApoAI, and ApoCIII levels, ApoB/ApoAI ratio, and PON1 activity were noticed compared with baseline, whereas CETP activity decreased. LDL-C/HDL-C ratio, ApoCII, and oxLDL levels, Lp-PLA 2 activity, and small dense LDL-C concentration were not altered. Brucella infection is associated with an atherogenic lipid profi le that is not fully restored 4 months following treatment. There is increasing evidence that a link exists between infection/infl ammation and atherosclerosis ( 1 ). Infections with chlamydia pneumoniae, cytomegalovirus,

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“…Generalised aggressive PD is associated with the putative pathogens Pg and Aa 14. It is demonstrated that patients with generalised aggressive periodontitis have twice the concentration of sd-LDL compared with subjects without PD 15. This essentially means the concentration of ApoB is doubled.…”

Section: Pathogenesis Part 1: Serum Lipoprotein Concentrationmentioning

confidence: 95%

High-risk periodontal pathogens contribute to the pathogenesis of atherosclerosis

Bale

Doneen

Vigerust

2016

Postgraduate Medical Journal

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Periodontal disease (PD) is generated by microorganisms. These microbes can enter the general circulation causing a bacteraemia. The result can be adverse systemic effects, which could promote conditions such as cardiovascular disease. Level A evidence supports that PD is independently associated with arterial disease. PD is a common chronic condition affecting the majority of Americans 30 years of age and older. Atherosclerosis remains the largest cause of death and disability. Studies indicate that the adverse cardiovascular effects from PD are due to a few putative or high-risk bacteria: Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis, Tannerella forsythia, Treponema denticola or Fusobacterium nucleatum. There are three accepted essential elements in the pathogenesis of atherosclerosis: lipoprotein serum concentration, endothelial permeability and binding of lipoproteins in the arterial intima. There is scientific evidence that PD caused by the high-risk pathogens can influence the pathogenesis triad in an adverse manner. With this appreciation, it is reasonable to state PD, due to high-risk pathogens, is a contributory cause of atherosclerosis. Distinguishing this type of PD as causal provides a significant opportunity to reduce arterial disease.

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

Cited by 23 publications

References 67 publications

Leptospirosis is Associated with Markedly Increased Triglycerides and Small Dense Low‐Density Lipoprotein and Decreased High‐Density Lipoprotein

Leptospirosis is Associated with Markedly Increased Triglycerides and Small Dense Low‐Density Lipoprotein and Decreased High‐Density Lipoprotein

Persistence of an atherogenic lipid profile after treatment of acute infection with brucella

High-risk periodontal pathogens contribute to the pathogenesis of atherosclerosis

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