Periodontal innate immune mechanisms relevant to atherosclerosis and obesity

Zelkha, Sami; Freilich, Robert W.; Amar, Salomon

doi:10.1111/j.1600-0757.2010.00358.x

Cited by 70 publications

(71 citation statements)

References 123 publications

(167 reference statements)

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“…Evidence is accumulating that distant bacterial infection is involved in the pathophysiology of local chronic inflammatory processes underlying atherosclerosis (17). The transfer of bacteria into the blood or lymph system from barrier organ surfaces has been suggested as a possible mechanism of atherosclerosis.…”

Section: Apoementioning

confidence: 99%

Pivotal role of NOD2 in inflammatory processes affecting atherosclerosis and periodontal bone loss

Yuan¹,

Zelkha²,

Burkatovskaya³

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

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Significance Apolipoprotein E −/− (ApoE −/− ) mice deficient in nucleotide binding oligomerization domain-containing protein 2 (NOD2) and subjected to an oral gavage of Porphyromonas gingivalis developed elevated serum inflammatory cytokines, cholesterol, alveolar bone loss, and atherosclerosis. Stimulation of NOD2 by Muramyl DiPeptide (MDP) in ApoE −/− mice reduced P. gingivalis -induced inflammatory cytokines, cholesterol, alveolar bone loss, and atherosclerosis by reducing the expression of inhibitor of NF-κB kinase-β, NF-κB, JNK mRNA, and TNF-α protein levels. A reduction in body weight gain was observed in ApoE −/− mice fed a high-fat diet (HFD) and injected with MDP compared to ApoE −/− mice fed a HFD but saline injected. MDP activation of NOD2 should be considered in the treatment of inflammatory processes affecting atherosclerosis, bone loss, and possibly, weight gain.

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Section: Apoementioning

confidence: 99%

Pivotal role of NOD2 in inflammatory processes affecting atherosclerosis and periodontal bone loss

Yuan¹,

Zelkha²,

Burkatovskaya³

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

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“…It was estimated that over 700 species of bacteria can colonize specific sites in the [67]. In addition, there are reports on the literature showing that bacteria present in the biofilm are more resistant to phagocytic activity of neutrophils and that their replication capacity is higher in this environment [68].…”

Section: Biofilm and Evasion Mechanisms Against Immune Cells In Periomentioning

confidence: 99%

Periodontal Disease: General Aspects from Biofilm to the Immune Response Driven by Periodontal Pathogens

Degasperi¹,

Etchegaray²,

Marcelino³

et al. 2018

AiM

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Periodontal disease is of inflammatory origin and affects the dental support tissues. The initial phase is characterized by the accumulation of biofilm, which is a predisposing factor for several oral pathologies. The combination of extrinsic factors such as lack of hygiene, smoking and diet, and intrinsic factors such as genetics, and major changes in the immune response associated with immune escape mechanisms of biofilm constituents are crucial to the development and progression of the disease, which when untreated entails local irreversible consequences that can lead to systemic changes. In this brief review, we describe general aspects of periodontal disease, its risk factors and ways of preventing the disease. In particular, we discuss some of the mechanisms of immune response to periodontal pathogens, as well as the escape mechanisms of these microorganisms.

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“…The human oral microbiota used to be substantially more diverse, but with the agricultural and industrial revolutions it underwent two major ecosystem shifts introducing the microbes associated with periodontal disease and caries respectively, with flour and sugar implicated in these shifts (47). An inappropriate innate immune response to these microbial changes is believed to underlie periodontitis, and may also exacerbate atherosclerosis (48,49), while limiting the sources of processed carbohydrate in diet can produce marked improvements in periodontal health (50,51). The small intestinal microbiota is proximal to both the satiety-sensing vagal afferents believed to play a key role in energy-homeostasis(52) (35), and to the immune system hub of the gut-associated lymphoid tissue (53,54).…”

Section: Microbes As Sensors Of Dietary Refinement -Dental and Systemmentioning

confidence: 99%

Dietary Refinement And The Upper Gut Microbiota: The Starting Point For Obesity And Non-Communicable Diseases?

Spreadbury¹

2017

jevohealth

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IntroductionThe epidemics of obesity and related non-communicable diseases remains a matter of the utmost concern for public health(1). While physical exercise has been shown able to provide concrete benefits(2,3), there is good reason to believe that it cannot fully compensate for the deleterious changes produced by poor diet(4). Opinions regarding optimal diet increasingly show elements of convergence, especially regarding the association of dietary refinement and ultra-processed foods with poorer health outcomes(5). Some proposed mechanisms underlying this epidemiology of junk food include the removal from diet of health-promoting compounds due to inadequate fruit and vegetable consumption(6), and the enhancement of glycemic responses by the refinement of foods(7-9). Consistent with the latter, ad libitum low-carbohydrate diets (<50 g / day) have been shown to produce weight loss(10,11) and improve cardiovascular risk profiles(12). However, some very high carbohydrate diets have also been shown to be compatible with population-wide optimal metabolic health in non-cereal agrarian populations(13-16). Likewise, the "paleolithic style" diets used to date in small clinical trials have achieved consensus diet-beating improvements in metabolic and cardiovascular-disease risk factors(17-21) despite not restricting total carbohydrate into the <50 g / day range. Similar short-term benefits have also been shown for "the McDougall Program" a low fat, high carbohydrate diet that places a strong emphasis on food quality and minimizes processed carbohydrates(22). This wide range of carbohydrate content for ad libitum diets that produce weight loss suggests that low glycemic index and minimized insulin release are not credible explanations for their effects, especially in light of the experimental variability in the glycemic index of foods between individuals and between meal contexts(23). However, one factor that these dietary regimens do have in common is minimal consumption of processed foods, milled flours and sugar. The present article is an outline of a recently proposed mechanism(24,25) that could explain the effects of food-quality upon weight and health, independent of overall macronutrient composition.

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Periodontal innate immune mechanisms relevant to atherosclerosis and obesity

Cited by 70 publications

References 123 publications

Pivotal role of NOD2 in inflammatory processes affecting atherosclerosis and periodontal bone loss

Pivotal role of NOD2 in inflammatory processes affecting atherosclerosis and periodontal bone loss

Periodontal Disease: General Aspects from Biofilm to the Immune Response Driven by Periodontal Pathogens

Dietary Refinement And The Upper Gut Microbiota: The Starting Point For Obesity And Non-Communicable Diseases?

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