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 Table of Contents  
REVIEW ARTICLE
Year : 2017  |  Volume : 9  |  Issue : 1  |  Page : 32-36

Nutrigenomics: A perio-nutrition interrelationship


Department of Periodontology, Subharti Dental College, Meerut, Uttar Pradesh, India

Date of Web Publication2-Mar-2017

Correspondence Address:
Chandni Gupta
Department of Periodontology, Subharti Dental College, Meerut - 250 002, Uttar Pradesh
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/2249-4987.201401

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  Abstract 

Periodontitis results from the loss of a delicate balance between microbial virulence factors and a proportionate host response. Nutrition may be important in redressing the balance between microbial challenge and the host response because it has been implicated in a number of inflammatory diseases and conditions, including type II diabetes mellitus, cardiovascular diseases, rheumatoid arthritis, and inflammatory bowel disease, all of which have also been associated with periodontal diseases. Nutrigenomics is concerned with the impact of dietary components on the genome, proteome (the sum total of all proteins), and metabolites (the sum of all metabolites). This article reviews the evidence for nutritional impact on periodontitis.

Keywords: Nutrigenomics, nutrition, periodontitis


How to cite this article:
Tomar N, Gupta C, Kaushik M, Wadhawan A. Nutrigenomics: A perio-nutrition interrelationship. J Oral Res Rev 2017;9:32-6

How to cite this URL:
Tomar N, Gupta C, Kaushik M, Wadhawan A. Nutrigenomics: A perio-nutrition interrelationship. J Oral Res Rev [serial online] 2017 [cited 2019 Sep 17];9:32-6. Available from: http://www.jorr.org/text.asp?2017/9/1/32/201401


  Introduction Top


Periodontal disease is an inflammatory process involving progressive, episodic loss of the periodontal attachment apparatus including gingiva, cementum, periodontal ligament, and alveolar bone, resulting ultimately in tooth loss in susceptible patients. National Oral Health Survey and Fluoride Mapping (2002–2003), DCI, New Delhi, 2004, did a first ever epidemiological survey in India and the prevalence of periodontal disease was 57%, 67.7%, 89.6%, and 79.9% in the age groups 12, 15, 35–44, and 65–74 years, respectively.[1],[2] There is an abundance of empirical evidence and substantial theoretical justification for accepting the widespread belief that periodontal diseases are of multifactorial etiology and also complex in nature.[3] The importance of successful management and treatment of periodontitis has gained added press in recent years with the recognition that periodontitis is a risk factor for a number of important systemic diseases, which include cardiovascular disease, diabetes, and rheumatoid arthritis.[4],[5] A risk factor can be defined as an occurrence or characteristic that has been associated with the increased rate of a subsequently occurring disease. It is important to make the distinction that risk factors are associated with a disease but do not necessarily cause the disease. Risk factors may be modifiable or nonmodifiable characterized as genetic, environmental (e.g., stress, bacterial challenge), and lifestyle/behavioral (e.g., exercise, nutrition, smoking).[6],[7] For many years, the literature has cited the importance of nutrition in a range of chronic inflammatory diseases, all of which are associated with periodontitis, but in recent years, there has been an increased research investigating this phenomenon; however, until recently, the role of nutrition in periodontal disease has gained attention.[8] Therefore, this article aims to discuss the impact of nutrition in periodontitis and how can individuals nutritional status effect this complex disease processes.


  Role of Nutrition Top


Nutrient is defined as a source of nourishment, such as food, that can be metabolized by an organism to give energy and build tissue whereas nutrition is the organic process by which an organism assimilates food and uses it for growth and maintenance. Nutrients can be divided into six major classes, i.e. fats, carbohydrates, proteins, minerals, vitamins, and water; these can be further subdivided into two broad categories, “macronutrients” (fats, carbohydrates, and proteins) which are required in large quantities from the diet and “micronutrients” (minerals, vitamins, trace elements, amino acids, and polyunsaturated fatty acids [PUFA]) which are only required in small quantities in the diet and which are essential for a range of biological processes important in supporting optimal health.[9] Common dietary chemicals act on the human genome, either directly or indirectly, to alter gene expression or structure. Genes are important in determining the function, but nutrition is able to modify the degree of gene expression.[10]


  Origin of Nutrigenomics Top


On April 14, 2003, it was believed that genomic era was born when Human Genome Project [3] was launched with the participation of former US President Bill Clinton and former British PM Tony Blair, which contained the complete sequencing of the human genome.

  • In 2004, NuGo (European Nutrigenomics Organization) was born and funded until June 2010
  • In 2007, Nestle Research Center joined the industrial platform of the Kluyver Centre for Genomics of Industrial Fermentation, The Netherlands
  • In 2008, the US Berkeley scientist predicted human genome tests within 5 years.[11]



  Nutrition and Periodontal Disease Top


Periodontal disease is a complex process characterized by the destruction of the periodontal attachment apparatus, following an inflammatory response.[12] Several studies support a role for nutrition in controlling periodontal inflammation. Research studies using an experimental gingivitis model have shown increased levels of bleeding on probing when participants were fed with a diet high in carbohydrates when compared to those on a low sugar diet.[13] This finding was further supported by another study investigating volunteers placed on a primitive diet which was high in fiber, antioxidants (AOs), and fish oils but low in refined sugars and with no oral hygiene measures. As would be expected, plaque levels increased significantly and classic periodontal pathogens emerged within the biofilm; however, unexpectedly, gingival bleeding significantly reduced from 35% to 13%.[14] Dang et al.[15] hypothesized that zinc supplements may alter periodontal disease progression through changes in expression of the ZnT8 transporter gene [Figure 1]. However, further studies investigating cross-susceptibility genes (including ZnT8) between periodontal disease, diabetes, and modulation by diet are required. Based on these study results, it can be assumed that nutrition imparts its effect on periodontal condition too just like other inflammatory disorders as till date the precise mechanism is not completely understood.
Figure 1: Possible role for nutrient regulation of genes associated with periodontal disease. The proposed model demonstrates the known central role of diet in the etiology of periodontal disease

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Inflammation is a localized protective response elicited by injury or destruction of tissues, which serves to destroy, dilute, or wall off both the injurious agent and the injured tissue. Chronic and nonresolving inflammation is destructive and is central to a number of chronic diseases, periodontitis being one of them [Figure 2]. Oxidative stress is a key driver of chronic inflammation and as a result has a central role in the pathogenesis of a wide range of chronic inflammatory diseases.[16] Periodontal attachment destruction is caused by hyperinflammatory response which fails to eradicate the causative pathogens and generates prolonged release of neutrophil proteolytic enzymes, pro-inflammatory mediators, and reactive oxygen species (ROS).[17] The term “ROS” has been adopted to include molecules such as hydrogen peroxide, hypochlorous acid, and singlet oxygen, which, though not radical in nature, are capable of radical transformation in the extra- and intra-cellular environments. Although most ROS have extremely short half-lives, they can cause substantial tissue damage by initiating free radical chain reactions. Therefore, the body contains a number of protective AO mechanisms, whose specific role is to remove harmful oxidants (ROS), as soon as they form, or to repair the damage caused by ROS in vivo.[18]
Figure 2: Oxidative stress is central to the pathogenesis of a number of systemic diseases including periodontitis and has been proposed as a potential mechanistic link with systemic disease

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  Effects of Reactive Oxygen Species on Periodontal Tissues and Components Top


The ROS cause periodontal tissue damage by:

  • Ground substance degradation
  • Collagenolysis either directly or indirectly or as a result of oxidation of proteases
  • Stimulation of excessive proinflammatory cytokine release through nuclear factor-κB (NF-κB) activation
  • PG-E2 production through lipid peroxidation and superoxide release, both of which have been linked with bone resorption
  • Since interleukin-1 (IL-1) and tumor necrosis factor alpha positively regulate their own production, the additive effects of endotoxin-mediated cytokine production and that arising from respiratory burst of polymorphonuclear leukocytes in response to the same organisms lead to periodontal inflammation and subsequent attachment loss.[17]



  Discussion Top


Nutrigenomics and periodontics

Changing concepts in periodontal microbiology might modify approach to mechanical therapy, and technologic advances might help to understand the exact nature of periodontal infections and to perform the treatment more effectively and easily.[19] Improved understanding of the mechanism behind periodontal tissue destruction, potential defensive role of nutrients, and advent of modern genomic measurement tools has led to an increased interest in the association between nutrition and periodontal disease.[15] Periodontitis is associated with low serum/plasma micronutrient levels that may result from dietary and/or lifestyle factors as well as nutrigenetic characteristics. Primary evidence suggests beneficial results from nutritional interventions, supporting the contention that daily intake of certain nutrients should be at the higher end of recommended daily allowances.[9]

Researchers have found irrefutable evidence that macronutrients and micronutrients modulate proinflammatory and anti-inflammatory cascades, which influence a person's baseline inflammatory status. The functionality of nutrients in human biology extends beyond fuels for energy production and cofactors in metabolism, the key macronutrients and micronutrients modulate inflammation and also act as molecular signals that are capable of modulating gene and protein expression at a molecular level.[20] A lack of nutrients does not cause gingival inflammation but may be a predisposing factor by disrupting the process of tissue repair. Adequate nutrients can hasten healing and repair processes. Controlling or modifying the etiological factors can reverse clinical characteristics. Nutritional interventions for varying severities of gingivitis are the same as those for promoting overall health by encouraging adequate intake of all food groups and analyzing fermentable carbohydrate intake to determine potentially damaging habits that intensify the gingivitis. Patients need to maintain adequate nutrient stores before periodontal surgery to support successful outcomes. This ensures an acceptable immunological response for optimal healing and can help prevent or minimize infections, thereby controlling the consumption of dietary sugars and fats will aid in reducing the levels of oxidative stress and minimizing the inflammatory sequelae. Elevated glucose and lipid levels generate ROS at a rate that exceeds endogenous AO defenses and oxidative stress results. Investigators have noted that this “postprandial dysmetabolism” plays a role in the genesis of inflammation. Multiple elevations in glucose eventually lead to chronic inflammatory pathologies.[21],[22] Furthermore, in states of oxidative stress, lipid peroxidation (a chain reaction induced by ROS attack on the PUFA side-chains of lipid membranes) arises,[17] low density lipoproteins are oxidized (oxLDL), and the oxLDLs bind to a group of pattern recognition receptors called “toll-like receptors-2/4” on inflammatory cell membranes, triggering NF-κB activation through the protein-kinase-C enzyme and other related pathways. NF-κB transcribes several proinflammatory cytokines.[23] In addition, researchers have proposed reduced glutathione (GSH), the key intracellular AO redox regulator of NF-κB as a novel approach to downregulation of hyperinflammatory events.[24] GSH levels appear depleted in periodontitis,[25] and methods of enhancing intracellular GSH may prove beneficial. PUFAs of the omega-3 form (ω-3 PUFAs) found in fish oils lower postprandial triglyceride levels [26] and findings observed by Yokoyama M et al. in their randomized control study oserved that it has anti-inflammatory and ardiovascular protective effects.[27] Kesavalu et al.[28] demonstrated that rats infected with Porphyromonas gingivalis and fed a diet rich in ω-3 PUFAs for 22 weeks experienced less bone loss than control rats fed a diet rich in n-6 PUFAs. One mode of action of PUFAs includes the downregulation of proinflammatory gene expression through the nuclear peroxisome proliferator-activated receptors others include inflammation-resolving mediators derived from ω-3 PUFAs (resolvins).[29] A recent randomized, double-blinded, clinical trial by Van der Velden et al.[9] investigated potential clinical benefits of a powdered fruit and vegetable juice concentrate on the treatment of patients with chronic periodontitis. The study assessed dietary intake and biochemical nutritional status (plasma ß-carotene). It was concluded that supplementation with the fruit and vegetable concentrate results in increased pocket depth reduction, following standard nonsurgical therapy when compared to a placebo control. Therefore, higher consumption of components/nutrients with AO capabilities has been associated with lower frequency of numerous human morbidities or mortalities as per many epidemiological studies. Diverse potential applications of AO/free radical manipulations in prevention or control of disease have been revealed by ongoing research.[30]

Further, as an adjunct to scaling and root planing, selected application of beneficial bacteria would also achieve and maintain periodontal health. Probiotics are live microorganisms administered in adequate amounts with beneficial health effects on the host. They repopulate the beneficial bacteria which can help kill pathogenic bacteria and fight against infection which in turn lowers the risk of developing periodontitis. Oral administration of probiotics may also benefit oral health by preventing the growth of harmful microbiota or by modulating mucosal immunity in the oral cavity.[31],[32] Probiotics are also known to produce AOs, which in turn prevent plaque formation by neutralizing the free electrons which are needed for the mineralization of plaque.[33] On the other hand, prebiotics are nondigestible oligosaccharides that affect the proliferation of resident commensal bacteria, which may exert beneficial effects on the host by directly stimulating expression of IL-10, interferon, enhancement of immunoglobulin A secretion, and modulation of inflammatory responses in pathogens.[34]

For inhibition and management of periodontitis, daily nutrition should include sufficient AOs, Vitamin D, and calcium. Insufficient AO levels may be managed by higher intake of vegetables, berries, and fruits (e.g., kiwi fruit) or by phytonutrient supplementation. AO micronutrient deficiencies can be met by a higher intake of vegetables, fruits, and berries.[9] The recommendations of the 2011 European workshop on periodontology suggest that the dental team should consider including advice to all patients to increase levels of fish oils, fiber, fruit, and vegetables and to reduce levels of refined sugars as part of a periodontal prevention/treatment regimen and a general health benefit message.[35]


  Conclusion Top


Diet is an important environmental factor that interacts with the genome to modulate disease risk. A clear understanding of these interactions has the potential to support disease prevention through optimization of dietary recommendations. The interaction between genetic and dietary influences can result in a higher risk of disease in certain individuals and populations. The future of nutrigenomic research promises to provide additional knowledge of biological function and individual response to diet. Based on the pathology of periodontal disease, the assumption is that specific nutrients which can modulate immune and inflammatory responses could in turn modulate periodontal health.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
  References Top

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26.
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Abstract
Introduction
Role of Nutrition
Origin of Nutrig...
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Effects of React...
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