Genomics of periodontal disease and tooth morbidity. KEYWORDS aggressive periodontitis, diagnosis, epidemiology, genetics, inflammation and innate immunity, IL-1 gene cluster single nucleotide polymorphisms cannot be considered a significant risk factor for all populations. This chapter will briefly discuss the various candidates’ gene approach in understanding the etiopathogenesis of periodontitis. Berglundh et al. It’s based on principles of collaboration, unobstructed discovery, and, most importantly, scientific progression. With cardiovascular disease (CVD) it has been shown that treating periodontal disease may lower a number of markers associated with risk of CVD, such as C-reactive protein and endothelial cell function, but there is no direct evidence that this results in decreased risk of cardiovascular events . It is encoded by the IL-6 gene localized on chromosome 7p21. Genetic research has focused on understanding how these responses work and also how these responses differ between different individuals. The study by Divaris et al. The reason for the large increase in publicati… Help us write another book on this subject and reach those readers. Brief introduction to this section that descibes Open Access especially from an IntechOpen perspective, Want to get in touch? These genes encode immune receptors and various molecules involved in the signal transduction pathways that play an essential role in up regulation or down regulation of the immune response essentially the inflammatory reaction in response to a stimuli. Built by scientists, for scientists. Periodontitis and Cardiovascular Diseases. By making research easy to access, and puts the academic needs of the researchers before the business interests of publishers. Epigenetics allows to perform dynamic analysis of different variations in gene expression, providing this great advantage to the static measurement provided by genetic markers. Use of the genetic risk score could be useful in assessing the susceptibility to periodontitis. Regardless of the patient's gum condition, investigators will also evaluate current and past dental x-rays to determine if there were signs of this disease in the past. How? Such individuals are up to 20 times more likely to develop advanced periodontitis than those without these genetic factors. The gene encoding vitamin D is located on 12q12-q14. In this critical review, we highlight recent progress in identifying genetic markers and variants associated with PD, present their overlap with CAD, and discuss functional aspects. Thus, the role of MMPs and TIMPs gene polymorphism with periodontitis has to be explored with further refined studies. These modifications express or repress certain genes. In the last 10 years, a rising number of epidemiological investigations have studied the possible association between chronic oral infections and cardiovascular diseases (CVD). Recent genome-wide association and large-scale candidate gene studies highlight that variations in >50 genes are associated with premature CAD, while variations in only 4 genes showing nominally significant associations with aggressive periodontitis and/or chronic periodontitis have so far been identified. 2015 Feb;8(1):159-67. doi: 10.1161/CIRCGENETICS.114.000554.  |  Applying the candidate gene approach, SNPs in IL1β (rs1143634) and KCNQ1 (rs2237892) were shown to be associated with comorbidity of rheumatoid arthritis and periodontal disease. 2020 Jun;83(1):26-39. doi: 10.1111/prd.12297. This chapter also throws some light on the relationship of the recent advances in genetic analysis like genome wide association studies, epigenetic regulation, and infectogenomics with periodontal destruction. In addition, we answer why a significant fraction of the heritability of PD is still missing, and we suggest approaches that may be taken to close the gap. Genetics of coronary artery disease: genome-wide association studies and beyond. The anaerobic bacteria have been implicated as the main etiological factor for periodontal destruction. Mashhadiabbas et al. postulated that a key determinant of whether individuals developed periodontitis or not was dependent on the way their bodies responded to the microbes [1]. Login to your personal dashboard for more detailed statistics on your publications. Genetic control of periodontal disease resistance or susceptibility could be exerted through many different biologic pathways. National Center for Biotechnology Information, Unable to load your collection due to an error, Unable to load your delegates due to an error. Other authors like Amirisetty et al., Masamatti et al. Thus, the host susceptibility to periodontal pathogens plays a significant role in the etiopathogenesis of periodontitis. Like many common chronic disorders, periodontitis (gum disease) involves an inflammatory response that varies from one individual to another. Infectogenomics refers to the association of the host genetic variants like single nucleotide polymorphisms with the composition of the microbial complexes in the host body. It is a proinflammatory cytokine produced by macrophages. This is essential for maintaining the normal tissue homeostasis. has shown an association of 13 host genetic variants with the red/orange complex bacteria in periodontitis. Periodontal disease (PD) and coronary artery disease (CAD) are common diseases characterized by an overaggressive inflammatory response to diverse stimuli. Few people, who do not have much contributing local factors such as plaque and calculus, still develop severe destruction of bone whereas some do not develop severe forms of periodontal diseases in spite of having a very poor oral hygiene. A variety of single nucleotide polymorphisms of various signaling factors, receptors, connective tissue components, enzymes involved in the host defense against the invading microbes have been reported by several researchers. Clipboard, Search History, and several other advanced features are temporarily unavailable. 2016 Feb;245:62-70. doi: 10.1016/j.atherosclerosis.2015.11.019. While many organs can be affected, iron overload is especially likely to affect the liver, heart, and pancreas.Early symptoms of hemochromatosis can include fatigue, weakness, and joint pain. We are IntechOpen, the world's leading publisher of Open Access books. A more detailed knowledge of the human oral microbiome could provide more information on its association with host genetic variants [31, 32]. Fifteen papers meeting selection criteria were included in the qualitative review; the authors determined that meta-analysis could not be … Keywords: have proposed that IL-1 cluster gene single nucleotide polymorphisms were associated with higher risk for periodontitis [3, 4]. Although there are several studies that associate various candidate gene polymorphisms to periodontitis, till date there is not much clarity in the genetic susceptibility to the disease since there are a multitude of etiological factors and epigenetic factors that contribute to the susceptibility as well as severity of periodontal disease. Genetic susceptibility to multifactorial diseases like periodontitis is usually due to several gene polymorphisms instead of a single, or few, gene mutations. 2013 Nov 15;22(22):4516-27. doi: 10.1093/hmg/ddt299. The genetic link with the etiopathogenesis of periodontitis was started with the initial finding of association of composite genotype (Interleukin-1α and IL-1β) with chronic periodontitis in Caucasian population by Kornman et al. It is an anti-inflammatory cytokine expressed by T helper cells. found an association between IFN-γ SNP in Iranian population, while Holla et al. Biofilm and periodontal microbiology 9. Along similar lines, DNA from periodontal pathogens, such as P. gingivalis, A. actinomycetemcomitans, Prevotella intermedia, and T. forsythia, was found in human atherosclerotic plaques, suggesting that these oral pathogens may migrate from … In its more serious form, called periodontitis, the gums can pull away from the tooth, bone can be lost, and the teeth may loosen or fall out. did not find any significant association [17]. in their meta-analysis based on 38 studies found an association of vitamin D receptor BsmI, TaqI, FokI, and ApaI polymorphisms with periodontitis [20]. Listing a study does not mean it has been evaluated by the U.S. Federal Government. Additional risk factors including other genetic markers, smoking, diabetes, and oral hygiene have an amplifying effect on disease progression and duration. Ninomiya M, Hashimoto M, Yamanouchi K, Fukumura Y, Nagata T, Naruishi K. Clin Oral Investig. Elevated levels of MMP-1, MMP-2, MMP-3, MMP-8, and MMP-9 have been detected in gingival crevicular fluid, peri-implant sulcular fluid, and gingival tissue of periodontitis patients. in their systematic analysis listed top genes NIN, ABHD12B, WHAMM, AP3B2, CPEB1, HGD, ZNF675, EMK1, TNFRSF10B, HTR4, WDR59, JDP2, OTOF, ANGEL2, etc. Matrix metalloproteinases (MMPs) are the key enzymes, which play a major role in the destruction of the collagenous and non-collagenous proteins of the connective tissue component. COVID-19 is an emerging, rapidly evolving situation. Vitamin D and Vitamin D receptor are important mediators of bone metabolism. These markers will also be evaluated in family members (parents, grandparents or siblings), when possible, to check for the likelihood of these members developing this disease. The current model of pathogenesis of periodontal disease underlines the complex interactions among plaque bacteria, the host's genetic factors, and acquired environmental stressors. 17, 128-131 Similar to other complex chronic diseases, it is important to … Author information: (1)Department of Obstetrics & Gynaecology, St Mary's Imperial NHS Trust, London, UK. Heidari et al. Markers of inflammation also declined to levels typical of younger animals. Tobacco users also are at increased risk for periodontal disease. Epub 2012 May 23. Rhodin et al. They did a meta-analysis of 17 studies [21]. Following him, lot of studies conducted in different ethnic races linking the association of composite genotype with periodontitis. Remarkably, 3 of the PD loci (75%) show shared associations with CAD ( ANRIL/CDKN2B-AS1, PLG, CAMTA1/VAMP3), suggesting involvement of common pathogenic mechanisms. For example, some people with severe periodontal disease have genetic factors that affect the immune factor interleukin-1 (IL-1), a cytokine involved in the inflammatory response. Another genetic study of human twins revealed significant genetic control of has shown an association of two genetic loci (KCNK1 and DAB2IP) with high colonization of red complex bacteria. This differential expression of periodontitis leads researchers to question if genetics and heritability played a major role. Loo et al. demonstrated the expression of miR-146a in infections caused by periodontopathic bacteria. Hemochromatosis is a disease in which too much iron builds up in the body.This is also called iron overload. Brett et al. The genetic basis of many aspects of the periodontal host response has been discussed in reference to genetic disorders predisposing to periodontal disease. GWAS is a recent development in the field of research. 2012 Nov;225(1):1-10. doi: 10.1016/j.atherosclerosis.2012.05.015. It is composed of two molecules, IL-1α and IL-1β. Epub 2014 Dec 2. Relationship of oral conditions to the incidence of infective endocarditis in periodontitis patients with valvular heart disease: a cross-sectional study. There has been a rapid increase in interest in understanding the relationship between periodontal disease and cancer risk; twice as many original observational studies were published with measures of periodontal disease (i.e., not including studies using tooth number as surrogate of periodontal disease) in the past few years (n = 12; 2011–2016) as were published during the 20 years prior to 2011 (n = 6) (Web Tables 1 and 2, available at http://aje.oxfordjournals.org/). Karimbux et al. 22,23 The endotoxin in the microorganisms could damage endothelial cells and induce smooth muscle proliferation. It is produced by inflammatory cells such as monocytes, macrophages, and dendritic cells, which play an important role in the regulation of immune and inflammatory responses to infections. Many GWAS in periodontitis has been carried out and has shown differential expression of varied genes [23, 24, 25, 26]. They seem to contribute to risk of periodontitis in Asian populations. Up to 30% of the population may have some genetic susceptibility to periodontal disease. Several studies have reported the influence of various microRNAs especially miR-146a, let-7a, miR-196a, miR-499a, and miR-125a in susceptibility to chronic periodontitis [27, 28, 29]. Epigenetic modifications such as DNA methylation, histone modifications and RNA-associated silencing (micro RNA) play a role in susceptibility to disease. The National Institutes of Health Biomarkers Definitions Working Group in 1998 defined a biomarker as “a substance that is measured objectively and evaluated as an indicator of normal biologic processes, pathogenic processes, or pharmacologic responses to a therapeutic intervention.” These biomarkers could be determined in various biological media like saliva, serum, and gingival crevicular fluid in health as well as disease. The genetic factor is the major determinant of the host susceptibility. According to Li et al., there was no significant association of MMP1, 8, 9, 12, 2, or 13 polymorphism with periodontitis. If you have a family history of gum disease, then you are more likely to have problems with your gums. However, the method is expensive and technique sensitive. This site needs JavaScript to work properly. 1 Bacteria can elicit inflammatory responses in different host cell populations through interactions of pathogen‐associated molecular patterns and pattern recognition receptors. Consensus Report. J Periodontol 2007;78:2289-302. We share our knowledge and peer-reveiwed research papers with libraries, scientific and engineering societies, and also work with corporate R&D departments and government entities. Our readership spans scientists, professors, researchers, librarians, and students, as well as business professionals. But the results were contradictory in nature. Interleukin-1 (IL-1) is a pro-inflammatory cytokine, which is encoded by IL-1 gene cluster at the chromosomal position 2q13–21. There are contradictory results and varied results of the association of various genetic loci of different genes with periodontitis in different ethnic populations. Open Access is an initiative that aims to make scientific research freely available to all. Thus, the genetic changes of the MMPs and TIMPs might play a role in the etiopathogenesis of periodontitis. Therefore, any alteration in FcyR expression and function would alter host immune responses against periodontal pathogens and hence susceptibility to periodontal diseases . Thus, the role of TNF-α SNP in the etiopathogenesis of periodontitis has to be explored with further studies. A genome-wide association study reveals susceptibility loci for myocardial infarction/coronary artery disease in Saudi Arabs. Priyanka et al. Amelogenesis imperfecta either causes problems in enamel hardening (mineralization) of normal amounts of enamel, or causes less than normal enamel production. Studies by Lavu et al., Hao et al. The gene is located on chromosome 12q24. These studies were based on the hypothesis that oral infections, including periodontitis may confer an independent risk for CVD. Different variations in frequency of some alleles in different populations have been observed. The role of dental calculus and other local predisposing factors 8. Kobayashi et al. 2020 Feb 3;15(1):1. doi: 10.5334/gh.400. Many investigators have, however, demonstrated a role for IL‐1 in the initiation and progression of periodontitis. In a meta-analysis by Nikolopoulos et al. A meta-analysis by Nikolopoulos et al., which based on 17 studies showed that there was no association of the TNF-α promoter −308G/A polymorphism with periodontitis while another meta-analysis by Song et al. in their study found TaqI, BsmI, FokI and ApaI SNPs were associated with periodontitis [18]. Cui et al. in their meta-analysis based on 15 studies found an association between TNF-α SNP and periodontitis in Asian and Caucasian population [16]. Dentinogenesis imperfecta is a genetic disorder causing defective formation of dentin, the mineralized material composing the majority of all tooth structure. Publishing on IntechOpen allows authors to earn citations and find new collaborators, meaning more people see your work not only from your own field of study, but from other related fields too. As periodontal diseases (PDs) are among the most prevalent chronic infections in humans, there is a mounting scientific interest and public awareness of these possible interactions, mainly due to the like… However, conflicting results have been obtained. By Gurumoorthy Kaarthikeyan and Swarna Meenakshi, Submitted: October 30th 2018Reviewed: June 14th 2019Published: November 11th 2019, Home > Books > Periodontal Disease - Diagnostic and Adjunctive Non-surgical Considerations. Whereas PD leads to destruction of the tooth-supporting structures, CAD is a chronic inflammatory condition ultimately causing myocardial infarction via narrowing and occluding of blood vessels. Prins BP, Lagou V, Asselbergs FW, Snieder H, Fu J. Atherosclerosis. Periodontitis and cardiovascular diseases: Consensus report. in their meta-analysis has found an association between IL-1α rs17561 and IL-1β rs 1143634 polymorphisms and periodontitis [11]. [2]. Although very prevalent, periodontal diseases are not evenly distributed across populations. Schaefer AS, Bochenek G, Jochens A, Ellinghaus D, Dommisch H, Güzeldemir-Akçakanat E, Graetz C, Harks I, Jockel-Schneider Y, Weinspach K, Meyle J, Eickholz P, Linden GJ, Cine N, Nohutcu R, Weiss E, Houri-Haddad Y, Iraqi F, Folwaczny M, Noack B, Strauch K, Gieger C, Waldenberger M, Peters A, Wijmenga C, Yilmaz E, Lieb W, Rosenstiel P, Doerfer C, Bruckmann C, Erdmann J, König I, Jepsen S, Loos BG, Schreiber S. Circ Cardiovasc Genet. It is encoded on gene at 1q31-q32. According to the American Dental Association, genetics is a risk factor for developing gum disease. Get the latest public health information from CDC: https://www.coronavirus.gov, Get the latest research information from NIH: https://www.nih.gov/coronavirus, Find NCBI SARS-CoV-2 literature, sequence, and clinical content: https://www.ncbi.nlm.nih.gov/sars-cov-2/. Scarel-Caminaga et al. In its early stage, called gingivitis, the gums become swollen, red, and may bleed. Sanz M, Del Castillo AM, Jepsen S, Gonzalez-Juanatey JR, D'Aiuto F, Bouchard P, Chapple I, Dietrich T, Gotsman I, Graziani F, Herrera D, Loos B, Madianos P, Michel JB, Perel P, Pieske B, Shapira L, Shechter M, Tonetti M, Vlachopoulos C, Wimmer G. Glob Heart. in their systematic review and meta-analysis studied 13 studies and found that IL-1α and IL-1β (IL-1α (−889) C > T, IL-1α (+4845) G > T, IL-1β (+3954) C > T, could be a significant contribution to the risk of developing periodontitis [10]. © 2019 The Author(s). Gene localized at 6p21.3. Periodontitis is a chronic inflammatory disease with multifactorial etiology. overall evaluation of periodontal disease. Although specific genetic markers have been identified in the uncommon juvenile forms of periodontitis, previous studies of specific genetic markers in adults with periodontitis have not been encouraging. 1 INTRODUCTION. atherosclerosis; coronary artery disease; genome-wide association study; long noncoding RNA; myocardial infarction; periodontitis. Zhang et al. did not find any significant association of VDR Taq1 polymorphism with periodontitis in south Indian population [19]. USA.gov. in their study showed that methylation of E-Cadherin and COX-2 was observed in periodontitis patients.  |  Genetic Testing. Schafer et al. It exists in three isoforms TGF-β1, β2, and β3. A meta-analysis by Mao et al., showed that IL-1β +3954 polymorphism increases the risk of periodontal disease [6]. which also included 17 studies found that TNF-α −308 A allele was associated with periodontitis in Brazilian, Asian, and Turkish populations [13]. Genetic evidence for PLASMINOGEN as a shared genetic risk factor of coronary artery disease and periodontitis. It activates and regulates the osteoclasts. NIH To date, at least 26 members of MMPs have been identified. Ding et al. Hum Mol Genet. did not find any significant association between interleukin-1β (+3954) polymorphism with chronic periodontitis in Indian population [9]. Wakil SM, Ram R, Muiya NP, Mehta M, Andres E, Mazhar N, Baz B, Hagos S, Alshahid M, Meyer BF, Morahan G, Dzimiri N. Atherosclerosis. Thus, this plays a major role in the susceptibility and progression of periodontal destruction. in their study found that Fok1 polymorphism was associated with periodontitis. Genetic factors and environmental factors determine the susceptibility to disease. in their meta-analysis found significant association between TGF-β SNP and periodontitis in Asian population. Specific bacteria are associated with the initiation of the periodontal disease. Genetic Biomarkers in Periodontal Disease Diagnosis, Periodontal Disease - Diagnostic and Adjunctive Non-surgical Considerations, Nermin Mohammed Ahmed Yussif, IntechOpen, DOI: 10.5772/intechopen.88058. in their study have found association of microRNA-125a and microRNA-499a polymorphisms with chronic periodontitis in south Indian population [30]. This review focuses on the genetic aspects of periodontal diseases wherein researchers are currently focusing on genetic evidences to explain the difference in susceptibility to periodontal disease in different individuals. Sanz M, Marco Del Castillo A, Jepsen S, Gonzalez-Juanatey JR, D'Aiuto F, Bouchard P, Chapple I, Dietrich T, Gotsman I, Graziani F, Herrera D, Loos B, Madianos P, Michel JB, Perel P, Pieske B, Shapira L, Shechter M, Tonetti M, Vlachopoulos C, Wimmer G. J Clin Periodontol. Evaluating polymorphisms in COX-2 and MMP-2, MMP-3, MMP-8, and MMP-9 genes, two meta-analysis are available in literature [ … It is a multifunctional cytokine that plays an important role in cellular differentiation, apoptosis and angiogenesis. This disease usually starts out as gingivitis, which is characterized by swollen, tender gums that may bleed during brushing. Contact our London head office or media team here. Research has indicated that some people may be genetically susceptible to gum disease. 2020 Feb;82(1):143-156. doi: 10.1111/prd.12320. in their study observed that miRNA-132 played a major role in pathogenesis induced by P. Gingivalis. However, conflicting results have been reported because of the heterogeneticity of the studies. Gurumoorthy Kaarthikeyan and Swarna Meenakshi (November 11th 2019). Kaarthikeyan et al. Bochenek G, Häsler R, El Mokhtari NE, König IR, Loos BG, Jepsen S, Rosenstiel P, Schreiber S, Schaefer AS. Typically the progression and severity of the disease depends upon the interaction of genetic and behavioral risk factors. Epub 2013 Jun 27. Licensee IntechOpen. Can a genetic test predict your risk of developing future cavities or severe gum disease? Periodontol 2000. In addition to playing a role in health, the genetic factors also plays a major role in disease susceptibility. Until recently, there was no reliable way to identify individuals who had an increased genetic risk for these diseases. Periodontitis is a chronic inflammatory disease with multifactorial etiology. Classical twin studies led to the conclusion that both complex diseases have a similar degree of heritability and that a significant fraction of the genetic factors accounting for this heritability is shared. The major regions of interleukin-10 single nucleotide polymorphisms studied were −1082, −819, and −592. reported a relationship between IL-1α −889 and IL-1β +3954 and the severity of periodontal disease [2]. Periodontal disease and bacterial vaginosis as genetic and environmental markers for the risk of spontaneous preterm labor and preterm birth. Available from: Diagnostic and Adjunctive Non-surgical Considerations, Department of Periodontics, Saveetha Dental College and Hospitals, Saveetha Institute of Medical and Technical Sciences (SIMATS), Chennai, India. Our team is growing all the time, so we’re always on the lookout for smart people who want to help us reshape the world of scientific publishing. Mustapha IZ, Debrey S, Oladubu M, Ugarte R. Markers of systemic bacterial exposure in periodontal disease and cardiovascular disease risk: a systematic review and meta-analysis. Both autosomal dominant and recessive forms of Mendelian transmission have been reported for PPP. Epub 2015 Nov 22. Epub 2019 Jun 13. SNPs or dysfunction could lead to bone resorption. Gross et al. The incidence of IL6 genotypes is reported to vary by ethnicity. Similarly, Yin et al. Kornman et al. NLM The first evidence that genetics played a role in periodontal diseases emerged in the 1990s. Diagnosis of Periodontal Disease Using Genetic Marker in Saliva The safety and scientific validity of this study is the responsibility of the study sponsor and investigators. demonstrated that Asians had a low carriage rate of IL-1α −889 R-allele compared to the other populations [5]. The large non-coding RNA ANRIL, which is associated with atherosclerosis, periodontitis and several forms of cancer, regulates ADIPOR1, VAMP3 and C11ORF10. ... Genetic sequencing of the animals’ oral bacteria showed that rapamycin also seemed to return their microbial makeup to a state resembling that of younger, healthier mice. did not find any significant association in the Caucasian population [15]. Accumulation of iron in the organs is toxic and can cause organ damage. Whereas the study by Kaarthikeyan et al. Future research should focus on the multitude of genes, their multiple interactions and the epigenetic regulation during different stages of periodontal disease pathogenesis is required to fully understand the molecular mechanisms behind the etiopathogenesis of periodontitis. Periodontal microorganisms have been found in atheromas. Generally, a combination of biomarkers is used in order to predict disease activity. The anaerobic bacteria have been implicated as the main etiological factor for periodontal destruction. The inheritance pattern of Ehlers-Danlos syndromes (EDS) varies by subtype. A drug targeting an aging-related molecule reversed periodontal disease in elderly mice. on cytokine gene polymorphisms such as IL-1α, IL-1β, IL-6, and TNF which included 53 studies, no significant association was detected between IL-6 and chronic periodontitis [13]. Not all the individuals having the similar amount of plaque and calculus develop the periodontitis. HHS be made in identifying a robust group of genetic, host, and microbial risk-markers associated with periodontal disease that can improve diagnostic capability in disease associated with juveniles, adolescents, and post-adolescent individuals. Not all the individuals having the similar amount of plaque and calculus develop the periodontitis. Khader YS, Albashaireh ZS, Alomari MA. Periodontal Disease A literature review 35 published in 2017 attempted to determine whether measurement of the inflammatory cytokines IL-1beta or TNF-alpha in saliva could be used as markers associated with clinical evidence of periodontal disease. suggested a strong association of IL-1β −511 and +3954 with chronic periodontitis in Indians [7, 8]. 2020 Mar;47(3):268-288. doi: 10.1111/jcpe.13189. Interleukin-6 is produced during inflammation by T cells.  |  The role of inflammation and genetics in periodontal disease. The condition may occur as part of a recognised syndrome or may occur as an isolated finding. IL-1 β is produced by a wide range of periodontal tissues and immune cells and, as such, is considered to have multiple roles in innate and adaptive immune responses to plaque bacteria which feature in the pathogenesis of periodontitis [ 49. that showed evidence of association with severity of periodontitis and colonization of microorganisms [22]. In periodontitis, this tissue homeostasis is altered with more destruction of connective tissue components and less inhibition by the TIMPs. This means that to be affected, a person needs to have a change (mutation) in only one copy of the disease-causing … This chapter is distributed under the terms of the Creative Commons Attribution 3.0 License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Studies have shown that tobacco use may be one of the most significant risk factors in the development and progression of periodontal disease. The recent meta-analysis by Nibali et al. The answer, at this point in time, is no. HeadquartersIntechOpen Limited5 Princes Gate Court,London, SW7 2QJ,UNITED KINGDOM. Epub 2020 Feb 3. Sanu O(1), Lamont RF. The interplay among the immune system, microbiota, and lifestyle habits like smoking, alcoholism, stress, and diet that leads to constant changes in the host is regulated by genes. 2020 Feb;24(2):833-840. doi: 10.1007/s00784-019-02973-2. On the basis of epidemiological studies in twins and in family studies with a high rate of early onset periodontitis, it can be concluded that in younger patients the genetic contribution may be as large as 50% to the total sum of causal factors, while in older patients the genetic contribution to the total of all causes is at most 25%. Please enable it to take advantage of the complete set of features! Periodontal diseases and the risk of coronary heart and cerebrovascular diseases: a meta-analysis. Whereas PD leads to destruction of the tooth-supporting structures, CAD is a chronic inflammatory condition ultimately causing myocardial infarction via narrowing and occluding of blood vessels. 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