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Year : 2015  |  Volume : 7  |  Issue : 1  |  Page : 18-23

Single nucleotide polymorphisms at interleukin (IL)-1β + 3954 and vitamin D receptor (VDR) TaqI in chronic periodontitis patients: A pilot study in North Indian population

1 Department of Periodontology, Faculty of Dentistry, Jamia Millia Islamia, New Delhi, India
2 Department of Biotechnology, Bundelkhand University, Jhansi, Uttar Pradesh, India
3 Professor, Periodontology, Career Dental College, Lucknow, Uttar Pradesh, India
4 Department of Periodontology, Faculty of Dental Sciences, Chhatrapati Shahuji Maharaj Medical University, Lucknow, Uttar Pradesh, India
5 Department of Genotoxicity Laboratory, Toxicology Division, Central Drug Research Institute, Lucknow, Uttar Pradesh, India

Date of Web Publication18-Mar-2015

Correspondence Address:
Dr. Anika Daing
Department of Periodontology, Jamia Millia Islamia, New Delhi - 110 025
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Source of Support: This work was supported by the CSIR, network project NWP0034. This bears communication number 170/2011/SKR of CDRI., Conflict of Interest: None

DOI: 10.4103/2231-0754.153490

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Background: Increasing evidences support the role of genetic factors in susceptibility to chronic periodontitis. The aim of the present pilot study was to explore the association of two potential single nucleotide polymorphisms (SNPs): Interleukin (IL)-1β + 3954 (rs1143634, C > T) and vitamin D receptor (VDR) TaqI (rs731236, T > C) with chronic periodontitis in a North Indian population. Materials and Methods: Twenty-eight chronic periodontitis subjects and 47 periodontally healthy controls were recruited. Individual samples of venous blood were obtained from each subject. Genotyping was done by polymerase chain reaction, followed by restriction fragment length polymorphism (PCR-RFLP). Logistic regression and chi square test were used for genetic association analysis and a P value less than 0.05 taken as statistical significance. Statistical Analysis Used: Chi square test and odds ratio (OR) was used. Results: Genotypes and alleles of SNP IL-1β + 3954 did not show a significant association (P > 0.05) with chronic periodontitis. Genotype CC and allele C of VDR TaqI were significantly associated with a higher risk for chronic periodontitis as compared to subjects with TT genotype (CC/TT OR = 4.615; 95% confidence interval [CI]: 1.17 to 18.078 P = 0.028) and allele T (C/T OR = 2.423; 95% CI: 1.179 to 4.980). Conclusion: In North Indian population, genotype CC and allele C of VDR TaqI were associated with risk of chronic periodontitis. No significant correlation was found for IL-1β + 3954 polymorphism and chronic periodontitis.

Keywords: Case control studies, chronic periodontitis, genetic polymorphisms, interleukin-1, receptor, receptor calcitriol, single nucleotide polymorphism, Taq polymerase, Vitamin D

How to cite this article:
Daing A, Singh SV, Saimbi CS, Khan MA, Rath SK. Single nucleotide polymorphisms at interleukin (IL)-1β + 3954 and vitamin D receptor (VDR) TaqI in chronic periodontitis patients: A pilot study in North Indian population. J Int Clin Dent Res Organ 2015;7:18-23

How to cite this URL:
Daing A, Singh SV, Saimbi CS, Khan MA, Rath SK. Single nucleotide polymorphisms at interleukin (IL)-1β + 3954 and vitamin D receptor (VDR) TaqI in chronic periodontitis patients: A pilot study in North Indian population. J Int Clin Dent Res Organ [serial online] 2015 [cited 2023 Feb 8];7:18-23. Available from: https://www.jicdro.org/text.asp?2015/7/1/18/153490

   Introduction Top

Chronic periodontitis is an inflammatory disease of multifactorial etiology. While its primary etiologic agent is accepted as bacterial, there is increasing evidence that susceptibility to the disease is dependent to a variable degree upon the host genetic factors. [1] A plethora of genetic factors including subtle combination of single nucleotide polymorphisms (SNPs) have been suggested to cause a functional change of the internal milieu, making individuals with aberrant genotypes more susceptible to the disease. In particular, SNPs in genes encoding molecules of the host defense system such as cytokines and factors which regulate cytokine expression have been targeted as potential genetic markers for chronic periodontitis. [2]

In this context, a considerable insight has been gained for variants of genes for interleukin (IL)-1 which is a key pro-inflammatory cytokine. IL-1 enables ingress of inflammatory cells into the sites of infection, causes eicosanoid release by monocytes and fibroblasts, stimulates matrix metalloproteinases, and contributes to the inflammatory cascades of microbial immune response. [3],[4],[5] IL-1 is known to be one of the most active stimulator of osteoclastic activity. It has been proposed that a particular genotype of IL-1 could predispose individuals to periodontal disease by enhancing the inflammatory process. [6]

Besides cytokines, mediators of bone metabolism also play a role in the pathophysiology of periodontitis. As alveolar bone loss is a key feature of chronic periodontitis, particular attention has been paid to the role of mediators of bone like vitamin D receptor (VDR) in the pathogenesis of the disease. [7] The mechanism by which VDR gene polymorphism influence the incidence of chronic periodontitis has not been clearly understood; however, investigators presume that VDR is involved in variety of biologic process including bone metabolism and the modulation of the immune response, a role in which it functions as a vitamin D 3 -dependent transcription factor. [8]

Several studies have been performed to investigate the possible association of IL-1and VDR gene polymorphism with chronic periodontitis in different ethnic and racial populations worldwide. [9],[10],[11],[12],[13],[14],[15],[16],[17],[18],[19],[20],[21],[22],[23],[24],[25] However, there are very few reports concerning the association of IL-1 gene polymorphism with chronic periodontitis in Indian population and particularly no documentation for VDR polymorphisms. [26],[27],[28],[29] Thus, the aim of the present endeavor was to study the association of two SNPs IL-1β + 3954 (rs1143634) and VDR TaqI (rs731236) with chronic periodontitis in a sample of North Indian population.

   Materials and Methods Top

Study design

Total 75 subjects (28 chronic periodontitis subjects and 47 controls) were recruited from the outpatient wing of Department of Periodontics for the present case control study. All the subjects who participated in the study were from North Indian subpopulations, belonging to the state of Uttar Pradesh. A written informed consent was obtained from each subject as per human ethics guidelines. Medical and dental histories of subjects were taken from the detailed questionnaire. The study protocol was reviewed and approved by the institution's ethical review board (CDRI/IEC/CEM/07-07-10).

Selection of subjects

A complete periodontal examination was carried out by single examiner using a UNC-15 probe (Hu-Friedy). Clinical periodontal parameters including probing pocket depth (PD), clinical attachment level (CAL), plaque index, calculus index, and gingival index were recorded. [30],[31],[32] A radiographic analysis was performed using an orthopantomogram to assess the bone level and confirm the clinical diagnosis. The study population was defined based on the clinical criteria proposed by the 1999 International world workshop for classification of periodontal diseases and conditions, [33] which was also adopted in previous studies. [34],[35] The subjects were categorized into chronic periodontitis group (n = 28) if exhibiting CAL ≥3 mm at >30% sites. The control group (n = 47) consisted of subjects exhibiting no sites with CAL and PD ≥ 3 mm. The selected control samples were of same ethnic origin. Exclusion criteria included: Systemic diseases like diabetes, hepatitis, immunosuppressive disorders, bleeding disorders; history of any disease known to severely compromise immune function; current pregnancy or lactation. Subjects who were tobacco smokers or smokeless tobacco users were also excluded.

Collection of blood samples

Blood samples (2 ml) were collected in tubes containing ethylenediaminetetraacetic acid (EDTA) from all the 75 subjects by venipuncture from anticubital fossa. The tubes were maintained in ice and transported to Genotoxicity Laboratory, Toxicology division of Central Drug Research Institute, Lucknow, Uttar Pradesh, India for isolation of genomic deoxyribonucleic acid (DNA) and SNP analysis.

DNA isolation

DNA was isolated from blood samples using Gene Elute TM blood genomic DNA kit (Sigma Aldrich) following manufacturers protocol, [36] quantified using spectrophotometer (Genequant, Amersham Biosciences) and stored at −20°C until further processing.

Selection of SNPs

SNP IL-1β + 3954 (rs1143634, C8967T, chromosome 2, C/T) on IL-1β gene and SNP VDR TaqI (rs731236, T65058C, chromosome 12, T/C) on VDR gene were selected for the study based on the available literature. [22],[37],[38]

Polymerase chain reaction (PCR)

Gradient PCR reaction was performed for standardization of DNA amplification condition and optimization of annealing temperature for the primer set (forward + reverse). Initially, the primer set was used to amplify a standard DNA template at different annealing temperatures (with increment of approximately 1°C each) and the temperature at which highest amount of PCR product was formed (as visualized from agarose gel) was considered the optimum annealing temperature for further PCR reactions. Further PCR reactions were performed using the optimized annealing temperatures.

All PCR reactions were performed in 200 μl transparent PCR tubes on a peltier-based thermal cycler (PTC100, MJ Research) using reagents from Fermentas Life Sciences (Fermentas, Lithuania) in a total reaction volume of 20 μl containing nearly 100 ng genomic DNA, 1.5 U Taq polymerase (New England biolabs) in 1X PCR buffer, 1.5 mM MgCl2, 10 pmol (0.5 μM) of each primer and 0.2 mM deoxynucleotide triphosphates (dNTPs). Primers used are shown in [Table 1]. Thermocycling conditions for IL-1β + 3954 are as follows: Initial denaturation at 95°C for 4 minutes followed by 35 cycles of denaturation at 95°C for 30 seconds, annealing at 59°C for 30 seconds, extension at 72°C for 30 seconds with final extension at 72°C for 7 minutes. Thermocycling conditions for VDR TaqI were same as mentioned above except the annealing temperature which was 61°C for 30 seconds. [22]
Table 1: PCR primers, restriction enzymes and lengths of fragments generated upon restriction digestion

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The PCR products were visualized by electrophoresis on 1.2% agarose gel. For gel electrophoresis, 5 μl of the amplified product was mixed with 1 μl of 6× gel loading buffer (analytical grade water containing 30% glycerol, 0.25% bromophenol blue, 0.25% xylene cynole) and resolved on 1.2% agarose gel in tris-acetate-EDTA (TAE) buffer at 80 volts for 2 hrs. Moreover, 50 base pair (bp) DNA markers were run with the amplified products as reference. PCR products were assessed based upon the presence of 194 bp product for IL-1β + 3954 and a 340 bp product for VDR TaqI.

Restriction fragment length polymorphism (RFLP)

Ten microliter PCR products from samples positive for IL-1β + 3954 and VDR TaqI were separately mixed with 2 μl buffer and 0.5 μl enzyme TaqI in a total reaction volume of 20 μl. The reaction mixture was incubated at 65°C overnight in a water bath. The resulting digestion products 97 + 85 + 12 bp (allele C, allele 1) and 182 + 12 bp (allele T, allele 2) for IL-1β + 3954; and 340 bp (allele T, allele 1) and 293 + 47 bp (allele C, allele 2) for VDR TaqI were visualized on 3% and 1.5% agarose gel electrophoresis with ethidium bromide staining [Table 1] and [Figure 1] and [Figure 2].
Figure 1: Restriction digestion pattern of PCR product [VDR TaqI] Marker- 50 bp (fermentas)

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Figure 2: Restriction digestion pattern of PCR product [IL beta + 3954] Marker- 50 bp (fermentas)

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For the present study, statistical analysis of data was performed using the computer softwares Statistical Package for the Social Sciences (SPSS) version 16.0 and GraphPad Prism 5. Hardy-Weinberg equilibrium was tested to compare the observed and expected genotype frequencies in control group. The distribution of genotypes and alleles frequency in the chronic periodontitis and the control group were compared using the standard chi square test. The risk associated with individual genotypes or alleles were calculated as Odds ratio (OR) with 95% confidence interval (CI) using logistic regression analysis. Age and gender distribution between diseased and control groups were respectively compared by independent t test and chi square test. All test used for the analysis were two-sided and a probability value < 0.05 was considered significant.

   Results Top

Age and gender were equally distributed among the study groups with no statistically significant difference (P > 0.05) [Table 2]. The frequency distribution of genotypes and alleles of SNP IL-1β + 3954 was not statistically significant (P > 0.05) both prior to and after adjustment for age and gender. For SNP VDR TaqI, an overall distribution of genotypes was not significant (P > 0.05) between the study groups [Table 3]. However, the relative risk analysis between the genotypes showed that genotype CC was more frequent in the chronic periodontitis group (28.6%) as compared to controls (8.5%), with a more than fourfold-associated risk when compared to genotype TT (CC/TT OR = 4.615;95% CI: 1.17 to18.078 P = 0.028). This risk associated with genotype CC further increased after adjusting for age and gender (CC/TT OR* = 4.956; 95% CI: 1.238-19.846, P = 0.024). Furthermore, C allele of VDR TaqI was more prevalent in subjects with chronic periodontitis (41.1%) as compared to controls (22.3%) and the associated risk was statistically significant (C/T OR = 2.423;95% CI:1.179 to 4.980).
Table 2: Characteristics of controls and chronic periodontitis (ChP) group

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Table 3: Distribution of genotype and allele of IL-1β + 3954 and VDR TaqI gene polymorphism in control and chronic periodontitis group

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   Discussion Top

The present study adds to the understanding of the role of genetic variants in the development of chronic periodontitis. New insights into genetic polymorphism provides with an altered paradigm of periodontal disease that emphasizes on the variation of host response in the pathogenesis of periodontitis. Present study is a pioneer endeavor to explore the association of IL-1β + 3954 and VDR TaqI polymorphism with chronic periodontitis in a sample of North Indian population.

On the basis of ethnic origin, Indian population can be sub-structured as four morphological types - Caucasoid, Mongoloid, Australoid, and Negrito; and on the basis of language families as: Indo European, Dravidian, Tibeto-Burman, and Austro Asiatic. Caucasoid morphological subtype and Indo linguistic group predominates in North Indian region. [39],[40] All subjects inducted in this study were recruited strictly from the North Indian subpopulation of Uttar Pradesh to keep the homogeneity within the ethnic group constituting mostly Caucasian morphological subtype of the Indo European linguistic group. [41] Smokers and smokeless tobacco users were excluded from the study as tobacco is a major risk factor in the development of periodontal diseases and previous studies have found that genetic association of chronic periodontitis was more evident when smokers were excluded. [15],[26],[27],[28]

Human genetic variants are found most commonly in the form SNPs with a frequency of 0.3 kb across human genome. [42],[43],[44] For this reason, SNPs were employed for the present genetic exploration. Both SNPs (IL-1β + 3954 and VDR TaqI) screened for the present study play a role in the inflammation and immunity, and as such might play a role in the altered inflammatory response leading to the development of symptoms seen in periodontal diseases. Both examined polymorphisms are functional and have effect on amount and/or activity of protein produced from each gene. This makes the two aforementioned SNPs an attractive candidate for current genetic association study.

In the present endeavor we examined IL-1β gene of Il-1 family (IL1- α, IL-1β, and IL-1RN) as previous studies have shown that IL-1β is 15 times more potent than IL-1α. [27],[45] The biological role of Il-1β + 3954 gene polymorphism in periodontal disease is that it directly influences production of Il-1β cytokine. Individuals homozygous for allele T produce an amount of Il-1β cytokine that is four times higher than subjects having CC genotype. [46] The genotypic and allelic distribution of IL-1β + 3954 revealed no statistically significant difference (P > 0.05) between chronic periodontitis and the control group in our study [Table 3]. These results of insignificance were consistent with findings in many different populations of South African, Polish, and Greek origin. [17],[18],[19] However, discordant with our results, several authors have found IL-1β + 3954 allele T to be a significant risk factor for chronic periodontitis in Caucasian, HanChinese, Chinese, and Brazilian populations. [9],[10],[11],[12],[13],[14]

In context to Indian population, varied results have been documented on association of Il-1β + 3954 gene polymorphism with chronic periodontitis. A study in Maharashtrian ethnicity and in a South Indian population reported an increased prevalence of T allele of IL-1β + 3954 in chronic periodontitis subjects whereas allele C was associated with increased risk of chronic periodontitis in Dravidian population. [26],[27],[29] A large variation in results within the Indian population can be possible explained due to differences in genetic makeup of ethnic groups residing in India.

Genotypes of VDR TaqI was not significantly (P > 0.05) distributed in control and chronic periodontitis group [Table 3]. However, on further analyzing it was observed that CC genotype was more prevalent in chronic peridontitis group (28.6%) than in controls (8.5%), showing a greater than fourfold risk for chronic periodontitis (OR = 4.615, P = 0.028). Associated risk with genotype CC increased (OR * = 4.956, P = 0.024) after adjusting for age and gender indicating that above factors were additive to the risk of SNP. Similarly, carriage of C allele was higher in chronic periodontitis (41.1%) subjects as compared to controls (23.3%), with a greater than two times associated risk for the disease (OR = 2.423, P = 0.0148). Our results were similar to those observed by de Brito et al., in a Brazilian population who also reported patients with C allele to be 2.4 times more susceptible to the disease. [20] In contrast to our findings Gunes et al., Brett et al., Wang et al., and Tachi et al., obtained a higher distribution of allele T and genotype TT in chronic periodontitis subjects in their respective Turkish, Caucasian, Chinese, and Japanese populations. [21],[22],[23],[24]

A large inconsistency shown by IL-1β + 3954 and VDR TaqI genotypes in different studies can be attributed to racial differences and also to confounding factors like clinical diagnosis, number of subjects enrolled, environmental variables, biologic plausibility, and logic of association studies. Because of the relatively small number of the subjects, results of the present study should be considered as preliminary and hypothesis generating. Further studies with a larger sample population and more elaborative study designs are needed to firmly establish the results.

To conclude, this study demonstrated a possible association of allele C and genotype CC of VDR TaqI polymporphism with chronic periodontitis in North Indian population; however, no association was found between Il-1β + 3954 gene polymorphism and chronic periodontitis in this pilot study.

   Acknowledgement Top

The work was supported by Council for Scientific and Industrial Research (CSIR), India, network project (NWP 0034).

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  [Figure 1], [Figure 2]

  [Table 1], [Table 2], [Table 3]

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