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BY 4.0 license Open Access Published by De Gruyter October 26, 2021

Association of bitter and sweet taste gene receptor polymorphisms with dental caries formation

[Farklı Acı ve Tatlı Tat Gen Reseptör Polimorfizmlerinin Diş Çürüğü Oluşumu ile İlişkisi]
Melis Yilmaz ORCID logo EMAIL logo , Senay Balci ORCID logo , Nazan Kocak Topbas ORCID logo , Didem Derici Yildirim ORCID logo and Lulufer Tamer ORCID logo



The aim of the study is to analyze the association of different bitter and sweet gene receptor polymorphisms and bitter and sweet food consumption on formation of dental caries in Turkish adult population.


This study included 205 adults whose detailed intraoral health examination was completed and decayed, missing, filled teeth (DMFT) index values were recorded. A mini questionnaire was applied to assess the consumption of bitter and sweet food. A venous blood sample from each participant was collected in Ethylenediamine tetraacetic acid (EDTA) tubes. Further, DNA samples were isolated from the blood samples by utilizing a DNA isolation kit, which were stored at +4 °C prior to the analysis. Taste receptor type 2 member 38 (TAS2R38; rs10246939, rs713598, rs1726866), Taste receptor type 1 member 2 (TAS1R2; rs35874116, rs9701796), and Taste receptor type 1 member 3 (TAS1R3; rs307355) gene polymorphisms were detected using real-time polymerase chain reaction (PCR).


There was no statistically significant association between the TAS2R38, TAS1R2, and TAS1R3 gene polymorphism and the DMFT index (p>0.05). No significant difference was found between the consumption of bitter and sweet food and the DMFT index (p>0.05).


TAS2R38 (rs10246939, rs713598, rs1726866), TAS1R2 (rs35874116, rs9701796), and TAS1R3 (rs307355) gene polymorphism may not be associated with the formation of dental caries in the Turkish adult population.



Bu çalışmanın amacı, farklı acı ve tatlı gen reseptör polimorfizmleri ile acı ve tatlı gıda tüketiminin diş çürüğü oluşumu üzerindeki ilişkisini değerlendirmektedir.


Çalışmaya detaylı ağız-diş sağlığı muayenesi yapılmış ve çürük, eksik, dolgulu dişler (DMFT) indeksi değerleri not edilen 205 yetişkin dahil edildi. Acı ve tatlı yiyeceklerin tüketimini değerlendirmek için mini bir anket uygulandı. Katılımcılardan EDTA tüplerine venöz kan örneği alındı. DNA izolasyon kiti ile kan örneklerinden DNA örnekleri izole edildi ve analiz gününe kadar + 4 °C’de saklandı. Tip 2 tat reseptörü üye 38 (TAS2R38; rs10246939, rs713598, rs1726866), Tip 1 tat reseptörü üye 2 (TAS1R2; rs35874116, rs9701796) ve Tip 1 tat reseptörü üye 3 (TAS1R3; rs307355) gen polimorfizmleri Real-Time PCR kullanılarak tespit edildi.


TAS2R38, TAS1R2 ve TAS1R3 gen polimorfizmi ile DMFT indeksi arasında istatistiksel olarak anlamlı bir ilişki yoktu (p>0.05). Acı ve tatlı gıda tüketimi ile DMFT indeksi arasında anlamlı bir fark bulunmadı (p>0.05).


TAS2R38 (rs10246939, rs713598, rs1726866), TAS1R2 (rs35874116, rs9701796) ve TAS1R3 (rs307355) gen polimorfizmleri, Türk yetişkin popülasyonunda diş çürüğü oluşumu ile ilişkili olmayabilir.


Complex environmental and numerous genetic factors are known to influence the occurrence and progression of dental caries [1]. The importance of genetic factors in the formation of caries is supported by twin studies. It is estimated that 40–60% of caries susceptibility is genetically determined [1], [2], [3], [4], [5], [6]. Animal studies also strongly support the genetic contribution to the risk of developing caries [7], [8], [9], [10]. Studies have demonstrated the importance of dietary habits, nutritional status, and chemically determined taste sensitivity in determining this risk [1, 4].

Studies in the last 15 years have allowed for the identification of proteins that act as taste receptors. There are five basic tastes that are consciously perceived as sweet, sour, salty, bitter, and umami [11].

Human sweet taste perception is mediated by the heterodimeric G-protein coupled receptor complex encoded by the TAS1R2 (taste receptor, type-1, member 2) and TAS1R3 (taste receptor, type-1, member 3) genes [1, 7, 12], [13], [14], [15]. The TAS1R gene family is mainly effective in sweet taste perception sensitization. TAS1R gene subunits are located on chromosome 1 as TAS1R1, TAS1R2, and TAS1R3 [7, 12]. The perception of bitter taste appears to be largely mediated by the TAS2R38 gene [13], [14], [15]. The TAS2R38 gene located on chromosome 7q36 is a member of the bitter unpleasant and pleasant sensations from alcohol [15]. All these three genes are of the protein coding kind and among their related pathways are taste transduction and peptide ligand-binding receptors [16]. Detailed information on taste receptor gene polymorphisms that were analyzed in this study has been outlined in Table 1.

Table 1:

Detailed information on the taste receptor gene polymorphisms.

Gene Position SO term Alleles MAF*
TAS1R2 rs35874116 chr1:18854899 (GRCh38.p13) Missense variant T>C C=0.319942
rs9701796 chr1:18859635 (GRCh38.p13) Missense variant G>C C=0.780938
TAS1R3 rs307355 chr1:1329774 (GRCh38.p12) 2 KB upstream variant T>C C=0.86580
TAS2R38 rs713598 chr7:141973545 (GRCh38.p13) Missense variant C>G G=0.422175
rs10246939 chr7:141972804 (GRCh38.p13) Missense variant T>C C=0.464881
rs1726866 chr7:141972905 (GRCh38.p13) Missense variant G>A A=0.528597
  1. *Global minor allel frequency data from dbSNP.

Sugar intake was found to be associated with sweet taste receptor (TAS1R2) alleles in humans [17]. In addition, the genetic variation of the bitter taste receptor TASR38 is found to be associated with the intake of vegetables, fat, and sweets [17], as dietary habits, nutritional status, and chemically determined taste sensitivity has been associated with the risk of caries [1, 4]. The different polymorphisms of TAS1R2, TAS2R38, and TAS1R3 and their possible associations with dental caries have been evaluated in the literature [18], [19], [20].

In the literature, there are few studies that have profoundly covered the association of taste genes and dental caries formation across different age ranges: TAS1R2 (ages 7–12) [7]; (ages 21–32) [21]; TAS1R2, TAS2R38, GNAT3 (guanine nucleotide binding protein, alpha transducing-3) (ages 1–42) [1]; CA6, TAS1R1, TAS1R3, TLR2, and TLR4 (ages 25–55) [19]; AMELX, CA6, DEFB1, and TAS2R38 (ages 20–60) [20]; TAS1R2 and GLUT2 (glucose transporter genes) (ages 18–65) [22]; TAS1R2 and GLUT2 (ages 11–13) [23]; and TAS1R1, TAS1R2, TAS1R3, TAS2R16, TAS2R38, TAS2R50, SLC2A2, SLC2A4, GNAT3, SCN1B, and TRPV1 (ages 18–23) [24].

There is no study in the literature that has evaluated the association between dental caries formation with three taste genes simultaneously in the Turkish population: a bitter gene with three polymorphisms (TAS2R38 (rs10246939, rs713598, rs1726866)) and two sweet taste genes with three polymorphisms (TAS1R2 (rs35874116, rs9701796) and TAS1R3 (rs307355)). In this study, we aim to investigate the possible effect of bitter and sweet food consumption and different bitter and sweet gene receptor polymorphisms on the formation of dental caries.

Materials and methods

The study protocol was approved by the local Ethical Committee of Mersin University (date: 13/04/2017; number: 102), and the written informed consent was obtained from all participants prior to data collection.

This study included 205 adults (18–45 years old; 91 men, 114 women), who attended the Faculty of Dentistry clinic at Mersin University for a routine dental examination. Clinical observations were made by two experienced dentists who had no knowledge of the individuals’ genotype. The patients were subjected to a detailed intraoral examination, and their decayed, missing and filled teeth (DMFT) scores were recorded after their teeth cleaning were performed with a brush and low abrasive polishing paste.

The DMFT index is used in accordance with the World Health Organization’s tooth decay evaluation criteria, and it evaluates the oral dental health of the population. It is used for permanent teeth. Further, a similar index used for primary teeth is expressed in small letters and referred to as the dmft index. The sample was surveyed through this mini questionnaire regarding their bitter or sweet taste preferences at the same appointment:

  1. If you consider your food consumption, which one do you prefer—bitter or sweet?

  2. When you are hungry, which food do you prefer to consume—bitter or sweet?

  3. If you consider your family’s food consumption, which one do you prefer—bitter or sweet?

Venous blood samples from each participant were drawn into EDTA tubes in the Medical Biochemistry Department. Furthermore, DNA samples were isolated from blood samples using a DNA isolation kit (Roche Diagnostics, GmbH, Germany), which were stored at +4 °C prior to the analysis. TAS2R38 (rs10246939, rs713598, rs1726866), TAS1R2 (rs35874116, rs9701796), and TAS1R3 (rs307355) gene polymorphisms were detected using real-time polymerase chain reaction (PCR) (LightCycler® 480 Instrument II – Diagnostics Roche GmbH, Germany) with a single nucleotide polymorphisms detection kit.

The inclusion and exclusion criteria for patient selection

This study included individuals aged between 18 and 45 years who visited Mersin University for a routine dental examination. Patients with general health problems such as anemia, diabetes mellitus, or any heart diseases; patients with amelogenesis imperfecta and dentinogenesis imperfecta; patients who do not have tooth brushing habits (those who brush less than twice a day); and patients with obesity were excluded from the study group.

Statistical analysis

Descriptive analyses were summarized as the mean ± standard deviation (SD). Additionally, categorical variables were summarized as counts and percentages. The chi-square test was used for categorical endpoints. An exact test was used when the probability of an expected count less than five was more than 25%. The Hardy-Weinberg equilibrium (HWE) of groups on account of genotypes was checked by the chi-square test and the frequencies of polymorphism were in HWE (p>0.05). A p-value of less than 0.05 was considered statistically significant.


The DMFT index values of 205 adults (aged 18–45 years (mean age 31.36 ± 8.25); 91 men, 114 women) were evaluated in the permanent dentition.

The basic description of participants is shown in Table 2. The education level of the samples is as follows: 47 participants (23%) had completed primary level, 79 of them (39.1%) secondary, and 76 of them (37.6%) graduate. The income level of the participants can be outlined as follows: 81 participants (39.5%) earn less than the minimum wage, 108 of them (52.7%) earn minimum wage, and 16 of them (7.8%) earn more than the minimum wage. There was no significant difference between the samples’ basic description. When the relationship between education or income and dental caries risk was analyzed, no statistically significant association was found.

Table 2:

Basic description of participants.

n %
Age, mean ± standard deviation, years 31.36 ± 8.25
Sex Male 91 44.4
Female 114 55.6
Education Primary 47 23.3
Secondary 79 39.1
Licentiate 76 37.6
Income <minimum wage 81 39.5
=minimum wage 108 52.7
>minimum wage 16 7.8
If you consider your food consumption, which one do you prefer, bitter or sweet? Equal 73 35.6
Bitter 60 29.3
Sweet 72 35.1
When you are hungry which food do you prefer to consume, bitter or sweet? Bitter 43 21.0
Sweet 75 36.6
Not matter 87 42.4
If you consider your family’s food consumption, which one do you prefer, bitter or sweet? Equal 86 42.0
Bitter 61 29.8
Sweet 58 28.3

In addition, according to the data obtained from the questionnaire completed by the participants, no significant association was found between the consumption of bitter and sweet food and DMFT index values (p>0.05).

Moreover, the taste gene receptor polymorphisms and DMFT index values were compared, and no statistically significant association was found between the individuals with TAS2R38, TAS1R2, and TAS1R3 gene polymorphisms and the DMFT index values (p>0.05) (Table 2).

The distribution of the major–minor allele in the population at stake is displayed in Table 3 and minor allele distribution is seen as TAS1R2 (rs35874116) C 31.5%, TAS1R2 (rs9701796) G 20%, TAS1R3 (rs307355) C 88.05%, TAS2R38 (rs713598) G 48.29%, TAS2R38 (rs10246939) C 52.68%, TAS2R38 (rs1726866) A 47.56%.

Table 3:

Association of taste gene receptor polymorphisms and caries risk groups within DMFT values and allele distribution.

DMFT p-Value
Low risk (0–3) Moderate risk (4–7) High risk (>8)
n, % n, % n, %
TAS1R3 (rs307355) CC 43 (26.7%) 56 (34.8%) 62 (38.5%) 0.548
CT 9 (23.1%) 13 (33.3%) 17 (43.6%)
TT 2 (40.0%) 0 (0.0%) 3 (60.0%)
Total 54 (100.0%) 69 (100.0%) 82 (100%)
C 95 (87.9%) 125 (90.6%) 141 (85.9%)
T 13 (12.1%) 13 (9.4%) 23 (14.1%)
TAS1R2 (rs35874116) CC 2 (9.1%) 11 (50.0%) 9 (40.9%) 0.055
CT 20 (24.7%) 32 (39.5%) 29 (35.8%)
TT 31 (31.0%) 25 (25.0%) 44 (44.0%)
Total 53 (100.0%) 68 (100.0%) 82 (100.0%)
C 24 (22.6%) 54 (39.7%) 47 (28.6%)
T 82 (77.4%) 82 (60.3%) 117 (71.3%)
TAS1R2 (rs9701796) CC 36 (27.5%) 44 (33.6%) 51 (38.9%) 0.986
CG 16 (24.2%) 22 (33.3%) 28 (42.4%)
GG 2 (25.0%) 3 (37.5%) 3 (37.5%)
Total 54 (100.0%) 69 (100.0%) 72 (100.0%)
C 88 (81.4%) 110 (79.7%) 130 (79.3%)
G 20 (18.6%) 28 (20.3%) 34 (20.7%)
TAS2R38 (rs713598) CC 15 (27.8%) 15 (27.8%) 24 (44.4%) 0.661
CG 28 (26.9%) 39 (37.5%) 37 (35.6%)
GG 11 (23.9%) 14 (30.4%) 21 (45.7%)
Total 54 (100.0%) 68 (100.0%) 82 (100.0%)
C 58 (53.7%) 69 (50.7%) 85 (51.8%)
G 50 (46.3%) 67 (49.3%) 79 (48.2%)
TAS2R38 (rs10246939) CC 14 (25.9%) 17 (31.5%) 23 (42.6%) 0.987
CT 29 (26.9%) 38 (35.2%) 41 (38.0%)
TT 11 (26.2%) 14 (33.3%) 17 (40.5%)
Total 54 (100.0%) 69 (100.0%) 81 (100.0%)
C 57 (52.7%) 72 (52.2%) 87 (53.7%)
T 51 (47.3%) 66 (47.8%) 75 (46.3%)
TAS2R38 (rs1726866) AA 11 (25.6%) 14 (32.6%) 18 (41.9%) 0.879
AG 29 (27.1%) 39 (36.4%) 39 (36.4%)
GG 14 (25.9%) 16 (29.6%) 24 (44.4%)
Total 54 (100.0%) 69 (100.0%) 81 (100.0%)
A 51 (47.2%) 67 (48.5%) 75 (46.3%)
G 57 (52.8%) 71 (51.4%) 87 (53.7%)
  1. The chi-square test was used for categorical endpoints. An exact test was used when the probability of an expected count less than five was more than 25%. Hardy-Weinberg equilibrium (HWE) of groups on account of genotypes was checked by chi-square test and the frequencies of polymorphism were in HWE (p>0.05).


Dental caries is a complex disease that is related to dietary habits, taste sensitivity, genetic factors, and teeth brushing habits [1], [2], [3], [4, 25]. The evaluated literature states that 40–60% cases of dental caries are affected by genetic factors [1], [2], [3], [4], [5], [6].

Evaluations of the relationships of dental caries, varying ages and genetic polymorphisms in different genes, such as TAS1R1, TAS1R2, TAS1R3, TAS2R16, TAS2R8, CA6, TLR2, TLR4, TAS2R50, AMELX, DEFB, SLC2A2, SLC2A4, GNAT3, SCN1B, TRPV1, and GLUT2, have been analyzed in various studies [1, 7, 19], [20], [21], [22], [23], [24].

This study is the first to evaluate the relationship between dental caries formation and both TAS1R2 and TAS1R3 sweet taste genes and the TAS2R38 bitter taste gene with six polymorphisms and food consumption in a sample group of the Turkish adult population.

The perception of sweet, umami, and bitter tastes is mediated via G-coupled protein receptors encoded by the TAS1R1 and TAS1R2 taste receptor gene families. The area of bitterness sensitivity is the most extensively researched of all taste qualities. The bitter compounds phenylthiocarbamide (PTC) and propylthiouracil (PROP) were first noted in the early 1930s. The TAS2R38 gene was found to be responsible for the majority of the variation in bitter taste sensitivity [25] and included the study with three polymorphisms.

The sweet taste was found to be mediated by two genes, TAS1R3 [25] and TAS1R2 [25, 26]. The TAS2R38 bitter taste gene has three common SNPs (rs10246939, rs713598, rs17268663), and all of them were included in the study plan. Further, TAS1R2 (rs35874116, rs9701796) and TAS1R3 (rs307355) gene polymorphisms were selected, similar to Haznedaroğlu et al.’s study, which evaluated the same population with different age groups [7].

There is no analysis encountered in the literature that has explored allele and minor allele distribution gene polymorphisms in the Turkish population but the frequency of global minor allele distribution has been known (Table 1). When the minor allele distribution frequency of this study and frequency of global minor allele distribution were evaluated together, our findings appeared to be similar to the TAS1R2 (rs35874116) C allele, TAS1R3 (rs307355) C allele, and all polymorphisms that have been explored of TAS2R38 gene (rs713598 G allele, rs10246939 C allele, rs1726866 A allele); yet, they are lower than the TAS1R2 (rs9701796) C allele.

In the literature, there is no caries risk classification for adults that performs its evaluation with DMFT caries scores. On the contrary, with reference to children, there is caries risk group classification with DMFT/dmft scores [7]. In the studies that investigate adults, the results were analyzed among gene polymorphisms by median and standard deviation [21, 22]. We analyzed the results of both DMFT caries risk groups and median–standard deviation and found no significant results again (data not shown).

In a family study, Wendell et al. evaluated the relationship between TAS2R38 (rs10246939, rs713598, rs17268663) as a bitter taste gene and TAS1R2 (rs4920566, rs9701796) as a sweet taste gene in caries formation. No statistically significant results were found between the DMFT index values of the TAS2R38 (rs10246939, rs713598, rs17268663) and TAS1R2 (rs9701796) genes in the permanent dentition group, although a statistically significant difference was found in the mixed dentition group [1]. Our study, on the other hand, was different from this study as it included the evaluation of TAS1R2 (rs35874116) and TAS1R3 (rs307355) polymorphisms. This is also true since the TAS1R2 (rs4920566) polymorphism was not included in our study design. However, in permanent dentition, our results and Wendell et al.’s results were similar with regard to the TAS2R38 (rs10246939, rs713598, rs17268663) and TAS1R2 (rs9701796) gene polymorphisms.

Haznedaroğlu et al. found no correlation between the DMFT index and TAS1R2 (rs35874116, rs9701796) and TAS1R3 (rs307355) gene polymorphisms in permanent dentition but found significant results between TAS1R2 (rs35874116) when compared with DMFT + dmft in mixed dentition and, in different age groups, in C/C in the high caries risk group [7]. This data is similar to our study results within the same population in permanent dentition. In addition, Holla et al. showed that the same polymorphism in TAS1R2 (rs35874116) was associated with the risk of dental caries formation, defined as DMFT scores ≥4 in permanent dentition (11–13 years) with children in their study, which evaluated the TAS1R2 gene (rs35874116) and the GLUT2 gene [23]. The study conducted by Kulkanie et al. reported a direct effect of TAS1R2 (rs35874116) and GLUT2 taste genes on caries formation in adults. Kulkanie’s results were different from those of Haznedaroğlu et al. and Holla et al., which showed the lowest caries scores in the TAS1R2 (rs35874116) group and our study as finding TAS1R2 (rs35874116) ineffective on caries formation [21]. In another study, Robino et al. evaluated the relationship between TAS1R2 (rs3935570) and GLUT2 in dental caries formation. They found that both TAS1R2 and GLUT2 were associated with dental caries risk or protection in adults [22].

In addition, no significant difference was found between the consumption of bitter and sweet food and DMFT index values (p>0.05) in this study. In the literature, another study evaluated bitter and sweet food preferences or intake and dental caries formation and similarly found no correlation with caries status and bitter and sweet food intake. However, it has also been reported that allelic variations in the GNAT3, SLC2A2, SLC2A4, TAS1R1, and TAS1R2 genes are associated with caries status [24].

In conclusion, we found that TAS2R38 (rs10246939, rs713598, rs17268663), TAS1R2 (rs9701796) and TAS1R3 (rs307355) gene polymorphisms have no effect on dental caries formation and bitter and sweet food consumption in the Turkish population.

It is known that candidate gene association studies have undergone various setbacks including false positives and poor control of population stratification [27]. Thus, the sample size was determined by power analysis where more participants were included in the study to overcome such a setback. The reasons for finding no association among polymorphisms as an outcome of the study might stem from the fact that this analysis was previously planned as a preliminary population study. It, thus, failed to impose control on all segments of the population, just like all genome-wide association studies (GWAS). Other reasons could be related with the fact that there is a lack of equal sampling on dental caries risk groups and that the patients involved have lower DMFT scores.

The results of this study show similarities and differences in the literature regarding the polymorphic changes by geographical region. The aim of this research was to investigate the taste receptors that have not been investigated in the Turkish population previously as a preliminary study. In the future, we aim to contribute to the literature with studies of different caries risk groups and different taste gene receptors and a more detailed analysis of the taste pathway mechanisms in relation with smoking and alcohol consumption.

Corresponding author: Melis Yilmaz, Department of Endodontics, School of Dentistry, Mersin University, Mersin, Turkey, Mobile: +905354415140, E-mail:

This study was presented as an Oral Presentation at the ‘First International Mediterranean Annual Symposium on the 1–3 November 2018 in Mersin, Turkey.

Funding source: Mersin Üniversitesi

Award Identifier / Grant number: 2017-2-AP4-2629

  1. Research funding: This project was supported by the Scientific Research Projects Unit of Mersin University (project code 2017-2-AP4-2629).

  2. Author contributions: Authors have accepted responsibility for the all content of this manuscript and approved its submission.

  3. Competing interests: The authors declare no conflicts of interest with respect to the research, authorship, and/or publication of this article.


1. Wendell, S, Wang, X, Brown, M, Cooper, M, DeSensi, RS, Weyant, RJ, et al.. Taste genes associated with dental caries. J Dent Res 2010;89:1198–202. in Google Scholar

2. Boraas, JC, Messer, LB, Till, MJ. A genetic contribution to dental caries, occlusion, and morphology as demonstrated by twins reared apart. J Dent Res 1988;67:1150–5. in Google Scholar

3. Conry, JP, Messer, LB, Boraas, JC, Aeppli, DP, Bouchard, TJJr. Dental caries and treatment characteristics in human twins reared apart. Arch Oral Biol 1993;38:937–43. in Google Scholar

4. Bretz, WA, Corby, PM, Melo, MR, Coelho, MQ, Costa, SM, Robinson, M, et al.. Heritability estimates for dental caries and sucrose sweetness preference. Arch Oral Biol 2006;51:1156–60. in Google Scholar PubMed

5. Bretz, WA, Corby, PM, Schork, NJ, Robinson, MT, Coelho, M, Costa, S, et al.. Longitudinal analysis of heritability for dental caries traits. J Dent Res 2005;84:1047–51. in Google Scholar PubMed PubMed Central

6. Wang, X, Shaffer, JR, Weyant, RJ, Cuenco, KT, DeSensi, RS, Crout, R, et al.. Genes and their effects on dental caries may differ between primary and permanent dentitions. Caries Res 2010;44:277–84. in Google Scholar PubMed PubMed Central

7. Haznedaroğlu, E, Koldemir-Gündüz, M, Bakır-Coşkun, N, Bozkuş, HM, Çağatay, P, Süsleyici-Duman, B, et al.. Association of sweet taste receptor gene polymorphisms with dental caries experience in school children. Caries Res 2015;49:275–81. in Google Scholar PubMed

8. Liu, H, Deng, H, Cao, CF, Ono, H. Genetic analysis of dental traits in 82 pairs of female-female twins. Chin J Dent Res 1998;1:12–6.Search in Google Scholar

9. Shuler, CF. Inherited risks for susceptibility to dental caries. J Dent Educ 2001;65:1038–45. in Google Scholar

10. Nariyama, M, Shimizu, K, Uematsu, T, Maeda, T. Identification of chromosomes associated with dental caries susceptibility using quantitative trait locus analysis in mice. Caries Res 2004;38:79–84. in Google Scholar PubMed

11. San Gabriel, AM. Taste receptors in the gastrointestinal system. Flavour 2015;4:14. in Google Scholar

12. Kim, UK, Wooding, S, Riaz, N, Jorde, LB, Drayna, D. Variation in the human TAS1R taste receptor genes. Chem Senses 2006;31:599–611. in Google Scholar PubMed

13. Opal, S, Garg, S, Jain, J, Walia, I. Genetic factors affecting dental caries risk. Aust Dent J 2015;60:2–11. in Google Scholar PubMed

14. Fushan, AA, Simons, CT, Slack, JP, Manichaikul, A, Drayna, D. Allelic polymorphism within the TAS1R3 promoter is associated with human taste sensitivity to sucrose. Curr Biol 2009;19:1288–93. in Google Scholar PubMed PubMed Central

15. Duffy, VB, Davidson, AC, Kidd, JR, Kidd, KK, Speed, WC, Pakstis, AJ, et al.. Bitter receptor gene (TAS2R38), 6-n-propylthiouracil (PROP) bitterness and alcohol intake. Alcohol Clin Exp Res 2004;28:1629–37. in Google Scholar PubMed PubMed Central

16. Alelyani, AA, Azar, PS, Khan, AA, Chrepa, V, Diogenes, A. Quantitative assessment of mechanical allodynia and central sensitization in endodontic patients. J Endod 2020;46:1841–8. in Google Scholar PubMed

17. Han, P, Keast, R, Roura, E. TAS1R1 and TAS1R3 polymorphisms relate to energy and protein-rich food choices from a buffet meal respectively. Nutrients 2018;10:1906. in Google Scholar PubMed PubMed Central

18. Chisini, LA, Cademartori, MG, Conde, MCM, Costa, FDS, Salvi, LC, Tovo-Rodrigues, L, et al.. Single nucleotide polymorphisms of taste genes and caries: a systematic review and meta-analysis. Acta Odontol Scand 2021;79:147–55. in Google Scholar PubMed

19. Yıldız Telatar, G, Saydam, F, Güzel, Aİ, Telatar, BC. Variants in taste genes on caries risk and caries activity status. Med Mol Morphol 2020;53:244–51. in Google Scholar PubMed

20. Yildiz, G, Ermis, RB, Calapoglu, NS, Celik, EU, Türel, GY. Gene-environment interactions in the etiology of dental caries. J Dent Res 2016;95:74–9. in Google Scholar PubMed

21. Kulkarni, GV, Chng, T, Eny, KM, Nielsen, D, Wessman, C, El-Sohemy, A. Association of GLUT2 and TAS1R2 genotypes with risk for dental caries. Caries Res 2013;47:219–25. in Google Scholar PubMed

22. Robino, A, Bevilacqua, L, Pirastu, N, Situlin, R, Di Lenarda, R, Gasparini, P, et al.. Polymorphisms in sweet taste genes (TAS1R2 and GLUT2), sweet liking, and dental caries prevalence in an adult Italian population. Genes Nutr 2015;10:485. in Google Scholar PubMed PubMed Central

23. Izakovicova Holla, L, Borilova Linhartova, P, Lucanova, S, Kastovsky, J, Musilova, K, Bartosova, M, et al.. GLUT2 and TAS1R2 polymorphisms and susceptibility to dental caries. Caries Res 2015;49:417–24. in Google Scholar PubMed

24. Eriksson, L, Esberg, A, Haworth, S, Holgerson, PL, Johansson, I. Allelic variation in taste genes is associated with taste and diet preferences and dental caries. Nutrients 2019;11:1491. in Google Scholar PubMed PubMed Central

25. Feeney, E, O’Brien, S, Scannell, A, Markey, A, Gibney, ER. Genetic variation in taste perception: does it have a role in healthy eating? Proc Nutr Soc 2011;70:135–43. in Google Scholar PubMed

26. Eny, KM, Wolever, TM, Fontaine-Bisson, B, El-Sohemy, A. Genetic variant in the glucose transporter type 2 is associated with higher intakes of sugars in two distinct populations. Physiol Genom 2008;33:355–60. in Google Scholar PubMed

27. Duncan, LE, Ostacher, M, Ballon, J. How genome-wide association studies (GWAS) made traditional candidate gene studies obsolete. Neuropsychopharmacology 2019;44:1518–23. in Google Scholar PubMed PubMed Central

Received: 2019-04-11
Accepted: 2020-11-06
Published Online: 2021-10-26

© 2021 Melis Yilmaz et al., published by De Gruyter, Berlin/Boston

This work is licensed under the Creative Commons Attribution 4.0 International License.

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