Do you know if you have children with Epilepsy in your practice?
Comparison of Dental Caries Experience in Children Suffering From Epilepsy with and without Administration of Long Term Liquid Oral Medication.
Sucrose is added as sweetening agent in liquid oral medication (LOM) to mask the acrid taste of medicines which may be potentially cariogenic. Many children under long term LOM therapy for treatment of epilepsy may be susceptible to dental caries.
To assess and compare dental caries experience in children under long term liquid oral medication with those not under such medication among 2-12 years old children suffering from epilepsy.
MATERIALS AND METHODS:
A cross-sectional study was undertaken on a total of 84 children aged 2-12 years, who were suffering from epilepsy receiving liquid oral medication for more than 3 months were selected (study group) and for comparison 106 children of similar age group and disease but on other forms of medication were included as control group. Dental caries was assessed using DMFT/DMFS (Decayed, Missing, Fillled Teeth / Surfaces), dmft/dft and dmfs/dfs indices. One-way ANOVA and t-test were used with p-value fixed at 0.05. Univariate logistic regression was applied.
Children on LOM were at increased risk of dental caries than those with other forms of medications (OR: 2.55, 95% CI (2.37-4.15) p=0.000, HS). Caries prevalence was high in the study group (76.1%) when compared to control group (55.6%).
Long term use of liquid medicines containing sucrose is a risk factor for dental caries among children with epilepsy.
We will be having part 2 of the webinar series with Dr. V. Kim Kutsch entitled: Dental Caries, a Disease of Choice? On August 23. If you have not had a chance to hear part 1 you can do so here.
Here is a snippet of information from the first webinar regarding the role genetics play in dental caries.
The NIH Consensus Development Program released a statement in 2001 and listed six major clinical caries research directions. One of these directions was the need for genetic studies to identify genes and genetic markers of diagnostic, prognostic and therapeutic value. This last decade has seen a steep increase in studies investigating the presence of genetic factors influencing individual susceptibility to caries. This review revisits recent caries human genetic studies and provides a perspective for future studies in order to fulfil their promise of revolutionizing our understanding of and the standard of care for the most prevalent bacteria-mediated non-contagious disease in the world. © 2014 S. Karger AG, Basel.
There is such a broad array of genetics that play a role in dental caries. Our capacity to study them has increased significantly over the past 10 years.
Current Dental Caries Genes
>Enamel Formation Genes: 7 (AMELX, ENAM)
>Immune Response Genes: 7 (BDEF1, CD14)
>Saliva Genes: 2 (AQP5, PRH1)
>Other Genes: 11 (TAS2R38, MMP13)
>34 Total at present
What we now know is that genetics loads the gun and the environment pulls the trigger so to speak.
As practitioners, we cannot change the genetic makeup of our patients, but we can help them understand their risk and make changes to their environment to help mitigate damage.
Interestingly, a study done on young adults; 77 caries active, 77 caries free looked at environmental and genetic factors. They found that:
“Based on stepwise multiple linear regression analyses, dental plaque amount, lactobacilli count, age, and saliva buffer capacity, as well as DEFB1, TAS2R38, and CA6 (Carbonic anhydrase) gene polymorphism, explained a total of 87.8% of the variations in DMFT scores.
What this tells us is these 7 factors explained almost 88% of what was going on in these patients. We need to be aware of the patterns that we can identify and alter.
To register for the live webinar with Dr. Kutsch and learn more about the advances in research SIGN UP HERE TODAY.
You won’t want to miss it!
By: Dr. V. Kim Kutsch, DMD
Dental floss made from silk thread first became a commercial product in 1882, and has probably been a controversial topic since that first introduction. The dental profession routinely recommends patients floss daily and dental hygienists daily instruct patients on flossing technique as a standard of care. Despite the profession’s continued efforts, self-care with dental floss has a very low adoption rate. The news media widely reported the results of a recent Associated Press examination of scientific evidence from a Freedom of Information Act request with the Human Health and Services. Upon receiving a letter from HHS acknowledging that this topic has not really been studied, the AP then examined 25 studies and found little or no scientific evidence to support flossing. So why floss?
The theory behind flossing is that tooth brushing does not reach into the interproximal region between teeth and daily flossing to disrupt the biofilm will improve the outcomes in dental caries and periodontal disease. While the theory is logical and intuitive, flossing is a difficult habit to establish, is technique sensitive and depends completely on patient adherence for any outcome. Unfortunately, the AP report was mostly right. There is little scientific evidence to support daily flossing providing any benefit.1,2 A search of Pubmed provides studies that demonstrate flossing adds little to no additional benefit to tooth brushing. One report did demonstrate a significant improvement with interdental brushing compared with flossing.3 A recent study even demonstrated improved outcomes in four patients with refractory periodontal disease when they stopped flossing.4 The evidence indicates one cannot simply brush and floss dental diseases away. So, should we all stop flossing? What is the risk versus the benefit?
Dental caries and periodontal disease are both multifactorial biofilm based diseases. They are frustrating diseases for both patients and the dental professionals treating them. Since the biofilm is one of the risk factors in both diseases, it still makes sense to disrupt that biofilm on a daily basis. While most studies demonstrate little to no evidence, there are a few that do.5 One study clearly demonstrated improved outcomes with dental caries bacteria6, while another study utilized daily professional flossing on students.7
Recognizing that the topic needs better scientific investigation, lack of evidence at this point should not be interpreted as lack of outcome. I will still floss and I will recommend it for my patients, but only as a part of my complete approach of risk assessment based care. I will still focus on helping patients understand the causes of their diseases, and helping them establish targeted therapies to reduce their risks.
- Berchier CE, Slot DE, Haps S, Van der Weijden GA. The efficacy of dental floss in addition to a toothbrush on plaque and parameters of gingival inflammation: a systematic review. Int J dent Hyg Nov 2008. 6(4):265-79.
- Dorri M, Dunne SM, Walsh T, Schwendicke F. Micro-invasive interventions for managing proximal dental decay in primary and permanent teeth. Cochrane Database Syst Rev 2015 Nov. 5(11).
- Salzer S, Slot DE, Van der Weijden FA, Dorfer CE. Efficacy of inter-dental mechanical plaque control in managing gingivitis—a meta-review. J Clin Periodontol April 2015. 42 Suppl 16:S92-105.
- Wilder RS, Bray KS. Improving periodontal outcomes: merging clinical and behavioral science. Periodontol 2000 June 2016. 71(1):65-81.
- Chapple IL, Van der Weijden F, Doerfer C, et al. Primary prevention of periodontitis: managing gingivitis. J Clin Periodontol April 2015. 42 Suppl 16:S71-6.
- Corby PM, Biesbrock A, Bartizek A, et al. Treatment outcomes of dental flossing in twins: molecular analysis of interproximal microflora. J Periodontol. August 2008. 79(8):1426-33.
- Hujoel PP, Cunha-Cruz J, Banting DW, Loesche WJ. Dental flossing and interproximal caries: a systematic review. JDR April 2006. 85(4):298-305.
The New York Times ran a story on July 11 titled: A Cavity-Fighting Liquid Lets Kids Avoid Dentists’ Drills
With the increasing national attention, and the fact that in Oregon, Medicaid patients are being reimbursed for SDF treatment, we wanted to make sure our readers were up to date on Dr. Kutsch’s thoughts posted in December. Have you noticed an increase of public awareness of Silver Diamine Fluoride by your patients? Have you been using it? Let us know in the comments below.
By V. Kim Kutsch, DMD, originally published December 22, 2015.
Silver Diamine Fluoride was market cleared by the FDA earlier this year as a “Cavity Varnish” for the treatment of hypersensitivity only in adults over the age of 21. But the use of the silver ion as an anti-cavity agent dates back to GV Black.1 He described the use of a silver nitrate solution painted onto lesions to arrest the process. I have personal experience with using silver nitrate in a technique modified by Dr. Steve Duffin. He immediately covered the lesion with fluoride varnish following the silver nitrate solution.2 I have used this technique for years with excellent outcomes. There is a drawback however, the silver ion turns the yellow to dark brown dentin lesion to black. It arrests the process, but turns the lesions black. So while effective, a technique that may not work for every patient. The good news, is that it does not stain sound enamel.
Most of the cases I have treated involved young children with SECC, whose parents didn’t want them subjected to sedation or general anesthesia to have restorative dentistry done. They were willing to compromise esthetics in the short term. These patients I then restored as the parents desired after the child was developmentally capable of having dentistry done with local anesthesia, or no anesthesia. Many of the lesions were never restored, but this provided a great service in my opinion. The other patients I have used this technique on were senior citizens in the end stages of life, where neither myself, the patient, or the family members were interested in putting the patient through extensive restorative procedures. It has worked fairly well with that demographic also.
Silver Diamine Fluoride has been used extensively for years in other countries with similar outcomes to silver nitrate. There have been numerous studies published on the topic and I believe it has gained popularity as a necessity with the increasing rates of SECC in the past two decades.3 Silver Diamine Fluoride provided better outcomes than fluoride varnish and GIC.4,5,6 I am now also using Silver Diamine Fluoride for the same types of patients that I have used silver nitrate with in the past. But in my experience contrary to some reports, it too turns the dark dentin lesions black. As long as that outcome is acceptable to the patient/parents/family, it too works very well. There is even evidence that once the silver ion kills a bacterial cell, it continues to kill other bacteria in what is described as a zombie-like state.7 For the right patient, this offers another option to their care.
One final note, these silver ion solutions do stain everything they come in contact with in the operatory, clothing, countertops etc. So just be very careful in handling the solution.
- Peng JJ, Botelho MG, Matinlinna JP. Silver compounds used in dentistry for caries management: a review. J Dent. 2012 Jul;40(7):531-41. 1966-2011 Sys Rev.
- Duffin S. Back to the future: the medical management of caries introduction. J Calif Dent Assoc. 2012 Nov;40(11):852-8.
- Chu CH, Lee AH, Zheng L, Mei ML, Chan GC. Arresting rampant dental caries with silver diamine fluoride in a young teenager suffering from chronic oral graft versus host disease post-bone marrow transplantation: a case report. BMC Res Notes. 2014 Jan 3;7:3.
- Chu CH, Lo EC, Lin HC. Effectiveness of silver diamine fluoride and sodium fluoride varnish in arresting dentin caries in Chinese pre-school children. J Dent Res. 2002 Nov;81(11):767-70.
- Rosenblatt A, Stamford TC, Niederman R. Silver diamine fluoride: a caries “silver-fluoride bullet”.J Dent Res. 2009 Feb;88(2):116-25.
- Zhi QH, Lo EC, Lin HC. Randomized clinical trial on effectiveness of silver diamine fluoride and glass ionomer in arresting dentine caries in preschool children. J Dent. 2012 Nov;40(11):962-7.
- Wakshlak R, Pedahzur R, Avnir D. Antibacterial activity of silver-killed bacteria: the “zombies” effect. Scientific Reports 5, Article number: 9555 doi:10.1038/srep09555.
Research taking place at the University of Alabama at Birmingham Department of Biology and School of Dentistry is showing the transmission of S. mutans not only occurs from mother to child, but from child-to-child (non-relatives) as well. Sharing spoons and toys in the daycare center or nursery at church may be the reason “72 percent of children harbored at least one strain of the cavity-causing Streptococcus mutans not found in any cohabiting family members.” Primary researcher Stephanie Momeni stated: “While the data supports that S. mutans is often acquired through mother-to-child interactions, the current study illuminates the importance of child-to-child acquisition of S. mutans strains and the need to consider these routes of transmission in dental caries risk assessments, prevention and treatment strategies.”
Educating parents on the importance of limiting sharing of things like pacifiers, utensils, sippy cups and straws at daycare and home may be beneficial to share based on these findings. Also, asking parents if their children participate in daycare-like settings may be worth considering as it appears to have the potential to be a significant risk factor for dental caries.
What do you think: Is this research evidence enough to consider in your practice?
Why do people hate fluoride so much?
As a kid, fluoride was the gold standard in preventing tooth decay and cavities. You had your fluoridated water, fluoride rinse, and bubble gum flavored treatment at the dentist. For the most part, it’s still just as prevalent today, with the exception of the ever-growing segment of the population that rejects it. But why?
Fluorosis is a cosmetic condition affecting teeth that have been overexposed to fluoride within the first 8 years of life when adult teeth are forming. Fluorosis can appear as various changes in the appearance of the tooth enamel, including white or dark spots on the teeth. Nobody wants that.
Crossing the line
Fluoride is the only chemical added to public water supplies for the purpose of medical treatment. Water fluoridation is argued to cross the line of “informed consent” that is standard practice for any medical treatment, and is the reason 97% of Western Europe has rejected water fluoridation.
It is argued that many children today exceed the recommended level of fluoride intake from toothpaste alone. The anti-fluoride camp argues the dosage for public water supply cannot be controlled, and combined with all the other fluoridated products, they think enough is enough.
In many communities with naturally high fluoride levels, we see dental fluorosis in children, and skeletal fluorosis in older adults. There is also evidence that excessive fluoride intake may harm other tissues including the brain and pineal gland, and may have a negative impact on IQ.
Today we are seeing a huge increase in the number of patients seeking holistic dentistry, which rejects the use of fluoride and other unnatural toxic materials like mercury. This trend toward a more natural, whole body approach to oral healthcare represents a paradigm shift in dentistry as we know it.
Where do you stand?
With the anti-fluoride camp seemingly growing every day, it’s important that you understand both sides of the coin. It is also important to have strategies in place to educate your patients, rather than discard their feelings or opinions. Most patients that are anti-fluoride aren’t trying to be difficult, they are just trying to do what is best for themselves and their families. As a team, know what your approach will be with these patients. Can you provide information on fluoride as an important protective factor? Can you effectively tell them why you think fluoride is important? Can you explain the different recommendations for different ages? Do you offer options for dental products that don’t contain fluoride, but contain other helpful protective factors like xylitol? If not, it may be time to sit down as a team and have the conversation. For information on fluoride as a protective factor, start here.
A study published this month in JDR by researchers from UCSF demonstrates the importance of CAMBRA and Caries Risk Assessment protocols for predicting the future of tooth decay in patients. In a recent press release about the findings, researcher B.W. Chaffee stated:
“Risk assessment is predictive – it tells you what kinds of outcomes are going to occur in a patient population… Together with other studies, our work has shown that providers are willing and able to use CAMBRA accurately, that it doesn’t take a lot of time to do it, and that it is effective.”
The findings of the study reinforce the importance of implementing CAMBRA protocols in office. Chaffee goes on: “CAMBRA has the potential to fundamentally change dentistry, but it won’t happen overnight, Chaffee said. “The traditional approach to dental caries for the last 100 years has been when a dentist sees a cavity to fill it and restore the tooth’s function, and that’s a critical aspect of what dentists should be doing,” Chaffee explained. “But in and of itself, this approach doesn’t do anything to prevent the disease from occurring again. It treats the symptom – the consequences of disease – but it doesn’t get after the causes of the disease.”
For further information we have included the study abstract below. Find the full study here.
Caries Risk Assessment Item Importance
Risk Designation and Caries Status in Children under Age 6
1. Department of Preventive and Restorative Dental Sciences, University of California San Francisco, San Francisco, CA, USA
2. Department of Orofacial Sciences, University of California San Francisco, San Francisco, CA, USA
B.W. Chaffee, Department of Preventive and Restorative Dental Sciences, University of California San Francisco, 3333 California St., Suite 495, Box 1361, San Francisco, CA 94143, USA. Email: email@example.com
Caries risk assessment (CRA) is widely recommended for dental caries management. Little is known regarding how practitioners use individual CRA items to determine risk and which individual items independently predict clinical outcomes in children younger than 6 y. The objective of this study was to assess the relative importance of pediatric CRA items in dental providers’ decision making regarding patient risk and in association with clinically evident caries, cross-sectionally and longitudinally. CRA information was abstracted retrospectively from electronic patient records of children initially aged 6 to 72 mo at a university pediatric dentistry clinic (n = 3,810 baseline; n = 1,315 with follow-up). The 17-item CRA form included caries risk indicators, caries protective items, and clinical indicators. Conditional random forests classification trees were implemented to identify and assign variable importance to CRA items independently associated with baseline high-risk designation, baseline evident tooth decay, and follow-up evident decay. Thirteen individual CRA items, including all clinical indicators and all but 1 risk indicator, were independently and statistically significantly associated with student/resident providers’ caries risk designation. Provider-assigned baseline risk category was strongly associated with follow-up decay, which increased from low (20.4%) to moderate (30.6%) to high/extreme risk patients (68.7%). Of baseline CRA items, before adjustment, 12 were associated with baseline decay and 7 with decay at follow-up; however, in the conditional random forests models, only the clinical indicators (evident decay, dental plaque, and recent restoration placement) and 1 risk indicator (frequent snacking) were independently and statistically significantly associated with future disease, for which baseline evident decay was the strongest predictor. In this predominantly high-risk population under caries-preventive care, more individual CRA items were independently associated with providers’ risk determination than with future caries status. These university dental providers considered many items in decision making regarding patient risk, suggesting that, in turn, these comprehensive CRA forms could also aid individualized care, linking risk assessment to disease management.
We all know that fluoride is one of the best ways to prevent tooth decay, but how much do you or your patients know of the history of water fluoridation? Here is a quick overview that may be of interest to you and your patient base. Feel free to share on your social media sites!
Water fluoridation became an official policy of the U.S. Public Health Services over 65 years ago. Today, approximately 75% of Americans live on a fluoridated water system. How did we get here?
Around the turn of the 20th century, the “brown stain” epidemic in Colorado Springs became a catalyst for the study and implementation of fluoridated water systems in America. Although the patients suffered unsightly staining, they showed a decreased rate of tooth decay. As it turns out, the brown stains was severe fluorosis caused by an excessive amount of naturally occurring fluoride in the water system. But the events spurred the question: If we could fluoridate the water system at a controlled level, could we decrease the rate of tooth decay, while avoiding fluorosis?
There are three essential periods of water fluoridation that got us to where we are today:
- Research into the cause of mottled tooth enamel: The Colorado Brown Stain. 1801 – 1933
- Research into the relationship between fluoride concentrations, fluorosis, and tooth decay found that moderate levels of fluoride prevents cavities. 1933 – 1945
- Fluoridated water supplies. 1945 – Present
The first fluoridated water supply in the world was in Grand Rapids, Michigan in 1945. During the last half of the 20th century, research was conducted on the effectiveness and side-effects of fluoridated water supplies. While there was evidence of decreased numbers of cavities, there was also an increase in the wide spread use of fluoridated oral healthcare products like toothpastes and rinses in 1960.
In 1960 water fluoridation became widely used in the U.S. Approximately 50 million people were now on fluoridated water systems. The rest of the world followed a similar pattern in researching and adopting the wide spread use of water fluoridation.
Today there is more debate than ever whether we still need fluoridated water systems, and if this is the best way to prevent tooth decay on a large scale; as many patients are leaning towards non-fluoride options, and fewer people actually drink tap water. There is evidence that water fluoridation decreases the decay rate among children in primary teeth, but there is not enough contemporary evidence supporting the same findings for adults.
Is this still something that’s effective and worthwhile for public health? Does each individual have the right to choose whether or not they ingest fluoride in their drinking water? I think it’s safe to say it’s time to sit down and discuss the future of fluoridated water in America. I look forward to that discussion and what the future of oral health has in store for us. But in the meantime…what’s in your cup?
A recent study demonstrates once again the popularity of acidic sports drinks and their detriment to the oral health of kids in Britain. The study highlights the low pH of these drinks: “Many sports drinks have a pH below 5.5, the critical pH for the demineralization of enamel, leading to erosion.”(1,2)
The study warns dental providers to pay attention to the consumption of these drinks and shares that most parents are unaware of the harm these beverages can do. Many kids reported consuming the beverages outside of a sporting event, and drinking them simply because they enjoy the taste. With the onset of summer, be sure to talk to parents about the consumption of acidic beverages including sports drinks.
For further reading:
British Dental Journal 220, 639 – 643 (2016)
Published online: 24 June 2016 | doi:10.1038/sj.bdj.2016.449
A survey of sports drinks consumption among adolescents
- Quantifies the consumption of sports drinks by high school children.
- Confirms that consumption is high and not always associated with sports activity.
- Taste was viewed as the prime reason for consumption.
- Enhancement of sporting ability was not stated as a reason for use.
- The popularity of these palatable high sugar and acidic drinks has implications for children’s oral health.
Background Sports drinks intended to improve performance and hydrate athletes taking part in endurance sport are being marketed to children, for whom these products are not intended. Popularity among children has grown exponentially. Worryingly they consume them socially, as well as during physical activity. Sports drinks are high in sugar and are acidic. Product marketing ignores the potential harmful effects of dental caries and erosion.
Results One hundred and sixty children responded (87% response rate): 89.4% (143) claimed to drink sports drinks, half drinking them at least twice a week. Lucozade Sport™ was the most popular brand. The main reason for consuming the drinks was attributed to the ‘nice taste’ (90%, 129/143). Most respondents purchased the drinks from local shops (80.4%, 115) or supermarkets (54.5%, 78). More boys claimed to drink sports drinks during physical activity (77.9% versus 48.6% girls, P <0.001). Whereas more girls claimed to drink them socially (51.4% versus 48.5% boys, NS).
Conclusion A high proportion of children consumed sports drinks regularly and outside of sporting activity. Dental health professionals should be aware of the popularity of sports drinks with children when giving health education advice or designing health promotion initiatives.
Have you ever tried to have a conversation with a young patient, always in the chair with decay and they (or their parent) constantly give the excuse: “Doc, she just has a sweet tooth!” or “Doc, I just don’t like vegetables!” Albeit an oversimplification, these patients may have a genetic variation that in fact has them prefer sweets and or averse to the phenols in coniferous veggies.
Consider this from a 2010 study:
“Dental caries is influenced by a complex interplay of genetic and environmental factors, including dietary habits. Previous reports have characterized the influence of genetic variation on taste preferences and dietary habits. Statistically, significant associations were seen in TAS2R38 (bitter) and TAS1R2 (sweet) for caries risk and/or protection.”
TAS2R38 gene is known as the supertasters, children avoid bitter tastes (broccoli) and prefer sweets. It was significantly associated with dental caries in primary dentition, TAS2R38 sensitivity is known to decrease with age, and in fact this gene was not related to caries in mixed and permanent dentitions.
So it appears having a ‘sweet tooth’ is in fact a legitimate genetically influenced thing (at least in young people). How does this impact our interaction with these patients? We can’t simply let them off the hook and throw in the towel can we? Knowing there may be genetic forces at play can be used to your advantage. We want our patients to own their disease; yet they consistently want to push ownership on us. If there is a third party present in the conversation (genetics) it could be the perfect imputes for change.
Let’s see how a conversation may play out:
Doc: “Susie, you know this is the fourth time you have missed school because of cavities right? Have you been able to do the things we talked about? Limiting treats and brushing and flossing?”
Susie: “I have been brushing, but I just have a sweet tooth! All I want to eat are sweets, and I just can’t help it!”
Doc: “Sweets are delicious. In fact, you may actually have a genetic predisposition to liking sweets more than most of your friends, which can make it much harder for you to say no. The problem is, if you do, you have a higher risk of tooth decay and other diseases of your mouth and body.”
Susie: “So my genes make me want sweet food?”
Doc: “Possibly. If that is the case you have to be even more careful about your food choices. Every time you want to have a treat, remind yourself that even though your brain or body seem to really want it, your teeth can’t handle it. Think you can try that?”
Susie: “Yeah, that makes sense.”
If anything, it allows the patient to name the struggle they are facing and instead of it simply being about willpower or rules, it becomes a predisposition to a certain behavior, which when made aware of the possibility, can help them stop and think before having the doughnut or drinking the soda.
Here is a more recent study regarding the association of TAS1R3 and TAS1R2 with dental caries:
Sweet taste is a powerful factor influencing food acceptance. The peripheral taste response to sugar is mediated by the TAS1R2/TAS1R3 taste receptors. The aim of the study was to determine the relationship between TAS1R2 (rs35874116 or rs9701796) and/or TAS1R3 (rs307355) single nucleotide polymorphisms with dental caries experience in schoolchildren. A total of 184 schoolchildren aged between 7 and 12 years (101 girls, 83 boys) were included in the study. Genomic DNA was extracted from saliva samples and the genotypes were identified by qPCR. The genotype frequencies were as follows: 6.6% for homozygous wild type, 41.8% for heterozygous and 51.6% for homozygous polymorphic genotype carriers of TAS1R2 gene rs35874116; 27.8% for heterozygous and 72.2% for homozygous polymorphic genotype carriers of TAS1R2 gene rs9701796, and 83.1% for homozygous wild type and 16.9% for heterozygous genotype carriers of TAS1R3 gene rs307355 polymorphism. A significant association was observed between total caries experience (dft + DMFT – decayed filled primary teeth + decayed, missing and filled permanent teeth) and TAS1R2 rs35874116 (p = 0.008) and TAS1R3 rs307355 (p = 0.04) gene polymorphisms but not for TAS1R2 gene rs9701796 polymorphism. TAS1R3 gene rs307355 polymorphism has been found to be an independent risk factor for dental caries experience by logistic regression analysis and to have increased the risk of caries. Moderate caries experience (4-7 caries) was found to be associated with TAS1R3 rs307355 heterozygous genotype, whereas high-risk caries experience (>8 caries) was found to be associated with TAS1R2 rs35874116 homozygous polymorphic genotype.
“Caries experience (4-7 caries) was found to be associated with TAS1R3 rs307355 heterozygous genotype, whereas high-risk caries experience (>8 caries) was found to be associated with TAS1R2 rs35874116 homozygous polymorphic genotype.”
What do you think? Can you think of any patients that could potentially have the genetic makeup that has them prefer sweets? Let us know in the comments below.
Wendell S, Wang X, Brown M, Cooper ME et al. Taste genes associated with dental caries. JDR November 2010. 89(11):1198-1202.
Haznedaroğlu E, Koldemir-Gündüz M, Bakır-Coşkun N, Bozkuş HM, et al.
Association of sweet taste receptor gene polymorphisms with dental caries experience in school children. Caries Res. 2015;49(3):275-81.
184 7-12 DMFT.