Measuring the Microscopic Structures of Human Dental Enamel Can Predict Caries Experience.
ABSTRACT: OBJECTIVES:The hierarchical structure of enamel gives insight on the properties of enamel and can influence its strength and ultimately caries experience. Currently, past caries experience is quantified using the decayed, missing, filled teeth/decayed, missing, filled surface (DMFT/DMFS for permanent teeth; dmft/dmfs for primary teeth), or international caries detection and assessment system (ICDAS) scores. By analyzing the structure of enamel, a new measurement can be utilized clinically to predict susceptibility to future caries experience based on a patient's individual's biomarkers. The purpose of this study was to test the hypothesis that number of prisms by square millimeter in enamel and average gap distance between prisms and interprismatic areas, influence caries experience through genetic variation of the genes involved in enamel formation. MATERIALS AND METHODS:Scanning electron microscopy (SEM) images of enamel from primary teeth were used to measure (i) number of prisms by square millimeter and interprismatic spaces, (ii) prism density, and (iii) gap distances between prisms in the enamel samples. The measurements were tested to explore a genetic association with variants of selected genes and correlations with caries experience based on the individual's DMFT+ dmft score and enamel microhardness at baseline, after an artificial lesion was created and after the artificial lesion was treated with fluoride. RESULTS:Associations were found between variants of genes including ameloblastin, amelogenin, enamelin, tuftelin, tuftelin interactive protein 11, beta defensin 1, matrix metallopeptidase 20 and enamel structure variables measured (number of prisms by square millimeter in enamel and average gap distance between prisms and interprismatic areas). Significant correlations were found between caries experience and microhardness and enamel structure. Negative correlations were found between number of prisms by square millimeter and high caries experience (r value= -0.71), gap distance between prisms and the enamel microhardness after an artificial lesion was created (r value= -0.70), and gap distance between prisms and the enamel microhardness after an artificial lesion was created and then treated with fluoride (r value= -0.81). There was a positive correlation between number of prisms by square millimeter and prism density of the enamel (r value = 0.82). CONCLUSIONS:Our data support that genetic variation may impact enamel formation, and therefore influence susceptibility to dental caries and future caries experience. CLINICAL RELEVANCE:The evaluation of enamel structure that may impact caries experience allows for hypothesizing that the identification of individuals at higher risk for dental caries and implementation of personalized preventative treatments may one day become a reality.
Project description:<h4>Objective</h4>To evaluate the influence of ultrapulsed CO<sub>2</sub> laser in combination with commercial fluoride products in order to verify the increase of microhardness of artificial enamel caries lesions.<h4>Materials and methods</h4>Bovine enamel specimens were prepared, and artificial enamel caries lesions were created. Teeth were randomly divided into 5 groups (n=10): treated with laser (L), laser + neutral fluoride gel 2% (LNF), laser + acidulated phosphate fluoride gel 1.23% (LAFG), laser + acidulated fluoride mousse 1.23% (LAFM), and laser + fluoride varnish 5% (LFV). Microhardness was evaluated at baseline, after caries induction, after CO<sub>2</sub> laser irradiation + fluoride treatment in the 1st week, and after fluoride treatment at 3rd and 5th week.<h4>Results</h4>There was a decrease in microhardness in all groups after artificial enamel caries lesion formation; no increase in microhardness was found in the first and third weeks in all groups (p > 0.05). In the fifth week, an increase in microhardness occurred in all groups (p < 0.05).<h4>Conclusion</h4>Although CO2 laser irradiation in combination with different commercial fluoride products was capable of increasing microhardness on enamel caries lesions in bovine tooth enamel it is necessary to confirm these results by testing the isolated effect of fluoride on enamel surface microhardness. Also, although microhardness was higher in the fluoride varnish group than in the other groups in the fifth week it is not possible to discard the best effect of fluoride varnish treatment on absence of artifacts that may occur with the other fluoride treatments.<h4>Clinical relevance</h4>In order to prove that CO2 laser may contribute to an increase in microhardness when applied to enamel lesions in combination with different commercial fluoride products it is necessary to conduct additional studies. Also, higher microhardness of fluoride varnish group should be carefully considered.
Project description:Clinically, primary and permanent teeth are distinct anatomically and the presentation of caries lesions differs between the two dentitions. Hence, the possibility exists that genetic contributions to tooth formation of the two dentitions are different. The purpose of this study was to test the hypothesis that genetic associations with an artificial caries model will not be the same between primary and permanent dentitions. Enamel samples from primary and permanent teeth were tested for microhardness at baseline, after carious lesion creation, and after fluoride application to verify association with genetic variants of selected genes. Associations were found between genetic variants of ameloblastin, amelogenin, enamelin, tuftelin, tuftelin interactive protein 11, and matrix metallopeptidase 20 and enamel from permanent teeth but not with enamel from primary teeth. In conclusion, our data continue to support that genetic variation may impact enamel development and consequently individual caries susceptibility. These effects may be distinct between primary and permanent dentitions.
Project description:There is evidence for a genetic component in caries susceptibility, and studies in humans have suggested that variation in enamel formation genes may contribute to caries. For the present study, we used DNA samples collected from 1,831 individuals from various population data sets. Single nucleotide polymorphism markers were genotyped in selected genes (ameloblastin, amelogenin, enamelin, tuftelin, and tuftelin interacting protein 11) that influence enamel formation. Allele and genotype frequencies were compared between groups with distinct caries experience. Associations with caries experience can be detected but they are not necessarily replicated in all population groups and the most expressive results was for a marker in AMELX (p=0.0007). To help interpret these results, we evaluated if enamel microhardness changes under simulated cariogenic challenges are associated with genetic variations in these same genes. After creating an artificial caries lesion, associations could be seen between genetic variation in TUFT1 (p=0.006) and TUIP11 (p=0.0006) with enamel microhardness. Our results suggest that the influence of genetic variation of enamel formation genes may influence the dynamic interactions between the enamel surface and the oral cavity.
Project description:<h4>Background</h4>Dental caries is the localized destruction of dental hard tissues (enamel and dentine). Decayed, Missing, and Filled Teeth (DMFT) index is the most commonly used dental caries index. Thickness of the outermost part of the tooth called the enamel is determined by the rate of deposition of enamel proteins. Relative enamel thickness (RET) gives a measure of enamel thickness with respect to dentine. Dental caries is influenced by a genetically determined factor called dermatoglyphics (DG). As the genes responsible for RET and DG lie on the same chromosome and develop during the same time of intrauterine life, it is biologically plausible to correlate RET and DG.<h4>Aims</h4>This study consists of two primary aims: (1) to assess RET using cone beam computed tomography images and correlate it with caries and (2) to correlate RET with DG.<h4>Materials and methods</h4>148 dental subjects were assessed for DMFT caries score and were categorized as Group 1 with DMFT = 0 and Group 2 with DMFT ≥ 1. Following this, their DG pattern was recorded digitally. The CBCT images of these subjects were assessed for RET, and the data were analyzed statistically.<h4>Results</h4>Mean RET in our sample population is 18.45 (SD 3.79) while mean DMFT is 5.34 (SD 5.13). Mean RET in Group 1 subjects was 19.82 (SD 4.05) while that in the Group 2 was 17.68 (SD 3.43). RET and DMFT showed a statistically significant negative correlation (<i>p</i> = 0.007). The "Single Loop" DG characteristic showed a statistically significant difference between males and females (<i>p</i> = 0.031). The "Simple Arch" type of DG was positively correlated with RET.<h4>Conclusion</h4>This is the first in vivo study to assess RET using CBCT images and correlate with DMFT and DG. RET is inversely related to DMFT while directly proportional to the "Simple arch" DG pattern. Males and females differed in their "Single Loop" DG characteristic.
Project description:The aims of this study were to assess the trends in dental caries experience in the permanent dentition (i.e., the number of decayed, missing, or filled teeth, DMFT) in Germany from 1997-2014 and to project caries experience to 2030. Components of caries experience (decayed teeth, DT, missing teeth, MT, filled teeth, FT) from repeated waves (1997, 2005, 2014) of the nationally representative German Oral Health Studies were analyzed in 12-, 35-44-, and 65-74-year-olds. Weighted means were interpolated cross-sectionally by fitting piecewise-cubic spline-curves and were then subjected to longitudinal regression and combined with population estimates. In 1997, children (12-year-olds) had a mean caries experience (decayed, missing, filled teeth, DMFT) of 1.7 teeth; this experience decreased to 0.5 teeth in 2014. For 2030, an experience of 0.2 teeth is projected. In adults (35-44-year-olds), a decrease was recorded (1997: 16.1 teeth; 2014: 11.2 teeth). This decrease is expected to continue until 2030 (to 7.7 teeth). Similarly, in seniors (65-74-year-olds), a decrease was recorded (1997: 23.6 teeth; 2014: 17.7 teeth); this decrease is expected to continue until 2030 (to 14.9 teeth). While the number of missing teeth has decreased consistently across age groups, the number of filled and decayed teeth has increased in seniors and is expected to continue to increase. The cumulative caries experience has decreased from 1.1 billion DMFT in 2000 to 867 million in 2015 and is expected to decrease to 740 million in 2030. Caries experience in the permanent dentition has been decreasing substantially, mainly due to a decrease in missing teeth. Younger age groups also show fewer decayed and filled teeth, while in older groups, restorative needs have not decreased, as more teeth are retained. Concepts for addressing the emanating morbidity shifts are required.
Project description:<h4>Objectives</h4>Behavioural and lifestyle factors, as oral hygiene and diet, are well-established risk factors in the pathogenesis of dental caries, though displaying large differences in susceptibility across individuals. Since enamel formation already starts in utero, pregnancy course and outcome may eventually play a role in enamel strength and caries susceptibility. Therefore, we studied the association between history of pregnancy complications and the caries experience in their six-year-old children. The pregnancy complications included small for gestational age (SGA), spontaneous preterm birth (sPTB), gestational hypertension (GH), pre-eclampsia (PE), individually, and a combination of those, designated as placental syndrome.<h4>Methods</h4>This study was embedded in Generation R, a prospective longitudinal Dutch multiethnic pregnancy cohort study. Information about pregnancy complications was obtained from questionnaires completed by midwives and obstetricians with cross-validation in medical records. These included SGA, sPTB, GH and PE. Caries experience was assessed with the decayed, missing and filled teeth (dmft) index at a mean age of six years. The association between dental caries experience and a history of pregnancy complications was studied by using hurdle negative binomial (HNB) models.<h4>Results</h4>We were able to assess the dmft index in 5323 six-year-old children (mean age 6.2 years, SD 0.5). We did not find an association between the different pregnancy complications and dental caries experience in childhood, whether for SGA, sPTB, GH, PE, or for the combined outcome placental syndrome (HNB estimates: OR 1.02, 95%CI 0.87 - 1.19; RR 0.90, 95%CI 0.78 - 1.04). Further adjustment of the models with different confounders did not alter the outcome.<h4>Conclusions</h4>Although it is expected that prenatal stress can be a risk factor for caries development later in life, our findings do not support this hypothesis. Therefore, we believe disparities in caries experience between children are probably not explained by early life events during a critical intrauterine period of development.
Project description:We have previously shown that AQP5 and BTF3 genetic variation and expression in whole saliva are associated with caries experience suggesting that these genes may have a functional role in protecting against caries. To further explore these results, we tested ex vivo if variants in these genes are associated with subclinical dental enamel mineral loss. DNA and enamel samples were obtained from 53 individuals. Enamel samples were analyzed for Knoop hardness of sound enamel, integrated mineral loss after subclinical carious lesion creation, and change in integrated mineral loss after remineralization. DNA samples were genotyped for single nucleotide polymorphisms using TaqMan chemistry. Chi-square and Fisher's exact tests were used to compare individuals above and below the mean sound enamel microhardness of the cohort with alpha of 0.05. The A allele of BTF3 rs6862039 appears to be associated with harder enamel at baseline (p = 0.09), enamel more resistant to demineralization (p = 0.01), and enamel that more efficiently regain mineral and remineralize (p = 0.04). Similarly, the G allele of AQP5 marker rs3759129 and A allele of AQP5 marker rs296763 are associated with enamel more resistant to demineralization (p = 0.03 and 0.05, respectively). AQP5 and BTF3 genetic variations influence the initial subclinical stages of caries lesion formation in the subsurface of enamel.
Project description:There is evidence for a genetic component in caries susceptibility, and studies in humans have suggested that variation in enamel formation genes and their interaction with Streptococcus mutans levels may contribute to caries. For the present study, we used DNA samples collected from 173 unrelated children from Istanbul: 91 children with 4 or more affected tooth surfaces and 82 caries-free children. Six single-nucleotide polymorphism markers were genotyped in selected candidate genes (ameloblastin, amelogenin, enamelin, tuftelin 1 and tuftelin interacting protein 11) that influence enamel formation. Allele and genotype frequencies were compared between groups with distinct caries experience. Regression analysis was used for the evaluation of individual gene effects, environmental effects and gene-environment interactions. Overrepresentation of the C allele of the amelogenin marker was seen in cases with dmft scores higher than 8 (p = 0.01) when compared to controls. Also, overrepresentation of the T allele of the ameloblastin marker was seen in cases with dmfs scores higher than 10 (p = 0.05) when compared to controls. In addition, the CT genotype of the tuftelin rs3790506 marker was overrepresented in cases with dmft scores higher than 5 (p = 0.05) and dmfs scores higher than 6 (p = 0.05) compared to controls. The best-fitting model showed that dmfs is increased when the following factors are present: (1) females and both the anterior and posterior teeth are affected simultaneously, (2) when the T allele of the tuftelin rs3790506 is involved, and (3) the C allele of the amelogenin rs17878486 is involved. Our study provides support that genes involved in enamel formation modify caries susceptibility in humans.
Project description:<h4>Background</h4>Dental caries inequalities still severely burden individuals' and society's health, even in countries where fluoride toothpastes are widely used and the incidence of dental caries has been decreasing. School-based fluoride mouth-rinse (S-FMR) programs, a population strategy for dental caries prevention, might decrease dental caries inequalities. This study investigated the association between S-FMR and decreasing dental caries prevalence and caries-related inequalities in 12-year-olds by Japanese prefecture.<h4>Methods</h4>We conducted an ecological study using multi-year prefecture-level aggregated data of children born between 1994 and 2000 in all 47 Japanese prefectures. Using two-level linear regression analyses (birth year nested within prefecture), the association between S-FMR utilization in each prefecture and 12-year-olds' decayed, missing, or filled permanent teeth (DMFT), which indicates dental caries experience in their permanent teeth, were examined. Variables that could explain DMFT inequalities between prefectures, such as dental caries experience at age 3 years, dentist density, and prefectural socioeconomic circumstances, were also considered.<h4>Results</h4>High S-FMR utilization was significantly associated with low DMFT at age 12 (coefficient -0.011; 95% confidence interval, -0.018 to -0.005). S-FMR utilization explained 25.2% of the DMFT variance between prefectures after considering other variables. Interaction between S-FMR and dental caries experience at age 3 years showed that S-FMR was significantly more effective in prefectures where the 3-year-olds had high levels of dental caries experience.<h4>Conclusions</h4>S-FMR, administered to children of all socioeconomic statuses, was associated with lower DMFT. Utilization of S-FMR reduced dental caries inequalities via proportionate universalism.
Project description:This study evaluated the effect of CO2 laser irradiation and topical fluoride therapy in the control of caries progression on primary teeth enamel. 30 fragments (3 × 3 × 2 mm) from primary canines were submitted to an initial cariogenic challenge that consisted of immersion on demineralizing solution for 3 hours and remineralizing solution for 21 hours for 5 days. Fragments were randomly assigned into three groups (n = 10): L: CO2 laser (λ = 10.6 μm), APF: 1.23% acidulated phosphate fluoride, and C: no treatment (control). CO2 laser was applied with 0.5 W power and 0.44 J/cm(2) energy density. Fluoride application was performed with 0.1 g for 1 minute. Cariogenic challenge was conducted for 5 days following protocol previously described. Subsurface Knoop microhardness was measured at 30 μm from the edge. Obtained data were subjected to analysis the variance (ANOVA) and Duncan test with significance of 5%. It was found that the L group showed greater control of deciduous enamel demineralization and were similar to those of APF group, while being statistically different from C group (P ≤ 0.05) that showed the lowest microhardness values. It was concluded that CO2 laser can be an additional resource in caries control progression on primary teeth enamel.