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Abstract Background Individuals born with cleft lip and/or palate who receive corrective surgery regularly have abnormal growth in the midface region such that they exhibit premaxillary hypoplasia. However, there are also genetic contributions to craniofacial morphology in the midface region, so although these individuals appear to have Class III skeletal discrepancy, their molar relationship may be Class I. Past genome-wide association studies (GWASs) on skeletal Class II and III malocclusion suggested that multiple genetic markers contribute to these phenotypes via a multifactorial inheritance model, but research has yet to examine the genetic markers associated with dental Class I malocclusion. Thus, our goal was to conduct a family based GWAS to identify genes across the genome that are associated with Class I malocclusion, as defined by molar relations, in humans with and without clefts. Methods Our cohort consisted of 739 individuals from 47 Filipino families originally recruited in 2006 to investigate the genetic basis of orofacial clefts. All individuals supplied blood samples for DNA extraction and genotyping, and a 5,766 single nucleotide polymorphism (SNP) custom panel was used for the analyses. We performed a transmission disequilibrium test for participants with and without clefts to identify genetic contributors potentially involved with Class I malocclusion. Results In the total cohort, 13 SNPs had associations that reached the genomic control threshold (p

Abstract Hurricane Maria was the worst recorded natural disaster to affect Puerto Rico. Increased stress in pregnant women during and in the aftermath of the hurricane may have induced epigenetic changes in their infants, which could affect gene expression. Stage of gestation at the time of the event was associated with significant differences in DNA methylation in the infants, especially those who were at around 20–25 weeks of gestation when the hurricane struck. Significant differences in DNA methylation were also associated with maternal mental status assessed after the hurricane, and with property damage. Hurricane Maria could have long lasting consequences to children who were exposed to this disaster during pregnancy.

Abstract Early-stage cancer diagnosis is critical for higher survival rates. Because early cancers can be difficult to detect, our focus is on the identification of cancer risk markers such as pleiotropic genes involved in the etiology of both craniofacial conditions and cancers. In this study we aimed to test if our previously detected association between ERN1 rs196929 marker and oral health outcomes would be detected in individuals diagnosed with cancer as well as in a subpopulation of individuals who also had one or more teeth missing due to dental caries, periodontal disease, or periapical lesions. We genotyped a total of 1,671 subjects and selected a subset of 1,421 subjects for stratified analysis of cancer types; three hundred and twelve self-reported a diagnosis of various cancer types and 1,109 reported never receiving a diagnosis of cancer. Our results showed a statistically significant association between the rs196929 in ERN1, and cancer overall in both the additive and dominant models (OR = 1.37, 95% C.I. 1.06–1.79, p = 0.014). When we stratified the analysis for each cancer type, our results show that the rs196929 ERN1 variant is associated with skin cancer (OR = 2.07, 95% C.I. 1.27–3.37, p = 0.003) and breast cancer (OR = 1.83, 95% C.I. 1.13–2.99, p = 0.013) in the subset of patients that had tooth loss. An additional nominal association between the rs196929 in ERN1 and male’s reproductive system cancers (OR = 1.96, 95% C.I. 1.07–3.59, p = 0.028) was identified. We hope that our study helps guide future genetic studies on these cancers and this specific genetic variant as well as drive attention to the potential for oral health outcomes to serve as indicators for cancer risk. The early identification of genetic markers and/or oral conditions that indicate increased cancer risk could positively impact cancer outcomes and survival rates with timely implementation of preventive and diagnostic measures. In conclusion, our results suggest that the genetic variant in ERN1 (rs196929) is associated with increased risk of skin and breast cancers.

Abstract Undernutrition is a public health challenge in sub-Saharan countries, including Uganda. In a previous randomized controlled trial (RCT) with a nutrition, hygiene and stimulation education intervention among mothers of 6 months’ old children, we found less caries in the intervention group when the children were 36 months of age. We now examined the effects of (i) the intervention on the microbiota, (ii) microbiota on caries, and (iii) the intervention and microbiota on caries. The original RCT comprised 511 mother/child pairs whereas in the current study we had access to data from 344/511 (67%) children aged 36 months. The saliva microbiota was determined using 16S rRNA gene sequencing. Carious lesions (a proxy for dental health) were identified using close-up intra-oral photographs of the upper front teeth. Statistical models were used to determine host-microbiota associations. The intervention had a significant effect on the microbiota, e.g. an increase in Streptococcus abundance and decreases in Alloprevotella and Tannerella. Significant associations between the microbiota and dental caries were identified: Positive associations of Capnocytophaga and Tannerella suggest that these taxa may be deleterious to dental health while negative associations of Granulicatella, Fusobacterium, and Abiotrophia suggest taxa potentially beneficial or benign contributors to dental health. Based on taxonomic profiles, the effects of the intervention and microbiota on dental health may be independent of one another. Educational interventions with emphasis on nutrition and oral hygiene may provide a feasible strategy to decrease progression of childhood caries in low-resource settings.

Trigeminal neuralgia is highly debilitating, and its etiology is still undefined. The goal of this work was to define associations between well-characterized trigeminal neuralgia cases and common genetic variants in the population. Two hundred and fifty-seven individuals diagnosed with classical trigeminal neuralgia were compared to 865 individuals without classical trigeminal neuralgia and with an assessment for lower or higher pain threshold based on the amount of anesthetic required for routine dental treatment. Genotypes of 24 variants marking genes in the VGSC (voltage-gated sodium channels) or GABA (gamma-aminobutyric acid) pathways were obtained using TaqMan chemistry end end-point analysis. Chi-square was used for all comparisons with an alpha of 0.002. An association between classical trigeminal neuralgia and individuals requiring less or more anesthetic for routine dental treatments showed associations with SCN8A rs1601012 and GPHN rs723432 (p = 0.0009 and p = 0.0002, respectively). In conclusion, classical trigeminal neuralgia is associated with SCN8A and GPHN and markers rs1601012 rs723432 may be useful to determine individual risks for the condition.

It is common to hear the assertion that Brazil’s dentistry is one the best in the world or that Brazil has the best dentists. These statements are based, in part, on the total number of scientific dentistry manuscripts produced in Brazil and on extrapolating the ranking of Brazilian faculty/courses compared to others in the world, which also uses the number of article publications produced by each institution as a parameter. Therefore, Dentistry in Brazil is among the best in the world, as this is a direct metric: more publications must be at the forefront of knowledge, and this transfers to classrooms and clinics where future dentists in training are learning dentistry. The result, in the end, should be better oral health for Brazilians.

The need to determine risk factors for complex diseases continues to drive efforts to identify etiological factors of common conditions. Molecular tools have created new opportunities to identify risk factors that may act interactively. The goal of this work was to explore potential interactions between oral microbial species and common genetic variants. Ninety-two 6- to 19-year-old individuals recruited through the University of Pittsburgh Dental Registry and DNA Repository project that had oral microbiome and genotyping of 44 single nucleotide polymorphism (SNP) data available were studied. Over-representation of alleles between individuals with or without particular microorganisms was determined using chi-square or Fisher's exact tests. An alpha of 0.001, to account for multiple testing (0.05/44), was considered statistically significant. Associations were found between Candida albicans and enamelin rs3796704 (p = 0.0006), and Staphylococcus epidermidis and tuftelin rs3828054 (p = 0.001). Microbiota and their metabolites might predispose to oral disease when interacting with the host genetic variation and future studies should address their causal roles in oral disease.

Abstract Background Dental caries is one of the most common chronic diseases and is influenced by a complex interplay of genetic and environmental factors. Most previous genetic studies of caries have focused on identifying genes that contribute to dental caries in specific ethnic groups, usually of European descent. Methods The aim of this study is to conduct a genome-wide association study (GWAS) to identify associations affecting susceptibility to caries in a large multiethnic population from Argentina, the Philippines, Guatemala, Hungary, and the USA, originally recruited for studies of orofacial clefts (POFC, N = 3686). Ages of the participants ranged from 2 to 12 years for analysis of the primary dentition, and 18–60 years for analysis of the permanent dentition. For each participant, dental caries was assessed by counts of decayed and filled teeth (dft/DFT) and genetic variants (single nucleotide polymorphisms, SNPs) were genotyped or imputed across the entire genome. Caries was analyzed separately for the primary and permanent dentitions, with age, gender, and presence/absence of any type of OFC treated as covariates. Efficient Mixed-Model Association eXpedited (EMMAX) was used to test genetic association, while simultaneously accounting for relatedness and stratification. Results We identified several suggestive loci (5 × 10−8

Introduction: The goal of this study was to test the impact of both diabetes type and control via the hemoglobin A1C biomarker on oral health outcomes. Materials & Methods: In this observational study, data were extracted from the University of Pittsburgh Dental Registry and DNA Repository and analyzed. From 6,026 subjects, 414 ones with a diagnosis of diabetes were matched by sex, age and ethnicity with 414 individuals without diabetes. A number of statistical approaches (chi-square, Fisher’s exact, Student’s t, Wilcox, and Mann Whitney tests) were used and all comparisons were set with an alpha of 0.05. Results: Patients with type 1 diabetes experienced xerostomia more often compared to non-diabetic matched pairs (p=0.02). Patients with diabetes (n=414) experienced temporomandibular joint (TMJ) discomfort more often than their non-diabetic matched pairs, as did type 1 diabetic patients alone, in comparison to both their matched pairs and type 2 diabetic patients (p=0.01, p=0.004, and p=0.02, respectively). Among patients grouped by diabetic control, all patients reporting control (n=39) experienced xerostomia more often than their non-diabetic matched pairs (p=0.05). Patients in poor diabetic control experienced restoration failure more often than patients in good control (p=0.04). The experience of restoration failure was no different between patients in good diabetic control and their matched controls (p=0.26). The number of restoration failures was higher in patients in poor control, as compared to their matched non-diabetic controls (p=0.03). Conclusion: Patients with diabetes experienced xerostomia but not necessarily more severe caries experience, and may be protected from TMJ discomfort. Patients in good control of their diabetes were at no greater risk for restoration failure as compared to non-diabetic patients; however, the patients in poor control were at higher risk for failed restorations.

Patient centeredness in planning treatment and research has become paramount. The goal of this report was to describe a complex case in which untreated chronic pain was not properly addressed to reflect on the need to establish alternative protocols for controlling chronic orofacial pain. When a female underwent orthognathic surgery to correct her occlusion, she not only ended up with a worse occlusion, she developed chronic orofacial pain that could not be treated by opioids and only improved after the use of neuropathic medication, and finally disappeared after the use of low-level laser therapy. There is a need to incorporate alternative nonpharmacological approaches to manage chronic pain. Further, what the patient’s goals are for their treatments should be given priority in case of elective procedures.

Background: Supernumerary teeth refer to extra teeth that exceed the usual number of dentitions. A mesiodens is a particular form of supernumerary tooth, which is located in the premaxilla region. The objective of the study was to investigate the genetic etiology of extra tooth phenotypes, including mesiodens and isolated supernumerary teeth. Methods: Oral and radiographic examinations and whole-exome sequencing were performed on every patient in our cohort of 122 patients, including 27 patients with isolated supernumerary teeth and 94 patients with mesiodens. A patient who had multiple supernumerary teeth also had odontomas. Results: We identified a novel (c.8498A>G; p.Asn2833Ser) and six recurrent (c.1603C>T; p.Arg535Cys, c.5852G>A; p.Arg1951His, c.6949A>T; p.Thr2317Ser; c.1549G>A; p.Val517Met, c.1921A>G; p.Thr641Ala, and c.850G>C; p.Val284Leu) heterozygous missense variants in FREM2 in eight patients with extra tooth phenotypes. Conclusions: Biallelic variants in FREM2 are implicated in autosomal recessive Fraser syndrome with or without dental anomalies. Here, we report for the first time that heterozygous carriers of FREM2 variants have phenotypes including oral exostoses, mesiodens, and isolated supernumerary teeth.

Excessive sugar consumption is the main cause of dental caries. Dental caries is highly prevalent and negatively impacts the quality of life at all stages. Furthermore, sugar consumption is associated with other noncommunicable conditions and diseases, such as obesity, diabetes, and cardiovascular diseases. The aim of this paper is to propose recommendations at the individual and population levels for health professionals, families, educators, stakeholders, and public officials to reduce the burden of dental caries and other noncommunicable diseases that are caused by the excessive sugar intake. A systematic search was performed in PubMed and Cochrane databases to investigate the effectiveness of strategies and policies aiming to reduce sugar consumption as well as the impact of different patterns of sugar consumption on the occurrence of dental caries. Reference list of the identified papers and practice guidelines were manually reviewed as well. Based on the best evidence available, the Brazilian Academy of Dentistry recommends not to offer sugars to children younger than 2 years of age, and to limit total sugar consumption to

BackgroundOur aim was to investigate the relationship between caries experience and erosive tooth wear in adolescents.MethodsWe compared the Decayed, Missing, and Filled Teeth (dmft/DMFT) data of 795 adolescents to their erosive tooth wear scores using diet as a covariate and determined whether dental caries and erosive tooth wear scores are associated with each other, using linear regression analysis. Diet data and oral hygiene habits were collected using self-reported surveys and erosive tooth wear scores were previously collected. We also compared patients' genotypes and phenotypes and looked for an association between erosive tooth wear experience and different single nucleotide polymorphisms (SNPs). A Bonferroni correction was implemented to correct multiple comparisons. Two-group comparisons were made depending on the phenotype definitions implemented, and both chi-square and linear regression analyses were used to the test association between genetic variants and caries definitions. All covariates were included in each model.ResultsFor four SNPs (rs17159702, rs10246939, rs1800972, and rs1676303), there was an association between a spike in caries experience of DMFT 4 or more between two time points and increased frequency of fruit juice intake. A fifth SNP rs2860216 was shown to be a protective factor against a caries spike when associated with more frequent yogurt consumption. We did not find significant associations between our dental caries phenotypes or our demographic data and erosive tooth wear status in our linear regression.ConclusionsDental caries and erosive tooth wear are two diseases that differ in mechanism and heritability.

Certain patients, despite receiving proper treatment, still show higher failure rates of restorative dental treatments. The aim of this work was to test if MMP2 and MMP3 alleles are overrepresented in individuals with secondary caries. A total of 1,089 individuals from the University of Pittsburgh School of Dental Medicine Dental Registry and DNA Repository project were selected for this study. From this total, 341 individuals were selected for having a record of secondary caries in any type of restoration and were matched with 748 individuals by sex, age, ethnicity, and restorative work in the same teeth that did not fail. Genomic DNA extracted from saliva was used to obtain genotypes in five markers of MMP2 and MMP3 using TaqMan chemistry and end-point analysis. Chi-square was used to test if differences in allele and genotype distributions were statistically different at an alpha of 0.05. The less common allele and homozygote genotype of MMP2 rs9923304 were less commonly found among individuals with secondary caries. The less common allele of MMP2 rs2287074 was also less frequent among individuals with secondary caries. These results provide statistical evidence for the role of MMP2 in failure of restorations due to secondary caries. We can conclude that MMP2 variation impacts the risk of having secondary caries, independent of the restorative material.

Care for individuals born with cleft lip and palate is done by a team approach, including dental medicine. However, oral health is not integrated in other situations that affect overall health. This perspective essay makes the case for a universal team approach, having dental medicine integrated regardless of the overall health issue, much like how cleft lip and palate is managed. Furthermore, future research agenda on the etiology of cleft lip and palate in particular will need to be adjusted for a major roadblock: the lack of more sophisticated clinical descriptions for the cases ascertained at birth.

Abstract Objectives Dental caries is a highly prevalent infectious disease that causes tooth decay. While no single bacterial species is causative of dental caries, the role of the oral microbiome in oral health and caries is gaining interest. The purpose of this study is to compare the major species present in whole saliva samples from caries‐free and caries‐active children using the IBIS Universal Biosensor. Material and Methods The abundant microbial species in ninety‐five whole saliva samples from caries‐free and caries‐active subjects were characterized using the IBIS Universal Biosensor. Results Twenty‐four genera and sixty‐five species were detected. Candida and Streptococcus were common across samples, and often the dominant genus. While we did not observe a strong association between the most abundant species and oral health, Bacteroides thetaiotaomicron and Rothia mucilaginosa were enriched in children with active caries; while, Staphylococcus epidermidis was enriched in caries‐free children. Conclusions These study trends observed suggest that microbial markers in saliva may serve as predictors of oral health and thus aid in diagnosis and treatments for prevention of caries. Consistent with competitive interactions, we also observed negative associations between Streptococcus pneumoniae and other streptococcal species, Staphylococcus aureus and S. epidermidis, Candida and Neisseria, and Saccharomyces and Streptococcus.

Abstract Introduction: Genetics has been suggested as an explanation for the etiology of malocclusions, although some questions, due to the perception that genetic inheritance is tied to a monogenic or Mendelian form of inheritance. Objective: This paper describes the inheritance of malocclusions, highlighting the areas of knowledge where research has explored mechanisms that explain deviations in patterns of craniofacial growth. Conclusion: Malocclusions have a complex or multifactorial pattern of inheritance, where more than one gene is involved in the development of the phenotype. There is also the possibility that the environment influences malocclusions.

Individuals with orofacial clefting (OFC) have a higher prevalence of tooth agenesis (TA) overall. Neither the precise etiology of TA, nor whether TA occurs in patterns that differ by gender or cleft type is yet known. This meta-analysis aims to identify the spectrum of tooth agenesis patterns in subjects with non-syndromic OFC and controls using the Tooth Agenesis Code (TAC) program. An indexed search of databases (PubMed, EMBASE, and CINAHL) along with cross-referencing and hand searches were completed from May to June 2019 and re-run in February 2022. Additionally, unpublished TAC data from 914 individuals with OFC and 932 controls were included. TAC pattern frequencies per study were analyzed using a random effects meta-analysis model. A thorough review of 45 records retrieved resulted in 4 articles meeting eligibility criteria, comprising 2182 subjects with OFC and 3171 controls. No TA (0.0.0.0) was seen in 51% of OFC cases and 97% of controls. TAC patterns 0.2.0.0, 2.0.0.0, and 2.2.0.0 indicating uni- or bi-lateral missing upper laterals, and 16.0.0.0 indicating missing upper right second premolar, were more common in subjects with OFC. Subjects with OFC have unique TA patterns and defining these patterns will help increase our understanding of the complex etiology underlying TA.

Orofacial clefts (OFCs) are among the most prevalent craniofacial birth defects worldwide and create a significant public health burden. The majority of OFCs are non-syndromic and vary in prevalence by ethnicity. Africans have the lowest prevalence of OFCs (~ 1/2,500), Asians have the highest prevalence (~1/500), Europeans and Latin Americans lie somewhere in the middle (~1/800 and 1/900, respectively). Thus, ethnicity appears to be a major determinant of the risk of developing OFC. The Pittsburgh Orofacial Clefts Multiethnic study was designed to explore this ethnic variance, comprising a large number of families and individuals (~12,000 individuals) from multiple populations worldwide: US and Europe, Asians, mixed Native American/Caucasians, and Africans. In this current study, we analyzed 2,915 OFC cases, 6,044 unaffected individuals related to the OFC cases, and 2,685 controls with no personal or family history of OFC. Participants were grouped by their ancestry into African, Asian, European, and Central and South American subsets, and genome-wide association run on the combined sample as well as the four ancestry-based groups. We observed 22 associations to cleft lip with or without cleft palate at 18 distinct loci with p-values < 1e-06, including 10 with genome-wide significance (

The goal of this study was to test if oral health outcomes are associated with the same genetic markers in Black and White individuals who did not have cancer. From a total of 6,100 subjects from the Dental Registry and DNA Repository project, 1,042 individuals who self-identified as White and 266 as Black without a history of cancer were included in this analysis. Genotyping data from IRE1—rs196929, RHEB—rs2374261 and rs1109089, AXIN2—rs2240308 and rs11867417, and RPTOR—rs4396582, present in cell regulatory pathways, were analyzed. We ran separate analyses in self-reported Black and White groups to reduce possible confounding effects of population stratification. Internal diagnostic codes from our dental registry were converted into Phecodes in order to run the analysis using the PheWAS package, installed in R Studio software. Periodontitis was associated with RHEB in both Black and White patients, with the minor allele increasing the likelihood of developing periodontitis in the White group and yielding a protective effect in the Black individuals. The presence of ulcers and gingivitis were associated with RPTOR and AXIN2, respectively, in the White group, but an association was not detected for the Black group. On the other hand, phenotypes such as dental fracture, diseases of the tongue, attrition, erosion, abrasion, fordyce granules, and torus and exostosis were uniquely associated with the Black group. Periodontitis associated with RHEB in both Black and White patients, and associations found in Black individuals may be the result of social disparities that lead to higher levels of stress, and these observed differences require further study.

The goal of the present work was to revisit published data to test if genetic variation in interferon regulatory factor 6 (IRF6) is associated with children born with cleft lip with or without cleft palate (CL/P) for cases with positive history of maternal smoking. From the 573 individuals originally studied, this reanalysis focused on 57 who had a positive history of maternal smoking during pregnancy (39 born with CL/P and 18 born without CL/P). Seven IRF6 markers (rs4844880, rs2235371, rs2013162, ra861019, rs2073487, rs642961, and rs658860) were tested for over-transmission of alleles and an alpha of 0.05 was considered statistically significant. All individuals born with CL/P were homozygous for the wild type allele of rs2235371 in comparison to just two individuals born without clefts (p = 0.0000001). For rs861019, individuals born with CL/P were more likely to have the variant allele (p = 0.006). A similar trend was seen for rs642961 (p = 0.09). The results suggest that statistical evidence of over-representation of IRF6 alleles in individuals born with CL/P may be unveiled only when maternal smoking during pregnancy is used as the inclusion criterion in the analysis.

Abstract Background The Met136Val mutation in SCN8A was described in a case of trigeminal neuralgia but no frequency among affected individuals was provided. Methods Direct sequencing of 123 individuals diagnosed with classic trigeminal neuralgia was performed aimed to detect the Met136Val change. Results No cases of classical trigeminal neuralgia studied had the Met136Val mutation in SCN8A. Conclusion Met136Val mutation in SCN8A is not a frequent cause of classical trigeminal neuralgia.

Abstract Background Dental caries is a common chronic disease among children and adults alike, posing a substantial health burden. Caries is affected by multiple genetic and environmental factors, and prior studies have found that a substantial proportion of caries susceptibility is genetically inherited. Methods To identify such genetic factors, we conducted a genome-wide linkage scan in 464 extended families with 2616 individuals from Iowa, Pennsylvania and West Virginia for three dental caries phenotypes: (1) PRIM: dichotomized as zero versus one or more affected primary teeth, (2) QTOT1: age-adjusted quantitative caries measure for both primary and permanent dentitions including pre-cavitated lesions, and (3) QTOT2: age-adjusted quantitative caries excluding pre-cavitated lesions. Genotyping was conducted for approximately 600,000 SNPs on an Illumina platform, pruned to 127,511 uncorrelated SNPs for the analyses reported here. Results Multipoint non-parametric linkage analyses generated peak LOD scores exceeding 2.0 for eight genomic regions, but no LOD scores above 3.0 were observed. The maximum LOD score for each of the three traits was 2.90 at 1q25.3 for PRIM, 2.38 at 6q25.3 for QTOT1, and 2.76 at 5q23.3 for QTOT2. Some overlap in linkage regions was observed among the phenotypes. Genes with a potential role in dental caries in the eight chromosomal regions include CACNA1E, LAMC2, ALMS1, STAMBP, GXYLT2, SLC12A2, MEGF10, TMEM181, ARID1B, and, as well as genes in several immune gene families. Our results are also concordant with previous findings from association analyses on chromosomes 11 and 19. Conclusions These multipoint linkage results provide evidence in favor of novel chromosomal regions, while also supporting earlier association findings for these data. Understanding the genetic etiology of dental caries will allow designing personalized treatment plans based on an individual’s genetic risk of disease.

Abstract Background Oral hygiene instruction is an intervention widely practiced but increased knowledge about oral health does not necessarily dramatically impact oral disease prevalence in populations. We aimed to measure plaque and bleeding in periodontal patients over time to determine patterns of patient response to oral hygiene instructions. Methods Longitudinal plaque and bleeding index data were evaluated in 227 periodontal patients to determine the impact of oral hygiene instructions. Over multiple visits, we determined relative plaque accumulation and gingival bleeding for each patient. Subsequently, we grouped them in three types of oral hygiene status in response to initial instructions, using the longitudinal data over the period they were treated and followed for their periodontal needs. These patterns of oral hygiene based on the plaque and gingival bleeding indexes were evaluated based on age, sex, ethnic background, interleukin 1 alpha and beta genotypes, diabetes status, smoking habits, and other concomitant diseases. Chi-square and Fisher’s exact tests were used to determine if any differences between these variables were statistically significant with alpha set at 0.05. Results Three patterns in response to oral hygiene instructions emerged. Plaque and gingival bleeding indexes improved, worsened, or fluctuated over time in the periodontal patients studied. Out of all the confounders considered, only ethnic background showed statistically significant differences. White individuals more often than other ethnic groups fluctuated in regards to oral hygiene quality after instructions. Conclusions There are different responses to professional oral hygiene instructions. These responses may be related to ethnicity.

Abstract Objectives To evaluate the association between hypoxia during embryo development and oral clefts in an animal model, and to evaluate the association between polymorphisms in the HIF-1A gene with oral clefts in human families. Material and Methods The study with the animal model used zebrafish embryos at 8 hours post-fertilization submitted to 30% and 50% hypoxia for 24 hours. At 5 days post-fertilization, the larvae were fixed. The cartilage structures were stained to evaluate craniofacial phenotypes. The family-based association study included 148 Brazilian nuclear families with oral clefts. The association between the genetic polymorphisms rs2301113 and rs2057482 in HIF-1A with oral clefts was tested. We used real time PCR genotyping approach. ANOVA with Tukey's post-test was used to compare means. The transmission/disequilibrium test was used to analyze the distortion of the inheritance of alleles from parents to their affected offspring. Results For the hypoxic animal model, the anterior portion of the ethmoid plate presented a gap in the anterior edge, forming a cleft. The hypoxia level was associated with the severity of the phenotype (p0.05). Conclusion Hypoxia is involved in the oral cleft etiology, however, polymorphisms in HIF-1A are not associated with oral clefts in humans.

Composite resins for posterior tooth restorations have become a viable alternative to dental amalgam. Failures sometimes cannot be easily explained, and we hypothesize that a genetic component may influence longevity of restorations. We aimed to determine if there is any evidence for a difference in the performance of amalgams versus composite resin in extensive posterior restorations. We also aimed to determine if risk factors such as age, sex, smoking tobacco, alcohol drinking, diabetes status, and periodontal health status may have a role in the failures of extensive anterior composite restorations. Finally, we investigated if genetic variation in matrix metalloproteinases that are present in the mineralized dentin is associated with failure of composite resin. The data used to perform this research were obtained from the Dental Registry and DNA Repository project after screening 4,856 patients. All restorations were evaluated at times of 1, 2, and 5 years after the restoration placement. 6,266 amalgam and 2,010 composite restorations were analyzed in a total of 807 patients in a period of approximately 10 years (period corresponding to the database existence). An additional 443 extensive direct composite resin restorations in anterior teeth were also studied. Failure rates of amalgam and composite restorations are similar, and by the end of 5 years, composites outperformed amalgams slightly. Failures of anterior composite restorations occurred more often in males who smoked tobacco (p = 0.05), despite a similar number of females and males that smoked tobacco in the sample (116 individuals smoked tobacco, 54 females and 62 males). Alcohol drinking increased failure rate within 2 years (p = 0.03). We found a statistically significant association between matrix metalloproteinase 2 rs9923304 and failure of composite restorations (p = 0.007). Composite resins can replace amalgam restorations. Smoking tobacco and drinking alcohol will increase the chance of restoration failure.

Aims. There is evidence of association between bruxism and the increasingly common central nervous system stimulants prescribed for attention deficit hyperactivity disorder (ADHD), as well as the selective serotonin reuptake inhibitors (SSRIs) often prescribed for depression or anxiety. However, the evidence is not clear on whether these medications inducing bruxism are directly associated with temporomandibular joint disorder (TMD). The aim of this work is to evaluate whether these medications are associated with TMD symptoms. Methods. Medical history and participant data were obtained for 469 patients from the University of Pittsburgh School of Dental Medicine, Dental Registry and DNA Repository, dating back to 2006. The chi-square test was used to determine any statistically significant associations. Results. There were no statistically significant associations between ADHD stimulant medications or SSRIs and reported TMD symptoms. However, there were significant differences seen between specific brands of medications and reported TMD symptoms. Individuals prescribed methylphenidate (Concerta) were less likely to report temporomandibular joint discomfort (p=0.01). Conversely, individuals prescribed citalopram (Celexa) were more likely to report temporomandibular joint discomfort (p=0.04). Conclusion. Signs and symptoms of temporomandibular joint dysfunction may be influenced by the use of certain medications prescribed for depression or attention deficit hyperactive disorder.

Characteristics of enamel may influence or modulate individual susceptibility to caries and erosion. These characteristics are defined during development, which is under strict genetic control, but can easily be modified in many ways by environmental factors. In the symposium, translational aspects of embryology, biochemistry, and genetics of amelogenesis were presented. The symposium provided unique insight into how basic sciences integrate with clinically relevant problems. The need for improved understanding of risks at the individual level, taking into consideration both environmental exposures and genetic background, was presented. The symposium was divided into four stepwise and interconnected topics as follows: 1) The Many Faces of Enamel Development; 2) Enamel Pathogenesis: Biochemistry Lessons; 3) Environmental Factors on Enamel Formation; and, 4) Genetic Variation in Enamel Formation Genes.

Objectives. Little evidence exists for the current standard of two annual preventative care visits. The purpose of this study was investigate this claim by modeling the potential savings of implementing a personalized care plan for high risk individuals in the Pittsburgh region. Methods. Using radiographs from 39 patients in the University of Pittsburgh Dental Registry and DNA Repository database, two models were created to analyse the direct savings of implementing a more aggressive preventative treatment plan and to view the longitudinal cost of increased annual yearly visits. Results. There is a significant decrease (p

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Many patients today are living longer with certain health issues like human immunodeficiency virus (HIV). These patients take numerous medications (HAART: highly active antiretroviral therapy) that cause xerostomia, which increases caries risk. There are particular challenges when treating HIV-positive patients with decreased immune systems, which can also accelerate the progression of periodontal disease. This paper discusses one such case that was followed from 2002 to 2010 at the University of Pittsburgh School of Dental Medicine, where an HIV patient lost all his teeth despite investing thousands of dollars. It is also common sense that just performing restorations to decayed teeth is not enough to control the disease, but recommending a personalized preventive maintenance program to the patient is a must.

The identification of individuals at a higher risk of developing caries is of great interest. Isolated forms of cleft lip and palate are among the most common craniofacial congenital anomalies in humans. Historically, several reports suggest that individuals born with clefts have a higher risk for caries. Caries continues to be the most common infectious noncontagious disease worldwide and a great burden to any health system. The identification of individuals of higher susceptibility to caries is of great interest. In this paper, we assessed caries experience of 1,593 individuals from three distinct populations. The study included individuals born with clefts, their unaffected relatives, and unrelated unaffected controls that were recruited from areas with similar cultural pressures and limited access to dental care. DMFT/dmft scores were obtained, and caries experience rates were compared among the three groups in each geographic area. Individuals born with clefts did not present higher caries experience in comparison to their unaffected relatives or unrelated unaffected controls. Women tend to present higher caries rates in comparison to men. Our work provides strong evidence that individuals born with clefts are not at higher risk to caries; however, women tend to have more severe caries experience.

Root caries is one of the most significant dental problems among older adults today. Many studies have demonstrated that older adults are at greater risk for developing root caries. Here we examine what risk factors older adults are prone to and explain how they contribute to higher rates of oral disease, in particular root caries. The elderly are at risk for root caries due to dentures, lack of dexterity, a shift from complex to simple sugars, and poor oral hygiene. Decreased salivary flow and its manifestations with other social/behavioral and medical factors may provide a more comprehensive explanation to a higher frequency of root caries in older adults.

Many studies have demonstrated that caries rates are higher in women than in men. This review attempts to provide an explanation for this trend by examining each factor which contributes to caries and how the factor differs in men and women. Evidence has been provided to demonstrate that caries risk factors for women include a different salivary composition and flow rate, hormonal fluctuations, dietary habits, genetic variations, and particular social roles among their family. Systemic diseases that have been found to be associated with caries have also been found to have an association with the female gender. An extended exposure to the oral cavity or a more cariogenic oral microflora has not been proven to contribute to higher caries in women. Further research in these areas could be done in the future to explain their contribution, or lack thereof, to a higher caries rate in women.