Studies have found both genetic and environmental influences on chronic periodontitis. The purpose of this study was to examine the relationships among previously identified genetic variants, smoking status, and two periodontal disease-related phenotypes (PSR1 and PSR2) in 625 Caucasian adults (aged 18–49 years). The PSR Index was used to classify participants as affected or unaffected under the PSR1 and PSR2 phenotype definitions. Using logistic regression, we found that the form of the relationship varied by single nucleotide polymorphism (SNP): For rs10457525 and rs12630931, the effects of smoking and genotype on risk were additive; whereas for rs10457526 and rs733048, smoking was not independently associated with affected status once genotype was taken into consideration. In contrast, smoking moderated the relationships of rs3870371 and rs733048 with affected status such that former and never smokers with select genotypes were at increased genetic risk. Thus, for several groups, knowledge of genotype may refine the risk prediction over that which can be determined by knowledge of smoking status alone. Future studies should replicate these findings. These findings provide the foundation for the exploration of novel pathways by which periodontitis may occur.

Objective

The purpose of this study is to identify barriers that early-adopting dentists perceive as common and challenging when implementing recommendations from evidence-based (EB) clinical guidelines.

Method

This is a cross-sectional study. Dentists who attended the 2008 Evidence-based Dentistry Champion Conference were eligible for inclusion. Forty-three dentists (34%) responded to a 22-item questionnaire administered online. Two investigators independently coded and categorized responses to open-ended items. Descriptive statistics were computed to assess the frequency of barriers and perceived challenges.

Results

The most common barriers to implementation are difficulty in changing current practice model, resistance and criticism from colleagues, and lack of trust in evidence or research. Barriers perceived as serious problems have to do with lack of up-to-date evidence, lack of clear answers to clinical questions, and contradictory information in the scientific literature.

Conclusions

Knowledge of barriers will help improve translation of biomedical research for dentists. Information in guidelines needs to be current, clear, and simplified for use at chairside; dentists’ fears need to be addressed.

Background

People in Appalachia experience some of the worst oral health in the United States. To develop effective intervention and prevention strategies in Appalachia, we must understand the complex relationships among the contributing factors and how they affect the etiology of oral diseases. To date, no such comprehensive analysis has been conducted. This report summarizes the characteristics of the sample and describes the protocol of a study determining contributions of individual, family, and community factors to oral diseases in Appalachian children and their relatives.

Methods/Design

Families participated in a comprehensive assessment protocol involving interviews, questionnaires, a clinical oral health assessment, a microbiological assessment, and collection of DNA. The design of the study is cross-sectional.

Conclusion

Due to its multilevel design and large, family-based sample, this study has the potential to greatly advance our understanding of factors that contribute to oral health in Appalachian children.

Background

Over 90% of adults aged 20 years or older with permanent teeth have suffered from dental caries leading to pain, infection, or even tooth loss. Although caries prevalence has decreased over the past decade, there are still about 23% of dentate adults who have untreated carious lesions in the US. Dental caries is a complex disorder affected by both individual susceptibility and environmental factors. Approximately 35-55% of caries phenotypic variation in the permanent dentition is attributable to genes, though few specific caries genes have been identified. Therefore, we conducted the first genome-wide association study (GWAS) to identify genes affecting susceptibility to caries in adults.

Methods

Five independent cohorts were included in this study, totaling more than 7000 participants. For each participant, dental caries was assessed and genetic markers (single nucleotide polymorphisms, SNPs) were genotyped or imputed across the entire genome. Due to the heterogeneity among the five cohorts regarding age, genotyping platform, quality of dental caries assessment, and study design, we first conducted genome-wide association (GWA) analyses on each of the five independent cohorts separately. We then performed three meta-analyses to combine results for: (i) the comparatively younger, Appalachian cohorts (N = 1483) with well-assessed caries phenotype, (ii) the comparatively older, non-Appalachian cohorts (N = 5960) with inferior caries phenotypes, and (iii) all five cohorts (N = 7443). Top ranking genetic loci within and across meta-analyses were scrutinized for biologically plausible roles on caries.

Results

Different sets of genes were nominated across the three meta-analyses, especially between the younger and older age cohorts. In general, we identified several suggestive loci (P-value ≤ 10E-05) within or near genes with plausible biological roles for dental caries, including RPS6KA2 and PTK2B, involved in p38-depenedent MAPK signaling, and RHOU and FZD1, involved in the Wnt signaling cascade. Both of these pathways have been implicated in dental caries. ADMTS3 and ISL1 are involved in tooth development, and TLR2 is involved in immune response to oral pathogens.

Conclusions

As the first GWAS for dental caries in adults, this study nominated several novel caries genes for future study, which may lead to better understanding of cariogenesis, and ultimately, to improved disease predictions, prevention, and/or treatment.

Background

Dental caries is the result of a complex interplay among environmental, behavioral, and genetic factors, with distinct patterns of decay likely due to specific etiologies. Therefore, global measures of decay, such as the DMFS index, may not be optimal for identifying risk factors that manifest as specific decay patterns, especially if the risk factors such as genetic susceptibility loci have small individual effects. We used two methods to extract patterns of decay from surface-level caries data in order to generate novel phenotypes with which to explore the genetic regulation of caries.

Methods

The 128 tooth surfaces of the permanent dentition were scored as carious or not by intra-oral examination for 1,068 participants aged 18 to 75 years from 664 biological families. Principal components analysis (PCA) and factor analysis (FA), two methods of identifying underlying patterns without a priori surface classifications, were applied to our data.

Results

The three strongest caries patterns identified by PCA recaptured variation represented by DMFS index (correlation, r = 0.97), pit and fissure surface caries (r = 0.95), and smooth surface caries (r = 0.89). However, together, these three patterns explained only 37% of the variability in the data, indicating that a priori caries measures are insufficient for fully quantifying caries variation. In comparison, the first pattern identified by FA was strongly correlated with pit and fissure surface caries (r = 0.81), but other identified patterns, including a second pattern representing caries of the maxillary incisors, were not representative of any previously defined caries indices. Some patterns identified by PCA and FA were heritable (h2 = 30-65%, p = 0.043-0.006), whereas other patterns were not, indicating both genetic and non-genetic etiologies of individual decay patterns.

Conclusions

This study demonstrates the use of decay patterns as novel phenotypes to assist in understanding the multifactorial nature of dental caries.

Objective

This report describes a model for the development, process and tracking methods of an interdisciplinary peer mentoring program, Peer-mentored Research Development Meeting (PRDM). PRDM was initiated in 2004 by a group of postdoctoral scholars and junior faculty from the Schools of the Health Sciences at the University of Pittsburgh.

Method

Case report. From February of 2004 through February of 2006, PRDM's first 5 members tracked and documented their research activity (e.g., manuscripts, grants) every 4 months. The defining features of PRDM are: 1) adherence to a structured frequency and format for meetings, 2) systematic tracking and evaluation of research development activities, and 3) maintenance of ongoing relationships with senior mentors.

Results

During the 24-month data collection period, members were involved in 91 research development projects including grant applications, journal article manuscripts, book chapters and conference abstracts. Members' productivity increased during the 24-month period, as did the efficiency and focus of the completed projects.

Conclusions

Members increased the efficiency and focus of their research development activities during the study period. Structured peer-mentoring groups have potential to enhance research productivity among junior investigators in research intensive environments.