Professional identity formation: The key contributors and dental students' concerns.

OBJECTIVES: This study aimed to explore the components of professional identity formation (PIF) and understand dental students' concerns toward their professional identity development so that research-informed recommendations can be made to improve dental professional programs. METHODS: This is a qualitative study. A total of 18 students of the whole graduating class (class size: 46) were interviewed about their progress through a newly designed curriculum specific for the dental students at a large public research university in Canada. The audio files were recorded, transcribed, and corrected by a research assistant. Using QSR International's NVivo (Version 12), the researchers of this study conducted a thematic analysis to generate overarching themes and extract the relevant components of PIF. RESULTS: Five themes emerged from the study as follows: (i) domain-specific self-efficacy, (ii) role modeling and mentoring, (iii) professional socialization with peers, (iv) learning environment (LE), and (v) reflection. We considered these to be the five key contributors to dental students' PIF. CONCLUSIONS: Understanding the main concerns for students and improving the LE are critical in helping students form their professional identity. The findings of this qualitative study identified some important aspects of the dental curricula for educators to consider. These results can be used by future research studies to explore models for professional identity assessment tools that can aid in guiding students' professional identity development.

Identification of Smad-dependent and -independent signaling with transforming growth factor-ß type 1/2 receptor inhibition in palatogenesis.

TGF-ß signaling is one of important function during palatal fusion. Three types of TGF-ß receptor (TßR1, TßR2, and TßR3) have been identified, and play essential roles in mechanisms leading to palatal fusion. However, the balance between Smad-dependent/-independent signaling during palatal fusion with inhibited TßR1/2 functions is not fully understood. The objective of this study was to investigate palatal fusion via TGF-ß signaling when TßR1 and TßR2, but not TßR3, were inhibited. In addition, the present study examined the functional balance between Smad-dependent/-independent signaling and related gene expression. Palatal organ cultures were treated with TßR1/2 inhibitor in vitro. Control palates were cultured without inhibitor. We observed histological phenotype of palatal fusion, and evaluation of expression pattern by Western blot or real time RT-PCR. Palatal organ cultures treated with the inhibitor did not fuse and the medial edge epithelium remained at embryonic 13 day +72 h in culture. The inhibitor decreased TßR1 and TßR2 expression by approximately 90%, but did not affect TßR3 expression. The expression of p-Smad2 and p-Smad3 was significantly decreased in treated palates compared with controls. The expression of p-Smad4 was slightly decreased in treated palates compared with controls. Smad-independent signaling was also affected by the inhibitor; p-ERK, p-JNK, and p-p38 expressions was significantly reduced in treated palates compared with controls. The expression of transcription factors (Runx1 and Msx1) and extracellular matrix proteins (MMP2/13) was also significantly decreased by inhibitor exposure. Treatment with TßR1/2 inhibitor altered the patterns of the Smad-dependent and -independent signaling pathways during palatal fusion.

SMAD2 overexpression rescues the TGF-ß3 null mutant mice cleft palate by increased apoptosis.

During palatal development, medial edge epithelium (MEE) disappearance is one of the crucial steps in the process of fusion. The fate of these cells is still debated, and controversies remain. During secondary palate fusion, TGF-ß3 signaling mediated in the cell through the SMAD2 protein plays an important role and leads to the disappearance of the midline epithelial seam (MES) and the confluence of the palatal mesenchyme. In mice, TGF-ß3 knock-out is lethal and mice are born with a cleft in the secondary palate. This phenotype has been rescued by targeted overexpression of SMAD2 in the medial edge epithelium (MEE). The goal of this research was to understand the mechanism of palatal fusion in the rescue mice. METHODS: The heads of embryos with four different genotypes (wild-type, K14-SMAD2/TGF-ß3(-/-), K14-SMAD2/TGF-ß3(±), and TGF-ß3 null) were collected at embryonic day E14.5, genotyped, fixed and embedded in paraffin. Serial sections were studied for detection of apoptosis and epithelial mesenchymal transition using immunofluorescence. RESULTS: TGF-ß3 null mice developed a cleft in the secondary palate while both mice with K14-SMAD2 overexpression had fusion of the secondary palate. The MEE of both the rescue mice and K14-SMAD2 overexpression had a much higher ratio of apoptotic cells than wild-type mice. The increase in apoptosis was correlated with increased phospho-SMAD2 in the MEE. CONCLUSION: SMAD2 overexpression rescued the cleft in the secondary palate by increasing apoptosis in the medial edge epithelium.

The Culture of Certainty in Dentistry and Its Impact on Dental Education and Practice.

With this essay, the authors encourage all dental educators to look at a common characteristic in our dental profession: the culture of certainty. They also urge educators to look beyond this culture of certainty for its impact on educational activities and clinical care.

Designing and Implementing a Competency-Based Formative Progress Assessment System at a Canadian Dental School.

Progress testing is an innovative formative assessment practice that has been found successful in many educational programs. In progress testing, one exam is given to students at regular intervals as they progress through a curriculum, allowing them to benchmark their increase in knowledge over time. The aim of this study was to assess the first two years of results of a progress testing system implemented in a Canadian dental school. This was the first time in North America a dental school had introduced progress testing. Each test form contains 200 multiple-choice questions (MCQs) to assess the cognitive knowledge base that a competent dentist should have by the end of the program. All dental students are required to complete the test in three hours. In the first three administrations, three test forms with 86 common items were administered to all DMD students. The total of 383 MCQs spanning nine domains of cognitive knowledge in dentistry were distributed among these three test forms. Each student received a test form different from the previous one in the subsequent two semesters. In the fourth administration, 299 new questions were introduced to create two test forms sharing 101 questions. Each administration occurred at the beginning of a semester. All students received individualized reports comparing their performance with their class median in each of the domains. Aggregated results from each administration were provided to the faculty. Based on analysis of students' responses to the common items in the first two administrations, progression in all domains was observed. Comparing equated results across the four administrations also showed progress. This experience suggests that introducing a progress testing assessment system for competency-based dental education has many merits. Challenges and lessons learned with this assessment are discussed.

Dental Faculty Members' Pedagogic Beliefs and Curriculum Aims in Problem-Based Learning: An Exploratory Study.

The aims of this exploratory study were to explore dental faculty members' views and beliefs regarding knowledge, the dental profession, and teaching and learning and to determine how these views related to their problem-based learning (PBL) instructional practices. Prior to a PBL in dental education conference held in 2011, all attendees were invited to complete a survey focused on their pedagogical beliefs and practices in PBL. Out of a possible 55 participants, 28 responded. Additionally, during the conference, a forum was held in which preliminary survey findings were shared and participants contributed to focus group data collection. The forum results served to validate and bring deeper understanding to the survey findings. The conference participants who joined the forum (N=32) likely included some or many of the anonymous respondents to the survey, along with additional participants interested in dental educators' beliefs. The findings of the survey and follow-up forum indicated a disconnect between dental educators' reported views of knowledge and their pedagogical practices in a PBL environment. The results suggested that the degree of participants' tolerance of uncertainty in knowledge and the discrepancy between their epistemological and ontological beliefs about PBL pedagogy influenced their pedagogical choices. These findings support the idea that learner-centered, inquiry-based pedagogical approaches such as PBL may create dissonance between beliefs about knowledge and pedagogical practice that require the building of a shared understanding of and commitment to curricular goals prior to implementation to ensure success. The methods used in this study can be useful tools for faculty development in PBL programs in dental education.

Trends in Basic Sciences Education in Dental Schools, 1999-2016.

The purpose of this study was to examine data published over the past two decades to identify trends in the basic sciences curriculum in dental education, provide an analysis of those trends, and compare them with trends in the basic sciences curriculum in medical education. Data published from the American Dental Association (ADA) Surveys of Dental Education, American Dental Education Association (ADEA) Surveys of Dental School Seniors, and two additional surveys were examined. In large part, survey data collected focused on the structure, content, and instructional strategies used in dental education: what was taught and how. Great variability was noted in the total clock hours of instruction and the clock hours of basic sciences instruction reported by dental schools. Moreover, the participation of medical schools in the basic sciences education of dental students appears to have decreased dramatically over the past decade. Although modest progress has been made in implementing some of the curriculum changes recommended in the 1995 Institute of Medicine report such as integrated basic and clinical sciences curricula, adoption of active learning methods, and closer engagement with medical and other health professions education programs, educational effectiveness studies needed to generate data to support evidence-based approaches to curriculum reform are lacking. Overall, trends in the basic sciences curriculum in medical education were similar to those for dental education. Potential drivers of curriculum change were identified, as was recent work in other fields that should encourage reconsideration of dentistry's approach to basic sciences education. This article was written as part of the project "Advancing Dental Education in the 21st Century."

Smad2 overexpression induces alveolar bone loss and up regulates TNF-α, and RANKL.

OBJECTIVE: The aim of the current study was to investigate whether Smad2 overexpression in JE cells induced alveolar bone loss, and to understand the mechanisms regulating the bone loss. METHODS: A mouse line was created that used a cytokeratin 14 (K14) promoter to overexpress Smad2 in the epithelium of the transgenic mice (K14-Smad2). Micro CT radiographs (µCT) were used to assess bone loss, bone volume, and bone density. The expression of Tnfα, Il1-ß, Ifγ, Rankl, and Opg were assessed by RT-PCR. Western blots were used to detect the protein levels of TNF-α and IL1-ß. Tartrate-resistant acid phosphatase (TRAP) was used as a marker for osteoclasts. Wild type (WT) mice were used as controls in all steps of the current study. RESULTS: K14-Smad2 mice had 52.5% (±4.2) root exposed compared to 32.4%(±3.2) in the WT mice. There was a significant difference in alveolar bone volume in the K14-Smad2 mice when compared to WT mice 2.65mm3 (±0.3) and 4.3mm3 (±0.35) respectively. K14-Smad2 mice also had reduced bone density 696.8mg/cc (±70) at 12 months when compared to WT mice 845.9mg/cc(±10). The mRNA levels of Tnfα and Rankl increased by 3.26- and 2.5-fold respectively in the K14-Smad2 mice when compared to controls. The protein level of TNF-α was also significantly increased to 2.8-fold in K14-Smad2 mice when compared to WT mice. Smad2 overexpression increased the total numbers of osteoclasts in K14-Smad2 mice (3.4±0.2)-fold when compared to WT mice. CONCLUSION: Smad2 overexpression induces alveolar bone loss and increases the numbers of osteoclasts. Also, Smad2 overexpression up-regulates TNF-α and RANKL.

Olmsted syndrome with oral involvement, including premature teeth loss.

INTRODUCTION: Olmsted syndrome is a rare palmoplantar keratodermal disease that has not previously been reported to have an association with periodontal disease. The aim of this study is to report and document a case of Olmsted syndrome with evidence of severe periodontal disease. CASE REPORT: A 38-year old Saudi male patient presented to the dental clinic diagnosed previously with Olmsted syndrome. Clinical and radiographic examinations were done and provided evidence of the typical clinical findings in Olmsted syndrome and evidence of severe periodontal disease. The patient had severe generalized hyperkeratotic lesions on the palms, soles, and perioral skin as well as hyperkeratosis of oral mucosa at multiple sites. CONCLUSION: This case report documents the first reported case of Olmsted syndrome to be associated with severe periodontal disease. The altered differentiation of oral mucosa linked to Olmsted syndrome may contribute to the periodontal disease. Patients diagnosed with this syndrome should receive a comprehensive oral examination to determine whether periodontal destruction is a significant component of their disease or not.

Palatal adhesion is dependent on Src family kinases and p38MAPK.

During secondary palate development, palatal shelves adhere to each other in the midline to form a midline epithelial seam leading to palatal closure. Cell-cell and cell-extracellular matrix adhesions, which are mediated by cell adhesion receptors, E-cadherin and integrins, are implicated in the process of adhesion of the palatal shelves. Src family kinases (SFK) function downstream of both receptors. In this study, we focused on the role of SFK in the process of palatal adhesion. During palatal adhesion, the expression of SFK mRNA, as well as localization and quantitation of the protein in the activated form, were examined by real-time qPCR and immunofluorescence. Palatal organ cultures were performed to identify the effect of pharmacological inhibition of SFK on palatal adhesion. Activated SFKs were found to be co-localized with adhesion receptors, E-cadherin and integrins in the palatal medial edge epithelium. Src, Fyn and Yes subfamily members were expressed in the palatal tissue. The expression of SFK mRNA and the quantity of the activated form of the protein were upregulated during palatal adhesion. An SFK inhibitor, PP2, blocked palatal adhesion, but another SFK inhibitor, SU6656 was not inhibitory. However, the combination of SU6656 and either of the p38MAPK inhibitors, SB203580 or BIRB0796, showed similar inhibitory effects on palatal adhesion compared to PP2 alone. The p38MAPK inhibitors alone did not alter palatal adhesion. Real-time qPCR revealed that p38MAPK alpha and delta were elevated during palatal adhesion. This study indicates that palatal cell adhesion is dependent on signaling from integrin receptors and E-cadherin through SFK and p38MAPK.

Functional role of TGF-ß receptors during palatal fusion in vitro.

OBJECTIVE: Reported expression patterns for TGF-ß receptors (TßR-I, -II, and -III) during palatogenesis suggest that they play essential roles in the mechanisms leading to palatal fusion. The purpose of this study was to compare the functions of the three TßRs during palatal fusion. METHODS: Using organ culture of mouse palatal shelves, expression levels of TßR-I, -II, and -III were suppressed by transfecting the siRNAs siTßR-I, -II, and -III, respectively. Phosphorylation of SMAD2 was examined as an indicator of downstream signalling via each TßR. Linkage between TGF-ß signalling and critical events in palatal fusion led to the use of, MMP-13 expression as an outcome measure for the function of the TGF-ß receptors. RESULTS: The siRNA treatment decreased the expression level of each receptor by more than 85%. When treated with either siTßR-I or -II, palatal shelves at E13+72 h were not fused, with complete clefting in the anterior and posterior regions. The middle palatal region following treatment with either siTßR-I or -II had fusion from one-half or one-third of the palatal region. Treatment with siTßR-III resulted in a persistent midline seam of medial edge epithelium (MEE) in the anterior region with islands of persistent MEE in the middle and posterior regions of the midline. Treatment with all three siTßRs altered the pattern of SMAD2 phosphorylation. Palatal shelf cultures treated with siTßR-I or -II, but not -III, showed altered MMP-13 expression levels. CONCLUSION: The ability to identify and recover MEE and palatal mesenchymal cells during palatal fusion will aid in the evaluation of the different mechanistic events regulated by each TßR during palatogenesis.

Personality preference distribution of dental students admitted to one dental school using different selection methods.

This study sought to determine whether using the Myers-Briggs Type Indicator (MBTI) would detect differences in personality preferences in first-year dental students admitted to the same dental school through different admission methods. First-year dental students admitted in 2000 and 2001 were given the MBTI instrument during orientation prior to the start of classes. In fall 2000, the Class of 2004 had 140 students, with 116 in the traditional track and twenty-four in the parallel problem-based learning (PBL) track. In fall 2001, the Class of 2005 had 144 students, all enrolled in the PBL curriculum. All students admitted to the PBL track had experienced a process that included evaluation of their participation in a small group. Students in the traditional track had individual interviews with faculty members. Both student groups were required to meet the same baseline grade point average and Dental Admission Test standards. In 2000, the PBL students showed personality preferences that were distinctly different from the personality preferences of traditional track students in the categories of Extroversion (89 percent PBL, 44 percent traditional) and Thinking (72 percent PBL, 39 percent traditional). In 2001, the all-PBL class retained the trend towards Extroversion (69 percent). This study suggests that admission method may effectively change the personality preference distribution exhibited by the students who are admitted to dental school.

Use of lecture recordings in dental education: assessment of status quo and recommendations.

This research project was part of a planned initiative at the University of Pittsburgh School of Dental Medicine to incorporate lecture recordings as standard educational support technologies. The goal of an institutional survey was 1) to gather current data about how dental educators across the United States and Canada use lecture recordings; 2) determine dental educators' perceived value and outcomes of using lecture recordings; and 3) develop recommendations based on #1 and #2 for the dental education community. Of the sixty-six North American dental schools at the time of the study, forty-five schools responded to the survey, for a 68 percent response rate. Of the respondents, twenty-eight schools were found to currently conduct lecture recording; these comprised the study sample. This study focused on the dental schools' past experiences with lecture recording; thus, those not currently engaged in lecture recording were excluded from further analysis. The survey questions covered a wide range of topics, such as the scope of the lecture recording, logistics, instructional design considerations, outcomes related to student learning, evaluation and reception, barriers to lecture recording, and issues related to copyright and intellectual property. The literature review and results from the survey showed that no common guidelines for best practice were available regarding lecture recordings in dental education. The article concludes with some preliminary recommendations based on this study.

Microtubule disassembly prevents palatal fusion and alters regulation of the E-cadherin/catenin complex.

During palatal fusion, the midline epithelial seam (MES) degrades to achieve mesenchymal confluence. Epithelial mesenchymal transition (EMT) is one mechanism which is active in MES degradation. TGF-ß induces EMT in medial edge epithelium (MEE) by down-regulation of an epithelial marker, E-cadherin. Microtubule disassembly impaired palatal fusion leading to a multi-layered MES in the mid-region. In this study, we investigated the effect of microtubule disruption on the regulation of the E-cadherin/catenin adhesion complex. Nocodazole (NDZ) enhanced the accumulation of the adhesion complex at cell-cell contacts in MEE, while loss of the adhesion complex was observed in the control. NDZ caused aberrant regulation of the E-cadherin transcriptional repressors (Snail and Zeb) and the activator (c-MYC) through inhibition of the TGF-ß/SMAD2 signaling pathway, which led to a failure in EMT. These results suggest that the microtubule cytoskeleton plays an important role in mediating TGF-ß/SMAD2 signals to control E-cadherin gene expression in MEE during palatal fusion.

Smad2 is involved in the apoptosis of murine gingival junctional epithelium associated with inhibition of Bcl-2.

OBJECTIVE: Gingival junctional epithelium (JE) actively contributes to the homeostasis of the periodontium. Altered activation of TGF-ß signalling is implicated in the epithelium from chronic periodontitis. However, little is known about the effects of TGF-ß signalling on the JE. In this study, we investigated the relationship between Smad2, which plays an important role in mediating TGF-ß signal, and induction of apoptosis in the JE. METHODS: K14-Smad2 transgenic mice were used to observe the effect of over-expression of Smad2 driven by CK14 promoter in the JE. We performed TUNEL technique to evaluate the epithelial apoptosis. Expression of apoptosis related genes was examined using real-time PCR and immunofluorescence. RESULTS: K14-Smad2 mice showed an increased number of phospho-Smad2 positive JE cells associated with an increase in TGF-ß1 expression. K14-Smad2 mice have a significantly higher percentage of TUNEL positive cells in the JE. Immunofluorescence double labelling revealed that TUNEL positive cells showed immunoreactivity to phospho-Smad2. Real-time PCR analysis of apoptosis related gene expression provided evidence of lower expression of Bcl-2 in the gingival tissue from K14-Smad2 mice. There was a strong positive reaction for Bcl-2 protein in the junctional epithelium of wild type mice, while the gingival tissue of K14-Smad2 transgenic mice had only a faint signal for Bcl-2. CONCLUSIONS: The present study provided evidence that Smad2 plays a crucial role in the induction of apoptosis in gingival JE through inhibition of Bcl-2.

Multi-layered hypertrophied MEE formation by microtubule disruption via GEF-H1/RhoA/ROCK signaling pathway.

BACKGROUND: Formation of the secondary palate is complex and disturbance during palatal fusion may result in cleft palate. The processes of adhesion, intercalation, and disappearance of medial edge epithelia (MEE) are characterized by morphological changes requiring dynamic cytoskeletal rearrangement. Microtubules are one of the cytoskeletal elements involved in maintenance of cell morphology. Microtubule-disrupting drugs have been reported to cause craniofacial malformations including cleft palate. The mechanisms underlying the failure of palatal fusion remain poorly understood. We evaluated the effect of nocodazole (NDZ), a drug that disrupts microtubules, on palatal fusion in organ culture. RESULTS: NDZ caused failure of palatal fusion due to the induction of a multi-layered hypertrophied MEE in the mid-region of the secondary palatal shelves. Microtubule disruption increased RhoA activity and stress fiber formation. Pharmacological inhibition of the RhoA/ROCK pathway blocked multi-layered MEE formation. Partial prevention of hypertrophied MEE was observed with Y27632 and cytochalasin, but not with blebbistatin. NDZ induced re-localization of GEF-H1 into cytoplasm from cell-cell junctions. CONCLUSIONS: The present study provided evidence that the GEF-H1/RhoA/ROCK pathway plays a pivotal role in linking microtubule disassembly to the remodeling of the actin cytoskeleton, which resulted in a multi-layered hypertrophied MEE and failure of palatal fusion.

Spatiotemporal localization of periostin and its potential role in epithelial-mesenchymal transition during palatal fusion.

The medial epithelial seam (MES) between the palatal shelves degrades during palatal fusion to achieve the confluence of palatal mesenchyme. Cellular mechanisms underlying the degradation of MES have been proposed, such as apoptosis, epithelial-mesenchymal transition (EMT) and migration of medial edge epithelia (MEE). Extracellular matrix components have been shown to play an important role in EMT in many model systems. Periostin (also known as osteoblast-specific factor-2) is a secreted mesenchymal extracellular matrix component that affects the ability of cells to migrate and/or facilitates EMT during both embryonic development and pathologic conditions. In this study, we evaluated the spatiotemporal expression patterns of periostin during mouse palatal fusion by in situ hybridization and immunofluorescence. Periostin mRNA and protein were present in the palatal mesenchyme, the protein being distributed in a fine fibrillar network and in the basement membrane, but absent from the epithelium. During MES degradation, the protein was strongly expressed in the basement membrane underlying the MES and in some select MEE. Confocal microscopic analysis using an EMT marker, twist1, and an epithelial marker, cytokeratin 14, provided evidence that select MEE were undergoing EMT in association with periostin. Moreover, the major extracellular matrix molecules in basement membrane, laminin and collagen type IV were degraded earlier than periostin. The result is that select MEE establish interactions with periostin in the mesenchymal extracellular matrix, and these new cell-matrix interactions may regulate MEE transdifferentiation during palatal fusion.

The expression of TGF-ß3 for epithelial-mesenchyme transdifferentiated MEE in palatogenesis.

The fate of the palatal medial edge epithelial (MEE) cells undergoes programming cell death, migration, and epithelial-mesenchymal transdifferentiation (EMT) coincident with the process of palatal fusion and disappearance of MEE. Mesenchymal cells in the palate have both cranial neural crest (CNC) and non-CNC origins. The objectives of this study were to identify the populations of palatal mesenchymal cells using ß-galactosidase (ß-gal) and DiI cell lineage markers, and to determine whether MEE-derived cells continued to express transforming growth factor-ß3 (TGF-ß3) and transforming growth factor-ß type III receptor (TßR-III), which were specific for MEE. A model has been developed using Wnt1 tissue specific expression of Cre-recombinase to activate ß-gal solely in the CNC. The expressions of TGF-ß3 and TßR-III in MEE were temporally correlated with critical events in palatogenesis. Three cell populations could be distinguished in the palatal mesenchymal CNC-derived, non-CNC derived and MEE-derived. After fusion, ß-gal⁻ and DiI+ mesenchymal cells continued to express TGF-ß3, however TßR-III was expressed only in the epithelial MEE, as well as keratin expression. In addition, we performed laser capture microdissection to identify mRNA expression of isolated DiI+ MEE cells. Both epithelial and transdifferentiated MEE have expressed TGF-ß3, however, TßR-III was only expressed in epithelium. Extracellular matrix, especially MMP13 has been expressed coincident with fused stage which can be strongly associated with TGF-ß3. These results demonstrate that combining a heritable marker and a cell lineage dye can distinguish different populations of mesenchymal cells in the developing palate. Furthermore, TGF-ß3 and MMP13 could be strongly associated with EMT in palatogenesis.