Teledentistry from research to practice: a tale of nineteen countries

AimThe COVID-19 pandemic has accelerated teledentistry research with great interest reflected in the increasing number of publications. In many countries, teledentistry programs were established although not much is known about the extent of incorporating teledentistry into practice and healthcare systems. This study aimed to report on policies and strategies related to teledentistry practice as well as barriers and facilitators for this implementation in 19 countries.MethodsData were presented per country about information and communication technology (ICT) infrastructure, income level, policies for health information system (HIS), eHealth and telemedicine. Researchers were selected based on their previous publications in teledentistry and were invited to report on the situation in their respective countries including Bosnia and Herzegovina, Canada, Chile, China, Egypt, Finland, France, Hong Kong SAR, Iran, Italy, Libya, Mexico, New Zealand, Nigeria, Qatar, Saudi Arabia, South Africa, United Kingdom, Zimbabwe.ResultsTen (52.6%) countries were high income, 11 (57.9%) had eHealth policies, 7 (36.8%) had HIS policies and 5 (26.3%) had telehealth policies. Six (31.6%) countries had policies or strategies for teledentistry and no teledentistry programs were reported in two countries. Teledentistry programs were incorporated into the healthcare systems at national (n = 5), intermediate (provincial) (n = 4) and local (n = 8) levels. These programs were established in three countries, piloted in 5 countries and informal in 9 countries.ConclusionDespite the growth in teledentistry research during the COVID-19 pandemic, the use of teledentistry in daily clinical practice is still limited in most countries. Few countries have instituted teledentistry programs at national level. Laws, funding schemes and training are needed to support the incorporation of teledentistry into healthcare systems to institutionalize the practice of teledentistry. Mapping teledentistry practices in other countries and extending services to under-covered populations increases the benefit of teledentistry

Expression of cyclin D1 and its correlation with p27KIP1 in non-neoplastic and non-dysplastic mucosa, oral epithelial dysplasia and oral squamous cell carcinoma

Background Oral and pharyngeal cancer accounts for one-sixth of the total cancers worldwide. An estimated 263,900 new cases and 128,000 deaths from oral cavity cancer (including lip cancer) occurred in 2008 worldwide. Smoking, alcohol use, smokeless tobacco products, and HPV infections are the major risk factors for head and neck cancers, with smoking and alcohol having synergistic effects. Squamous cell carcinoma of the oral cavity is driven by a multistep process of accumulation of genetic mutations related to cell proliferation and differentiation. Increasing evidence suggests that cyclins, cyclin dependent kinases (CDKs), and cyclin dependent kinases inhibitors (CDKIs) either are themselves targets for genetic change in cancer or are disrupted secondarily by other oncogenic events. Cyclin D1 and p27KIP1 are two important regulators for the cell cycle G1/S checkpoint. Normally, cyclin D1 at G1 is constant or at a very low level and its excessive expression may be associated with disordered proliferation of cells leading to malignant change. On the other hand, p27KIP1 is an anti-oncogene and under the regulation of TGF-β, p27KIP1 inhibits activity of oncogenes and controls the transition of G1/S phase mainly by the interaction with CDK and CDK-Cyclin, so as to inhibit cell proliferation and give cells opportunities to repair DNA. No study, to date, has clearly determined the expression of cyclin D1 and its correlation with in p27KIP1 in non-neoplastic and non-dysplastic mucosa, oral dysplasia, and oral squamous cell carcinoma. Aim The purpose of this research is to determine cyclin D1 and p27KIP1 intensity of expression, location and pattern in oral epithelial dysplasia and oral squamous cell carcinoma by standard immunohistochemistry. Methodology Formalin-fixed, paraffin-embedded (FFPE) tissue biopsies of the oral mucosa with a diagnosis of non-neoplastic tissue (Gingivitis) (n=10), oral epithelial dysplasia (mild and moderate)(n=12) and oral squamous cell carcinoma (n=11) for the period from 2005 to 2013 were obtained from the histopathology-archived records of the University of Otago, School of Dentistry, Medlab Dental Oral Pathology Diagnostic Laboratory. All the specimens were prepared and stained using immunohistochemistry following confirmation of diagnosis on H&E stained sectioned. Scanning software was used to determine cyclin D1 and p27KIP1 intensity of expression, location and pattern. Result A significant increase in expression of cyclin D1 and a decrease in expression of p27KIP1 proteins were observed with the severity of oral epithelial dysplasia and in less well-differentiated OSCC in this study. In the control groups, scattered cells showing cyclin D1 protein expression were seen in the parabasal and basal epithelial layers. In contract to the distribution in the control group, there was a more diffuse distribution of cells showing cyclin D1 protein expression extending from the basal cell layer into the prickle cell layers in epithelial dysplasia. Diffuse distribution of cyclin D1 positive cells was observed within the OSCC. In the control group, positive p27KIP1 stained cells were found in the superficial and intermediary thirds, associated with epithelial differentiation and maturation compartments. Cases of oral epithelial dysplasia showed moderate infrequent expression of p27KIP1. There were no p27KIP1 positive cells in OSCC. In addition, we observed the percentage of cells with both nuclear and cytoplasmic cyclin D1 staining was higher in oral squamous cell carcinoma specimens than control groups and oral epithelial dysplasia. Conclusion These results suggest that the characteristic expression of both cyclin D1 and p27KIP1 correlate with the grade of oral epithelial dysplasia and degree of oral squamous cell carcinoma differentiation. Both nuclear and cytoplasmic cyclin D1 staining was observed in more oral squamous cell carcinoma than non-neoplastic and non-dysplastic epithelium. The exact mechanism remains unknown, but it may due to presence of two different isoforms of cyclin D1

Expression of cyclin D1 and its correlation with p27KIP1 in non-neoplastic and non-dysplastic mucosa, oral epithelial dysplasia and oral squamous cell carcinoma

Background Oral and pharyngeal cancer accounts for one-sixth of the total cancers worldwide. An estimated 263,900 new cases and 128,000 deaths from oral cavity cancer (including lip cancer) occurred in 2008 worldwide. Smoking, alcohol use, smokeless tobacco products, and HPV infections are the major risk factors for head and neck cancers, with smoking and alcohol having synergistic effects. Squamous cell carcinoma of the oral cavity is driven by a multistep process of accumulation of genetic mutations related to cell proliferation and differentiation. Increasing evidence suggests that cyclins, cyclin dependent kinases (CDKs), and cyclin dependent kinases inhibitors (CDKIs) either are themselves targets for genetic change in cancer or are disrupted secondarily by other oncogenic events. Cyclin D1 and p27KIP1 are two important regulators for the cell cycle G1/S checkpoint. Normally, cyclin D1 at G1 is constant or at a very low level and its excessive expression may be associated with disordered proliferation of cells leading to malignant change. On the other hand, p27KIP1 is an anti-oncogene and under the regulation of TGF-β, p27KIP1 inhibits activity of oncogenes and controls the transition of G1/S phase mainly by the interaction with CDK and CDK-Cyclin, so as to inhibit cell proliferation and give cells opportunities to repair DNA. No study, to date, has clearly determined the expression of cyclin D1 and its correlation with in p27KIP1 in non-neoplastic and non-dysplastic mucosa, oral dysplasia, and oral squamous cell carcinoma. Aim The purpose of this research is to determine cyclin D1 and p27KIP1 intensity of expression, location and pattern in oral epithelial dysplasia and oral squamous cell carcinoma by standard immunohistochemistry. Methodology Formalin-fixed, paraffin-embedded (FFPE) tissue biopsies of the oral mucosa with a diagnosis of non-neoplastic tissue (Gingivitis) (n=10), oral epithelial dysplasia (mild and moderate)(n=12) and oral squamous cell carcinoma (n=11) for the period from 2005 to 2013 were obtained from the histopathology-archived records of the University of Otago, School of Dentistry, Medlab Dental Oral Pathology Diagnostic Laboratory. All the specimens were prepared and stained using immunohistochemistry following confirmation of diagnosis on H&E stained sectioned. Scanning software was used to determine cyclin D1 and p27KIP1 intensity of expression, location and pattern. Result A significant increase in expression of cyclin D1 and a decrease in expression of p27KIP1 proteins were observed with the severity of oral epithelial dysplasia and in less well-differentiated OSCC in this study. In the control groups, scattered cells showing cyclin D1 protein expression were seen in the parabasal and basal epithelial layers. In contract to the distribution in the control group, there was a more diffuse distribution of cells showing cyclin D1 protein expression extending from the basal cell layer into the prickle cell layers in epithelial dysplasia. Diffuse distribution of cyclin D1 positive cells was observed within the OSCC. In the control group, positive p27KIP1 stained cells were found in the superficial and intermediary thirds, associated with epithelial differentiation and maturation compartments. Cases of oral epithelial dysplasia showed moderate infrequent expression of p27KIP1. There were no p27KIP1 positive cells in OSCC. In addition, we observed the percentage of cells with both nuclear and cytoplasmic cyclin D1 staining was higher in oral squamous cell carcinoma specimens than control groups and oral epithelial dysplasia. Conclusion These results suggest that the characteristic expression of both cyclin D1 and p27KIP1 correlate with the grade of oral epithelial dysplasia and degree of oral squamous cell carcinoma differentiation. Both nuclear and cytoplasmic cyclin D1 staining was observed in more oral squamous cell carcinoma than non-neoplastic and non-dysplastic epithelium. The exact mechanism remains unknown, but it may due to presence of two different isoforms of cyclin D1

Expression of cyclin D1 correlates with p27KIP1 and regulates the degree of oral dysplasia and squamous cell carcinoma differentiation

Objectives: The aim of this study was to identify an association or link between cyclin D1 and p27 protein expression and dysplastic changes or progression. Study Design: Oral mucosal biopsies with a diagnosis of non-neoplastic tissue (gingivitis) (n = 10), mild to moderate oral epithelial dysplasia (n = 12), and oral squamous cell carcinoma (n = 11) were evaluated by using immunohistochemistry. Scanning software was used to determine cyclin D1 and p27 intensity of expression, location, and pattern. Results: A significant increase in expression of cyclin D1 and a decrease in expression of p27 proteins were identified in oral epithelial dysplasia and less differentiated oral squamous cell carcinoma (OSCC). There was a more diffuse distribution of cyclin D1 protein expression extending from the basal cell layer into the prickle cell layers in epithelial dysplasia and extending within all epithelial layers in OSCC. Cases of oral epithelial dysplasia had moderate infrequent expression of p27. There were no p27-positive cells in OSCC. The percentage of cells with both nuclear and cytoplasmic cyclin D1 staining was higher in OSCC specimens than control groups and oral epithelial dysplasia. Conclusions: The expression of both cyclin D1 and p27 correlated with the grade of oral epithelial dysplasia and degree of OSCC differentiation. The results obtained will be verified through a basic follow-up of the cases to determine the prognosis/progression of oral dysplasia

Effect of the Rho-Kinase/ROCK Signaling Pathway on Cytoskeleton Components

The mechanical properties of cells are important in tissue homeostasis and enable cell growth, division, migration and the epithelial-mesenchymal transition. Mechanical properties are determined to a large extent by the cytoskeleton. The cytoskeleton is a complex and dynamic network composed of microfilaments, intermediate filaments and microtubules. These cellular structures confer both cell shape and mechanical properties. The architecture of the networks formed by the cytoskeleton is regulated by several pathways, a key one being the Rho-kinase/ROCK signaling pathway. This review describes the role of ROCK (Rho-associated coiled-coil forming kinase) and how it mediates effects on the key components of the cytoskeleton that are critical for cell behaviour

Naringenin promotes SDF-1/CXCR4 signaling pathway in BMSCs osteogenic differentiation

Introduction. Naringenin, a dihydro-flavonoid compound that shows chemotactic activity, may have a good application prospect in repairing bone tissue, but its specific mechanism in bone regeneration, especially the osteogenic differentiation of stem cells, needs for a further study. The aim of this study was to investigate the effect of naringenin on the osteogenic differentiation and its roles in the C-X-C chemokine receptor type 4/stromal cell-derived factor 1 (SDF-1/CXCR4) signal pathway of bone marrow-derived mesenchymal stem cells (BMSCs). Material and methods. BMSCs were harvested from the femurs and tibias of 4-to-6-week-old male Sprague-Dawley rats. Cell Counting kit-8 assay was used to determine cytotoxicity of naringenin. Alkaline phosphatase (ALP) activity was measured in cell’s precipitates and alizarin-red staining was performed to determine the osteogenic differentiation capacity of the BMSCs. Real-time polymerase chain reaction, enzyme-linked immunosorbent assay and western blotting were adopted to determine the expression of genes and proteins. Results. The cellular morphology was spindle-shaped, and arranged in radial and whorled patterns. The flow cytometric analysis have confirmed the presence of characteristic surface proteins in the harvested BMSCs. Different concentrations (0–200 μg/ml) of naringenin have no influence on the viability and proliferation rate of the BMSCs. The highest ALP activity was found at culture day 7 and 9 when the concentration of naringenin was 75 and 100 μg/ml. Positive red or dark red stained cells with mineralized nodules can be observed on day 14. The expression of ALP, Runt-related transcription factor 2, CXCR4 and SDF-1a at the gene and protein levels in naringenin-treated cells were significantly higher than those in the control cells. Moreover, AMD3100, an inhibitor of CXCR4, suppressed the expression of the studied genes and proteins. Conclusions. Naringenin does not show toxic effect on BMSCs. Naringenin promotes the expression of the SDF-1a gene and protein via the SDF-1/CXCR4 signaling pathway. A better understanding of the mechanisms of naringenin action would be helpful for developing specific therapeutic strategies to improve bone regeneration after injuries

Final year dental students' career plans, work patterns, work-life balance and domestic life in New Zealand and Australia

Having insight into final year dental students' career planning is vital in maintaining and enhancing the quality of dental education. The aim of this study was to investigate final year dental students' career plans, work patterns, work-life balance, and domestic life, in New Zealand and Australia.The design of the study was a two-centred cross-sectional study.A total of 148 students, including 95 females (64%) and 53 males (36%), completed the survey (response rate=87%). The mean age of students across two Australasian universities was 23± 3 years. Findings from this study demonstrate that students prefer their first job is an urban, full-time and salary-based with a good mentor. However, when describing their long-term planning, work-life balance becomes more important. The growth in the number of female dentists will continue to shape the future patterns of our dental profession.The current study has highlighted several similarity and differences in career plans, work patterns, work-life balance and domestic life between two Australasian universities. The information might be useful for the policymakers involved in future workforce planning and infrastructure and for those involved in the delivery of dental education

Measuring Changes in Jaw Opening Forces to Assess the Degree of Improvement in Patients with Temporomandibular Disorders

Background: Currently, the degree of improvement in patients with TMDs is measured through subjective questionnaires and clinical examination This study aimed to investigate the properties of an objective quantitative measure of jaw-opening forces to assess clinical improvement in temporomandibular disorder (TMD) patients following treatment. Methods: Baseline jaw-opening forces were recorded for TMD-patients (n = 62) and a comparison group of TMD-free participants (n = 56), using a jaw-opening forces measuring device. TMD patients were divided into three subcategories (myofascial pain, disc-displacement, and myofascial pain and disc-displacement combined) and received a combination of treatment for six months; meanwhile, TMD-free participants did not receive treatment. Jaw-opening forces for each participant in both groups were measured at their six-month review appointment. Results: Jaw-opening forces were reliable at baseline (single measure ICC 0.98, 95% CI 0.97–0.98, ICC ≥ 0.94 for all groups and subcategories). Jaw-opening forces increased in the TMD group following treatment at six-months (18.6 N at baseline and 32.4 N at six-months, p p = 0.002). However, the myofascial-pain and myofascial-pain-and-disc-displacement groups showed significant improvement following treatment (93.5% higher forces, p p < 0.001; respectively). Conclusion: This study demonstrated that the measurement of jaw-opening forces could potentially be used to assess the clinical improvement in TMD patients following diagnosis and treatment

Measuring Changes in Jaw Opening Forces to Assess the Degree of Improvement in Patients with Temporomandibular Disorders

Background: Currently, the degree of improvement in patients with TMDs is measured through subjective questionnaires and clinical examination This study aimed to investigate the properties of an objective quantitative measure of jaw-opening forces to assess clinical improvement in temporomandibular disorder (TMD) patients following treatment. Methods: Baseline jaw-opening forces were recorded for TMD-patients (n = 62) and a comparison group of TMD-free participants (n = 56), using a jaw-opening forces measuring device. TMD patients were divided into three subcategories (myofascial pain, disc-displacement, and myofascial pain and disc-displacement combined) and received a combination of treatment for six months; meanwhile, TMD-free participants did not receive treatment. Jaw-opening forces for each participant in both groups were measured at their six-month review appointment. Results: Jaw-opening forces were reliable at baseline (single measure ICC 0.98, 95% CI 0.97&ndash;0.98, ICC &ge; 0.94 for all groups and subcategories). Jaw-opening forces increased in the TMD group following treatment at six-months (18.6 N at baseline and 32.4 N at six-months, p &lt; 0.001) and did not change significantly in the TMD-free group (49 N at baseline and 48.3 N at six-months). There was a small improvement in the disc displacement group (27.8% higher forces, p = 0.002). However, the myofascial-pain and myofascial-pain-and-disc-displacement groups showed significant improvement following treatment (93.5% higher forces, p &lt; 0.001; 91.1% higher forces, p &lt; 0.001; respectively). Conclusion: This study demonstrated that the measurement of jaw-opening forces could potentially be used to assess the clinical improvement in TMD patients following diagnosis and treatment