The Presence of Women in the Dental Profession: A Global Survey.

OBJECTIVES: The aim of this research was to acquire knowledge about the female dental workforce, identifying factors to pursue specialty training and career choices and working in dental institutions/associations. METHODS: An original online questionnaire was developed, validated (n = 22), and sent to 189 member associations in 133 countries of the Women Dentists Worldwide section of the FDI World Dental Federation. RESULTS: In all, 3232 female dentists from 81 countries participated. Results were divided into 5 geographic areas by continent. Difference in proportion amongst questionnaire items was evaluated with χ2 test or Fisher exact test. Ordinal multinomial linear regression analysis was performed to evaluate the association of questionnaire items with total work experience in dentistry (in years), motivation to study dentistry, type of specialisation, working hours per week, perception of female dentists about working hours, sex-based inequalities, job security after maternity leaves, as well as involvement in political organisations within their country of residence and their role in dental associations. A majority of participating female dentists are self-employed (57.7%), and 60.0% have 10 to 30 years of experience. The most popular form of practice is the single private practice (29.7%), followed by the group private practice (28.8%). Further, 44.8% work 31 to 40 h/wk, 29.1% part-time up to 30 h/wk, and 26.0% more than 40 h/wk. CONCLUSIONS: Women are still poorly represented in professional organisations, and few are officers in representative assemblies, members of the board, or president. Family life with children influences perceptions and has an impact on professional life, especially in academia and political/professional associations, so that taking on leadership positions poses additional challenges.

Development of Tooth Brushing Recommendations Through Professional Consensus.

INTRODUCTION: Despite being a largely preventable disease, untreated caries of permanent teeth is estimated to affect almost 2 billion people worldwide, which is followed by severe periodontal disease. The aim of this work was to provide a professional consensus on tooth brushing methods and associated oral hygiene behaviours and develop evidence-informed recommendations. METHODS: An initial scoping search was undertaken to identify systematic reviews of relevance and key questions. This was followed by comprehensive evidence mapping of the literature focussing on systematic reviews and clinical guidelines. Electronic searches of several databases including MEDLINE (via Ovid), Embase (via Ovid), Epistemonikos, and The Cochrane Library were undertaken from 2000 to May 2022, alongside a guideline repository search. Considered Judgement Forms were developed detailing the underpinning evidence, balance between benefits and harms, potential impact on the population, and feasibility of implementation. An online survey comprising 22 draft recommendations was distributed to international members of all FDI committees, including the FDI Council. Participants were asked to indicate to what level they agreed or disagreed with for each recommendation and to provide feedback. The Considered Judgement Forms were provided for reference. RESULTS: Three hundred ten records were identified and mapped to different aspects of tooth brushing methods and associated behaviours. Research literature informed 7 Considered Judgement Forms comprising 12 questions with draft recommendations. Twenty-five participants from Asia, Europe, North and South America, Africa, and Australia provided feedback on the recommendations. More than 70% of respondents showed agreement with 21 of the 22 draft recommendations. Final recommendations were drafted with associated strength of recommendation. CONCLUSION: Using a robust methodology and an international professional consensus, a set of evidence-informed recommendations was developed. These recommendations provide clinicians with practical guidance to facilitate communications with patients that may help to reinforce individual-level preventive strategies.

Alveolar bone morphology in patients with a unilateral palatally displaced maxillary lateral incisor: A cone-beam computed tomography study.

INTRODUCTION: Lingual displacement of the maxillary anterior teeth is 1 of the most common forms of malocclusion. The labial alveolar bone is thinner for the maxillary lateral incisor than for the central incisor and canine; however, the alveolar bone width at the actual position of the maxillary lateral incisor has not been examined. We investigated the morphologic characteristics of the alveolar bone around palatally displaced maxillary lateral incisors using cone-beam computed tomography and a split-mouth model. METHODS: Twenty-seven patients with a unilateral palatally displaced maxillary lateral incisor were included. Axial, sagittal, and horizontal measurements were recorded at 3 levels (ie, 25%, 50%, and 75% of the root length) using cone-beam computed tomography. All obtained data were statistically analyzed using paired t tests. RESULTS: The labial alveolar bone width at 25% of root length was significantly lesser on the affected side. At all 3 levels, the distance between a line tangential to the labial alveolar bone of the central incisor and canine and the position of the labial alveolar bone of the lateral incisor was significantly greater on the affected side. At 50% and 75% of root length, the horizontal distance between the posterior nasal spine and the labial alveolar bone of the lateral incisor was significantly lesser on the affected side. CONCLUSIONS: Palatal displacement of maxillary lateral incisors is significantly associated with decreased alveolar bone width at the apical level and asymmetry. However, a further elaborate investigation is necessary to determine the clinical relevance of the study.

Runx2 haploinsufficiency ameliorates the development of ossification of the posterior longitudinal ligament.

Ossification of the Posterior Longitudinal Ligament (OPLL) is a disease that is characterized by the ectopic calcification of the ligament; however, the pathogenesis of OPLL remains to be investigated. We attempted to identify the in vivo role of Runx2, a master regulator of osteoblast differentiation and skeletal mineralization, in the pathogenesis of OPLL. The expression of Runx2 in the ligament was examined using in situ hybridization and immunohistochemistry and by monitoring the activity of a LacZ gene that was inserted into the Runx2 gene locus. To investigate the functional role of Runx2, we studied ENPP1(ttw/ttw) mice, a mouse model of OPLL, that were crossed with heterozygous Runx2 mice to decrease the expression of Runx2, and we performed histological and quantitative radiological analyses using 3D-micro CT. Runx2 was expressed in the ligament of wild-type mice. The induction of Runx2 expression preceded the development of ectopic calcification in the OPLL-like region of the ENPP1(ttw/ttw) mice. Runx2 haploinsufficiency ameliorated the development of ectopic calcification in the ENPP1(ttw/ttw) mice. Collectively, this study demonstrated that Runx2 is expressed in an OPLL-like region, and its elevation is a prerequisite for developing the complete OPLL-like phenotype in a mouse model of OPLL.

Vitamin E decreases bone mass by stimulating osteoclast fusion.

Bone homeostasis is maintained by the balance between osteoblastic bone formation and osteoclastic bone resorption. Osteoclasts are multinucleated cells that are formed by mononuclear preosteoclast fusion. Fat-soluble vitamins such as vitamin D are pivotal in maintaining skeletal integrity. However, the role of vitamin E in bone remodeling is unknown. Here, we show that mice deficient in α-tocopherol transfer protein (Ttpa(-/-) mice), a mouse model of genetic vitamin E deficiency, have high bone mass as a result of a decrease in bone resorption. Cell-based assays indicated that α-tocopherol stimulated osteoclast fusion, independent of its antioxidant capacity, by inducing the expression of dendritic-cell-specific transmembrane protein, an essential molecule for osteoclast fusion, through activation of mitogen-activated protein kinase 14 (p38) and microphthalmia-associated transcription factor, as well as its direct recruitment to the Tm7sf4 (a gene encoding DC-STAMP) promoter. Indeed, the bone abnormality seen in Ttpa(-/-) mice was rescued by a Tm7sf4 transgene. Moreover, wild-type mice or rats fed an α-tocopherol-supplemented diet, which contains a comparable amount of α-tocopherol to supplements consumed by many people, lost bone mass. These results show that serum vitamin E is a determinant of bone mass through its regulation of osteoclast fusion.

Runx1 and Runx2 cooperate during sternal morphogenesis.

Chondrocyte differentiation is strictly regulated by various transcription factors, including Runx2 and Runx3; however, the physiological role of Runx1 in chondrocyte differentiation remains unknown. To examine the role of Runx1, we generated mesenchymal-cell-specific and chondrocyte-specific Runx1-deficient mice [Prx1 Runx1(f/f) mice and alpha1(II) Runx1(f/f) mice, respectively] to circumvent the embryonic lethality of Runx1-deficient mice. We then mated these mice with Runx2 mutant mice to obtain mesenchymal-cell-specific or chondrocyte-specific Runx1; Runx2 double-mutant mice [Prx1 DKO mice and alpha1(II) DKO mice, respectively]. Prx1 Runx1(f/f) mice displayed a delay in sternal development and Prx1 DKO mice completely lacked a sternum. By contrast, alpha1(II) Runx1(f/f) mice and alpha1(II) DKO mice did not show any abnormal sternal morphogenesis or chondrocyte differentiation. Notably, Runx1, Runx2 and the Prx1-Cre transgene were co-expressed specifically in the sternum, which explains the observation that the abnormalities were limited to the sternum. Histologically, mesenchymal cells condensed normally in the prospective sternum of Prx1 DKO mice; however, commitment to the chondrocyte lineage, which follows mesenchymal condensation, was significantly impaired. In situ hybridization analyses demonstrated that the expression of alpha1(II) collagen (Col2a1 - Mouse Genome Informatics), Sox5 and Sox6 in the prospective sternum of Prx1 DKO mice was severely attenuated, whereas Sox9 expression was unchanged. Molecular analyses revealed that Runx1 and Runx2 induce the expression of Sox5 and Sox6, which leads to the induction of alpha1(II) collagen expression via the direct regulation of promoter activity. Collectively, these results show that Runx1 and Runx2 cooperatively regulate sternal morphogenesis and the commitment of mesenchymal cells to become chondrocytes through the induction of Sox5 and Sox6.

A microRNA regulatory mechanism of osteoblast differentiation.

Growing evidence shows that microRNAs (miRNAs) regulate various developmental and homeostatic events in vertebrates and invertebrates. Osteoblast differentiation is a key step in proper skeletal development and acquisition of bone mass; however, the physiological role of non-coding small RNAs, especially miRNAs, in osteoblast differentiation remains elusive. Here, through comprehensive analysis of miRNAs expression during osteoblast differentiation, we show that miR-206, previously viewed as a muscle-specific miRNA, is a key regulator of this process. miR-206 was expressed in osteoblasts, and its expression decreased over the course of osteoblast differentiation. Overexpression of miR-206 in osteoblasts inhibited their differentiation, and conversely, knockdown of miR-206 expression promoted osteoblast differentiation. In silico analysis and molecular experiments revealed connexin 43 (Cx43), a major gap junction protein in osteoblasts, as a target of miR-206, and restoration of Cx43 expression in miR-206-expressing osteoblasts rescued them from the inhibitory effect of miR-206 on osteoblast differentiation. Finally, transgenic mice expressing miR-206 in osteoblasts developed a low bone mass phenotype due to impaired osteoblast differentiation. Our data show that miRNA is a regulator of osteoblast differentiation.

Central control of bone remodeling by neuromedin U.

Bone remodeling, the function affected in osteoporosis, the most common of bone diseases, comprises two phases: bone formation by matrix-producing osteoblasts and bone resorption by osteoclasts. The demonstration that the anorexigenic hormone leptin inhibits bone formation through a hypothalamic relay suggests that other molecules that affect energy metabolism in the hypothalamus could also modulate bone mass. Neuromedin U (NMU) is an anorexigenic neuropeptide that acts independently of leptin through poorly defined mechanisms. Here we show that Nmu-deficient (Nmu-/-) mice have high bone mass owing to an increase in bone formation; this is more prominent in male mice than female mice. Physiological and cell-based assays indicate that NMU acts in the central nervous system, rather than directly on bone cells, to regulate bone remodeling. Notably, leptin- or sympathetic nervous system-mediated inhibition of bone formation was abolished in Nmu-/- mice, which show an altered bone expression of molecular clock genes (mediators of the inhibition of bone formation by leptin). Moreover, treatment of wild-type mice with a natural agonist for the NMU receptor decreased bone mass. Collectively, these results suggest that NMU may be the first central mediator of leptin-dependent regulation of bone mass identified to date. Given the existence of inhibitors and activators of NMU action, our results may influence the treatment of diseases involving low bone mass, such as osteoporosis.