Faculty Bibliography

Rapid palatal expansion is an orthodontic procedure widely used to correct the maxillary arch. However, its outcome is significantly influenced by factors that show a high degree of variability amongst patients. The traditional treatment methodology is based on an intuitive and heuristic treatment approach because the forces applied in the three dimensions are indeterminate. To enable optimal and individualized treatment, it is essential to measure the three-dimensional (3D) forces and displacements created by the expander. This paper proposes a method for performing these 3D measurements using a single embedded strain sensor, combining experimental measurements of strain in the palatal expander with 3D finite element analysis (FEA). The method is demonstrated using the maxillary jaw from a freshly euthanized pig (Sus scrofa) and a hyrax-design rapid palatal expander (RPE) appliance with integrated strain gage. The strain gage measurements are recorded using a computer interface, following which the expansion forces and extent of expansion are estimated by FEA. A total activation of 2.0 mm results in peak total force of about 100 N-almost entirely along the direction of expansion. The results also indicate that more than 85% of the input activation is immediately transferred to the palate and/or teeth. These studies demonstrate a method for assessing and individualizing expansion magnitudes and forces during orthopedic expansion of the maxilla. This provides the basis for further development of smart orthodontic appliances that provide real-time readouts of forces and movements, which will allow personalized, optimal treatment.

A common problem in clinical dentistry is the significant and rapid bone loss that occurs after tooth extraction. Currently there is no solution for the long-term preservation of alveolar bone. Previously, we showed that high-frequency acceleration (HFA) has an osteogenic effect on healthy alveolar bone. However, it is not known if HFA can preserve alveolar bone after extraction without negatively affecting wound healing. The purpose of this study was to evaluate the effect of HFA on alveolar bone loss and the rate of bone formation after tooth extraction. Eighty-five adult Sprague-Dawley rats were divided into 3 groups: control, static (static load), and HFA. In all groups, the maxillary right third molar was extracted. The HFA group received HFA for 5 min/d, applied through the second molar. The static group received the same magnitude of static load. The control group did not receive any stimulation. Some animals received fluorescent dyes at 26 and 54 d. Samples were collected on days 0, 7, 14, 28, and 56 for fluorescence microscopy, micro-computed tomography, histology, RNA, and protein analyses. We found that HFA increased bone volume in the extraction site and surrounding alveolar bone by 44% when compared with static, while fully preserving alveolar bone height and width long-term. These effects were accompanied by increased expression of osteogenic markers and intramembranous bone formation and by decreased expression of osteoclastic markers and bone resorption activity, as well as decreased expression of many inflammatory markers. HFA is a noninvasive safe treatment that can be used to prevent alveolar bone loss and/or accelerate bone healing after tooth extraction.

BACKGROUND: Orai1 is a plasma membrane protein that forms the pore of the calcium release activated calcium channel. Humans with mutated Orai1 present with hereditary combined immunodeficiency, congenital myopathy and anhidrotic ectodermal dysplasia. Consistent with the ectodermal dysplasia phenotype, enamel formation and mineralization is also abnormal in Orai1 deficient patients. The expression pattern and potential functions of Orai1 in enamel formation remains unclear. To contribute toward understanding the role of Orai1 in amelogenesis we characterized ORAI1 protein developmental pattern in comparison with other ectodermal organs. We also examined the effects of Orai1 down-regulation in ameloblast cell proliferation and differentiation. RESULTS: Our data show strong expression of ORAI1 protein during the ameloblast secretory stage, which weans at the end of the maturation stage. In salivary glands, ORAI1 is expressed mainly in acini cells. ORAI1 expression is also found in hair follicle and oral epithelium. Knockdown of Orai1 expression decreases cell proliferation and results in RNA expression levels changes of key ameloblast genes regulating enamel thickness and mineralization. CONCLUSIONS: This study provides insights in the anhidrotic ectodermal dysplasia phenotype due to Orai1 mutation and highlights the importance of calcium signaling in controlling ameloblast differentiation and maturation during tooth development.

Understanding the biology of tooth movement has great importance for developing techniques that increase the rate of tooth movement. Based on interpretations of data on the biology of tooth movement, the resulting accelerating techniques can be divided into two main groups: one group stimulates upstream events to indirectly activate downstream target cells, while the other group bypasses the upstream events and directly stimulates downstream target cells. In both approaches, there is a general consensus that the rate of tooth movement is controlled by the rate of bone resorption, which in turn is controlled by osteoclast activity. Therefore, to increase the rate of tooth movement, osteoclasts should be the target of treatment. In this article, both approaches will be reviewed and the biological limitations of each group will be discussed. (C) 2015 Elsevier Inc. All rights reserved.

Safe, minimally invasive, and cost-effective treatments are being sought to shortened orthodontic treatment time. Based on the well-known principle that orthodontic force triggers inflammatory pathways and osteoclast activity, we hypothesized that controlled micro-trauma in the form of micro-osteoperforations (MOPs) will amplify the expression of inflammatory markers that are normally expressed during orthodontic treatment and that this amplified response will accelerate both bone resorption and tooth movement. We tested our hypothesis in an animal model and in a human clinical trial. In adult rats, MOPs treatment significantly increased molar protraction with concomitant increase in inflammatory cytokine expression, osteoclastogenesis, and alveolar bone remodeling. Likewise, in human subjects, MOPs increased the rate of canine retraction concomitant with increased TNF alpha and IL-1 beta levels in gingival crevicular fluid. Moreover, MOPs treatment did not produce additional pain or discomfort in the patients tested. Our data supports our conclusion that MOPs offers a safe, minimally invasive, and easy mechanism to accelerate orthodontic tooth movement. (C) 2015 Elsevier Inc. All rights reserved.

Since its introduction into dentistry in 1998, cone beam computed tomography (CBCT) has become increasingly utilized for orthodontic diagnosis, treatment planning and research. The utilization of CBCT for these purposes has been facilitated by the relative advantages of 3D over two-dimensional radiography. Despite CBCTs many suggested indications, scientific evidence that its utilization improves diagnosis and treatment plans or outcomes has only recently begun to emerge for some of these applications. This manuscript provides a comprehensive and current review of key studies on the applications of CBCT in orthodontic therapy and for research to decipher treatment outcomes and 3D craniofacial anatomy. The current diagnostic and treatment planning indications for CBCT include impacted teeth, cleft lip and palate and skeletal discrepancies requiring surgical intervention. Use of CBCT in these and other situations such as root resorption, supernumerary teeth, TMJ pathology, asymmetries and alveolar boundary conditions should be justified on the basis of the merits relative to risks of imaging. CBCT has also been used to assess 3D craniofacial anatomy in health and disease and of treatment outcomes including that of root morphology and angulation; alveolar boundary conditions; maxillary transverse dimensions and maxillary expansion; airway morphology, vertical malocclusion and obstructive sleep apnea; TMJ morphology and pathology contributing to malocclusion; and temporary anchorage devices. Finally this manuscript utilizes findings of these studies and current voids in knowledge to provide ideas for future research that could be beneficial for further optimizing the use of CBCT in research and the clinical practice of orthodontics.