A Novel Rat Model of Orthodontic Tooth Movement Using Temporary Skeletal Anchorage Devices: 3D Finite Element Analysis and In Vivo

The aim of this animal study was to develop a model of orthodontic tooth movement using a microimplant as a TSAD in rodents. A finite element model of the TSAD in alveolar bone was built using μCT images of rat maxilla to determine the von Mises stresses and displacement in the alveolar bone surrounding the TSAD. For in vivo validation of the FE model, Sprague-Dawley rats (n=25) were used and a Stryker 1.2 × 3 mm microimplant was inserted in the right maxilla and used to protract the right first permanent molar using a NiTi closed coil spring. Tooth movement measurements were taken at baseline, 4 and 8 weeks. At 8 weeks, animals were euthanized and tissues were analyzed by histology and EPMA. FE modeling showed maximum von Mises stress of 45 Mpa near the apex of TSAD but the average von Mises stress was under 25 Mpa. Appreciable tooth movement of 0.62 ± 0.04 mm at 4 weeks and 1.99 ± 0.14 mm at 8 weeks was obtained. Histological and EPMA results demonstrated no active bone remodeling around the TSAD at 8 weeks depicting good secondary stability. This study provided evidence that protracted tooth movement is achieved in small animals using TSADs

Computer-assisted detection of cemento-enamel junction in intraoral ultrasonographs

The cemento-enamel junction (CEJ) is an important reference point for various clinical measurements in oral health assessment. Identifying CEJ in ultrasound images is a challenging task for dentists. In this study, a computer-assisted detection method is proposed to identify the CEJ in ultrasound images, based on the curvature change of the junction outlining the upper edge of the enamel and cementum at the cementum–enamel intersection. The technique consists of image preprocessing steps for image enhancement, segmentation, and edge detection to locate the boundary of the enamel and cementum. The effects of the image preprocessing and the sizes of the bounding boxes enclosing the CEJ were studied. For validation, the algorithm was applied to 120 images acquired from human volunteers. The mean difference of the best performance between the proposed method and the two raters’ measurements was an average of 0.25 mm with reliability ≥ 0.98. The proposed method has the potential to assist dental professionals in CEJ identification on ultrasonographs to provide better patient care

Central Role of Pyrophosphate in Acellular Cementum Formation

Background: Inorganic pyrophosphate (PPi) is a physiologic inhibitor of hydroxyapatite mineral precipitation involved in regulating mineralized tissue development and pathologic calcification. Local levels of PPi are controlled by antagonistic functions of factors that decrease PPi and promote mineralization (tissue-nonspecific alkaline phosphatase, Alpl/TNAP), and those that increase local PPi and restrict mineralization (progressive ankylosis protein, ANK; ectonucleotide pyrophosphatase phosphodiesterase-1, NPP1). The cementum enveloping the tooth root is essential for tooth function by providing attachment to the surrounding bone via the nonmineralized periodontal ligament. At present, the developmental regulation of cementum remains poorly understood, hampering efforts for regeneration. To elucidate the role of PPi in cementum formation, we analyzed root development in knock-out ((-/-)) mice featuring PPi dysregulation. Results: Excess PPi in the Alpl(-/-) mouse inhibited cementum formation, causing root detachment consistent with premature tooth loss in the human condition hypophosphatasia, though cementoblast phenotype was unperturbed. Deficient PPi in both Ank and Enpp1(-/-) mice significantly increased cementum apposition and overall thickness more than 12-fold vs. controls, while dentin and cellular cementum were unaltered. Though PPi regulators are widely expressed, cementoblasts selectively expressed greater ANK and NPP1 along the root surface, and dramatically increased ANK or NPP1 in models of reduced PPi output, in compensatory fashion. In vitro mechanistic studies confirmed that under low PPi mineralizing conditions, cementoblasts increased Ank (5-fold) and Enpp1 (20-fold), while increasing PPi inhibited mineralization and associated increases in Ank and Enpp1 mRNA. Conclusions: Results from these studies demonstrate a novel developmental regulation of acellular cementum, wherein cementoblasts tune cementogenesis by modulating local levels of PPi, directing and regulating mineral apposition. These findings underscore developmental differences in acellular versus cellular cementum, and suggest new approaches for cementum regeneration

"Inhibition of mineralization in bones and teeth following ectopic expression of matrix Gla protein"

Matrix Gla Protein (MGP) inhibits mineralization of arteries and cartilage. To determine its mineral-inhibiting potential in hard tissues, MGP was ectopically expressed in bones and teeth of mice using an osteoblast/odontoblast-specific 2.3kb proximal promoter for type 1 collagen. Mandibles and long bones of Col1a1-Mgp mice and wild-type littermates were analyzed by Faxitron(TM) radiography, PIXImus(TM) dual-energy x-ray absorptiometry (DEXA) and micro-computed tomography (mu-CT). In addition, light microscopy (LM) and transmission electron microscopy (TEM) were performed. While bone and tooth extracellular matrices (ECMs) appeared normally established in Col1a1-Mgp mice, examination of the mineral phase by radiography, DEXA and mu-CT, together with histological mineral localization by LM after von Kossa staining of undecalcified tissue sections, and by TEM, revealed massive hypomineralization of bone and tooth ECMs. In the skeleton of Col1a1-Mgp mice, alveolar bone of the mandible was most heavily affected (compared to long bones), showing a 50% increase in the unmineralized osteoid volume compared to wild-type littermates. For teeth, mineralization was virtually absent in root dentin of both incisors and molars, and absent in molar cellular cementum, whereas crown dentin showed localized "breakthrough" areas of mineralization. Acellular cementum formation and mineralization was absent in the Col1a1-Mgp mice. Immunohistochemical staining of bone and tooth ECM proteins in Col1a1-Mgp mice showed variations in staining relative to wild-type tissues, with immunostaining generally restricted to areas of mineralization. In conclusion, these results confirm in vivo that ECM proteins can act as inhibitors of bone and tooth mineralization

Impact of bisphosphonate drug burden in alveolar bone during orthodontic tooth movement in a rat model: A pilot study

INTRODUCTION: The aim of this pilot study was to investigate the effect of long-term bisphosphonate drug use (bone burden) on orthodontic tooth movement in a rat model. METHODS: Sprague Dawley rats were used for orthodontic protraction of the maxillary first molars with nickel-titanium coil springs and temporary anchorage devices as anchorage. Four groups of 5 rats each were included in the study; the first 2 groups were dosed with alendronate or a vehicle during concurrent orthodontic tooth movement. The third and fourth groups were pretreated for 3 months with alendronate or vehicle injections, and bisphosphonate drug treatment was discontinued before orthodontic tooth movement. Tooth movement measurements were obtained at 0, 4, and 8 weeks using high-resolution in-vivo microcomputed tomography, and the tissues were analyzed with histology and dynamic labeling of bone turnover. RESULTS: Appreciable tooth movement was achieved during the 8-week duration of this study with nickel-titanium coil springs and temporary anchorage devices. Both bisphosphonate treatment groups exhibited reduced tooth movement compared with the vehicle-dosed controls with a tendency toward more severe reduction in the bisphosphonate predosed group. Concurrent dosing of the bisphosphonate drug resulted in 56% and 65% reductions in tooth protraction at the 4-week and 8-week times, respectively. The impact of bisphosphonate bone burden in retarding tooth movement was even greater, with 77% and 86% reductions in tooth movement at 4 and 8 weeks, respectively. CONCLUSIONS: In this study, we used a robust rat model of orthodontic tooth movement with temporary anchorage devices. It has provided evidence that the bone burden of previous bisphosphonate use will significantly inhibit orthodontic tooth movement