The Experts below are selected from a list of 270 Experts worldwide ranked by ideXlab platform
John D. Bartlett - One of the best experts on this subject based on the ideXlab platform.
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beta catenin is essential for ameloblast movement during Enamel development
European Journal of Oral Sciences, 2016Co-Authors: Xiaomu Guan, Sarah E Millar, John D. BartlettAbstract:Beta-catenin is a multifunctional protein that plays key roles in cadherin-based cell adherens junctions and in the Wnt signaling pathway. The canonical Wnt/β-catenin pathway can regulate transcription factors that control cell movement/invasion. We investigated whether β-catenin regulates ameloblast movement through canonical Wnt signaling. The morphological and physical properties of Enamel were assessed in Enamel from control and β-catenin conditional knockout (cKO) mice. Ameloblast-lineage cells (ALC) were used to investigate the potential roles of β-catenin in cell migration and in E-cadherin expression. Compared with controls, incisors from β-catenin cKO mice were short, blunt, and where Enamel was present, it was soft and malformed. Scanning electron microscopy revealed a dysplastic Rod pattern within the Enamel of incisors from β-catenin cKO mice, and Vickers microhardness measurements confirmed that mice with β-catenin ablated from their Enamel organ had Enamel that was significantly softer than normal. Amelogenesis was disrupted in the absence of β-catenin and the ameloblasts did not differentiate properly. We further demonstrated that migration of ALCs was inhibited in vitro and that E-cadherin expression was significantly up-regulated when ALCs were treated with the β-catenin inhibitor, ICG-001. Beta-catenin ablation causes Enamel malformation in mice and this phenotype may occur, in part, by a lack of ameloblast differentiation and/or movement necessary to form the decussating Enamel Rod structure.
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E-Cadherin Can Replace N-Cadherin during Secretory- Stage Enamel Development
2015Co-Authors: Xiaomu Guan, Felicitas B. Bidlack, Nicole Stokes, John D. BartlettAbstract:Background: N-cadherin is a cell-cell adhesion molecule and deletion of N-cadherin in mice is embryonic lethal. During the secretory stage of Enamel development, E-cadherin is down-regulated and N-cadherin is specifically up-regulated in ameloblasts when groups of ameloblasts slide by one another to form the Rodent decussating Enamel Rod pattern. Since N-cadherin promotes cell migration, we asked if N-cadherin is essential for ameloblast cell movement during Enamel development. Methodology/Principal Findings: The Enamel organ, including its ameloblasts, is an epithelial tissue and for this study a mouse strain with N-cadherin ablated from epithelium was generated. Enamel from wild-type (WT) and N-cadherin conditional knockout (cKO) mice was analyzed. mCT and scanning electron microscopy showed that thickness, surface structure, and prism pattern of the cKO Enamel looked identical to WT. No significant difference in hardness was observed between WT and cKO Enamel. Interestingly, immunohistochemistry revealed the WT and N-cadherin cKO secretory stage ameloblasts expressed approximately equal amounts of total cadherins. Strikingly, E-cadherin was not normally down-regulated during the secretory stage in the cKO mice suggesting that E-cadherin can compensate for the loss of N-cadherin. Previously it was demonstrated that bone morphogenetic protein-2 (BMP2) induces E- and N-cadherin expression in human calvaria osteoblasts and we show that the N-cadherin cKO Enamel organ expressed significantly more BMP2 an
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E-cadherin can replace N-cadherin during secretory-stage Enamel development.
PloS one, 2014Co-Authors: Xiaomu Guan, Felicitas B. Bidlack, Nicole Stokes, John D. BartlettAbstract:Background N-cadherin is a cell-cell adhesion molecule and deletion of N-cadherin in mice is embryonic lethal. During the secretory stage of Enamel development, E-cadherin is down-regulated and N-cadherin is specifically up-regulated in ameloblasts when groups of ameloblasts slide by one another to form the Rodent decussating Enamel Rod pattern. Since N-cadherin promotes cell migration, we asked if N-cadherin is essential for ameloblast cell movement during Enamel development.
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kallikrein related peptidase 4 klk4 role in Enamel formation and revelations from ablated mice
Frontiers in Physiology, 2014Co-Authors: John D. Bartlett, James P. SimmerAbstract:Enamel development occurs in stages. During the secretory stage, a soft protein rich Enamel layer is pRoduced that expands to reach its final thickness. During the maturation stage, proteins are removed and the Enamel matures into the hardest substance in the body. KLK4 is expressed during the transition from secretory to the maturation stage and its expression continues throughout maturation. KLK4 is a glycosylated chymotrypsin-like serine protease that cleaves Enamel matrix proteins prior to their export out of the hardening Enamel layer. Mutations in KLK4 can cause autosomal recessive, non-syndromic Enamel malformations in humans and mice. Klk4 ablated mice initially have normal-looking teeth with Enamel of full thickness. However, the Enamel is soft and protein-rich. Three findings are notable from Klk4 ablated mice: First, Enamel Rods fall from the interRod Enamel leaving behind empty holes where the Enamel fractures near the underlying dentin surface. Second, the ~10,000 crystallites that normally fuse to form a solid Enamel Rod fail to grow together in the ablated mice and can fall out of the Rods. Third, and most striking, the crystallites grow substantially in width and thickness (a- and b-axis) in the ablated mice until they almost interlock. The crystallites grow in defined Enamel Rods, but interlocking is prevented presumably because too much protein remains. Conventional thought holds that Enamel proteins bind specifically to the sides of Enamel crystals to inhibit growth in width and thickness so that the thin, ribbon-like Enamel crystallites grow predominantly in length. Results from Klk4 ablated mice demonstrate that this convention requires updating. An alternative mechanism is proposed whereby Enamel proteins serve to form a mold or support structure that shapes and orients the mineral ribbons as they grow in length. The remnants of this support structure must be removed by KLK4 so that the crystallites can interlock to form fully hardened Enamel.
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mmp20 modulates cadherin expression in ameloblasts as Enamel develops
Journal of Dental Research, 2013Co-Authors: Xiaomu Guan, John D. BartlettAbstract:Matrix metalloproteinase-20 (Enamelysin, MMP20) is essential for dental Enamel development. Seven different MMP20 mutations in humans cause non-syndromic Enamel malformations, termed amelogenesis imperfecta, and ablation of Mmp20 in mice results in thin brittle Enamel with a dysplastic Rod pattern. Healthy Enamel formation requires the sliding movement of ameloblasts in rows during the secretory stage of development. This is essential for formation of the characteristic decussating Enamel Rod pattern observed in Rodents, and this is also when MMP20 is secreted into the Enamel matrix. Therefore, we propose that MMP20 facilitates ameloblast movement by cleaving ameloblast cell-cell contacts. Here we show that MMP20 cleaves the extracellular domains of the E- and N-cadherin adherens junction proteins, that both E- and N-cadherin transcripts are expressed at significantly higher levels in Mmp20 null vs. wild-type (WT) mice, and that in Mmp20 ablated mice, high-level ameloblast N-cadherin expression persists during the maturation stage of development. Furthermore, we show that E-cadherin gene expression is down-regulated from the pre-secretory to the secretory stage, while N-cadherin levels are up-regulated. This E- to N-cadherin switch supports epithelial migration in other tissues and may be an important event necessary for the ameloblasts to start moving in rows that slide by one another.
M V Swain - One of the best experts on this subject based on the ideXlab platform.
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elastic modulus and stress strain response of human Enamel by nano indentation
Biomaterials, 2006Co-Authors: Li Hong He, Naoki Fujisawa, M V SwainAbstract:Abstract Nano-indentation with a sharp (Berkovich) and two spherical indenters with nominal tip radii of 5 and 20 μm was used to determine the elastic modulus and stress–strain response of human Enamel. Indentation tests were made over a wide range of peak loads from 1 to 450 mN in two orthogonal directions, i.e., parallel and perpendicular to Enamel prisms. The elastic modulus and hardness (mean contact pressure) versus depth of penetration were determined for the three indenters. From the spherical indentation data, stress–strain curves ( H− tan θ curve) of Enamel were determined in the two orthogonal directions and were found to be different. The elastic modulus showed load dependence for both orientations of the Enamel Rod structure that depended on the indenter. However, these differences could be normalized upon considering the contact diameter. The indented sample was imaged with an SEM to investigate the near surface damage. In conclusion, prism-sheath structure played an important role in determining the mechanical properties as well as the localized fracture of Enamel.
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elastic modulus and stress strain response of human Enamel by nano indentation
Biomaterials, 2006Co-Authors: Naoki Fujisawa, M V SwainAbstract:Nano-indentation with a sharp (Berkovich) and two spherical indenters with nominal tip radii of 5 and 20 microm was used to determine the elastic modulus and stress-strain response of human Enamel. Indentation tests were made over a wide range of peak loads from 1 to 450 mN in two orthogonal directions, i.e., parallel and perpendicular to Enamel prisms. The elastic modulus and hardness (mean contact pressure) versus depth of penetration were determined for the three indenters. From the spherical indentation data, stress-strain curves (H-tantheta curve) of Enamel were determined in the two orthogonal directions and were found to be different. The elastic modulus showed load dependence for both orientations of the Enamel Rod structure that depended on the indenter. However, these differences could be normalized upon considering the contact diameter. The indented sample was imaged with an SEM to investigate the near surface damage. In conclusion, prism-sheath structure played an important role in determining the mechanical properties as well as the localized fracture of Enamel.
Charles E Smith - One of the best experts on this subject based on the ideXlab platform.
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Quantitative analysis of the core 2D arrangement and distribution of Enamel Rods in cross-sections of mandibular mouse incisors.
Journal of anatomy, 2018Co-Authors: Charles E Smith, James P. SimmerAbstract:Considerable descriptive information about the overall organization of mouse mandibular incisor Enamel is available but almost nothing is known about the quantitative characteristics of Enamel Rod arrangement and distribution in these teeth. This has important implications concerning cell movement during the secretory stage because each ameloblast makes one Enamel Rod. Knowing how many Enamel Rods are cut open in a cross‐section of the Enamel layer could provide insights into understanding the dynamics of how groups of ameloblasts form the Enamel layer. In this study, cross‐sections of fully mineralized Enamel were cut on 24 mandibular mouse incisors, polished and etched, and imaged by scanning electron microscopy in backscatter mode. Montaged maps of the entire Enamel layer were made at high magnification and the Enamel Rod profiles in each map were color‐coded based upon Rod category. Quantitative analyses of each color layer in the maps were then performed using standard routines available in imagej. The data indicated that that there were on average 7233 ± 575 Enamel Rod profiles per cross‐section in mandibular incisors of 7‐week‐old mice, with 70% located in the inner Enamel layer, 27% located in the outer Enamel layer, and 3% positioned near the mesial and lateral cementoEnamel junctions. All Enamel Rod profiles showed progressive increases in tilt angles, some very large in magnitude, from the lateral to mesial sides of the Enamel layer, whereas only minor variations in tilt angle were found relative to Enamel thickness at given locations across the Enamel layer. The decussation angle between alternating rows of Rod profiles within the inner Enamel layer was fairly constant from the lateral to central labial sides of the Enamel layer, but it increased dramatically in the mesial region of the Enamel layer. The packing density of all Rod profiles decreased from lateral to central labial regions of the Enamel layer and then in progressing mesially, decreased slightly (inner Enamel, mesial tilt), increased slightly (outer Enamel layer) or almost doubled in magnitude (inner Enamel, lateral tilt). It was concluded that these variations in Rod tilt angle and packing densities are adaptations that allow the tooth to maintain a sharp incisal edge and shovel‐shape as renewing segments formed by around 7200 ameloblasts are brought onto the occluding surface of the tooth by continuous renewal.
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Modulation of Cell-Cell Junctional Complexes by Matrix Metalloproteinases:
Journal of Dental Research, 2012Co-Authors: John D. Bartlett, Charles E SmithAbstract:The ameloblast cell layer of the Enamel organ is in contact with the forming Enamel as it develops into the hardest substance in the body. Ameloblasts move in groups that slide by one another as the Enamel layer thickens. Each ameloblast is responsible for the formation of one Enamel Rod, and the Rods are the mineralized trail that moving ameloblasts leave behind. Matrix metalloproteinases (MMPs) facilitate cell movement in various tissues during development, and in this review we suggest that the tooth-specific MMP, Enamelysin (MMP20), facilitates ameloblast movements during Enamel development. Mmp20 null mice have thin brittle Enamel with disrupted Rod patterns that easily abrades from the underlying dentin. Strikingly, the Mmp20 null mouse Enamel organ morphology is noticeably dysplastic during late-stage development, when MMP20 is no longer expressed. We suggest that in addition to its role of cleaving Enamel matrix proteins, MMP20 also cleaves junctional complexes present on ameloblasts to foster the cell movement necessary for formation of the decussating Enamel Rod pattern. Therefore, inactivation of MMP20 would result in tight ameloblast cell-cell attachments that may cause maturation-stage Enamel organ dysplasia. The tight ameloblast attachments would also preclude the ameloblast movement necessary to form decussating Enamel Rod patterns.
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mmp20 promotes a smooth Enamel surface a strong dej and a decussating Enamel Rod pattern
European Journal of Oral Sciences, 2011Co-Authors: John D. Bartlett, Ziedonis Skobe, Antonio Nanci, Charles E SmithAbstract:Mutations of the Matrix metalloproteinase-20 (MMP20, Enamelysin) gene cause autosomal recessive amelogenesis imperfecta and Mmp20 ablated mice also have malformed dental Enamel. Here we show that Mmp20 null mouse secretory stage ameloblasts maintained a columnar shape and were present as a single layer of cells. However, the null maturation stage ameloblasts covered extraneous nodules of ectopic calcified material formed at the Enamel surface. Remarkably, nodule formation occurs in null mouse Enamel when MMP20 is normally no longer expressed. The malformed Enamel in Mmp20 null teeth was loosely attached to the dentin and the entire Enamel layer tended to separate from the dentin indicative of a faulty DEJ. The Enamel Rod pattern was also altered in Mmp20 null mice. Each Enamel Rod is formed by a single ameloblast and is a mineralized record of the migration path of the ameloblast that formed it. The Mmp20 null mouse Enamel Rods were grossly malformed or were absent indicating that the ameloblasts do not migrate properly when backing away from the DEJ. Thus, MMP20 is required for ameloblast cell movement necessary to form the decussating Enamel Rod patterns, for the prevention of ectopic mineral formation, and to maintain a functional DEJ.
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Matrix metalloproteinase 20 promotes a smooth Enamel surface, a strong dentino-Enamel junction, and a decussating Enamel Rod pattern: Mmp20 null mouse Enamel
European Journal of Oral Sciences, 2011Co-Authors: John D. Bartlett, Ziedonis Skobe, Antonio Nanci, Charles E SmithAbstract:Mutations of the Matrix metalloproteinase-20 (MMP20, Enamelysin) gene cause autosomal recessive amelogenesis imperfecta and Mmp20 ablated mice also have malformed dental Enamel. Here we show that Mmp20 null mouse secretory stage ameloblasts maintained a columnar shape and were present as a single layer of cells. However, the null maturation stage ameloblasts covered extraneous nodules of ectopic calcified material formed at the Enamel surface. Remarkably, nodule formation occurs in null mouse Enamel when MMP20 is normally no longer expressed. The malformed Enamel in Mmp20 null teeth was loosely attached to the dentin and the entire Enamel layer tended to separate from the dentin indicative of a faulty DEJ. The Enamel Rod pattern was also altered in Mmp20 null mice. Each Enamel Rod is formed by a single ameloblast and is a mineralized record of the migration path of the ameloblast that formed it. The Mmp20 null mouse Enamel Rods were grossly malformed or were absent indicating that the ameloblasts do not migrate properly when backing away from the DEJ. Thus, MMP20 is required for ameloblast cell movement necessary to form the decussating Enamel Rod patterns, for the prevention of ectopic mineral formation, and to maintain a functional DEJ.
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Matrix metalloproteinase 20 promotes a smooth Enamel surface, a strong dentino–Enamel junction, and a decussating Enamel Rod pattern
European Journal of Oral Sciences, 2011Co-Authors: John D. Bartlett, Ziedonis Skobe, Antonio Nanci, Charles E SmithAbstract:Mutations of the matrix metalloproteinase 20 (MMP20, Enamelysin) gene cause autosomal-recessive amelogenesis imperfecta, and Mmp20 ablated mice also have malformed dental Enamel. Here we showed that Mmp20 null mouse secretory-stage ameloblasts maintain a columnar shape and are present as a single layer of cells. However, the maturation-stage ameloblasts from null mouse cover extraneous nodules of ectopic calcified material formed at the Enamel surface. Remarkably, nodule formation occurs in null mouse Enamel when MMP20 is normally no longer expressed. The malformed Enamel in Mmp20 null teeth was loosely attached to the dentin and the entire Enamel layer tended to separate from the dentin, indicative of a faulty dentino-Enamel junction (DEJ). The Enamel Rod pattern was also altered in Mmp20 null mice. Each Enamel Rod is formed by a single ameloblast and is a mineralized record of the migration path of the ameloblast that formed it. The Enamel Rods in Mmp20 null mice were grossly malformed or absent, indicating that the ameloblasts do not migrate properly when backing away from the DEJ. Thus, MMP20 is required for ameloblast cell movement necessary to form the decussating Enamel Rod patterns, for the prevention of ectopic mineral formation, and to maintain a functional DEJ.
Xiaomu Guan - One of the best experts on this subject based on the ideXlab platform.
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beta catenin is essential for ameloblast movement during Enamel development
European Journal of Oral Sciences, 2016Co-Authors: Xiaomu Guan, Sarah E Millar, John D. BartlettAbstract:Beta-catenin is a multifunctional protein that plays key roles in cadherin-based cell adherens junctions and in the Wnt signaling pathway. The canonical Wnt/β-catenin pathway can regulate transcription factors that control cell movement/invasion. We investigated whether β-catenin regulates ameloblast movement through canonical Wnt signaling. The morphological and physical properties of Enamel were assessed in Enamel from control and β-catenin conditional knockout (cKO) mice. Ameloblast-lineage cells (ALC) were used to investigate the potential roles of β-catenin in cell migration and in E-cadherin expression. Compared with controls, incisors from β-catenin cKO mice were short, blunt, and where Enamel was present, it was soft and malformed. Scanning electron microscopy revealed a dysplastic Rod pattern within the Enamel of incisors from β-catenin cKO mice, and Vickers microhardness measurements confirmed that mice with β-catenin ablated from their Enamel organ had Enamel that was significantly softer than normal. Amelogenesis was disrupted in the absence of β-catenin and the ameloblasts did not differentiate properly. We further demonstrated that migration of ALCs was inhibited in vitro and that E-cadherin expression was significantly up-regulated when ALCs were treated with the β-catenin inhibitor, ICG-001. Beta-catenin ablation causes Enamel malformation in mice and this phenotype may occur, in part, by a lack of ameloblast differentiation and/or movement necessary to form the decussating Enamel Rod structure.
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E-Cadherin Can Replace N-Cadherin during Secretory- Stage Enamel Development
2015Co-Authors: Xiaomu Guan, Felicitas B. Bidlack, Nicole Stokes, John D. BartlettAbstract:Background: N-cadherin is a cell-cell adhesion molecule and deletion of N-cadherin in mice is embryonic lethal. During the secretory stage of Enamel development, E-cadherin is down-regulated and N-cadherin is specifically up-regulated in ameloblasts when groups of ameloblasts slide by one another to form the Rodent decussating Enamel Rod pattern. Since N-cadherin promotes cell migration, we asked if N-cadherin is essential for ameloblast cell movement during Enamel development. Methodology/Principal Findings: The Enamel organ, including its ameloblasts, is an epithelial tissue and for this study a mouse strain with N-cadherin ablated from epithelium was generated. Enamel from wild-type (WT) and N-cadherin conditional knockout (cKO) mice was analyzed. mCT and scanning electron microscopy showed that thickness, surface structure, and prism pattern of the cKO Enamel looked identical to WT. No significant difference in hardness was observed between WT and cKO Enamel. Interestingly, immunohistochemistry revealed the WT and N-cadherin cKO secretory stage ameloblasts expressed approximately equal amounts of total cadherins. Strikingly, E-cadherin was not normally down-regulated during the secretory stage in the cKO mice suggesting that E-cadherin can compensate for the loss of N-cadherin. Previously it was demonstrated that bone morphogenetic protein-2 (BMP2) induces E- and N-cadherin expression in human calvaria osteoblasts and we show that the N-cadherin cKO Enamel organ expressed significantly more BMP2 an
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E-cadherin can replace N-cadherin during secretory-stage Enamel development.
PloS one, 2014Co-Authors: Xiaomu Guan, Felicitas B. Bidlack, Nicole Stokes, John D. BartlettAbstract:Background N-cadherin is a cell-cell adhesion molecule and deletion of N-cadherin in mice is embryonic lethal. During the secretory stage of Enamel development, E-cadherin is down-regulated and N-cadherin is specifically up-regulated in ameloblasts when groups of ameloblasts slide by one another to form the Rodent decussating Enamel Rod pattern. Since N-cadherin promotes cell migration, we asked if N-cadherin is essential for ameloblast cell movement during Enamel development.
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mmp20 modulates cadherin expression in ameloblasts as Enamel develops
Journal of Dental Research, 2013Co-Authors: Xiaomu Guan, John D. BartlettAbstract:Matrix metalloproteinase-20 (Enamelysin, MMP20) is essential for dental Enamel development. Seven different MMP20 mutations in humans cause non-syndromic Enamel malformations, termed amelogenesis imperfecta, and ablation of Mmp20 in mice results in thin brittle Enamel with a dysplastic Rod pattern. Healthy Enamel formation requires the sliding movement of ameloblasts in rows during the secretory stage of development. This is essential for formation of the characteristic decussating Enamel Rod pattern observed in Rodents, and this is also when MMP20 is secreted into the Enamel matrix. Therefore, we propose that MMP20 facilitates ameloblast movement by cleaving ameloblast cell-cell contacts. Here we show that MMP20 cleaves the extracellular domains of the E- and N-cadherin adherens junction proteins, that both E- and N-cadherin transcripts are expressed at significantly higher levels in Mmp20 null vs. wild-type (WT) mice, and that in Mmp20 ablated mice, high-level ameloblast N-cadherin expression persists during the maturation stage of development. Furthermore, we show that E-cadherin gene expression is down-regulated from the pre-secretory to the secretory stage, while N-cadherin levels are up-regulated. This E- to N-cadherin switch supports epithelial migration in other tissues and may be an important event necessary for the ameloblasts to start moving in rows that slide by one another.
Dar-bin Shieh - One of the best experts on this subject based on the ideXlab platform.
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Human Enamel Rod presents anisotropic nanotribological properties.
Journal of the mechanical behavior of biomedical materials, 2010Co-Authors: Yeau-ren Jeng, Tsung Ting Lin, Hsiu Ming Hsu, Hsin-ju Chang, Dar-bin ShiehAbstract:The AFM combined nanoindentation was performed to observe the ultrastructure of Enamel Rod from various section plans and positions while probing their mechanical and tribological properties of the area. The nanohardness and the elastic modulus of the head region of the Enamel Rods are significantly higher than that of the tail region and the axial-sectional plane. Both nanohardness and elastic modulus gradually decrease from Enamel surface toward dentino-Enamel junction. Such a variation correlates well with the decreasing trend of calcium composition from our element analysis. The friction coefficient and nanowear of the Enamel showed an inversed trend to the hardness with respect to their relative topological position in the long axis of Enamel Rod toward DEJ. The relationship between the nanowear depth and the distance from the outer Enamel surface to DEJ presented exponential function. The results presented clarify the basic nanomechanical and nanotribological properties of human Enamel Rods and provide a useful reference for the future development of dental restorative materials.
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Nanotribological characterization of tooth Enamel Rod affected by surface treatment.
Journal of biomechanics, 2009Co-Authors: Yeau-ren Jeng, Tsung Ting Lin, Dar-bin ShiehAbstract:Tooth Enamel is a hybrid organic-inorganic bionanocomposite comprised predominantly of Enamel Rods. Understanding the effects of anti-caries treatment on the biomechanical properties of these Rods is essential in developing effective caries prevention strategies. Calcium fluoride-like deposits play an important role in caries prevention and their nanotribological properties have a direct effect upon their long-term effectiveness. Accordingly, this study utilizes a variety of techniques, namely nanoindentation, nanoscratch tests, nanowear tests and atomic force microscopy (AFM), to characterize the mechanical and tribological properties of single Enamel Rods before and after topical fluoride application. The results show that the CaF(2)-like deposits formed on the Enamel surface following fluoride application increase the coefficient of friction of the Enamel Rods, but decrease their critical load and nanohardness. As a result, the nanowear depth of the treated Enamel surface is around six times higher than that of the native Enamel surface under an applied load of 300 microN. Following the removal of the surface deposits, however, the modulus of elasticity and wear depth of the underlying Enamel surface are found to be similar to those of the original Enamel surface. However, a notable increase in the surface roughness is observed.