ライフサイエンスコーパス: enamel

1 the prevention and restoration of defective enamel.

2 Homozygous mutant mice failed to produce enamel.

3 are essential for the proper development of enamel.

4 ation of apatite crystals observed in mature enamel.

5 l surface in comparison with the hypoplastic enamel.

6 plate the growth of apatite mineral in human enamel.

7 s group of genetic disorders affecting tooth enamel.

8 nd microstructure in hypoplastic and healthy enamel.

9 n and showed that Mmp20(+/+)Tg mice had soft enamel.

10 amelogenin interaction in the maturing mouse enamel.

11 malian diets from isotopic analyses of tooth enamel.

12 ess organized texture in the rostrum than in enamel.

13 each results in formation of hypomineralized enamel.

14 logenesis imperfecta (AI) with almost absent enamel.

15 terozygous mice secreted structurally normal enamel.

16 produces lactic acid to degrade the tooth's enamel.

17 rized by the demineralization of the tooth's enamel.

18 imetic approach to the regeneration of human enamel.

19 at were more consistent with wear types than enamel.

20 matrix and formation of properly structured enamel.

21 Dental enamel, a hierarchical material composed primarily of hy

22 In the pigmented enamel, a mixture of ferrihydrite and amorphous iron-cal

23 ate that delta(66)Zn values in both bone and enamel allow a clear distinction between carnivores and

24 The use of Ca isotope analysis in tooth enamel allows microsampling and offers an independent ap

25 secretory stage 1.8-fold more than wild-type enamel and containing less chloride (suggesting more bic

26 There were no differences in enamel and dentin densities between GACI and control tee

27 lization, gap progress could be seen on both enamel and dentin even after irradiation; furthermore, t

28 s, including supernumerary or missing teeth, enamel and dentin hypoplasia, or teeth crowding.

29 oved the differentiation of lesions for both enamel and dentin in polished or natural surfaces.

30 SP, BF, and SB had significantly lower enamel and dentin initial gaps than the control and GB (

31 The percentages of sealed enamel and dentin interface area (E%, D%) were calculate

32 ound [no lesion; control]) and 2 substrates (enamel and dentin).

33 assified up to 84% and 94% of the lesions on enamel and dentin, respectively.

34 assified up to 81% and 91% of the lesions in enamel and dentin, respectively.Asfc, Sa, and Tfv were a

35 asion, and erosion-abrasion lesions on human enamel and dentin.

36 structural and compositional alterations in enamel and dentine that coincided with elemental signatu

37 or each posterior group) for 2 tissue types (enamel and dentine).

38 a lower mineral density compared to control enamel and exhibited structural defects at least some of

39 me, characterized by kinky hair, thin-pitted enamel and increased bone density.

40 utes 90% of the protein matrix in developing enamel and plays a central role in guiding the hierarchi

41 pithelium by K14-cre resulted in hypoplastic enamel and reduced density in X-ray radiography as well

42 ly destructive surface acid etching of tooth enamel and subsequent identification of sex chromosome-l

43 ins in mediating the structural hierarchy of enamel and that contribute to our efforts to design and

44 in equatorial Africa were sampled for tooth enamel and, together with vegetation and feces, analyzed

45 metals present in large quantity in bone and enamel apatite, providing that biologically mediated fra

46 ooth sensitivity and demineralization of the enamel are, however, common side effects associated with

47 itions are recorded in human deciduous tooth enamel as marked variations in Ca isotope ratios (delta(

48 the morphology and microstructure changes in enamel, as well as the expression pattern of enamel matr

49 trate that delta(26)Mg incorporated in tooth enamel becomes heavier from strict herbivores to omnivor

50 tribute to our efforts to design and develop enamel biomimetic material.

51 PEHB+40ACP had higher bracket-enamel bond strength and ion release and rechargeability

52 aining ACP was developed with a high bracket-enamel bond strength and the ability to be repeatedly re

53 cement did not adversely affect the bracket-enamel bond strength.

54 portant role not only in mineralizing dental enamel but also in regulating the expression of EMPs.

55 Moreover, the enamel Ca/P ratio and microhardness were markedly reduce

56 Among the main elements found in enamel, Ca(2+) is the most abundant ion, yet how amelobl

57 lly, the surface of ENAM-mutated hypoplastic enamel can appear to be normal, yet severe sub-nano and

58 The affected enamel can be hypoplastic and/or hypomineralized.

59 Enamel carbon isotope values from teeth of human-hunted

60 rom caries-free tooth surfaces (PF) and from enamel carious lesions (PE) and dentin carious lesions (

61 the mechanisms mediating Ca(2+) dynamics in enamel cells are unclear.

62 In an enamel protein intake assay, enamel cells transfected with miR-153 show a decreased a

63 Investigating primary murine enamel cells, we found that key components of CRAC chann

64 t be an important Ca(2+) uptake mechanism in enamel cells.

65 remineralization of S. mutans-demineralized enamel compared with controls.

66 Tooth enamel comprises parallel microscale and nanoscale ceram

67 Tooth is made of an enamel-covered crown and a cementum-covered root.

68 he nondestructive 3D imaging and analysis of enamel crack behavior in whole human teeth in vitro.

69 f this study was to nondestructively analyze enamel crack behavior on different areas of teeth using

70 use in clinical studies for the analysis of enamel crack behavior.

71 each arch ( n = 80 teeth) were inspected for enamel crack patterns on functional, contact and nonfunc

72 stage of enamel formation when nucleation of enamel crystallites occurs.

73 SEM) have been used to measure and correlate enamel crystallography and microstructure in hypoplastic

74 Enamel crystals form de novo in a rich extracellular env

75 that ACP transformation to ordered arrays of enamel crystals may be regulated in part by the proteoly

76 ntially interacts with ab surfaces of mature enamel crystals, inhibiting their directional growth, th

77 hat MMP-20 prevents protein occlusion inside enamel crystals, we hypothesized that addition of MMP-20

78 promoting linear growth along the c-axis of enamel crystals.

79 egulate the shape and orientation of growing enamel crystals.

80 ORAI1-deficient patients have dental enamel defects and anhidrosis, representing a new form o

81 was ubiquitously inactivated, had dentin and enamel defects as well as hypophosphatemic rickets.

82 The A-Tg+ and A-Tg++ mice displayed severe enamel defects in spite of the expression level of trans

83 These results indicated that the enamel defects in the Sox2-Cre;Fam20C(fl/fl) mice were i

84 Fam20C-knockout mice showed severe enamel defects very similar to those in the ameloblastin

85 h, aberrant crown and root morphologies, and enamel defects, although the underlying mechanistic link

86 e D-Tg+ and D-Tg++ mice showed minor to mild enamel defects, indicating that the D-Tg transgenes dist

87 e;Fam20C(fl/fl) mice were independent of the enamel defects.

88 (WD) in terrestrial environments using tooth enamel delta(18)O values, and use this approach to addre

89 ects of metabolic and dietary changes on the enamel delta(26)Mg composition remain to be explored but

90 White spot lesions (WSL) due to enamel demineralization are major complications for orth

91 rtant integument that protects teeth against enamel demineralization, and abrasion.

92 ic oral bacteria to flourish and to generate enamel-demineralizing acids.

93 Enamel density was reduced in preeruption Irf6-cKO mice,

94 se was searched with the terms amelogenesis, enamel, dental, and tooth, and all results were screened

95 lesions confined to enamel (not reaching the enamel-dentin junction), 21% (95% confidence interval [C

96 For proximal lesions extending up to the enamel-dentin junction, 48% (95% CI, 40%-56%) of dentist

97 ns: those confined to enamel or reaching the enamel-dentin junction.

98 AM plays the greatest functional role at the enamel-dentine junction (EDJ), as it was the region that

99 Using enamel-dentine junction morphology, enamel thickness and

100 cluding hardness, are comparable to those of enamel despite the nanocomposites having a smaller hard-

101 8 (PN8) induced AI-like pathologies when the enamel development reached maturity (PN12).

102 relieve ER stress or modulate the UPR during enamel development to ameliorate the clinical phenotype.

103 matrix mineralization in the final stage of enamel development, and is strongly expressed, almost ex

104 s a paradigm shift from the current model of enamel development.

105 most abundant during the maturation stage of enamel development.

106 For occlusal lesions with enamel discoloration/cavitation but no clinical/radiogra

107 fect the diffusivity of peroxide through the enamel discs.

108 howed a very large force of interaction with enamel (e.g., compared with mucin and casein) and signif

109 amelogenin degradation product in developing enamel (e.g., P148) primarily serves to prevent uncontro

110 that Lanzhousaurus had a rapid rate of tooth enamel elongation or amelogenesis at 0.24 mm/day with de

111 Its capacity to protect against initial enamel erosion was also tested in vitro via changes in s

112 n of the three solutions against citric acid enamel erosion, enamel specimens were immersed in the co

113 nd casein) and significantly reduced initial enamel erosion.

114 tal products might confer protection against enamel erosion.

115 local, given that the isotopic ratio of the enamel falls within the local range and is comparable wi

116 Enamel matrix proteins (EMPs) play a role in enamel formation and the development of the periodontium

117 tant mice we recently generated, we analyzed enamel formation in the mouse incisor.

118 , transit-amplifying cell proliferation, and enamel formation in the mouse incisor.

119 ndicating that the D-Tg transgenes disturbed enamel formation less than the A-Tg transgenes did.

120 known genotype expands the understanding of enamel formation processes and can aid better clinical d

121 Dental enamel formation requires large quantities of Ca(2+) yet

122 bances in adhesion and polarity, and delayed enamel formation was confirmed immunohistochemically.

123 in colocalized during the secretory stage of enamel formation when nucleation of enamel crystallites

124 Fam20A, a Fam20C paralog, is essential for enamel formation, but the biochemical function of Fam20A

125 dental abnormalities, including hypomorphic enamel formation, has been reported in patients with EvC

126 Amelogenesis is the process of dental enamel formation, leading to the deposition of the harde

127 , determining tooth number, crown shape, and enamel formation.

128 c conditions that result in defective dental enamel formation.

129 a proton sensor that is required for proper enamel formation.

130 nherited conditions associated with abnormal enamel formation.

131 eostasis, which further leads to hypomorphic enamel formation.

132 of cell function during different stages of enamel formation; cell movement and attachment; regulati

133 no measurable variation in delta(44/42)Ca of enamel formed during this time.

134 chromosome-linked isoforms of amelogenin, an enamel-forming protein, by nanoflow liquid chromatograph

135 n isotope analysis to human and faunal tooth enamel from four late Pleistocene-to-Holocene archaeolog

136 ted the evolution of (44)Ca/(42)Ca ratios in enamel from in utero development to first months of post

137 carbon isotope ratios (delta(13)C) in canine enamel from individuals that lived between 1960-2000 ind

138 a sequential microsampling method along the enamel growth axis, we collected more than 150 enamel mi

139 logenin supramolecular structures and mature enamel has yet to be described, in part because the prot

140 Defects in tooth enamel have been used to reconstruct stress but the meth

141 Our abiotic enamels have viscoelastic figures of merit (VFOM) and we

142 t Evc2 mutant mice had smaller incisors with enamel hypoplasia.

143 ne encoding the enamelin protein, results in enamel hypoplasia.

144 ng that amelogenins could regulate the pH in enamel in situ.

145 Here we performed ex vivo replication of enamel-inspired columnar nanocomposites by sequential gr

146 and the initiation of new cracks within the enamel (internal cracks) were observed as bright areas.

147 Biomimetic synthesis of artificial enamel is a promising strategy for the prevention and re

148 Enamel is an acellular material formed by the intricate

149 t, little is known regarding how hypomorphic enamel is formed in patients with EvC.

150 ate various molecules and resins into dental enamel is highly desirable in dentistry, yet transportin

151 The formation of human enamel is highly regulated at the molecular level and in

152 stry, yet transporting materials into dental enamel is limited by the nanometric scale of their pores

153 Dental enamel is one of the most remarkable examples of matrix-

154 Fully mineralized enamel is the hardest tissue found in vertebrates owing

155 Tooth enamel is the hardest tissue in the human body and survi

156 Enamel is unique.

157 ABL was calculated by measuring cemento-enamel junction and alveolar crest distance.

158 Cracks originating from the dental-enamel junction and enamel tufts, crack deflections, and

159 %-28% 3D RSA bone loss apical to the cemento-enamel junction corresponded to a CRR of 1:1, relating t

160 aphic bone fill as measured from the cemento-enamel junction to base of bony defect and 2) change in

161 red, including: 1) distance from the cemento-enamel junction to the bone crest; 2) tooth torque (TT);

162 ne loss of 1.01 +/- 0.06 mm from the cemento-enamel junction, whereas all doses of SIM/SIM-mPEG reduc

163 ormation of the tooth signalling centre, the enamel knot (EK), which maintains dental mesenchymal con

164 Bmp4, a known inducer of enamel knots and dental epithelial differentiation, down

165 Enamel knots are signaling centers that define the posit

166 infiltrate which nearly replaced the entire enamel layer.

167 (without acid etching)-deep into the normal enamel layer.

168 Enamel lesion progress was slower in the fluoride-releas

169 differentiated erosion and erosion-abrasion enamel lesions (allP< 0.05).

170 uped as caries free (CF), caries active with enamel lesions (CAE), and caries active with dentin cari

171 es were allowed to etch and extract HAp from enamel, light-cured in situ, and stored in the dark, aft

172 full-length amelogenin during the growth of enamel-like crystals on an etched enamel surface.

173 on, the formation of well-aligned bundles of enamel-like hydroxyapatite (HA) crystals was promoted in

174 calcium phosphate is effective in forming an enamel-like layer that has a seamless interface with nat

175 A thin layer of enamel-like material remained over the dentin and at the

176 gnificant production of organized dentin and enamel-like tissues was observed in dTB-recell and nTB i

177 einaceous microenvironments depending on the enamel location.

178 operties of enamel resulting in irreversible enamel loss.

179 n developing teeth and MMP20 mutations cause enamel malformation.

180 We show that enamel matrices stain positive for amyloids and we ident

181 ible for the transportation and secretion of enamel matrix components, and proteases processing ename

182 Enamel matrix derivative (EMD) and collagen membranes (C

183 Enamel matrix derivative (EMD) and recombinant human pla

184 sidering xenogeneic collagen matrix (CM) and enamel matrix derivative (EMD) characteristics, it is su

185 The enamel matrix derivative (EMD) contains hundreds of pept

186 In periodontal therapy enamel matrix derivative (EMD) has been successfully use

187 Although enamel matrix derivative (EMD) has been used to promote

188 ith a xenogenous collagen matrix (CM) and/or enamel matrix derivative (EMD) in combination with a cor

189 Acellular dermal matrix graft (ADMG) or enamel matrix derivative (EMD) in conjunction with a cor

190 Use of enamel matrix derivative (EMD) when dealing with non-con

191 of periodontal regeneration treatments with enamel matrix derivative (EMD), a commercial formulation

192 Enamel matrix derivatives (EMDs) have demonstrated proof

193 n the pH range that occurs in the developing enamel matrix during amelogenesis.

194 -X-Y motif, the molecular mechanism by which enamel matrix proteins (EMPs) assemble into the organic

195 Enamel matrix proteins (EMPs) play a role in enamel form

196 ns constitute the major portion of secretory enamel matrix proteins and are known to be highly altern

197 Differentiated ameloblasts synthesizing enamel matrix proteins and odontoblasts expressed the ge

198 t data that support cooperative functions of enamel matrix proteins in mediating the structural hiera

199 activity and promotes the phosphorylation of enamel matrix proteins in vitro and in cells.

200 work is needed to further incorporate other enamel matrix proteins into the system, this study bring

201 to investigate the adsorption properties of enamel matrix proteins to bone grafts after surface coat

202 Although the expression of multiple enamel matrix proteins was down-regulated in the mutant

203 the surface of bone grafting materials when enamel matrix proteins were delivered in either a liquid

204 ta (AI) can be caused by the deficiencies of enamel matrix proteins, molecules responsible for the tr

205 dues in the Ser-x-Glu/pSer motifs in several enamel matrix proteins.

206 matrix components, and proteases processing enamel matrix proteins.

207 enamel, as well as the expression pattern of enamel matrix proteins.

208 miR-exon4, with no changes in expression of enamel matrix-related genes.

209 ndary revealed the "fish net" pattern of the enamel matrix.

210 ntrolled changes to the pH of the developing enamel matrix.

211 sported from ameloblasts into the developing enamel matrix.

212 interactions between their fragments during enamel maturation.

213 mel rods and eventual contribution to unique enamel mechanical properties.

214 amel growth axis, we collected more than 150 enamel microsamples from 51 deciduous teeth of 12 differ

215 miR-224 plays a pivotal role in fine tuning enamel mineralization by modulating SLC4A4 and CFTR to m

216 channel genes STIM1 and ORAI1 show abnormal enamel mineralization, we hypothesized that CRAC channel

217 ey buffering ion transporters, in modulating enamel mineralization.

218 CFTR to maintain pH homeostasis and support enamel mineralization.

219 Stable isotope analysis of herbivore tooth enamel (n = 86) from this site reveals, instead, extensi

220 For proximal carious lesions confined to enamel (not reaching the enamel-dentin junction), 21% (9

221 The enamel of AmelX(-/-) mice was 10-fold thinner, mineraliz

222 onary advantage of the columnar motif in the enamel of living species.

223 The outermost enamel of the human tooth and the rostrum of the whale M

224 We present the Sr isotopic composition of enamel of the most ancient deciduous tooth ever discover

225 delta(66)Zn) in bioapatite (bone and dental enamel) of animals from a modern food web in the Koobi F

226 ntum volume ( P = 0.002), with no changes in enamel or dentin.

227 f "early" carious lesions: those confined to enamel or reaching the enamel-dentin junction.

228 ibles confirmed localization of GPR68 in the enamel organ at all stages of amelogenesis.

229 Mmp20(+/+)Tg mice had decreased enamel organ cadherin levels compared to the Mmp20 ablat

230 The means by which the enamel organ regulates pH during amelogenesis is largely

231 ance a new model for Ca(2+) transport by the enamel organ.

232 t of cell types which combined represent the enamel organ.

233 self-assembly causes disorganization of the enamel organic matrix and yields enamel with disordered

234 s most highly amplified from wild-type mouse enamel organs at the secretory stage.

235 e amount of Slc26a6 protein was unchanged in enamel organs of Ae2a,b- and Cftr-null mice but reduced

236 In enamel organs of Slc26a6-null mice, Dra and pendrin prot

237 is group of inherited disorders resulting in enamel pathologies.

238 m natural saliva on tooth surfaces, acquired enamel pellicle (AEP), protects against erosive wear.

239 The acquired enamel pellicle is an oral, fluid-derived protein layer

240 The functional properties of the acquired enamel pellicle will therefore be mostly dictated by the

241 ied as an acid-resistant protein in acquired enamel pellicle; it could therefore be included in oral

242 itance in Man (OMIM) that have an associated enamel phenotype and whether a causative gene has been i

243 Such enamel phenotype was consistent with the diagnosis of hy

244 screened by 2 individuals to determine if an enamel phenotype was identified.

245 ected to a significant degree the underlying enamel prism pattern.

246 In an enamel protein intake assay, enamel cells transfected wi

247 R-153 show a decreased ability to endocytose enamel proteins.

248 phate (PPi) to control the onset and rate of enamel regeneration and the use of leucine-rich amelogen

249 em function and to facilitate the biomimetic enamel regrowth, matrix metalloproteinase-20 (MMP-20) wa

250 tudy brings us one step closer to biomimetic enamel regrowth.

251 d to obtain spatially resolved DC across the enamel-resin interface.

252 sives consistently scored ~80% DC across the enamel-resin interface.

253 wear undermines the structural properties of enamel resulting in irreversible enamel loss.

254 is important for support and maintenance of enamel rods and eventual contribution to unique enamel m

255 ty in X-ray radiography as well as shortened enamel rods under scanning electron microscopy.

256 eruption Irf6-cKO mice, and some shearing of enamel rods was noted in posteruption incisors.

257 ndicular or parallel to the direction of the enamel rods, were exposed to a PPi-stabilized supersatur

258 in fragments created a discontinuity between enamel rods, which we suggest is important for support a

259 at were cut parallel to the direction of the enamel rods.

260 surfaces that were cut perpendicular to the enamel rods.

261 of known dietary histories, as well as nine enamel samples from permanent third molars.

262 However, enamel secreted thereafter was structurally abnormal; pr

263 ffects are restricted to the early stages of enamel secretion.

264 Specimens were tested for bracket-enamel shear bond strength, water sorption, CaP release,

265 Chemical comparison of rostrum and enamel shows bioapatite in the rostrum to be enriched in

266 in Na, Mg, CO3, and S, whereas the outermost enamel shows only a slightly enriched Cl concentration.

267 >99% of S. mutans in planktonic cultures, 8 enamel slabs were harvested from a single tooth.

268 and Slc26a6 to secrete bicarbonate into the enamel space in exchange for Cl(-).

269 of mineral ions and regulation of pH in the enamel space.

270 olutions against citric acid enamel erosion, enamel specimens were immersed in the corresponding solu

271 development of a new approach to regenerate enamel structure and properties.

272 bout the consequence of ENAM mutation on the enamel structure at a crystallographic level.

273 ed greater organization in line with healthy enamel, suggesting its effects are restricted to the ear

274 growth of enamel-like crystals on an etched enamel surface.

275 ition was reversed by the presence of etched enamel surfaces and led to the formation of large, rando

276 the effect of chewed food particles on tooth enamel surfaces and reflects dietary signals over time.

277 Acid-etched enamel surfaces of extracted human molars, cut perpendic

278 little to no crystal formation was found on enamel surfaces that were cut parallel to the direction

279 t abundant protein species in forming dental enamel, taken to regulate crystal shape and crystal grow

280 ibes a group of inherited diseases of dental enamel that have major clinical impact.

281 ary teeth from an affected family member had enamel that was of a lower mineral density compared to c

282 In the maturing mouse enamel, the association of these residual protein fragme

283 Enamel, the outermost layer of teeth, is an acellular mi

284 orus content of mineral tissue in dentin and enamel; they show a lack of signal from pulp tissue and

285 Using enamel-dentine junction morphology, enamel thickness and comparative morphology, we show tha

286 o characterize the structure of ENAM-mutated enamel to develop a deeper understanding of the role of

287 When applied to enamel, TPO-only adhesives had ~80% DC in resin, which g

288 ginating from the dental-enamel junction and enamel tufts, crack deflections, and the initiation of n

289 the removal of matrix proteins in the mutant enamel was drastically delayed, which was coincided with

290 The ability of CaneCPI-5 to bind to dental enamel was evaluated using atomic force microscopy.

291 drogen peroxide through 1-mm discs of bovine enamel was measured at steady-state conditions, and the

292 rs from mice as a model for maturation-stage enamel, we identified the ~17-kDa ameloblastin (Ambn-N)

293 r to, or higher than, those of natural tooth enamels-we achieve values that exceed the traditional ma

294 oth the modulus and hardness of the repaired enamel were significantly increased (1.8- and 2.4-fold,

295 resin, which gradually descended to ~50% in enamel, whereas TPO+4E adhesives consistently scored ~80

296 tion of the enamel organic matrix and yields enamel with disordered hydroxyapatite crystallites.

297 tion of the crystallographic properties from enamel with known genotype expands the understanding of

298 nd Amtn knockout mouse models have defective enamel with no other associated phenotypes, highlighting

299 ring into context the mechanical behavior of enamel with the developmental process of amelogenesis an

300 We hypothesized that without amelogenins the enamel would acidify unless ameloblasts were buffered by