ライフサイエンスコーパス: tooth

1 t teeth; RR: 1.84 for AL and BOP in the same tooth).

2 t secrete dentine throughout the life of the tooth.

3 sorption images of the interior regions of a tooth.

4 s on the lateral expansion of the developing tooth.

5 to the bone and soft tissues surrounding the tooth.

6 ue index were measured at four sites of each tooth.

7 ace teeth through shedding of the functional tooth.

8 tion determination in such ancient deciduous tooth.

9 cal wall was compared with the contralateral tooth.

10 mutations are associated with developmental tooth abnormalities and adolescent onset of a broad rang

11 al-specific deletion of Evc2 phenocopied the tooth abnormalities in Evc2 mutants.

12 enic variants in candidate disease genes for tooth agenesis in 10 multiplex Turkish families.

13 than 1 gene were identified segregating with tooth agenesis in 2 families, suggesting oligogenic inhe

14 Tooth agenesis is a common craniofacial abnormality in h

15 Tooth agenesis is complex, and variations in about a doz

16 Tooth agenesis is one of the most common developmental a

17 ed that the mutations co-segregated with the tooth agenesis phenotype (with exception of families in

18 le for WNT pathways genes in the etiology of tooth agenesis while revealing new candidate genes.

19 pite significant progress in the genetics of tooth agenesis, many gaps in knowledge exist in refining

20 standing of the genetic etiology of familial tooth agenesis.

21 identified as likely pathogenic in isolated tooth agenesis.

22 otype-phenotype correlation between PAX9 and tooth agenesis.

23 ss of function of the PAX9 protein underlies tooth agenesis.

24 genic in 2 families with suspected syndromic tooth agenesis.

25 nces between groups in time taken to achieve tooth alignment (mean [SD] 158.7 [75.3] d; P = 0.486).

26 wed from start of treatment to completion of tooth alignment with fixed orthodontic appliances.

27 Primary outcome was time taken to complete tooth alignment, while secondary outcomes included rate

28 um lingual and buccal depth of space between tooth and bone, periosteal reaction, serpentine bone res

29 um lingual and buccal depth of space between tooth and bone, periosteal reaction, serpentine grooving

30 demonstrate this technique can be applied on tooth and brain tissue samples.

31 Such cements remain in the tooth and fail to degrade and thus normal mineral volume

32 rkers, and the microbiome of subject-matched tooth and implant sites during native inflammation and i

33 critical for patterning and morphogenesis of tooth and taste buds.

34 icrobiomes in kogiid hosts compared to other toothed and baleen whales, driven by differences in symb

35 analysis was performed around one incisional tooth, and color data were expressed in terms of L*, a*,

36 Tooth- and implant-supported fixed restorations from com

37 ng related to long-term clinical outcomes of tooth- and implant-supported high-strength ceramic resto

38 Furthermore, a sharper tooth angle results in a higher preferential formation o

39 The OPL appeared to have a saw-tooth appearance ("intraretinal peaks") in 12 eyes (75%)

40 orporated into clinical literature regarding tooth autotransplantation.

41 like its hadrosauriform relatives possessing tooth batteries of many small teeth, Lanzhousaurus utili

42 Since the success of whole tooth bioengineering is predicated on the availability o

43 bite forces and tooth pressures, and studied tooth-bone contacts to provide the answer.

44 les not associated with breastfeeding (e.g., tooth brushing), as can be guided using tools such as di

45 finding that the developing mandibular molar tooth bud mesenchyme expresses significantly higher leve

46 nificantly upregulated and expanded into the tooth bud mesenchyme in Inhba(-/-) embryos in comparison

47 We hypothesize that decellularized tooth buds (dTBs) created from unerupted porcine tooth b

48 h buds (dTBs) created from unerupted porcine tooth buds (TBs) can be used to guide reseeded dental ce

49 ing bleeding from the periapical area of the tooth can be challenging and in turn may deleteriously a

50 Ancient DNA from the saber-toothed cat Homotherium reveals that the late Pleistocen

51 Saber-toothed cats (Machairodontinae) are among the most widel

52 volutionary history of two lineages of saber-toothed cats (Smilodon and Homotherium) in relation to l

53 ew ancient-DNA studies have focused on saber-toothed cats [1-3], and they have been restricted to sho

54 oximately 36,000 to 10,000 years ago), saber-toothed cats, American lions, dire wolves, and coyotes c

55 tRNA synthetases implicated in Charcot-Marie-Tooth (CMT) disease suggests a common mechanism, a defec

56 tly been shown to cause axonal Charcot-Marie-Tooth (CMT) disease, but the cellular function of MORC2

57 history study of children with Charcot-Marie-Tooth (CMT) disease.

58 However, little attention has been paid to tooth color, whose origin remains unknown.

59 (AAAs) in proteins-might be responsible for tooth color.

60 cance in promoting the synthesis of advanced tooth-colored materials and furthering our understanding

61 gments in the odontoblast-like cells and the tooth compartments.

62 wn dentin formation points to a new concept: tooth crown and root have different control mechanisms.

63 Axin2 is rapidly upregulated in response to tooth damage and that these Axin2-expressing cells diffe

64 rative dentinogenesis using an in vivo mouse tooth damage model.

65 Dental caries (tooth decay) is a polymicrobial biofilm disease driven b

66 tans biofilms in the oral cavity can lead to tooth decay.

67 Forty single-tooth dental implants inserted after placement of biogla

68 lecular mechanisms of human craniofacial and tooth development and disease and will ultimately lead t

69 dings demonstrate that MMP9 is important for tooth development and DSP is a novel target of MMP9 duri

70 for FGF3 and FGF11, genes related to ear and tooth development and hypoxia, respectively.

71 epithelium and mesenchyme at early stages of tooth development and later during cell differentiation

72 s through processing substrates, its role in tooth development and whether DSP is a substrate of MMP9

73 dentin formation have been a major focus in tooth development for several decades.

74 d the impact of disrupted cilia signaling on tooth development in ciliopathies.

75 In this study, the function of MMP9 in the tooth development was examined by observation of Mmp9 kn

76 During tooth development, ephrinB1, and EphB2 were expressed in

77 to uncover the mechanism leading to abnormal tooth development, little is known regarding how hypomor

78 ormed an array of genetic analyses in murine tooth development, where Lrp4 and Wise play important ro

79 detected in dental mesenchymal cells during tooth development.

80 BBS due to abnormal embryonic orofacial and tooth development.

81 ng the Hippo-Yap pathway in craniofacial and tooth development.

82 surrounds the tooth germ in early stages of tooth development.

83 vidence implicates primary cilia function in tooth development.

84 inical and genetic spectrum of Charcot-Marie-Tooth disease (CMT) caused by mutations in the neurofila

85 Charcot-Marie-Tooth disease type 1A (CMT1A) is caused by duplication o

86 yelinating neuropathy known as Charcot-Marie-Tooth disease type 1A (CMT1A) is linked with duplication

87 Charcot-Marie-Tooth disease type 1A (CMT1A) is the most common heritab

88 Charcot-Marie-Tooth disease type 1A (CMT1A) is the most common inherit

89 gene, have been shown to cause Charcot Marie Tooth Disease type 2 (CMT-2) or distal hereditary motor

90 Charcot-Marie-Tooth disease type 2D (CMT2D) is a peripheral nerve diso

91 al nerve toxicity resulting in Charcot-Marie-Tooth disease type 2D (CMT2D) is still largely unresolve

92 disease, Huntington's disease, Charcot-Marie-Tooth disease, heart failure, schizophrenia, epilepsy, c

93 posita and her mother also had Charcot-Marie-Tooth disease.

94 ns in the GDAP1 gene can cause Charcot-Marie-Tooth disease.

95 However, at 1 wk, initial tooth displacement was significantly increased in the ob

96 The use of Ca isotope analysis in tooth enamel allows microsampling and offers an independ

97 inimally destructive surface acid etching of tooth enamel and subsequent identification of sex chromo

98 transitions are recorded in human deciduous tooth enamel as marked variations in Ca isotope ratios (

99 Tooth enamel comprises parallel microscale and nanoscale

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

101 infer that Lanzhousaurus had a rapid rate of tooth enamel elongation or amelogenesis at 0.24 mm/day w

102 ce of the effect of chewed food particles on tooth enamel surfaces and reflects dietary signals over

103 similar to, or higher than, those of natural tooth enamels-we achieve values that exceed the traditio

104 ntoblastic processes until the completion of tooth eruption.

105 h as ankylosis and root resorption up to the tooth exfoliation have occurred frequently.

106 h type, and the location of the crack on the tooth exhibited a strong correlation.

107 Here, using mammalian tooth explants cultured in isolation, we investigate sel

108 mputational modeling of cusp patterning, and tooth explants cultured with small braces show that corr

109 Tooth extraction and dental disease have been strongly a

110 phasize the importance of dental disease and tooth extraction in ONJ pathogenesis and help delineate

111 Second, osteotomies were produced in healed tooth extraction sites and therefore represented the pla

112 one grafting in maxillary, non-molar, single-tooth extraction sites were recruited.

113 for use in alveolar ridge preservation after tooth extraction.

114 xamination, and data on number and timing of tooth extractions as well as pre-extraction diagnoses an

115 root size and the generation of a whole "bio-tooth" for therapeutic purposes.

116 ]) promoting crack propagation in bones, (2) tooth form and dental arcade configurations that concent

117 This relatively strong correlation validates tooth form as a proxy for neutral genomic markers.

118 Furthermore, tooth form is considered to be highly heritable and sele

119 y do not lose their ability to contribute to tooth formation and differentiate into odontoblasts.

120 populations can contribute to bioengineered tooth formation but only as cells that respond to tooth-

121 dental mesenchyme cells are unable to induce tooth formation, they can contribute to tooth induction

122 enchymal cells renders them unable to induce tooth formation, they do not lose their ability to contr

123 toblasts, and at ratios of 1:1, they inhibit tooth formation.

124 butions of cell populations to bioengineered tooth formation.

125 embryonic dental mesenchyme cells to induce tooth formation.

126 cells, however, lose all tooth-inducing and tooth-forming capacity following in vitro expansion, and

127 date of 286 +/- 32 thousand years ago for a tooth from the Irhoud 3 hominin mandible.

128 ently been found to be linked to multirooted tooth furcation formation.

129 of ectomesenchymal cells that surrounds the tooth germ in early stages of tooth development.

130 olar tooth germs while their maxillary molar tooth germs completed morphogenesis.

131 The degree of mineralization of permanent tooth germs in dental age assessment has been an area of

132 developmental arrest of the mandibular molar tooth germs while their maxillary molar tooth germs comp

133 ce exhibit early developmental arrest of all tooth germs.

134 minerals are thought to be indispensable for tooth-hardening and durability.

135 HERSs fail to reach toward the center of the tooth in the normal furcation region, and taurodont teet

136 of half-mouth registration at six sites per tooth including probing depth (PD) and clinical attachme

137 Postnatal pulp cells, however, lose all tooth-inducing and tooth-forming capacity following in v

138 numbers of cells, in vitro cell expansion of tooth-inducing cell populations is an essential requirem

139 duce tooth formation, they can contribute to tooth induction and formation if combined with noncultur

140 formation but only as cells that respond to tooth-inductive signals.

141 Tooth injury in mice with odontoblast-specific IGF-1 rec

142 In a model of tooth injury with pulp exposure, ephrinB1 was strongly e

143 ed in odontoblastic processes 2 wk following tooth injury without pulp exposure, whereas EphB2 was ex

144 ays significant roles in the early stages of tooth injury.

145 This jaw-tooth integration of a specific aspect of the tooth phen

146 Tooth is made of an enamel-covered crown and a cementum-

147 most unexpected one is the change from fully toothed jaws in the hatchling and juvenile individuals t

148 s by using detailed clinical measures at the tooth level, including both periodontal measurements and

149 terns in the population at an individual and tooth level.

150 a postcranial dermal skeleton consisting of tooth-like "denticles" embedded within their skin.

151 .1% and 1.7% increases in the probability of tooth loss (probit coefficients were 0.469 (95% confiden

152 deregulated immune response and resulting in tooth loss and various systemic conditions.

153 treatment strategies may influence long-term tooth loss are hard to find.

154 by sex and age, to estimate familial risk of tooth loss as well as estimates of heritability.

155 on and housing damage due to the disaster on tooth loss by fitting an instrumental variable probit mo

156 ase severity based on alveolar bone loss and tooth loss during follow-up.

157 n and housing damage due to the disaster and tooth loss in a cohort of community-dwelling residents (

158 tory bone disorder and the greatest cause of tooth loss in adults.

159 d that family background importantly affects tooth loss in both the middle-aged and the older populat

160 ssess risk for periodontitis progression and tooth loss in dental patients.

161 eolar vestiges and indicate that ontogenetic tooth loss in Limusaurus is a gradual, complex process.

162 Tooth loss is a common health concern in older adults.

163 that a substantial part of the variation in tooth loss is explained by genetic as well as environmen

164 Tooth loss is the ultimate negative consequence of perio

165 Tooth loss was common, but actual number of teeth lost,

166 rporated in the collection were examined for tooth loss, cavity occurrence, average and maximum lingu

167 Alterations following tooth loss, itself a major risk factor for oral cancer,

168 red community composition and function after tooth loss, with smaller alterations in current tobacco

169 including both periodontal measurements and tooth loss.

170 abetes can increase the risk and severity of tooth loss.

171 ect size relative to microbiome shifts after tooth loss.

172 eteriorating socioeconomic circumstances and tooth loss.

173 those who smoke, suffer from a high rate of tooth loss.

174 ecrosis, arrested tooth-root development and tooth loss.

175 itf that has previously been associated with tooth malformations.

176 Using validated tooth-matrix biomarkers, we estimate pre- and post-natal

177 lthough in vitro cell expansion of embryonic tooth mesenchymal cells renders them unable to induce to

178 pression of Inhba and Bmp4 in the developing tooth mesenchyme is independent of each other, Bmp4(ncko

179 of Dkk2 than the developing maxillary molar tooth mesenchyme, these data indicate that Bmp4 and acti

180 ularly Dkk2, in the maxillary and mandibular tooth mesenchyme.

181 including Dkk2 and Sfrp2, in the developing tooth mesenchyme.

182 urcation involvements and/or Grade II or III tooth mobility were also detected in the sextant than wh

183 sting of probing depth, bleeding on probing, tooth mobility, gingival index, and plaque index was per

184 signaling on maxillary and mandibular molar tooth morphogenesis are mainly due to the differential e

185 KK inhibitor IIIC3a rescued mandibular molar tooth morphogenesis in Inhba(-/-) embryos.

186 pathway control the bud-to-cap transition of tooth morphogenesis through antagonistic regulation of e

187 tion of the Wnt signaling pathway to promote tooth morphogenesis through the bud-to-cap transition an

188 g possibly affected the evolution of jaw and tooth morphology.

189 year clinical outcome of therapy in terms of tooth mortality between groups of patients treated with

190 reatment approaches in patients where buccal tooth movement (expansion) is planned in the anterior ma

191 r bone alterations influenced by orthodontic tooth movement and can help determine risk assessment pr

192 t, while secondary outcomes included rate of tooth movement and change in clinical parameters (plaque

193 mineral metabolism contributing to disrupted tooth movement and exfoliation.

194 patients had a significantly higher rate of tooth movement compared with normal-weight patients (+0.

195 ry dentofacial therapy involving orthodontic tooth movement in the management of malocclusion with as

196 ounding natural teeth undergoing orthodontic tooth movement or influenced by orthopedic forces throug

197 ry teeth, ankylosis, and/or slow orthodontic tooth movement, suggesting altered mineral metabolism co

198 herapies for patients undergoing orthodontic tooth movement.

199 stigate the effect of obesity on orthodontic tooth movement.

200 tients and associated with observed rates of tooth movement.

201 Here we report a new species of toothed mysticete, Coronodon havensteini, from the Oligo

202 t the glycosylation site cause Charcot-Marie-Tooth neuropathy, has abundant GlcNAc-6-O-sulfated N-gly

203 is stage, development can be arrested if the tooth organ is damaged by either trauma or caries.

204 The heterophylly, evolved from linear to toothed-ovate shape, showed the significant difference i

205 or dentine hypersensitivity and inflammatory tooth pain.

206 ooth integration of a specific aspect of the tooth phenotype indicates that organs may outsource spec

207 des of Lrp4 function are supported by severe tooth phenotypes of mice carrying a human mutation known

208 s bite forces (8,526-34,522 newtons [N]) and tooth pressures (718-2,974 megapascals [MPa]) promoting

209 an pulverize skeletal elements by generating tooth pressures between occluding teeth that exceed cort

210 om trace evidence, estimated bite forces and tooth pressures, and studied tooth-bone contacts to prov

211 n and definition of distinct periodontal and tooth profile classes (PPCs/TPCs) among a cohort of indi

212 ile classes (PPCs A to G) and seven distinct tooth profile classes (TPCs A to G) ranging from health

213 stent clinical treatment decisions affecting tooth prognosis (as measured by defect fill, improvement

214 ls, we are able to identify the formation of tooth pulp cells and odontoblasts in bioengineered teeth

215 e mobilisation of resident stem cells in the tooth pulp.

216 Whole tooth regeneration approaches currently are limited by o

217 e potential use of dTBs for functional whole tooth regeneration.

218 a potential off-the-shelf scaffold for whole tooth regeneration.

219 rdinary properties of teeth have resulted in tooth repair and the generation of novel materials.

220 of Wnt/beta-catenin signaling is pivotal for tooth repair in exposed pulp injury, and the pathway can

221 This simple, rapid natural tooth repair process could thus potentially provide a ne

222 ssil fish demonstrate that shedding involved tooth resorption, a primitive feature in bony fishes, bu

223 tentially provide a new approach to clinical tooth restoration.

224 In this study, we used tooth root development as a model with which to investig

225 the critical gaps in our understanding about tooth root formation but will aid future research regard

226 t and NFIC-independent signaling pathways in tooth root formation.

227 cellular and molecular mechanisms underlying tooth root formation.

228 role of Hertwig's epithelial root sheath in tooth root formation.

229 The tooth root is an integral, functionally important part o

230 lenging and in turn may deleteriously affect tooth root maturation.

231 de aggregate was used to seal one end of the tooth root segment, while the other was left open.

232 e methods to regenerate pulp-like tissues in tooth root segments (RSs).

233 egarding the identifying factors controlling tooth root size and the generation of a whole "bio-tooth

234 fections, leading to pulp necrosis, arrested tooth-root development and tooth loss.

235 Thus, apical revascularization facilitates tooth-root development but lacks consistency in promotin

236 Post-operative tooth-root development in immature permanent teeth repre

237 ts perceived ability to enable postoperative tooth-root growth, is being accepted worldwide.

238 Tooth-root lengths lacked significant postoperative gain

239 ented greater risk of AL and BOP in the same tooth (RR: 2.16) and percentage of BOP (RR: 1.37).

240 ent teeth (RR: 1.47), AL and BOP in the same tooth (RR: 2.77), and percentage of BOP (RR: 1.49).

241 equently produces lactic acid to degrade the tooth's enamel.

242 characterized by the demineralization of the tooth's enamel.

243 and finite-element modeling for probing the tooth's mechanical properties, spatially resolved small-

244 portion to macroscale deformations along the tooth's normal is maximized when the architecture is col

245 Using fluorescence immunostaining on human tooth sections in vivo and on primary human pulp fibrobl

246 Tooth sensitivity and demineralization of the enamel are

247 e causing subtle but consistent variation in tooth shape resembling variation in nature.

248 ains, we show the effect of the Mitf gene on tooth shape.

249 of the developing jaw than other aspects of tooth shape.

250 dentify five genomic regions associated with tooth shape; one region contained the gene microphthalmi

251 hantavirus identified from the Ussuri white-toothed shrews (Crocidura lasiura) in the Republic of Ko

252 ed for the body, skull and brain size of red-toothed shrews and some mustelids [3-5].

253 Red-toothed shrews exhibit a rare exception, where the shape

254 ctive brain malformation known as the "molar tooth sign" on axial MRI.

255 d superior cerebellar peduncles (mild "molar tooth sign"), typical cranio-facial dysmorphisms (hypert

256 Patient/tooth/site-associated variables were recorded for each p

257 ry, differences existed between implants and tooth sites in microbiome evolution during OH abstention

258 when used in ridge preservation of non-molar tooth sites.

259 en trends in brain enlargement and posterior tooth size reduction in some hominin species.

260 Tooth slices of human healthy extracted third molars wer

261 ly distantly related to the well-known saber-toothed Smilodon.

262 occus sanguinis is an early colonizer of the tooth surface and competes with oral pathogens such as S

263 sucrose to initiate biofilm formation on the tooth surface and consequently produces lactic acid to d

264 luid-derived protein layer that forms on the tooth surface.

265 teeth (OR = 0.86; 95% CI, 0.60 to 1.22) and tooth surfaces (OR = 0.85; 95% CI, 0.59 to 1.21) were ex

266 Plaque samples from caries-free tooth surfaces (PF) and from enamel carious lesions (PE)

267 val dental plaque differ substantially among tooth surfaces and children of different caries activiti

268 Tooth surfaces are exposed to different proteinaceous mi

269 For instance, tooth surfaces close to the gingival sulcus contact seru

270 g a split-mouth design, with half the buccal tooth surfaces coated with serum and the other half with

271 S. sanguinis, which yields understanding of tooth surfaces colonization and contributions to dental

272 tion time points, the microbiomes of healthy tooth surfaces differed substantially from those found d

273 protein layer formed from natural saliva on tooth surfaces, acquired enamel pellicle (AEP), protects

274 r that has a seamless interface with natural tooth surfaces.

275 one anatomy, mobility patterns, and ultimate tooth survival)?

276 interventions did not reverse the arrest in tooth, thymus, and parathyroid gland development, sugges

277 ayer components in Tannerella forsythia, and tooth tissue-degrading enzymes in the oral pathogen Porp

278 conducive to acid damage of the mineralized tooth tissue.

279 The autogenous tooth transplantation approach to replace missing teeth

280 Some independent variables, such as age, tooth type, and GRD at T1 seem to influence GRD and KT c

281 We found that crack pattern, tooth type, and the location of the crack on the tooth e

282 inherited neuropathies such as Charcot-Marie-Tooth type-2, distal hereditary motor neuropathies, spin

283 nique, to determine the (87)Sr/ (86)Sr intra-tooth variability of a human deciduous incisor from the

284 dentists with clinically significant erosive tooth wear and increased esophageal acid exposure by 24-

285 tudinal studies of reflux-associated erosive tooth wear and of reflux characteristics have been repor

286 longitudinal study in patients with erosive tooth wear and oligosymptomatic GERD receiving esomepraz

287 antly associated with progression of erosive tooth wear at follow-up.

288 receiving esomeprazole for one year, erosive tooth wear did not progress further in the majority of p

289 follow-up, no further progression in erosive tooth wear was observed in 53 (74%) of patients.

290 Predictive factors for erosive tooth wear were assessed by logistic regression.

291 nal course of GERD and of associated erosive tooth wear, as well as factors predictive of its progres

292 early detection and management of pathologic tooth wear.

293 tion of the causal role of reflux in erosive tooth wear.

294 periodontal examinations with six sites per tooth were conducted at baseline and after 5 years.

295 tacean lineages uniquely associated with the toothed whales or Odontoceti (arginine at 156) and balee

296 his motif emerged by convergent evolution in toothed whales, the only other mammals with a prolonged

297 s differed from those previously reported in toothed whales, which exhibited low diversity communitie

298 to 3.15%), in patients showing at least one tooth with >/=2 mm of AL progression (2.24%, 95% CI: 1.5

299 in the autotransplantation of a multirooted tooth with completed root formation.

300 rm a versatile damage-tolerant protein-based tooth, with a stiffness similar to mineralized mammalian