ライフサイエンスコーパス: bone formation

1 bone (resorption) and the laying down of new bone (formation).

2 ing, neurotransmission, lipid transport, and bone formation.

3 s, suggesting an indirect effect of c-Kit on bone formation.

4 contrast, decreases serum IGF-1 and inhibits bone formation.

5 functions of FGF signaling during postnatal bone formation.

6 ts in cartilage development and endochondral bone formation.

7 Msx1 and Msx2 play a major role in tooth and bone formation.

8 n has been proposed as a potent inhibitor of bone formation.

9 f adenosine A2A receptors (A2ARs) stimulates bone formation.

10 OCLs to increase ephrinB2-EphB4 coupling and bone formation.

11 can stimulate osteoblast differentiation and bone formation.

12 ng trauma, and their presence may facilitate bone formation.

13 beta-catenin pathway are major regulators of bone formation.

14 that bone resorption normalizes earlier than bone formation.

15 DLX3 involving the senescence regulation of bone formation.

16 molecules, resulting in accelerated in vitro bone formation.

17 retion into broader programs of craniofacial bone formation.

18 , without a decrease in osteoblast number or bone formation.

19 are essential for FCSC-derived vascularized bone formation.

20 izes the heterogeneity of the mineral during bone formation.

21 to increased bone resorption and suppressed bone formation.

22 ve feedback mechanism that limits Wnt-driven bone formation.

23 icantly decreased or inhibited extraskeletal bone formation.

24 ansport blockade with dipyridamole regulates bone formation.

25 bolism or Gcn2 deletion suppressed excessive bone formation.

26 Rather, short-term ALN treatment enhanced bone formation.

27 ransform into bone cells during endochondral bone formation.

28 art to the inhibition of skeletal growth and bone formation.

29 regulator of osteoblast differentiation and bone formation.

30 FGFRL1 and hsa-miR-140-5p are important for bone formation.

31 enchymal cells inhibited skeletal growth and bone formation.

32 g may play an important role in EPO-mediated bone formation.

33 rging on shared nuclear targets that promote bone formation.

34 ytes undergo apoptosis prior to endochondral bone formation.

35 ogical process with similarities to skeletal bone formation.

36 ALN exhibited no negative effect on bone formation.

37 by osteocytes and is a negative regulator of bone formation.

38 h subcortical necrosis and subperiosteal new bone formation.

39 ved and non-conserved features in vertebrate bone formation.

40 oclast activity, and an increase in alveolar bone formation.

41 nd suggest a therapeutic approach to promote bone formation.

42 (Vegfa) has important roles in endochondral bone formation.

43 a critical anabolic pathway for osteoblastic bone formation.

44 sheep spine leads to significant increase in bone formation.

45 lead to endochondral or intramembranous-like bone formation.

46 ed control, with little sign of endochondral bone formation.

47 tivity may be a target for the regulation of bone formation.

48 effect of the distance from the calvaria on bone formation.

49 prevent unwanted and detrimental heterotopic bone formation.

50 iocompatibility and the potential to support bone formation.

51 cytes undergo programmed cell death prior to bone formation.

52 ning the balance between bone resorption and bone formation.

53 e a key group of growth factors that enhance bone formation.

54 helial cell interactions during vascularized bone formation.

55 ing an imbalance between bone resorption and bone formation.

56 eted and sustained delivery of E2 to promote bone formation.

57 -threatening cervical swelling and cyst-like bone formation.

58 s underlying the role of FCSCs in regulating bone formation.

59 is required to achieve maximal load-induced bone formation.

60 for osteoporosis that increases the rate of bone formation.

61 osteoclastic bone resorption and suppressed bone formation.

62 eocyte-specific Wnt antagonist that inhibits bone formation.

63 or function may also interfere with coupled bone formation.

64 nitors" (MMPs), are essential for cancellous bone formation.

65 this study is to histologically evaluate new bone formation 8 to 10 weeks versus 18 to 20 weeks after

66 till survive and actively participate in new bone formation 8 weeks after implantation.

67 membrane exposure and a noteworthy, ectopic bone formation above the mesh in 72% of sites.

68 s neither due to the changes in osteoblastic bone formation activity nor osteoclastic bone resorption

69 s two separate processes during endochondral bone formation after birth, recent studies have demonstr

70 MPs) show promise in therapies for improving bone formation after injury; however, the high supraphys

71 of HFA on alveolar bone loss and the rate of bone formation after tooth extraction.

72 ver, little is known about how EPO regulates bone formation, although several studies suggested that

73 ologous bone graft and bone bed improved new bone formation and bone consolidation.

74 regulator (CFTR) is associated with reduced bone formation and bone loss in mice.

75 ct, thus leading to a net effect of impaired bone formation and bone loss.

76 molecule SIK inhibitor YKL-05-099 increases bone formation and bone mass.

77 on of osteogenic markers and intramembranous bone formation and by decreased expression of osteoclast

78 It also significantly reduced both reactive bone formation and cortical bone destruction by CM from

79 injection of aptamer-antagomiR-188 increased bone formation and decreased bone marrow fat accumulatio

80 estored trabecular bone volume by increasing bone formation and decreasing bone resorption.

81 and prevent bone loss but fail to influence bone formation and do not replace lost bone, so patients

82 e therapeutic strategies employed to enhance bone formation and fracture repair, but the mechanisms e

83 ymal progenitors responsible for both normal bone formation and fracture repair.

84 in long-term colonized mice, an increase in bone formation and growth plate activity predominates, r

85 t then contributes in a major way to overall bone formation and growth.

86 ic overexpression of miR-188 in mice reduced bone formation and increased bone marrow fat accumulatio

87 their lineage allocation in vivo, inhibiting bone formation and inducing marrow adipogenesis.

88 , Scl-Ab treatment appears to both stimulate bone formation and inhibit bone resorption in humans.

89 Given its dual role in promoting bone formation and inhibiting bone resorption, our resul

90 altered hematological parameters, increased bone formation and lipid accumulation in metabolically c

91 (miR-31) is known to play a role in cancer, bone formation and lymphatic development.

92 Skeletal bone formation and maintenance requires coordinate funct

93 ntation of EPC/otMSCs significantly improved bone formation and mineral density.

94 isorder resulting in variable alterations of bone formation and mineralization that are caused by mut

95 e mOSM receptor (Osmr(-/-)) also had reduced bone formation and osteoblast number within the injury s

96 bbits to test their application in promoting bone formation and osteointegration at the implant-bone

97 an efficient and facile method for promoting bone formation and osteointegration in bone repair.

98 cular bones in developmental origin, mode of bone formation and pathological bone resorption.

99 , alternatively, could result from defective bone formation and patterning.

100 V), are known to be associated with alveolar bone formation and periodontal improvements.

101 ed surgically and dramatically increased new bone formation and regeneration of the periodontal organ

102 receptor (PTHR) is central to the process of bone formation and remodeling.

103 iological responses of mechanical loading on bone formation and remodeling.

104 inhibition during the repair phase disturbed bone formation and remodeling.

105 ational potential of coimplantation to speed bone formation and repair.

106 HU MAT- mice had elevated cancellous bone formation and resorption compared to other treatmen

107 han in lumbar vertebrae, suggesting enhanced bone formation and resorption in OVX-Diet rats.

108 ergoes continuous remodeling due to balanced bone formation and resorption mediated by osteoblasts an

109 We show that maxillary growth remodelling (bone formation and resorption) of the Devil's Tower (Gib

110 de of type I collagen (CTX-I) are markers of bone formation and resorption, respectively, that are re

111 gen-free (SPF) gut microbiota increases both bone formation and resorption, with the net effect of co

112 vates receptors on osteocytes to orchestrate bone formation and resorption.

113 skeleton, circadian rhythm helps coordinate bone formation and resorption.

114 25(OH)D3 deficiency results in failure in bone formation and skeletal deformation.

115 tion of beta-catenin significantly increased bone formation and slightly hindered bone resorption.

116 bone-forming osteoblasts results in reduced bone formation and subsequent bone weakening, which lead

117 ned with ovariectomy recapitulates decreased bone formation and substandard matrix mineralization in

118 ion between denervation-induced reduction of bone formation and TGF-beta gene expression, we measured

119 nce that a WWOX-p53 network regulates normal bone formation and that disruption of this network in os

120 iR-874-3p expression during weaning enhances bone formation and that this miRNA may become a therapeu

121 p38alpha ablation resulted in a decrease in bone formation and the number of bone marrow mesenchymal

122 to determine the effect of short-term ALN on bone formation and tooth extraction wound healing.

123 ism, and simultaneously increased trabecular bone formation and trabecular connectivity, and decrease

124 found to significantly increase load-induced bone formation and Wnt/beta-catenin activity in osteocyt

125 binds to and inhibits sclerostin, increases bone formation, and decreases bone resorption.

126 s in bone mass, impaired osteoblast-mediated bone formation, and enhanced bone marrow fat accumulatio

127 om the imbalance between bone resorption and bone formation, and restoring the normal balance of bone

128 ed with increased bone resorption, decreased bone formation, and significant bone loss.

129 d by increased bone resorption and decreased bone formation, and significantly decreased bone strengt

130 eeks, DOX (61.11%) also had the highest mean bone formation, and statistical differences were observe

131 active WNT signaling and enhanced periosteal bone formation, and the combined outcome is generalized

132 implicated in osteoblast differentiation and bone formation are involved in vascular calcification.

133 eltaF508-CFTR mutation causes alterations in bone formation are poorly known.

134 eotomy site viability, leading to faster new bone formation around implants.

135 nanorods on their surface to promote the new bone formation around the implants.

136 maintained (trabecular) or higher (cortical) bone formation as compared to vehicle-treated mice.

137 g endogenous adenosine levels stimulates new bone formation as well as BMP-2 and represents a novel a

138 anscription factor 2 (RUNX2) is critical for bone formation as well as chondrocyte maturation.

139 volume quantification demonstrated a similar bone formation at 4weeks that was significantly increase

140 osteopenia with elevated bone resorption and bone formation at 6- and 9-week-old.

141 ty regulated bone regeneration, with optimal bone formation at 60 kPa.

142 ) demonstrated evidence of subperiosteal new bone formation at CT, with a subtle focus of new ossific

143 ti-inflammation effects in vivo and promotes bone formation at the lesion site of osteomyelitis.

144 Regarding new bone formation, at the end of 8 weeks, DOX (61.11%) also

145 Stained ground sections showed complete bone formation between bone and implant surface in the P

146 There was no significant difference in new bone formation between the cortical and cancellous FDBA

147 well tolerated and resulted in increases in bone formation biomarkers and bone mineral density, sugg

148 trongly suppressed sclerostin and stimulated bone formation but did not induce RANKL, suggesting that

149 ascular invasion was apparent at the time of bone formation but not earlier.

150 Knee loading promotes bone formation, but its effects on OA have not been well

151 osed as skeletal anabolic therapy to enhance bone formation, but the mechanisms underlying the contri

152 teins (Bmp) are well known to induce ectopic bone formation, but the physiological effect of Bmp sign

153 ediated primarily through the stimulation of bone formation, but with parallel notable reductions in

154 layed senescence of BMSCs leads to increased bone formation by compensating decreased osteogenic pote

155 Finally, miR-101 also promotes in vivo bone formation by hBMSCs.

156 WNT signaling stimulates bone formation by increasing both the number of osteobla

157 t1 overexpression from osteocytes stimulated bone formation by increasing osteoblast number and activ

158 roteasomal degradation of Runx2 and promotes bone formation by inhibiting another function of AMPK.

159 neage cells increases bone mass by elevating bone formation by OBs and reducing bone resorption by OC

160 the role of the endolysosomal system in both bone formation by osteoblasts and bone resorption by ost

161 n share their receptors in the regulation of bone formation by osteoblasts.

162 t is mainly due to defective intramembranous bone formation by osteoblasts.

163 uct of macrophages, sustains intramembranous bone formation by signaling through Osmr and Stat3, acti

164 ne mass is determined by the balance between bone formation, carried out by mesenchymal stem cell-der

165 megaly, cytopenia, hypercytokinemia, and the bone-formation defect of human GD1 through conditional d

166 osteogenic markers with no adverse effect on bone formation, demonstrating that PDK4 is a therapeutic

167 Bone formation during fracture repair inevitably initiat

168 ability and to adjust to the kinetics of new bone formation during healing.

169 hereby promote bone destruction and reactive bone formation during the acute phase of S. aureus osteo

170 the animal body environment and the immature bone formation during the fourth months of implantation

171 also enhances osteoblast differentiation and bone formation from mesenchymal stem cells.

172 nsity, structure, and strength by uncoupling bone formation from resorption.

173 e the differentiation of chondrocytes during bone formation, from their initial induction from mesenc

174 wever, targeting tumor-derived modulators of bone formation has had limited success.

175 ever, a role for Raf kinases in endochondral bone formation has not been identified.

176 r than 100%, the cause of such low levels of bone formation has rarely been investigated.

177 harvested at each timepoint and analyzed for bone formation, hydrogel mineralization and tissue respo

178 The implication of WNT1 in the control of bone formation identifies a potential new target for the

179 cific Plekho1 gene silencing, which promoted bone formation, improved bone microarchitecture, increas

180 in bone mass were associated with increased bone formation in 6-week-old p47(phox-/-) mice but decre

181 nding tissues over time and to influence new bone formation in a 3 mm femur osteoporotic defect model

182 ols, were tested for their ability to induce bone formation in a calvarial induction assay.

183 his study establishes a key role for Osx for bone formation in a non-mammalian species, and reveals c

184 R-195 stimulates CD31(hi)Emcn(hi) vessel and bone formation in aged mice.

185 Thus, abnormal bone formation in areas of subarticular ossification may

186 Dietary factors during early life program bone formation in female rats.

187 r osteoblast dedifferentiation in reparative bone formation in fish and indicate that adult fish oste

188 We hypothesized that controlled, rapid bone formation in large, critical-size defects could be

189 Bone formation in mammals requires continuous production

190 required for osteoblast differentiation and bone formation in mice.

191 TrkA signaling is essential for load-induced bone formation in mice.

192 opose a new model that contrasts the mode of bone formation in much of the mandibular ramus (chondroc

193 of sclerostin and DKK-1 leads to synergistic bone formation in rodents and non-human primates.

194 esis in Runx2-null osteoblasts and initiates bone formation in Runx2-deficient embryos.

195 rable degrees of osteolysis and reactive new bone formation in the acute phase of osteomyelitis.

196 emonstrated that EPO efficiently induces new bone formation in the alveolar bone regeneration model.

197 he defect bridging but left little space for bone formation in the defect site.

198 the cleft site with diminished capacity for bone formation in the expanded palate, more than 80% of

199 ecifically in Hh-responding cells diminishes bone formation in the mouse embryo.

200 ANKL-binding peptide, promotes BMP-2-induced bone formation in the murine maxilla using an injectable

201 The local bone formation in the OP3-4-BMP-2-injected group was ana

202 proof of principle, we study early stages of bone formation in the zebrafish (Danio rerio) larvae bec

203 as a whole in osteoblast differentiation and bone formation in vivo remains unknown.

204 eoblast and osteoclast function and promotes bone formation in vivo via an adenosine-dependent mechan

205 ized material capable of stimulating de novo bone formation in vivo.

206 X2 to promote osteoblast differentiation and bone formation in vivo.

207 administration of PTHrP1-17 augments ectopic bone formation in vivo.

208 Bone formation in vossicles was significantly enhanced i

209 S1P receptor agonist FTY720 causes increased bone formation in wild-type, but not in S1P3-deficient m

210 of osteoblasts, and reduced serum markers of bone formation, including osteocalcin and procollagen ty

211 multiple defects in skeletal patterning and bone formation, including shortened forelimbs, craniosyn

212 or without rMSC aggregates resulted in less bone formation, indicating a prominent role of DA in eff

213 Gq/11 (D/D mice), PTH significantly enhanced bone formation, indicating that phospholipase C activati

214 rathyroid hormone (PTH) levels and decreased bone formation indices and were associated with an impai

215 was found to greatly attenuate load-induced bone formation induced by axial forelimb compression.

216 Bone formation is a complex process that requires concer

217 thesis that denervation-induced reduction of bone formation is a result of inhibition of TGF-beta gen

218 nding the role of burn injury on heterotopic bone formation is an important first step toward the dev

219 fractures, bone resorption is increased, and bone formation is decreased.

220 Bone formation is dependent on the differentiation of os

221 ces support the hypothesis that osteoblastic bone formation is impaired, a clear pathogenetic mechani

222 However, the effect of ALN on bone formation is not as clear as its effect on resorpti

223 hypoxic in the body, but how hypoxia affects bone formation is not known.

224 In extant species, bone formation is restricted to vertebrate species.

225 e JCI, Joeng and colleagues demonstrate that bone formation is under the control of WNT1 produced by

226 The balance between bone resorption and bone formation is vital for maintenance and regeneration

227 has demonstrated extraordinary potential in bone formation, its clinical applications require suprap

228 scular calcification is a process similar to bone formation leading to an inappropriate deposition of

229 ne-specific alkaline phosphatase, which is a bone-formation marker, was detected between 0 and 20 g f

230 hypertrophic, hypertrophic, and subsequently bone formation markers in a sequential manner in euthyro

231 Transient increases in the bone formation markers procollagen type-I N-terminal pro

232 erum analysis showed decreases in OA and the bone-formation markers alkaline phosphatase and osteocal

233 uggest that denervation-induced reduction of bone formation may be regulated by glucocorticoids via i

234 ing, which is amenable to subsequent dynamic bone formation measurements.

235 obtain mineralized bone sections for dynamic bone formation measures.

236 nt increases in the speed and quality of new bone formation occur when siRNA-Sema4d is delivered via

237 While the majority of new bone formation occurred around the HCCS-PDA particulates

238 In the TG, a small amount of bone formation occurred compared with the CG between 3 a

239 dy indicates significantly greater new vital bone formation occurs after tooth extraction and ridge p

240 evels on these respective surfaces, and that bone formation occurs only above a given cell density.

241 s (chondrocyte-derived) with intramembranous bone formation of the mandibular body (non-chondrocyte-d

242 In vivo testing confirmed enhanced bone formation of the OP-1 loaded graft after 8 weeks of

243 of hMSC to a bone cell phenotype and promote bone formation on modified surfaces.

244 However, how to promote bone formation on their surface and their consequent per

245 Avpr2 inhibitor, tolvaptan, does not affect bone formation or bone mass, suggesting that Avpr2, whic

246 with autologous bone tissue did not improve bone formation or defect bridging compared to the empty

247 nstrating no significant difference in vital bone formation or dimensional changes among 50%/50% cort

248 Pathologic extraskeletal bone formation, or heterotopic ossification (HO), occurs

249 Analogous to bone formation, osteogenic cells are thought to be recru

250 ments revealed that both bone resorption and bone formation parameters were increased in male Erk5 (f

251 The current concept regarding endochondral bone formation postulates that most hypertrophic chondro

252 from the sclerostin null mice show improved bone formation potential even after exposure to Pb.

253 l telopeptides of type I collagen (CTX)) and bone formation (procollagen type I amino-terminal peptid

254 drocytes resulted in increased bone mass and bone formation rate (normalized to tissue volume) in lon

255 one density was associated with an increased bone formation rate and reduced bone resorption.

256 in antibody increased osteoblast numbers and bone formation rate but did not inhibit bone resorption

257 gnificantly increased osteoblast numbers and bone formation rate in both control and P-Gsalpha(OsxKO)

258 a decrease in the number of osteoblasts and bone formation rate while the osteoclasts remained relat

259 At 24 months, bone formation rate, trabecular thickness, and bone volu

260 , but had no change in osteoblast numbers or bone formation rate.

261 d bone mineral density, volume fraction, and bone formation rate; decreased expressions of osterix, c

262 icated increased osteogenesis and higher new bone formation rates in both Prkar1a(+/-)Prkar2a(+/-) an

263 d previously unknown Chd7 targets, including bone formation regulators Osterix (also known as Sp7) an

264 rtebrate lineages, its role in non-mammalian bone formation remains elusive.

265 Cell-based approaches for bone formation require instructional cues from the surro

266 rformed to determine percentage of new vital bone formation, residual graft, and connective tissue (C

267 vivo imaging with a fluorescent dye for new bone formation revealed a strong fluorescent signal in t

268 y shown to play key roles in normal alveolar bone formation), significant loss in alveolar bone mass

269 factor during development and essential for bone formation, skeletal growth and postnatal homeostasi

270 the rate of bone resorption exceeds that of bone formation, so we investigated the role of the osteo

271 cks heterotopic ossification, a pathological bone formation that mostly occurs in the skeletal muscle

272 smaller, with reduced fat mass and increased bone formation that was accompanied by elevated bone res

273 y contribution of the PDL in normal alveolar bone formation, the pathologic changes of the Ocys in pe

274 that Bmpr1a signaling suppresses trabecular bone formation through effectors beyond Smad4.

275 sed protein synthesis of factors involved in bone formation through NMP4-mediated dampening of Gadd34

276 aling couples increased bone resorption with bone formation through osteoclast-derived Wnt 10 b.

277 lveolar bone lineage differentiation and new bone formation through WNT, bone morphogenetic protein,

278 tiation during development and the extent of bone formation throughout life.

279 wn mesenchymal cell markers and promoted new bone formation to heal critical-size calvarial defects i

280 Stimulating bone formation to increase bone mass and fracture resist

281 modest but persistent programming effects on bone formation to prevent OVX-induced bone loss in adult

282 modest but persistent programming effects on bone formation to prevent OVX-induced bone loss in adult

283 rowth plate cartilage, the template for long bone formation, to gain insights into this process.

284 on-osteogenic C4-2b PCa cells led to ectopic bone formation under subcutaneous implantation.

285 cells directly participated in endochondral bone formation via their differentiation into chondrocyt

286 New bone formation was associated with increased uptake at N

287 ntly higher percentage (47.41%) of new vital bone formation was found in the long-term healing group

288 e concluded that the material resorption and bone formation was highly impacted by the particle-speci

289 Ectopic bone formation was monitored by micro-computed tomograph

290 Bone formation was not impeded by short-term ALN treatme

291 f Saa3 by PTH may explain the suppression of bone formation when PTH is applied continuously and may

292 in Cpdm mice is solely explained by impaired bone formation, whereas osteoclastogenesis is unaffected

293 bperiosteal injection promoted BMP-2-induced bone formation, which could lead to the development of a

294 e have increased osteoblast numbers and high bone formation, which results in high bone mass in the a

295 ination allograft results in increased vital bone formation while providing similar dimensional stabi

296 irst histologic evidence showing greater new bone formation with a combination mineralized/deminerali

297 The nHA-LC (38% HA content) paste supported bone formation with a high defect bridging-rate.

298 lecular phenamil synergized osteogenesis and bone formation with BMP2 in a rat critical size mandibul

299 eointegration, translating to highly regular bone formation with minimal fibrous tissue and increased

300 poencephalocele in an adult patient with new bone formation within it which was not associated with a