ライフサイエンスコーパス: resorption

1 ions of Vn, especially those related to bone resorption.

2 significantly larger and exhibited enhanced resorption.

3 ession and causes muscle catabolism and bone resorption.

4 s a tunable decision between deciliation and resorption.

5 d JE degeneration, PDL destruction, and bone resorption.

6 for diseases associated with excessive bone resorption.

7 ible for physiological and pathological bone resorption.

8 cial for osteoclast differentiation and bone resorption.

9 sorption but also osteocytes and perilacunar resorption.

10 low IQ, and defective kidney proximal tubule resorption.

11 se in bone formation and an increase in bone resorption.

12 adhesion, actin cytoskeletal remodeling and resorption.

13 al bone formation and increased endocortical resorption.

14 t 3 years, coincident with complete scaffold resorption.

15 obisphosphonate and potent inhibitor of bone resorption.

16 d the 3-year time point of complete scaffold resorption.

17 damage, fetal growth restriction, and fetal resorption.

18 latter is due in large part to elevated bone resorption.

19 e side effects such as hypocalcemia and bone resorption.

20 ed bone formation and slightly hindered bone resorption.

21 of IFT-B through cilia decapitation precedes resorption.

22 ml CSC neonatally had increased rates of pup resorption.

23 oclast differentiation and inflammatory bone resorption.

24 tomography analysis was used to assess bone resorption.

25 strogen deficiency leads to accelerated bone resorption.

26 Ts changes during flagellar regeneration and resorption.

27 microCT analysis was used to assess bone resorption.

28 tant gatekeepers of estrogen-controlled bone resorption.

29 tment, reduced IL-6 and RANKL, and less bone resorption.

30 undergoes continual cycles of formation and resorption.

31 ific genes via NFATc1, which facilitate bone resorption.

32 ied data that provide new insights into root resorption.

33 tegerin (OPG) signaling associated with bone resorption.

34 t, and reduced bone mass with increased bone resorption.

35 d strength by uncoupling bone formation from resorption.

36 severely osteopenic because of enhanced bone resorption.

37 main HIF-regulated pathway that drives bone resorption.

38 al knockout mice alleviated progressive bone resorption.

39 increases bone formation, and decreases bone resorption.

40 , plays an essential role in regulating bone resorption.

41 anced osteoclastogenesis, and increased bone resorption.

42 to bone tissue by inducing osteoclastic bone resorption.

43 ncreasing bone formation and decreasing bone resorption.

44 t osteoclast precursors to induce local bone resorption.

45 lasts, is a major negative regulator of bone resorption.

46 1 antisense RNA to control pathological bone resorption.

47 ase increased when cells underwent flagellar resorption.

48 sertion to minimize future peri-implant bone resorption.

49 ced osteoclastogenesis and inflammatory bone resorption.

50 rtical bone osteopenia due to increased bone resorption.

51 of Ac45 in periapical inflammation and bone resorption.

52 events that are caused by osteoclastic bone resorption.

53 rrelated with the difference in palatal bone resorption.

54 Boldine inhibited the alveolar bone resorption.

55 tion factor on osteoclast formation and bone resorption.

56 t that promotes both bone formation and bone resorption.

57 ation, extracellular acidification, and bone resorption.

58 ed bone formation and osteoclast-driven bone resorption.

59 ish demonstrate that shedding involved tooth resorption, a primitive feature in bony fishes, but abse

60 teoclasts are the cells responsible for bone resorption, a process that is essential for the maintena

61 C. acnes significantly decreased the resorption ability of osteoclasts with a major impact by

62 d bone, periosteal reaction, serpentine bone resorption, abscess formation, and root penetration of t

63 in vivo phenotype as its multinucleation and resorption activities determine quantifiable skeletal tr

64 one formation activity nor osteoclastic bone resorption activity in vivo.

65 Osteoclast differentiation and resorption activity was enhanced in Gnas(+/p-) cells.

66 ibitor reduced both osteoclast formation and resorption activity while siRNA targeting MMP9 also inhi

67 expression of osteoclastic markers and bone resorption activity, as well as decreased expression of

68 ardiomyocyte hypertrophy and osteoclast bone resorption activity.

69 ifferentiation although had little effect on resorption activity.

70 eeth with DBBM-C tended to exhibit less root resorption, although it was not statistically significan

71 based on histochemical, gene expression, and resorption analysis.

72 sociated with a significant decrease in bone resorption and a marked reduction in number of osteoclas

73 sociated with a significant decrease in bone resorption and a marked reduction in the number of osteo

74 ated animals, resulting in less buccal plate resorption and a wider alveolar ridge by day 21.

75 h an increase in osteoclastogenesis and bone resorption and an increase in the pool of monocytes.

76 ltaneously inhibits osteoclast-mediated bone resorption and attenuates dendritic cell-mediated inflam

77 tein (PTHrP) is a critical regulator of bone resorption and augments osteolysis in skeletal malignanc

78 L administered at ART initiation blunts bone resorption and BMD loss at key fracture-prone anatomical

79 L administered at ART initiation blunts bone resorption and BMD loss at key fracture-prone anatomical

80 hometry measurements revealed that both bone resorption and bone formation parameters were increased

81 We concluded that the material resorption and bone formation was highly impacted by the

82 osis results from the imbalance between bone resorption and bone formation, and restoring the normal

83 role in determining the balance between bone resorption and bone formation.

84 , thereby creating an imbalance between bone resorption and bone formation.

85 esting that Hdac3 regulates coupling of bone resorption and bone formation.

86 AT1-mTORC1 axis plays a pivotal role in bone resorption and bone homeostasis by modulating NFATc1 in

87 In terms of bone resorption and bone quality parameters, no implant mater

88 Aberrant serum-induced ciliary resorption and cold-induced depolymerization in ARMC9 an

89 e remodeling, as confirmed by increased bone resorption and decreased bone formation, and significant

90 Osteoporosis is caused by increased bone resorption and decreased bone formation.

91 Enhanced osteoclast-mediated bone resorption and diminished formation may promote bone los

92 mor growth and osteolysis by inhibiting bone resorption and enhancing bone formation.

93 CLP promoted OC formation and bone resorption and expression of OC-associated genes.

94 In normal aging, the balance between bone resorption and formation can be shifted.

95 he discovery of key pathways regulating bone resorption and formation has identified new approaches t

96 t activation and unbalanced coupling between resorption and formation, which induces a thinning of tr

97 is characterized by focal and dramatic bone resorption and formation.

98 ey insights into mechanisms that couple bone resorption and formation.

99 t osteoclasts (OCLs) block both pagetic bone resorption and formation; therefore, PD offers key insig

100 Alveolar bone resorption and gingival collagen fibers were histologica

101 of periodontitis by measuring alveolar bone resorption and gingival IL-17 expression as outcomes of

102 licated in sterile inflammation-induced bone resorption and has been shown to increase the bone-resor

103 ic matrix deposition and osteoclastic tissue resorption and immunomodulation for tissue development.

104 ts PKCzeta activity, cell polarity, and bone resorption and increases secretion of bone-forming Cthrc

105 Tooth extraction results in alveolar bone resorption and is accompanied by postoperative swelling

106 hich are characterized by high rates of bone resorption and loss of bone mass, may benefit from treat

107 nistered orally, inhibited the alveolar bone resorption and modulated the Th17/Treg imbalance during

108 ntly influence hydrogel functions, including resorption and molecular delivery when injected into hea

109 ch is determined by osteoclast-mediated bone resorption and osteoblast-mediated bone formation, repre

110 lyinosinic:polycytidylic acid promotes fetal resorption and placental abnormalities in wild-type but

111 ts in pathologies characterized by embryonic resorption and placental fusion.

112 phosphonates used for treatment inhibit bone resorption and prevent bone loss but fail to influence b

113 eoclasts, VAOs are dispensable for cartilage resorption and regulate anastomoses of type H vessels.

114 -like cells and unusual patterns of cementum resorption and repair.

115 (+) M2-like macrophages associated with root resorption and root surface repair processes linked to t

116 ion of Ocy-derived factors that promote bone resorption and suppress bone formation.

117 e is mediated by increased osteoclastic bone resorption and suppressed bone formation.

118 f periapical tissues, leading to severe bone resorption and tooth loss.

119 ises two processes: the removal of old bone (resorption) and the laying down of new bone (formation).

120 collagen-degrading enzyme activity, infarct resorption, and adverse structural remodeling (r>0.5).

121 epithelial lipid transporters, reduced lipid resorption, and changes in body fat homeostasis.

122 hage recruitment, osteoclast formation, bone resorption, and cortical and trabecular bone loss.

123 xtensive peri-implantitis with advanced bone resorption, and extensive inflammation with granulation

124 ing enhanced plant growth, plant N uptake, N resorption, and fine root biomass, suggesting higher pla

125 ses including cell invasion, migration, bone resorption, and immune surveillance.

126 ion, reduced osteoclast recruitment and bone resorption, and impaired osteoblast-mediated bone format

127 Bacterial colonization, bone resorption, and implant inflammation were evaluated by p

128 very high interfacial strains, marginal bone resorption, and no improvement in implant stability.

129 stimulating bone formation, inhibiting bone resorption, and promoting angiogenesis in OVX mice.

130 ligament (PDL) disintegration, alveolar bone resorption, and ultimately tooth loss.

131 apsulation induces more severe alveolar bone resorption, and whether this bone loss is associated wit

132 cated to attenuate physiologic alveolar bone resorption as a consequence of tooth extraction.

133 adopting the amount of palatal alveolar bone resorption as a dependent variable demonstrated that the

134 f markers for osteoclast differentiation and resorption, as well as osteoblast-stimulating 'clastokin

135 llografts, in vitro gene expression and bone resorption assays.

136 the inflammatory response and alveolar bone resorption associated with ligature-induced periodontal

137 Caspase-1 in inflammation and alveolar bone resorption associated with periodontitis.

138 cient to significantly inhibit alveolar bone resorption associated with the experimental periodontal

139 ays a relevant role in inflammation and bone resorption associated with the LPS model of experimental

140 Linear changes of facial soft-tissue resorption at immediately placed implants were independe

141 al, high alkaline phosphatase, and high bone resorption biomarker.

142 older people and may lead to increased bone resorption, bone loss, and increased falls and fractures

143 k, a process that involves osteoclastic bone resorption but also osteocytes and perilacunar resorptio

144 steoporosis drugs that not only inhibit bone resorption but also stimulate bone formation, such as po

145 HIF-2alpha knockdown did not affect bone resorption but moderately inhibited osteoclast formation

146 iency did not increase serum markers of bone resorption, but elevated serum markers of bone formation

147 NKL and BMPs, in osteoclastogenesis and bone resorption by ablating p38alpha MAPK in LysM+monocytes.

148 rmine whether boldine inhibits alveolar bone resorption by modulating the Th17/Treg imbalance during

149 ting bone formation by OBs and reducing bone resorption by OCs.

150 Excessive bone resorption by osteoclasts (OCs) can result in serious cl

151 estosterone (T), which thereby inhibits bone resorption by osteoclasts and stimulates bone formation

152 estosterone in bone, thereby inhibiting bone resorption by osteoclasts and stimulating bone formation

153 Bone remodeling consists of resorption by osteoclasts followed by formation by osteo

154 Bone resorption by osteoclasts is essential for bone homeosta

155 gand (RANKL), an essential cytokine for bone resorption by osteoclasts.

156 tivity of DOCK5, which is essential for bone resorption by osteoclasts.

157 ed matrix formation and increased osteoclast resorption by PolgA(mut/mut) cells.

158 ctedly enhanced their tonic firing, as water resorption by supporting cells reduced the extracellular

159 one matrix, pharmacologic inhibition of bone resorption by zoledronate attenuates inflammasome activa

160 ith blood lead and plasma biomarkers of bone resorption (C-terminal telopeptides of type I collagen (

161 xisting leaf-trait databases, since nutrient resorption can cause traits of litter and green leaves t

162 h decreased fusion events, and their mineral resorption capacity was significantly reduced, indicatin

163 nstream signaling resulting in impaired bone resorption capacity.

164 ymal stem cell-derived osteoblasts, and bone resorption, carried out by monocyte-derived osteoclasts.

165 mineralization inhibition, impaired mineral resorption, cellular senescence and extracellular vesicl

166 from 14 teeth (7 with and 7 without signs of resorption) collected from 11 cats.

167 e had elevated cancellous bone formation and resorption compared to other treatment groups as well as

168 ncoupled and disorganized bone formation and resorption continued for the duration of the study resul

169 l sources of variability, including feeding (resorption decreases) and recent fracture (all markers i

170 Outcomes assessed were bone resorption, detection of tartrate-resistant acid phospha

171 in osteoblasts and osteocytes decreases bone resorption due to an increased secretion of Semaphorin 3

172 treated with drugs that inhibit further bone resorption due to estrogen deficiency.

173 ieve coordination between bone formation and resorption during bone remodeling.

174 External apical root resorption during orthodontic treatment implicates speci

175 ople with SRA itself are predisposed to root resorption during orthodontic treatment.

176 ever, the effect of boldine on alveolar bone resorption during periodontitis has not been elucidated

177 Glucocorticoids mainly increase bone resorption during the initial phase (the first year of t

178 training session attenuated markers of bone resorption, effects that are independent of energy avail

179 during and after HIT running attenuates bone resorption, effects that are independent of energy avail

180 Osteopenia occurs where the rate of bone resorption exceeds that of bone formation, so we investi

181 Palatal alveolar bone thickness changes and resorption factors were identified and analyzed.

182 ce of the balance between bone formation and resorption factors.

183 at there was a significant reduction in bone resorption following 3 months of SPI supplementation tha

184 Hence, its actions on alveolar bone resorption, gingival collagen content and key inflammato

185 ylated on arginine residues during flagellar resorption; however, the function is not understood.

186 from the same cat with and without signs of resorption identified 1,732 differentially expressed gen

187 to assess its role in inflammation and bone resorption in a murine model of lipopolysaccharide (LPS)

188 to assess its role in inflammation and bone resorption in a murine model of lipopolysaccharide (LPS)

189 rexpression in the ethiopathogenesis of bone resorption in aggressive and chronic periodontitis.

190 nts compromised their ability to induce bone resorption in an ex vivo organ culture system.

191 Siglec-15 as a regulator of pathologic bone resorption in arthritis and highlight its potential as a

192 kness is a strong predictor of alveolar bone resorption in both groups.

193 ymal dental pulp cells in attenuating dentin resorption in homeostasis are also reviewed.

194 mass in mice and osteoclast multinucleation/resorption in humans with strong correlation between the

195 ckdown only affected glucose uptake and bone resorption in hypoxic conditions.

196 expression of RANKL indicated increased bone resorption in irisin lacking mice.

197 rgement and recovery points to a reduced CSF resorption in microgravity as the underlying cause.

198 itive feedback mechanism that amplifies bone resorption in pathologic conditions of accelerated bone

199 vides a potential strategy for treating bone resorption in patients with myeloma by counteracting tum

200 The exact mechanisms of bone resorption in periodontitis have not been fully elucidat

201 markers (BTMs) demonstrated presence of bone resorption in PIM; between comparable diagnostic ranges

202 osteoclast number and size and enhanced bone resorption in pit formation assays.

203 ms mediate the coupling of bone formation to resorption in remodeling.

204 zed osteopenia associated with enhanced bone resorption in the cancellous bone compartment and with s

205 Therefore, bone resorption in the mother becomes elevated during these p

206 dysbiosis led to a local inhibition of bone resorption in the presence of ligature-induced periodont

207 The importance of osteoclast-mediated bone resorption in the process of osseointegration has not be

208 it suppressed actin-ring formation and bone resorption in these assays.

209 on or viability, it efficiently blocked bone resorption in vitro and in vivo and consequently amelior

210 rbate synovial inflammation in vivo and bone resorption in vitro, suggesting that LTB4 and BLT1 could

211 nt doses of CMC2.24 on inflammation and bone resorption in vivo and also to describe on the effects o

212 a significant role in inflammation and bone resorption in vivo and that Caspase-1 has a pro-resorpti

213 ic drug-eluting stents, followed by complete resorption in ~3 years with recovery of vascular structu

214 tly decarboxylated and activated during bone resorption, inactivation of furin in osteoblasts in mice

215 press genes required in osteoclasts for bone resorption, including cathepsin K (Ctsk), and lactation

216 ivalis plays a key role in the alveolar bone resorption induced during periodontitis, and this bone l

217 odel of P. gingivalis-induced calvarial bone resorption, injection of mmu-miR-155-5p or anti-mmu-miR-

218 ntic treatment can lead to inflammatory root resorption (IRR) through an unclear mechanism.

219 The alveolar bone resorption is a distinctive feature of periodontitis pro

220 Bone resorption is a severe consequence of inflammatory disea

221 This resorption is preceded by elevation of PGF(2~) but is no

222 Inhibition of CatK-mediated bone resorption is validated in human osteoclasts.

223 in the central region of each pouch undergo resorption, leaving behind the region at the rim to form

224 as well as a transient decrease in the bone resorption marker C-telopeptide of type I collagen (CTX-

225 Primary outcome was change in bone resorption marker C-terminal telopeptide of collagen (CT

226 Compared to male WT mice, serum bone resorption marker in male Keap1 Ht mice was significantl

227 ent and modeling, rather than excessive bone resorption, may be the underlying pathophysiology of the

228 emodeling due to balanced bone formation and resorption mediated by osteoblasts and osteoclasts, resp

229 Our data indicate that the increase in bone resorption observed in states of estrogen deficiency in

230 plants demonstrated a peri-implant mean bone resorption of 2.96 mm increased bone loss, yielding a cu

231 This was underlined by a decreased resorption of a hydroxyapatite-like coating.

232 ing this process is that osteoclast-mediated resorption of a quantum of bone is followed by osteoblas

233 ersal of uremia, because of a lack of active resorption of apatite.

234 two novel mouse models show that the lack of resorption of BB xenografts renders them inadequate for

235 ary to determine the time taken for complete resorption of bone graft materials and their replacement

236 der, characterized by defective osteoclastic resorption of bone that results in increased bone densit

237 poorly understood but are thought to involve resorption of ciliary components into the cell body.

238 Here we show that bone resorption of differentiated osteoclasts heavily relies

239 This can be explained by resorption of earlier-formed sulfides, which might play

240 Extensive resorption of graft particles was observed in group DBG,

241 s in embryonic/neonatal lethality with rapid resorption of homozygous mutants, hampering additional s

242 We propose a molecular mechanism for resorption of NaCl by MRCs during development, and concl

243 bstrate restores osteoclastogenesis and bone resorption of Phlpp1-deficient osteoclasts.

244 Additionally, non-resorption of the canal pouch in Ntn1(-/-) mutants is pa

245 hickness and find the factors related to the resorption of the palatal alveolar bone caused by tooth

246 dation of beta-TCP and BBM, accelerating the resorption of these materials.

247 Irisin also increased bone resorption on several substrates in situ.

248 alendronic acid, a potent inhibitor of bone resorption, optimally linked through a differentially hy

249 bone formation rate but did not inhibit bone resorption or reduce tumor burden.

250 l (e.g. the nutrient uptake from litter, the resorption, or the storage of nutrients in the biomass),

251 CMC2.24 inhibited bone resorption, osteoclastogenesis, and tumor necrosis facto

252 Excessive bone resorption over bone formation is the root cause for bon

253 resorbable scaffold (MgBRS) presents a short resorption period (<1 year) and have the potential of be

254 as osteoclastogenic gene expression and bone resorption pit are increased.

255 Bone resorption pits in calvaria, observed by micro-computed

256 ic cell adhesion in the external apical root resorption process and the specific role of alpha/beta i

257 olved in cartilage damage, bone erosion, and resorption processes during osteoarthritis.

258 gradation of ARL13b that occurs during cilia resorption, raising the possibility that the sensitivity

259 e mean value of mid-facial linear 3D spatial resorption ranged from 0.1 to 0.7 mm.

260 Resorption rate of the remaining biomaterial was improve

261 ta T cells but were designed to inhibit bone resorption rather than treating cancer and have limited

262 The ZOL arm had a 65% reduction in bone resorption relative to the placebo arm at 24 weeks (0.11

263 hways; and (3) regulatory mechanisms of root resorption repair by cementum at the proteomic and trans

264 en (CTX-I) are markers of bone formation and resorption, respectively, that are recommended for clini

265 mechanism for progenitor recruitment to bone resorption sites and Cxcl9l and Cxcr3.2 as potential dru

266 esis, the number of nuclei per cell and bone resorption, suggesting a defect in cell fusion.

267 to increase differentiation and promote bone resorption, supporting the tenet that irisin not only st

268 s had increased osteoclast activity and bone resorption surrounding the extracted molar.

269 of P. gingivalis induced less alveolar bone resorption than the encapsulated W50 wild-type strain.

270 entiation but prevented the increase in bone resorption that occurs under hypoxic conditions.

271 in the bone promote osteoclast-mediated bone resorption that releases TGF-beta, which restrains T(h)1

272 one remodelling, with increased osteoclastic resorption the primary feature of the disease.

273 t alveolar bone, hyperloading activates bone resorption, the peak of which is followed by a bone form

274 oblastogenesis and inhibit osteoclastic bone resorption, thus promoting tissue regeneration.

275 codes netrin 1), which is required for canal resorption, to be ectopically expressed at the canal rim

276 Tooth resorption (TR) in domestic cats is a common and painful

277 ss pathologic analysis showed gradual device resorption until 32 weeks after deployment.

278 re: complications such as ankylosis and root resorption up to the tooth exfoliation have occurred fre

279 We then calculated the root resorption volume and examined periodontal tissue cathep

280 Gradual resorption was also observed, as well as events in which

281 Alveolar bone resorption was analyzed using microcomputed tomography a

282 well as events in which a period of gradual resorption was followed by rapid deciliation.

283 eas the expression of genes involved in bone resorption was higher in the AT-MSC group.

284 The amount of palatal alveolar bone resorption was measured and various parameters were anal

285 Bone resorption was measured by uCT and osteoclast number was

286 presence adjacent to the BB particles, no BB resorption was observed.

287 Likewise, volumetric bone resorption was significantly higher in the control group

288 Bone resorption was significantly reduced in Casp1-KO but not

289 raditionally thought to occur solely through resorption, we show that an acute loss of IFT-B through

290 tal complications or evidence of severe root resorption were reported for both groups.

291 ased by 25-40%, and the osteoclasts and bone resorption were suppressed by 50% in NTAP-Ti in vivo.

292 nt hypernucleated osteoclasts, enhanced bone resorption when cultured on bone slices, and altered mRN

293 formation of osteoclasts and excessive bone resorption, which can be assessed by live imaging.

294 mab fully inhibits teriparatide-induced bone resorption while allowing for continued teriparatide-ind

295 catib, a cathepsin K inhibitor, reduces bone resorption while maintaining bone formation.

296 We hypothesize that increased bone resorption with DMPA use allows for mobilization of the

297 eting senescent cells were due to lower bone resorption with either maintained (trabecular) or higher

298 The NC group exhibited internal root resorption with periapical lesions.

299 loss mediated by excessive osteoclastic bone resorption without affecting osteoblastic activity in bo

300 c podosomal organization, and dentine matrix resorption without any cytotoxicity.