ライフサイエンスコーパス: bone resorption

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

2 sponsible for physiological and pathological bone resorption.

3 e crucial for osteoclast differentiation and bone resorption.

4 ecrease in bone formation and an increase in bone resorption.

5 aminobisphosphonate and potent inhibitor of bone resorption.

6 cause side effects such as hypocalcemia and bone resorption.

7 creased bone formation and slightly hindered bone resorption.

8 The latter is due in large part to elevated bone resorption.

9 puted tomography analysis was used to assess bone resorption.

10 ted estrogen deficiency leads to accelerated bone resorption.

11 microCT analysis was used to assess bone resorption.

12 osteoclast differentiation and inflammatory bone resorption.

13 important gatekeepers of estrogen-controlled bone resorption.

14 ecruitment, reduced IL-6 and RANKL, and less bone resorption.

15 gement, and reduced bone mass with increased bone resorption.

16 -specific genes via NFATc1, which facilitate bone resorption.

17 eoprotegerin (OPG) signaling associated with bone resorption.

18 s the main HIF-regulated pathway that drives bone resorption.

19 ANKL), plays an essential role in regulating bone resorption.

20 are severely osteopenic because of enhanced bone resorption.

21 itional knockout mice alleviated progressive bone resorption.

22 tin, increases bone formation, and decreases bone resorption.

23 , enhanced osteoclastogenesis, and increased bone resorption.

24 ze into bone tissue by inducing osteoclastic bone resorption.

25 by increasing bone formation and decreasing bone resorption.

26 ttract osteoclast precursors to induce local bone resorption.

27 -induced osteoclastogenesis and inflammatory bone resorption.

28 steoblasts, is a major negative regulator of bone resorption.

29 umor-1 antisense RNA to control pathological bone resorption.

30 re insertion to minimize future peri-implant bone resorption.

31 nd cortical bone osteopenia due to increased bone resorption.

32 catenin pathway and Runx2 that contribute to bone resorption.

33 marrow stromal cells and systemic effects on bone resorption.

34 homeostatic bone remodeling and pathological bone resorption.

35 ation in osteoclasts, a process required for bone resorption.

36 lays a key role in bacteria-induced alveolar bone resorption.

37 ely regulates osteoclast differentiation and bone resorption.

38 gin, mode of bone formation and pathological bone resorption.

39 ifferentiation and inhibition of OC-directed bone resorption.

40 stimulated RANKL in osteoblasts and parietal bone resorption.

41 ccharide (LPS) from P. gingivalis stimulates bone resorption.

42 to augmented osteoclast differentiation and bone resorption.

43 h, in turn, increases osteoclastogenesis and bone resorption.

44 s PTH-induced osteoclast differentiation and bone resorption.

45 mass as the result of defective osteoclastic bone resorption.

46 e formation that was accompanied by elevated bone resorption.

47 growth in the bone environment and inhibited bone resorption.

48 iodontitis in mice, as evidenced by alveolar bone resorption.

49 ynamic MTs and podosomes interact to control bone resorption.

50 acrophages into gingival tissue and alveolar bone resorption.

51 an increased bone formation rate and reduced bone resorption.

52 nt cells (MGCs) of the monocytic lineage, is bone resorption.

53 d by osteoclasts, plays an important role in bone resorption.

54 organized in a belt, a feature critical for bone resorption.

55 ensity and bone formation and with decreased bone resorption.

56 and oestrogen deficiency-mediated pathologic bone resorption.

57 ion, Wnt4 inhibited osteoclast formation and bone resorption.

58 ction of Ac45 in periapical inflammation and bone resorption.

59 bolic events that are caused by osteoclastic bone resorption.

60 ly correlated with the difference in palatal bone resorption.

61 Boldine inhibited the alveolar bone resorption.

62 scription factor on osteoclast formation and bone resorption.

63 opment that promotes both bone formation and bone resorption.

64 dification, extracellular acidification, and bone resorption.

65 ediated bone formation and osteoclast-driven bone resorption.

66 progression and causes muscle catabolism and bone resorption.

67 caused JE degeneration, PDL destruction, and bone resorption.

68 rgets for diseases associated with excessive bone resorption.

69 Osteoclasts are the cells responsible for bone resorption, a process that is essential for the mai

70 tory cytokines and its influence on alveolar bone resorption (ABR) in rats.

71 th and bone, periosteal reaction, serpentine bone resorption, abscess formation, and root penetration

72 During bone resorption, abundant factors previously buried in t

73 tic bone formation activity nor osteoclastic bone resorption activity in vivo.

74 st, in functional osteo-assays, we show that bone resorption activity of D2J osteoclasts is dramatica

75 eased expression of osteoclastic markers and bone resorption activity, as well as decreased expressio

76 for cardiomyocyte hypertrophy and osteoclast bone resorption activity.

77 as associated with a significant decrease in bone resorption and a marked reduction in number of oste

78 as associated with a significant decrease in bone resorption and a marked reduction in the number of

79 Tgif2 deletion reduces bone resorption and abolishes miR-34a regulation.

80 d with an increase in osteoclastogenesis and bone resorption and an increase in the pool of monocytes

81 simultaneously inhibits osteoclast-mediated bone resorption and attenuates dendritic cell-mediated i

82 d protein (PTHrP) is a critical regulator of bone resorption and augments osteolysis in skeletal mali

83 of ZOL administered at ART initiation blunts bone resorption and BMD loss at key fracture-prone anato

84 of ZOL administered at ART initiation blunts bone resorption and BMD loss at key fracture-prone anato

85 ells and/or T cells, accompanied by enhanced bone resorption and BMD loss.

86 (sh) mice exhibited osteopenia with elevated bone resorption and bone formation at 6- and 9-week-old.

87 The balance between bone resorption and bone formation is vital for maintena

88 omorphometry measurements revealed that both bone resorption and bone formation parameters were incre

89 eoporosis results from the imbalance between bone resorption and bone formation, and restoring the no

90 ipal role in determining the balance between bone resorption and bone formation.

91 ation, thereby creating an imbalance between bone resorption and bone formation.

92 suggesting that Hdac3 regulates coupling of bone resorption and bone formation.

93 the LAT1-mTORC1 axis plays a pivotal role in bone resorption and bone homeostasis by modulating NFATc

94 ls had impaired ability to protect mice from bone resorption and bone loss in response to high-dose r

95 tosis of osteocytes and osteoblasts precedes bone resorption and bone loss with reduced mechanical st

96 In terms of bone resorption and bone quality parameters, no implant

97 ent significantly inhibits regional alveolar bone resorption and contributes to periodontal healing i

98 d bone remodeling, as confirmed by increased bone resorption and decreased bone formation, and signif

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

100 generally sufficient to prevent increases in bone resorption and decreases in BMD in men.

101 Enhanced osteoclast-mediated bone resorption and diminished formation may promote bon

102 es tumor growth and osteolysis by inhibiting bone resorption and enhancing bone formation.

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

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

105 The discovery of key pathways regulating bone resorption and formation has identified new approac

106 (PD) is characterized by focal and dramatic bone resorption and formation.

107 ers key insights into mechanisms that couple bone resorption and formation.

108 target osteoclasts (OCLs) block both pagetic bone resorption and formation; therefore, PD offers key

109 Alveolar bone resorption and gingival collagen fibers were histol

110 model of periodontitis by measuring alveolar bone resorption and gingival IL-17 expression as outcome

111 ay 14, there were no differences in alveolar bone resorption and gingival RANKL expression between mi

112 s implicated in sterile inflammation-induced bone resorption and has been shown to increase the bone-

113 atin (ATV) are known to inhibit osteoclastic bone resorption and have been proposed to have osteostim

114 inflammation associated with aging promotes bone resorption and impairs bone formation.

115 isrupts PKCzeta activity, cell polarity, and bone resorption and increases secretion of bone-forming

116 hould decrease calcium excretion by reducing bone resorption and increasing renal calcium reabsorptio

117 Tooth extraction results in alveolar bone resorption and is accompanied by postoperative swel

118 is, which are characterized by high rates of bone resorption and loss of bone mass, may benefit from

119 administered orally, inhibited the alveolar bone resorption and modulated the Th17/Treg imbalance du

120 Alveolar bone resorption and myeloperoxidase activity were statis

121 , which is determined by osteoclast-mediated bone resorption and osteoblast-mediated bone formation,

122 Bisphosphonates used for treatment inhibit bone resorption and prevent bone loss but fail to influe

123 generation by inhibiting osteoclast-mediated bone resorption and promoting osteoblast-mediated osteog

124 ckout and heterozygous mice exhibit elevated bone resorption and reduced bone mass.

125 pression of Ocy-derived factors that promote bone resorption and suppress bone formation.

126 isease is mediated by increased osteoclastic bone resorption and suppressed bone formation.

127 ic lesions that rarely heal due to increased bone resorption and suppressed bone formation.

128 prone to pathologic changes and, ultimately, bone resorption and tooth loss.

129 ion of periapical tissues, leading to severe bone resorption and tooth loss.

130 comprises two processes: the removal of old bone (resorption) and the laying down of new bone (forma

131 eoclastogenic cytokine production, stimulate bone resorption, and cause trabecular bone loss, demonst

132 acrophage recruitment, osteoclast formation, bone resorption, and cortical and trabecular bone loss.

133 ct, extensive peri-implantitis with advanced bone resorption, and extensive inflammation with granula

134 rocesses including cell invasion, migration, bone resorption, and immune surveillance.

135 ecretion, reduced osteoclast recruitment and bone resorption, and impaired osteoblast-mediated bone f

136 Bacterial colonization, bone resorption, and implant inflammation were evaluated

137 used very high interfacial strains, marginal bone resorption, and no improvement in implant stability

138 ng on stimulating bone formation, inhibiting bone resorption, and promoting angiogenesis in OVX mice.

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

140 s encapsulation induces more severe alveolar bone resorption, and whether this bone loss is associate

141 indicated to attenuate physiologic alveolar bone resorption as a consequence of tooth extraction.

142 ysis adopting the amount of palatal alveolar bone resorption as a dependent variable demonstrated tha

143 ivo allografts, in vitro gene expression and bone resorption assays.

144 ES on the inflammatory response and alveolar bone resorption associated with ligature-induced periodo

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

146 sufficient to significantly inhibit alveolar bone resorption associated with the experimental periodo

147 ty plays a relevant role in inflammation and bone resorption associated with the LPS model of experim

148 normal, high alkaline phosphatase, and high bone resorption biomarker.

149 iated with the severity of periodontitis and bone resorption biomarkers.

150 d between the periodontal parameters TOS and bone resorption biomarkers.

151 on in older people and may lead to increased bone resorption, bone loss, and increased falls and frac

152 e milk, a process that involves osteoclastic bone resorption but also osteocytes and perilacunar reso

153 et, osteoporosis drugs that not only inhibit bone resorption but also stimulate bone formation, such

154 HIF-2alpha knockdown did not affect bone resorption but moderately inhibited osteoclast form

155 deficiency did not increase serum markers of bone resorption, but elevated serum markers of bone form

156 PD-associated mutation, exhibited increased bone resorption, but not formation.

157 ng RANKL and BMPs, in osteoclastogenesis and bone resorption by ablating p38alpha MAPK in LysM+monocy

158 Enhanced bone resorption by infiltrating macrophages has been pro

159 blocks PTH-induced osteoclast formation and bone resorption by its additional effect to inhibit RANK

160 reduced P. gingivalis infection and alveolar bone resorption by modulating the host immune response.

161 determine whether boldine inhibits alveolar bone resorption by modulating the Th17/Treg imbalance du

162 elevating bone formation by OBs and reducing bone resorption by OCs.

163 Excessive bone resorption by osteoclasts (OCs) can result in serio

164 and testosterone (T), which thereby inhibits bone resorption by osteoclasts and stimulates bone forma

165 and testosterone in bone, thereby inhibiting bone resorption by osteoclasts and stimulating bone form

166 Bone resorption by osteoclasts is essential for bone hom

167 OC-iTcREG also limit bone resorption by osteoclasts, forming a negative feedb

168 aB ligand (RANKL), an essential cytokine for bone resorption by osteoclasts.

169 em in both bone formation by osteoblasts and bone resorption by osteoclasts.

170 n the bone remodeling process and stimulates bone resorption by osteoclasts.

171 ge activity of DOCK5, which is essential for bone resorption by osteoclasts.

172 by mature OCs but is critically involved in bone resorption by stimulating extracellular acidificati

173 imulates periosteal osteoclast formation and bone resorption by stimulating RANKL in osteoblasts via

174 uggested that the inhibition of osteoclastic bone resorption by these compounds did not result from t

175 rom bone matrix, pharmacologic inhibition of bone resorption by zoledronate attenuates inflammasome a

176 ime with blood lead and plasma biomarkers of bone resorption (C-terminal telopeptides of type I colla

177 These cytokines enhanced the bone resorption capacity of uninfected mature osteoclast

178 d downstream signaling resulting in impaired bone resorption capacity.

179 senchymal stem cell-derived osteoblasts, and bone resorption, carried out by monocyte-derived osteocl

180 cantly (p < 0.01) less P. gingivalis-induced bone resorption compared with controls in BALB/c and C57

181 trabecular bone in vivo was due to decreased bone resorption, consistent with the reduced receptor ac

182 ice, arthritis was associated with increased bone resorption, decreased bone formation, and significa

183 Outcomes assessed were bone resorption, detection of tartrate-resistant acid ph

184 gif1 in osteoblasts and osteocytes decreases bone resorption due to an increased secretion of Semapho

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

186 However, the effect of boldine on alveolar bone resorption during periodontitis has not been elucid

187 collagen degradation, is a key biomarker of bone resorption during the bone remodeling process.

188 Glucocorticoids mainly increase bone resorption during the initial phase (the first year

189 ore, during and after HIT running attenuates bone resorption, effects that are independent of energy

190 acute training session attenuated markers of bone resorption, effects that are independent of energy

191 Osteopenia occurs where the rate of bone resorption exceeds that of bone formation, so we in

192 es that there was a significant reduction in bone resorption following 3 months of SPI supplementatio

193 Hence, its actions on alveolar bone resorption, gingival collagen content and key infla

194 nhibited osteoclast actin-ring formation and bone resorption in a dose-dependent manner.

195 bitor to assess its role in inflammation and bone resorption in a murine model of lipopolysaccharide

196 used to assess its role in inflammation and bone resorption in a murine model of lipopolysaccharide

197 2 overexpression in the ethiopathogenesis of bone resorption in aggressive and chronic periodontitis.

198 patients compromised their ability to induce bone resorption in an ex vivo organ culture system.

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

200 thickness is a strong predictor of alveolar bone resorption in both groups.

201 TNF-alpha to induce osteoclast formation and bone resorption in DAP12-deficient animals.

202 ystemic melatonin administration on alveolar bone resorption in experimental periodontitis in rats.

203 to both stimulate bone formation and inhibit bone resorption in humans.

204 F knockdown only affected glucose uptake and bone resorption in hypoxic conditions.

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

206 d positive feedback mechanism that amplifies bone resorption in pathologic conditions of accelerated

207 y provides a potential strategy for treating bone resorption in patients with myeloma by counteractin

208 The exact mechanisms of bone resorption in periodontitis have not been fully elu

209 over markers (BTMs) demonstrated presence of bone resorption in PIM; between comparable diagnostic ra

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

211 t cell pool, osteoclast differentiation, and bone resorption in response to receptor activator of nuc

212 eralized osteopenia associated with enhanced bone resorption in the cancellous bone compartment and w

213 Therefore, bone resorption in the mother becomes elevated during th

214 Furthermore, CX3CR1 knockout mice resist bone resorption in the oral cavity following challenge w

215 oral dysbiosis led to a local inhibition of bone resorption in the presence of ligature-induced peri

216 The importance of osteoclast-mediated bone resorption in the process of osseointegration has n

217 bers, it suppressed actin-ring formation and bone resorption in these assays.

218 tiation or viability, it efficiently blocked bone resorption in vitro and in vivo and consequently am

219 exacerbate synovial inflammation in vivo and bone resorption in vitro, suggesting that LTB4 and BLT1

220 fferent doses of CMC2.24 on inflammation and bone resorption in vivo and also to describe on the effe

221 play a significant role in inflammation and bone resorption in vivo and that Caspase-1 has a pro-res

222 iciently decarboxylated and activated during bone resorption, inactivation of furin in osteoblasts in

223 es express genes required in osteoclasts for bone resorption, including cathepsin K (Ctsk), and lacta

224 gingivalis plays a key role in the alveolar bone resorption induced during periodontitis, and this b

225 use model of P. gingivalis-induced calvarial bone resorption, injection of mmu-miR-155-5p or anti-mmu

226 The alveolar bone resorption is a distinctive feature of periodontiti

227 Bone resorption is a severe consequence of inflammatory

228 reas in modern humans extensive osteoclastic bone resorption is found in the same regions.

229 peri-implant bone develops micro-fractures, bone resorption is increased, and bone formation is decr

230 Because bone resorption is largely unaltered, OSM could represen

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

232 eads to superfluous osteoclast formation and bone resorption, is widespread in the pathologic bone lo

233 Although chloroquine had no effect on basal bone resorption, it inhibited parathyroid hormone- and o

234 The 11 days of ligature induced bone resorption, low levels of BALP, leukocyte infiltrat

235 aded mice exhibited high serum levels of the bone resorption marker C-telopeptide fragments of type I

236 rmone as well as a transient decrease in the bone resorption marker C-telopeptide of type I collagen

237 Primary outcome was change in bone resorption marker C-terminal telopeptide of collage

238 Compared to male WT mice, serum bone resorption marker in male Keap1 Ht mice was signifi

239 The pattern of bone resorption markers was consistent with accelerated

240 elopment and modeling, rather than excessive bone resorption, may be the underlying pathophysiology o

241 loss mouse model and RANKL-injection-induced bone resorption model, we found that administration of X

242 arkers after parathyroidectomy suggests that bone resorption normalizes earlier than bone formation.

243 ice had increased mechanical loading-induced bone resorption, number of osteoclasts, and expression o

244 Our data indicate that the increase in bone resorption observed in states of estrogen deficienc

245 15 implants demonstrated a peri-implant mean bone resorption of 2.96 mm increased bone loss, yielding

246 Here we show that bone resorption of differentiated osteoclasts heavily re

247 Bone resorption of osteoclasts from subchondral bone and

248 udosubstrate restores osteoclastogenesis and bone resorption of Phlpp1-deficient osteoclasts.

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

250 , and alendronic acid, a potent inhibitor of bone resorption, optimally linked through a differential

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

252 lium, periodontal pocket formation, alveolar bone resorption, osteoclast activation, bacterial invasi

253 P. gingivalis and four other TLR2 ligands on bone resorption, osteoclast formation, and gene expressi

254 CMC2.24 inhibited bone resorption, osteoclastogenesis, and tumor necrosis

255 e in promoting bone formation and inhibiting bone resorption, our results suggest that Wnt4 signaling

256 Excessive bone resorption over bone formation is the root cause fo

257 tion as osteoclastogenic gene expression and bone resorption pit are increased.

258 assessed by using an osteologic plate assay (bone resorption pit formation).

259 Bone resorption pits in calvaria, observed by micro-comp

260 madelta T cells but were designed to inhibit bone resorption rather than treating cancer and have lim

261 ivation of matrix TGF-beta during osteoclast bone resorption recruits MSCs to bone-resorptive sites.

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

263 inflammatory diseases, their direct role in bone resorption remains unclear.

264 as PTH stimulation of RANKL, a stimulator of bone resorption, requires CRTC2.

265 steoblast activity and diminishes osteoclast bone resorption, shifting the balance of bone homeostasi

266 fy a mechanism for progenitor recruitment to bone resorption sites and Cxcl9l and Cxcr3.2 as potentia

267 ltifaceted processes of immunoregulation and bone resorption such as they occur in rheumatoid arthrit

268 nt rise in sympathetic output that increases bone resorption sufficiently to counteract its local ant

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

270 tors to increase differentiation and promote bone resorption, supporting the tenet that irisin not on

271 utants had increased osteoclast activity and bone resorption surrounding the extracted molar.

272 rains of P. gingivalis induced less alveolar bone resorption than the encapsulated W50 wild-type stra

273 ifferentiation but prevented the increase in bone resorption that occurs under hypoxic conditions.

274 mors in the bone promote osteoclast-mediated bone resorption that releases TGF-beta, which restrains

275 jacent alveolar bone, hyperloading activates bone resorption, the peak of which is followed by a bone

276 ated that XN inhibits osteoclastogenesis and bone resorption through RANK/TRAF6 signaling pathways.

277 osteoblastogenesis and inhibit osteoclastic bone resorption, thus promoting tissue regeneration.

278 disease initiated by bacteria, resulting in bone resorption, tooth loss, and systemic inflammation.

279 ts and C-terminal telopeptide release during bone resorption under distinct conditions.

280 Alveolar bone resorption was analyzed using microcomputed tomogra

281 whereas the expression of genes involved in bone resorption was higher in the AT-MSC group.

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

283 Bone resorption was measured by uCT and osteoclast numbe

284 t increase in osteoclast differentiation and bone resorption was observed with an increase in IL-17 l

285 Likewise, volumetric bone resorption was significantly higher in the control

286 Bone resorption was significantly reduced in Casp1-KO bu

287 ng a TNF-alpha-induced model of inflammatory bone resorption, we determined that RBP-J deficiency ena

288 increased by 25-40%, and the osteoclasts and bone resorption were suppressed by 50% in NTAP-Ti in viv

289 f giant hypernucleated osteoclasts, enhanced bone resorption when cultured on bone slices, and altere

290 entify and map fields of bone deposition and bone resorption, which affect the development of the fac

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

292 zation of these bone defects revealed active bone resorption, which is suppressed by Wnt activation i

293 enosumab fully inhibits teriparatide-induced bone resorption while allowing for continued teriparatid

294 Odanacatib, a cathepsin K inhibitor, reduces bone resorption while maintaining bone formation.

295 disrupted c-Kit signaling couples increased bone resorption with bone formation through osteoclast-d

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

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

298 bone loss mediated by excessive osteoclastic bone resorption without affecting osteoblastic activity

299 ealed an increased number of osteoclasts and bone resorption, without a decrease in osteoblast number

300 its pharmacologic action as an inhibitor of bone resorption, yet CT-deficient mice display increased