ライフサイエンスコーパス: bone resorption

1 creased bone formation and slightly hindered bone resorption.

2 ely regulates osteoclast differentiation and bone resorption.

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

4 ifferentiation and inhibition of OC-directed bone resorption.

5 ted estrogen deficiency leads to accelerated bone resorption.

6 stimulated RANKL in osteoblasts and parietal bone resorption.

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

8 to augmented osteoclast differentiation and bone resorption.

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

10 s PTH-induced osteoclast differentiation and bone resorption.

11 mass as the result of defective osteoclastic bone resorption.

12 e formation that was accompanied by elevated bone resorption.

13 growth in the bone environment and inhibited bone resorption.

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

15 ynamic MTs and podosomes interact to control bone resorption.

16 acrophages into gingival tissue and alveolar bone resorption.

17 an increased bone formation rate and reduced bone resorption.

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

19 microCT analysis was used to assess bone resorption.

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

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

22 ensity and bone formation and with decreased bone resorption.

23 and oestrogen deficiency-mediated pathologic bone resorption.

24 ion, Wnt4 inhibited osteoclast formation and bone resorption.

25 important gatekeepers of estrogen-controlled bone resorption.

26 cantly correlated with the level of alveolar bone resorption.

27 ss, whereas excess mechanical stress induces bone resorption.

28 is lifted and hypertrophied on initiation of bone resorption.

29 Cs to generate a list of genes implicated in bone resorption.

30 OC migration, SZ formation, and, ultimately, bone resorption.

31 as opposed to most other cancers that induce bone resorption.

32 ival connective tissue and reducing alveolar bone resorption.

33 Cs, which in turn would lead to more intense bone resorption.

34 rtant for osteoclastogenesis and TNF-induced bone resorption.

35 to, and patterning of, podosomes and reduced bone resorption.

36 metabolism via the H2 receptor, stimulating bone resorption.

37 rapeutic approach to diseases with increased bone resorption.

38 esulted in significantly reduced periodontal bone resorption.

39 blast number and function, but no changes in bone resorption.

40 nce for reduced bone formation and increased bone resorption.

41 ficient to induce neutrophil recruitment and bone resorption.

42 gingivalis infection-associated periodontal bone resorption.

43 increased LPS-induced osteoclastogenesis and bone resorption.

44 P5KIgamma-transduced osteoclasts compromises bone resorption.

45 ay be a risk factor for oxidative damage and bone resorption.

46 duction was largely attributable to elevated bone resorption.

47 lates the actin superstructures required for bone resorption.

48 llular acidification and osteoclast-mediated bone resorption.

49 ns against endocortical, but not cancellous, bone resorption.

50 culatory levels of pyridinoline, a marker of bone resorption.

51 de collagen and other matrix proteins during bone resorption.

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

53 id osteoclast formation/differentiation with bone resorption.

54 somal biogenesis-a necessary step for proper bone resorption.

55 el of osteoclast maturation and inflammatory bone resorption.

56 cell proliferation, and osteoclast-mediated bone resorption.

57 present a novel target to block pathological bone resorption.

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

59 ytokines, and a marked reduction in alveolar bone resorption.

60 ologic diseases is associated with excessive bone resorption.

61 iated bone formation and osteoclast-mediated bone resorption.

62 evels and bone mass apparently by inhibiting bone resorption.

63 ation, impairing proliferation, and delaying bone resorption.

64 amic equation between new bone formation and bone resorption.

65 asing the bone formation rate and depressing bone resorption.

66 eoprotegerin (OPG) signaling associated with bone resorption.

67 are severely osteopenic because of enhanced bone resorption.

68 itional knockout mice alleviated progressive bone resorption.

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

70 , enhanced osteoclastogenesis, and increased bone resorption.

71 ze into bone tissue by inducing osteoclastic bone resorption.

72 by increasing bone formation and decreasing bone resorption.

73 ttract osteoclast precursors to induce local bone resorption.

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

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

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

77 puted tomography analysis was used to assess bone resorption.

78 catenin pathway and Runx2 that contribute to bone resorption.

79 marrow stromal cells and systemic effects on bone resorption.

80 homeostatic bone remodeling and pathological bone resorption.

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

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

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

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

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

86 During bone resorption, abundant factors previously buried in t

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

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

89 Bone resorption activity was investigated by using a hum

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

91 y increasing OC formation and the consequent bone resorption activity.

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

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

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

95 e in trabecular bone volume due to decreased bone resorption and an increase in cortical bone due to

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

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

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

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

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

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

102 mal bone turnover requires tight coupling of bone resorption and bone formation to preserve bone quan

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

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

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

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

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

108 l effects on histopathological parameters of bone resorption and cartilage damage.

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

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

111 ce exhibit a severe osteopenia with elevated bone resorption and decreased bone mineralization.

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

113 decreased osteoblast activity and increased bone resorption and developed osteopenia at 6 months of

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

115 athyroidism, in which the transition between bone resorption and formation occurs optimally.

116 filtration and several parameters related to bone resorption and formation.

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

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

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

120 own of Atp6i/TIRC7 gene expression to target bone resorption and gingival inflammation simultaneously

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

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

123 overexpressing transgenic mice exhibit lower bone resorption and higher bone mass.

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

125 ed muscle contraction reversed elevations in bone resorption and increased Wnt signaling in bone-deri

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

127 esented immunomodulatory effects, decreasing bone resorption and inflammatory responses in a periodon

128 3rd principal stress range to promote direct bone resorption and insignificant OERR was between -9.92

129 sterone synthesis is positively regulated by bone resorption and insulin signaling in osteoblasts.

130 Increased bone resorption and largely unchanged bone formation res

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

132 Alveolar bone resorption and myeloperoxidase activity were statis

133 cell cultures and gavage with BaP stimulated bone resorption and osteoclastogenesis in vivo.

134 pression to simultaneously target periapical bone resorption and periapical inflammation.

135 herapeutic effects on inhibition of alveolar bone resorption and periodontal tissue destruction.

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

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

138 in triple knockout mice resulted in reduced bone resorption and recapitulated the high bone mass phe

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

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

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

142 d critical suppressor of osteoclastogenesis, bone resorption and the bone metastatic niche.

143 a potential strategy to prevent inflammatory bone resorption and to treat bone diseases.

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

145 mic resolution that made the localization of bone resorption and tumor extension detectable between d

146 hosphonate, is known to inhibit osteoclastic bone resorption and was proposed to have osteostimulativ

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

148 s gingivalis resulted in infection, alveolar bone resorption, and a significant increase in F4/80(+)

149 itis and loss of osseointegration), marginal bone resorption, and biologic complications (membrane pe

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

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

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

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

154 can inhibit endodontic disease development, bone resorption, and inflammation, indicating for the fi

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

156 y increased without significant increases in bone resorption, and their inhibition only partially res

157 nfection-induced gingival inflammation, oral bone resorption, and tooth loss.

158 ived S1P may recruit osteoblasts to sites of bone resorption as an initial step in replacing lost bon

159 Mice lacking Nod1 exhibit reduced bone resorption as well as impaired recruitment of neutr

160 completely rescues actin ring formation and bone resorption, as does VCL(P878A), which is incapable

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

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

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

164 teoclastogenesis, and prevented osteoclastic bone resorption but did not impair osteoblast differenti

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

166 mice from P. gingivalis infection-stimulated bone resorption by >85% and decreased the T-cell number

167 erapy reduced bacterial infection-stimulated bone resorption by 80% in the mouse model of endodontic

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

169 ssion in osteoblasts from male mice enhanced bone resorption by co-cultured splenocytes and induced i

170 Enhanced bone resorption by infiltrating macrophages has been pro

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

172 t RhoE is indispensable for OC migration and bone resorption by maintaining fast actin turnover in po

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

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

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

176 BE bound to bone slices and inhibited bone resorption by osteoclasts on BE-coated bone slices

177 Bone resorption by osteoclasts requires a large number o

178 Bone remodeling requires bone resorption by osteoclasts, bone formation by osteob

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

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

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

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

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

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

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

186 ts and that canonical Wnt signaling controls bone resorption by two different mechanisms.

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

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

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

190 d downstream signaling resulting in impaired bone resorption capacity.

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

192 During bone resorption, CatK and C4-S are co-localized at the r

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

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

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

196 Osteoclastic bone resorption depends upon the cell's ability to organ

197 Here, we observed increased bone resorption despite normal Opg production and a resi

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

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

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

201 The mean +/- SD bone resorption for all implants was 1.37 +/- 0.5 mm.

202 fter surgery, and values of implant marginal bone resorption for considered follow-ups.

203 phatemic rickets, and hypophosphatasia), and bone resorption (Gorham-Stout disease).

204 ading are known to cause osteoclast-mediated bone resorption; however, we hypothesize that osteocytic

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

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

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

208 nib (CP-690,550) affects osteoclast-mediated bone resorption in a rat adjuvant-induced arthritis (AIA

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

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

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

212 ggest that simvastatin prevents inflammatory bone resorption in experimental periodontitis, which may

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

214 al changes in bone associated with increased bone resorption in osteoporotic post-menopausal women.

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

216 it-C substances in the treatment of alveolar bone resorption in periodontal diseases.

217 Edema, inflammation, and osteoclast-mediated bone resorption in rats with AIA were dramatically reduc

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

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

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

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

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

223 on, we present evidence that the decrease in bone resorption in TPH(1)(-/-) mice is cell-autonomous.

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

225 s, and also between osteoclast formation and bone resorption in vitro.

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

227 In all mice, bone resorption induced by ligation plus P. gingivalis i

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

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

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

231 Because bone resorption is largely unaltered, OSM could represen

232 gingivalis infection-associated periodontal bone resorption is RANKL dependent and is accompanied by

233 ablished between bone-associated tumours and bone resorption is the central problem with therapeutic

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

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

236 Global deletion of Ctsk in mice decreases bone resorption, leading to osteopetrosis, but also incr

237 Increased osteoclastic bone resorption leads to periarticular erosions and syst

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

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

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

241 rmation markers and sustained decreases in a bone-resorption marker.

242 The pattern of bone resorption markers was consistent with accelerated

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

244 ) mice displayed extensive root and alveolar bone resorption, mediated by increased RANKL and the pre

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

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

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

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

249 15 implants demonstrated a peri-implant mean bone resorption of 2.96 mm increased bone loss, yielding

250 Bone resorption of osteoclasts from subchondral bone and

251 apped technique seemed to show less vertical bone resorption on the buccal aspect than the flapless t

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

253 tion of Ctsk in osteoblasts had no effect on bone resorption or BFR, demonstrating that the increased

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

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

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

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

258 nce in the amount of vertical and horizontal bone resorption (P >0.05) between groups.

259 gingival tissues (P < 0.01) and periodontal bone resorption (P < 0.05) were significantly elevated a

260 ased number of mature osteoclasts and higher bone resorption per osteoclast.

261 evels of MMP-13 are associated with alveolar bone resorption, periodontal ligament breakdown, and gin

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

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

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

265 the low-resorption graft material, and a low bone-resorption rate around implants was found.

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

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

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

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

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

271 increasing bone formation and inhibition of bone resorption, resulting in greater bone strength.

272 led to reduced bone formation and increased bone resorption, resulting in suboptimal peak bone mass

273 Male sex, high levels of bone resorption (serum type I collagen C-telopeptide), l

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

275 we determined the role of IL-17RA signal in bone resorption stimulated by dentoalveolar infections.

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

277 therapeutic target for diseases of excessive bone resorption, such as osteoporosis and arthritis.

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

279 ice had higher levels of horizontal alveolar bone resorption than sham-infected mice and an associate

280 the chemokine S1P couples bone formation to bone resorption through activation of kinase signaling p

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

282 carbon receptor (Ahr) to induce osteoclastic bone resorption through the activation of cytochrome P45

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

284 osteoblastic bone formation and osteoclastic bone resorption to maintain normal bone mass.

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

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

287 roles of TLR2 and TLR4 signaling in alveolar bone resorption, using a Porphyromonas gingivalis-associ

288 igature-induced, RANKL-dependent periodontal bone resorption via differential regulation of TLR2 and

289 in osteoblast number and function, although bone resorption was not affected.

290 rmed around the implant, and inflammation or bone resorption was not evident for both groups.

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

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

293 In contrast, osteoclast formation and bone resorption were both reduced in Avpr1alpha(-/-) cul

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

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

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

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

298 potently inhibited PTH-induced osteoclastic bone resorption with simultaneous new osteoid/bone forma

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