ライフサイエンスコーパス: bone remodeling

1 grades; grades ranged from 0 (healthy) to 6 (bone remodeling).

2 sociated from the later phase (activation of bone remodeling).

3 olytic functions in antigen presentation and bone remodeling.

4 hanisms of IL-33/ST2 in mechanically induced bone remodeling.

5 regulators of osteoclast differentiation and bone remodeling.

6 hannels is detrimental to cell viability and bone remodeling.

7 formation, temporally and spatially coupling bone remodeling.

8 nes and chemokine receptors as regulators of bone remodeling.

9 signaling for osteoclast differentiation and bone remodeling.

10 se findings are presumed to represent normal bone remodeling.

11 se mice substantially rescued the defects of bone remodeling.

12 Thus, bisphosphonate drastically inhibited bone remodeling.

13 e in mediating the effects of fatty acids on bone remodeling.

14 way because of its common role in cancer and bone remodeling.

15 hich the sympathetic nervous system controls bone remodeling.

16 e of sympathetic nerves in the regulation of bone remodeling.

17 rizzled 8 (Fzd8) as a candidate regulator of bone remodeling.

18 ed by osteolytic bone lesions with uncoupled bone remodeling.

19 with respect to the mathematical modeling of bone remodeling.

20 inking endothelium-dependent vasodilation to bone remodeling.

21 between chronic heart failure and catabolic bone remodeling.

22 on, but has minimal effects on physiological bone remodeling.

23 normalities of postnatal skeletal growth and bone remodeling.

24 protein, is essential for proper control of bone remodeling.

25 ntal ligaments may link mechanical strain to bone remodeling.

26 n the regulation of skeletal development and bone remodeling.

27 rder characterized by focal abnormalities of bone remodeling.

28 ked by the common themes of inflammation and bone remodeling.

29 eir progenitors does not contribute to adult bone remodeling.

30 mits rapid exchange of factors important for bone remodeling.

31 ration of cells involved in osteogenesis and bone remodeling.

32 between bone formation and resorption during bone remodeling.

33 process on local bone formation and resident bone remodeling.

34 ability to suppress osseous angiogenesis and bone remodeling.

35 e mechanical loading, which is essential for bone remodeling.

36 ce relevant bone formation but also resident bone remodeling.

37 ferent from those that affect later marginal bone remodeling.

38 system, play a crucial role in force-induced bone remodeling.

39 vivo variable state of phosphorylation with bone remodeling.

40 essential for proper osteoblast activity and bone remodeling.

41 etion in osteoblasts only does not influence bone remodeling.

42 hat TSHRs have a critical role in regulating bone remodeling.

43 ofound inhibition of osteoclast function and bone remodeling.

44 appaB ligand stimulation to initiate greater bone remodeling.

45 r-derived MT1-MMP may contribute directly to bone remodeling.

46 99m)Tc-methylene diphosphonate (MDP) reflect bone remodeling.

47 ion and function, which has consequences for bone remodeling.

48 MD at other sites and biochemical markers of bone remodeling.

49 lastic cells and therefore in the process of bone remodeling.

50 d by bone density and biochemical markers of bone remodeling.

51 ntional osteoclast precursors in homeostatic bone remodeling.

52 at acts as a novel osteoclastic inhibitor in bone remodeling.

53 m the aspect of microdamage accumulation and bone remodeling.

54 ot accurately distinguish osteomyelitis from bone remodeling.

55 ty, calcium kinetics studies, and markers of bone remodeling.

56 not only for long bone growth, but also for bone remodeling.

57 nt (bone modeling) that persist during adult bone remodeling.

58 HD) increase sympathetic tone and may affect bone remodeling.

59 hesize that OCLs participate in pathological bone remodeling.

60 (PTHR) regulates mineral-ion homeostasis and bone remodeling.

61 kidney, does not have a significant role in bone remodeling.

62 be removed by initiating endogenous targeted bone remodeling.

63 y a central role in skeletal development and bone remodeling.

64 Osteoprotegerin (OPG) is a key regulator of bone remodeling.

65 the unique and primary role of osteocytes in bone remodeling, a basic tenet of bone biology, raising

66 Bone remodeling, a coupled process involving bone resorp

67 The hormone leptin is a regulator of bone remodeling, a homeostatic function maintaining bone

68 apts to the change of mechanical stimulus by bone remodeling activities.

69 monstrated higher numbers of osteoclasts and bone remodeling activity in the OFP group, accompanied b

70 the absence of cystinosin primarily affects bone remodeling activity, apart from the influences of t

71 hem potent inhibitors of bone resorption and bone remodeling activity, with limited potential for sid

72 cid phosphatase in KO mice confirmed reduced bone remodeling activity.

73 etween different BM compartments in terms of bone-remodeling activity (BRA), blood volume fraction (B

74 Previous studies assessed bone remodeling after a single tooth extraction; however

75 e suitable noninvasive techniques to monitor bone remodeling after MR imaging-guided HIFU ablation.

76 ation with the primary tumor would result in bone remodeling alterations, and that platelets could fa

77 ith regard to the mechanical signals driving bone remodeling and adaptation through natural selection

78 udy identifies Tgif1 as a novel regulator of bone remodeling and an essential component of the PTH an

79 in the mechanical loading on improvement of bone remodeling and angiogenesis in a postmenopausal ost

80 capacity, playing key roles in steady-state bone remodeling and arthritic bone erosion.

81 eta or PTH signaling may reestablish coupled bone remodeling and be a potential therapy.

82 T cells are involved in bone remodeling and can induce osteoclastic resorption.

83 aving an important role in the regulation of bone remodeling and cancer progression and metastasis.

84 SMAD3 gene, which is known to play a role in bone remodeling and cartilage maintenance.

85 tion of TGF-beta alters MSC fate, uncoupling bone remodeling and causing skeletal disorders.

86 their impaired osteolytic activity distorts bone remodeling and contributes to the induction of oste

87 sults confirm the specific role of Sema4d in bone remodeling and demonstrate that significant increas

88 dentifies ESL-1 as an important regulator of bone remodeling and demonstrates that the modulation of

89 proteinase-13 (MMP-13), which is involved in bone remodeling and early stages of endochondral bone fo

90 ast-derived DPP4 as a potential link between bone remodeling and energy metabolism.

91 Despite its key role in bone remodeling and for being a highly sought-after drug

92 its receptor RANK are the key regulators for bone remodeling and for the activation of osteoclasts.

93 Postnatal bone remodeling and fracture healing provide evidence th

94 nd osteopontin (OPN) play important roles in bone remodeling and fracture healing.

95 synaptotagmin VII plays an important role in bone remodeling and homeostasis by modulating secretory

96 A stromal gene signature reflecting bone remodeling and immune-related pathways was upregula

97 cer patients showed extensive suppression of bone remodeling and implant failure.

98 s histologically observed, and modulated key bone remodeling and inflammatory mediators in rats with

99 as Sae-regulated factors promote pathologic bone remodeling and intraosseous bacterial survival.

100 ve osteoclastic bone erosion disrupts normal bone remodeling and leads to bone loss in many skeletal

101 nitor directly measured GFR, ensure that the bone remodeling and mineral effects are sustained, and d

102 cells that are important for maintenance of bone remodeling and mineral homeostasis.

103 d hormone levels and proteinuria, attenuated bone remodeling and mineral loss, and reduced eGFR in re

104 sion level of osteopontin, a known factor of bone remodeling and osteoblast differentiation, were red

105 NO regulates normal bone remodeling and pathological bone loss in part throu

106 ive cells that are important for homeostatic bone remodeling and pathological bone resorption.

107 significant differences in osseointegration, bone remodeling and periosteal reactions between groups

108 factor-beta1 (TGF-beta1) is released during bone remodeling and plays a part in maintenance of CML L

109 ing proper periodontal function and alveolar bone remodeling and point to dental dysfunction as causa

110 or inhibitor partially rescued the uncoupled bone remodeling and prevented the fractures.

111 identifies a dual mode of action of SSRIs on bone remodeling and suggests a therapeutic strategy to b

112 er, this study broadens our understanding of bone remodeling and suggests potential therapies to incr

113 relationship was found between the amount of bone remodeling and the location of the rough-smooth bor

114 The effects of c-Abl on BMP-2-induced bone remodeling and the underlying mechanisms are not we

115 ions of cortical bone, increases the rate of bone remodeling and tooth movement.

116 cell homeostasis, it plays central roles in bone remodeling and tumor invasiveness, making it a key

117 e concept that similar pathways control both bone remodeling and vascular calcification is widely acc

118 n implicated as a regulator of tumor growth, bone remodeling, and bone pain.

119 ilar markers, leading to tooth misalignment, bone remodeling, and craniofacial abnormalities.

120 l space and are needed for bone development, bone remodeling, and fracture repair.

121 ins as new players in osteoclastogenesis and bone remodeling, and highlight a potential regulation of

122 g innate immune responses trigger changes in bone remodeling, and how model systems can be leveraged

123 siologic processes, such as axonal guidance, bone remodeling, and immune cell development and traffic

124 indings suggest that MAGP1 is a regulator of bone remodeling, and its absence results in osteopenia a

125 ding restores OPOA by regulating subchondral bone remodeling, and may provide an effective method for

126 sts (OCs) and osteoblasts play a key role in bone remodeling, and MF monocytes, the OC precursors, ar

127 ells that is essential for fracture healing, bone remodeling, and osteogenesis.

128 ng pathways participate in the regulation of bone remodeling, and pathological negative balance in th

129 PPR signaling in osteocytes is required for bone remodeling, and receptor signaling in osteocytes is

130 iple mechanisms underlying the regulation of bone remodeling, and these involve not only the osteobla

131 meostasis, feeding behavior, fat deposition, bone remodeling, and vascular contractility.

132 has been shown that the dental follicle and bone remodeling are essential for tooth eruption.

133 iota immunomodulatory actions on physiologic bone remodeling are highly relevant in advancing the und

134 sis have shown that tumor-induced changes in bone remodeling are likely mediated by alterations in th

135 hic investigation is to analyze the alveolar bone remodeling around immediate implants placed in acco

136 The aim of this animal study is to analyze bone remodeling around platform-switching (PS) implants

137 Deletion of beta-catenin disturbed bone remodeling, as confirmed by increased bone resorpti

138 2) ITAM-coupled receptor plays a key role in bone remodeling, as patients with TREM-2 mutations exhib

139 iological pathway linking CHF with catabolic bone remodeling associated with an increased osteoporoti

140 mechanical insults, and may be important in bone remodeling associated with orthodontic tooth moveme

141 notch width in the DH animals indicates that bone remodeling at the ACL insertion site is a response

142 Until recently many studies of bone remodeling at the cellular level have focused on th

143 hat Prkaa1(-/-) mice had an elevated rate of bone remodeling because of increases in bone formation a

144 NK and osteoprotegerin are key regulators of bone remodeling but also influence cellular functions of

145 ng the tenet that irisin not only stimulates bone remodeling but may also be an important counter-reg

146 mily members not only regulate physiological bone remodeling but they are also implicated in the path

147 at lymphocyte RANKL is not involved in basal bone remodeling, but B cell RANKL does contribute to the

148 many of the existing mathematical models for bone remodeling, but can be used to explore aspects of t

149 Osteoclasts are essential for physiological bone remodeling, but localized excessive osteoclast acti

150 The regulation of bone remodeling by an adipocyte-derived hormone implies

151 hOSM and mLIF stimulate bone remodeling by both reducing osteocytic sclerostin a

152 vE1 modulates osteoclast differentiation and bone remodeling by direct actions on bone, rescuing OPG

153 ized that knee loading regulates subchondral bone remodeling by suppressing osteoclast development, a

154 n thought to be limited to the regulation of bone remodeling by the gonads.

155 Such bone remodeling caused disturbed bone mineralization and

156 Furthermore, we showed that bone remodeling compartment canopies arise from a mesenc

157 iginate from bone marrow perivascular cells, bone remodeling compartment canopy cells, or bone lining

158 Bone remodeling compartments (BRCs) were recently recogn

159 Bone remodeling comprises balanced activities between os

160 Bone remodeling consists of resorption by osteoclasts fo

161 Finally (18)F-fluoride, a marker of bone remodeling, correlated with the osteoblastic phenot

162 st that elevated [Ca2+]o following increased bone remodeling could facilitate metastatic localization

163 is a critical regulator of both arms of the bone remodeling cycle, its absence causing structural ch

164 k able to reproduce aspects of the different bone remodeling defective dynamics of osteomyelitis and

165 stablish a murine model for pathogen-induced bone remodeling, define Sae as critical for osteomyeliti

166 Bone remodeling depends on the precise coordination of b

167 Bone remodeling depends upon proper osteoblast and osteo

168 Lingual bone remodeling did not reveal any significant differenc

169 activity could be an effective treatment for bone remodeling diseases.

170 Thus, although inhibition of bone remodeling disturbed the bone marrow plasma cell ni

171 at the material's surface which facilitates bone remodeling due to binding of biomolecule moieties i

172 of c-Abl tyrosine kinase often show reduced bone remodeling due to impaired osteoblast and osteoclas

173 ry cytokines, including TNF, interferes with bone remodeling during inflammation through Ca(2+)-depen

174 ted tomography (microCT) method to visualize bone remodeling during S. aureus infection and discover

175 ibition of defined mediators of osteoclastic bone remodeling (e.g. receptor activator of nuclear fact

176 The short- (bone healing) and long-term (bone remodeling) effects of initial implant micromotion

177 recurrent fever, objective signs of abnormal bone remodeling, elevated CRP level or leukocytosis, and

178 We review the major diseases of bone remodeling, emphasizing our current understanding o

179 al and bone metastatic spread and subsequent bone remodeling events is highly relevant to successful

180 outlined by a cellular canopy separating the bone remodeling events on the bone surface from the marr

181 Although secondary osteonal bone remodeling existed in the C3H and B6 alveolar bone,

182 tion 3 (STAT3)-dependent osteoblast-mediated bone remodeling, explains why dysregulation of IL-23 res

183 emplifies an interesting class of targetable bone-remodeling factors expressed by normal and malignan

184 The drug may inhibit bone remodeling (formation and resorption), even in pati

185 Cherubism, a case of bone remodeling gone haywire, is associated with mutatio

186 ndamental understanding of the mechanisms of bone remodeling has led to the prospect of mechanism-bas

187 t signaling pathways are critical for normal bone remodeling; however, it is unclear if dysfunctional

188 Bone cells controlling bone remodeling (i.e. osteoblasts, osteoclasts, and oste

189 e unique anatomical structures implicated in bone remodeling in a widespread disease, such as post-me

190 local catabolic and anabolic signals during bone remodeling in addition to implying distinct mechani

191 the role of CCR3 in osteoclast formation and bone remodeling in adult mice is unknown.

192 is physiologically an important regulator of bone remodeling in adults.

193 bility through reduced tumor cell growth and bone remodeling in an intratibial mouse model.

194 osteogenesis and suggest that the defects in bone remodeling in faciogenital dysplasia may persist th

195 e therefore decided to investigate in detail bone remodeling in growing and mature TPH(1) knockout mi

196 bone mineral density (BMD) and biomarkers of bone remodeling in HIV/HCV coinfected patients.

197 significant changes in BMD nor biomarkers of bone remodeling in HIV/HCV-coinfected persons.

198 on of Keap1 improved bone mass by regulating bone remodeling in male mice.

199 , HEY2 decreases skeletal mass and regulates bone remodeling in male mice.

200 the transcription of many genes involved in bone remodeling in osteoblasts.

201 racterized by cartilage loss and subchondral bone remodeling in response to abnormal mechanical load.

202 Continuous bone remodeling in response to mechanical loading is cri

203 ion in osteocytes plays an important role in bone remodeling in response to mechanical loading; howev

204 t joint loading elicits abnormal subchondral bone remodeling in temporomandibular joint (TMJ) osteoar

205 on contrast material-enhanced MR images, and bone remodeling in the cortex was measured on CT images.

206 roup, thereby demonstrating a higher rate of bone remodeling in the presence of MSCs.

207 Hence the 2 h surface provided optimal bone remodeling in vitro conditions while reducing infec

208 FVIII.VWF complex is not required for normal bone remodeling in vivo.

209 tical for skeletal homeostasis and regulates bone remodeling, in part, by modulating the expression o

210 lay important roles in the cycle of targeted bone remodeling, in serving as a significant source of R

211 Changes in bone remodeling induced by pharmacological and genetic m

212 Bone remodeling involves the removal of old or damaged b

213 Healthy bone remodeling is a balanced and dynamic equation betwe

214 Bone remodeling is a balanced process between bone synth

215 Bone remodeling is a complex process that must be precis

216 Bone remodeling is a continuous process of osteoblastic

217 Bone remodeling is age-dependently regulated and changes

218 Bone remodeling is characterized by tethering of the act

219 Bone remodeling is controlled by dual actions of osteocl

220 Bone remodeling is essential for the repair and replacem

221 rmation, and restoring the normal balance of bone remodeling is highly desirable for identification o

222 Advancing the hypothesis that bone remodeling is intimately linked to metabolic homeos

223 st recruitment during adult human cancellous bone remodeling is lacking.

224 relevance of IL-33 and its receptor ST2 for bone remodeling is not well-defined.

225 Buccal bone remodeling is significantly more extensive around i

226 but delineating the role of this receptor in bone remodeling is still pending.

227 Increased bone remodeling, leading to microarchitectural deteriora

228 sion and pathophysiologic involvement of the bone remodeling ligand RANKL in this disease and the pot

229 lates numerous physiologic processes such as bone remodeling, lymph node organogenesis, central therm

230 emic status affects the relationship between bone remodeling markers and periodontal status.

231 condary endpoints included percent change in bone remodeling markers and vertebral volumetric BMD (vB

232 . gingivalis inoculation (P < 0.01), whereas bone remodeling markers OC, CTX, and P1NP were lowest in

233 osis and bone cell counts, and expression of bone remodeling markers, respectively.

234 sts, display high bone mass, suggesting that bone remodeling may also be subject to circadian regulat

235 n in diabetic skeleton and the corresponding bone remodeling mechanisms remain poorly understood.

236 the expression of Notch signaling molecules, bone remodeling mediators, and pro-inflammatory cytokine

237 cells and the cells directly responsible for bone remodeling, namely osteoclasts and osteoblasts.

238 insights into the role of the IGF-I gene in bone remodeling occur through several distinct mechanism

239 in general, clinically significant marginal bone remodeling occurred between the time of implant pla

240 ne mineral density consistent with increased bone remodeling occurred in MK-677 recipients.

241 at bone forming osteoblasts recruited during bone remodeling originate from bone marrow perivascular

242 this therapy did not influence tumor-induced bone remodeling, osteoblast proliferation, osteoclastoge

243 por signaling in osteoblasts is important in bone remodeling, particularly trabecular bone and endoge

244 The healing phase is followed by the bone-remodeling phase.

245 egulates osteogenesis during development and bone remodeling postnatally.

246 It participates in the bone remodeling process and stimulates bone resorption b

247 the importance of targeting both arms of the bone remodeling process for therapy of bone metastasis,

248 A growing understanding of the bone remodeling process suggests that inflammation signi

249 The bone remodeling process within the spine was assessed by

250 ntly increased the bone mass and delayed the bone remodeling process, resulting in slightly impaired

251 on of osteoclast-like cells, paralleling the bone remodeling process.

252 oclasts were regulated by T cells during the bone remodeling process.

253 key biomarker of bone resorption during the bone remodeling process.

254 accumulation of Ti particles may act on the bone-remodeling process and impact both long- and short-

255 vealed a strong positive correlation between bone remodeling rates, mitotic activity, and osteotomy s

256 ays affects skeletal development, as well as bone remodeling, regeneration, and repair during a lifes

257 Bone remodeling remained stable with a slight increase,

258 Normal bone remodeling requires a tight coupling of bone resorp

259 Bone remodeling requires bone resorption by osteoclasts,

260 Bone remodeling requires osteoclasts to generate and mai

261 ontrols mineralized cartilage resorption and bone remodeling, respectively.

262 ls in bone, are thought to initiate adaptive bone remodeling responses via osteoblasts and osteoclast

263 s under conditions which dissociates the two bone remodeling stages, viz., resorption by osteoclasts

264 t IGF-1 released from the bone matrix during bone remodeling stimulates osteoblastic differentiation

265 maximal strain but in a region of potential bone remodeling, suggesting that dendrite elongation may

266 inical study is to evaluate the radiographic bone remodeling, survival rate, and soft tissue health s

267 retion and blood pH balance, male fertility, bone remodeling, synaptic transmission, olfaction and he

268 Here we develop a cell population model of bone remodeling that includes the role of osteocytes, sc

269 be used to explore aspects of the process of bone remodeling that were previously beyond the scope of

270 Osteocytes are master orchestrators of bone remodeling; they control osteoblast and osteoclast

271 hyroid hormone (PTH) is a hormone regulating bone remodeling through its actions on both bone formati

272 may recruit osteoprogenitors to the site of bone remodeling through SIP and BMP6 and stimulate bone

273 ), one of the most-prescribed SSRIs, acts on bone remodeling through two distinct mechanisms.

274 , an essential process for the initiation of bone remodeling to maintain healthy bone mass and struct

275 Tumor cells disrupt normal bone remodeling to promote bone destruction and its asso

276 rolonged bisphosphonate therapy may suppress bone remodeling to the extent that normal bone repair is

277 herefore identified new regulatory events in bone remodeling under inflammatory conditions.

278 ms have been developed to model the adaptive bone remodeling under mechanical loads for orthopedic an

279 low and nerve-derived norepinephrine (NE) to bone remodeling under pathophysiological conditions rema

280 In contrast, resident bone remodeling was significantly influenced by the rhBM

281 ual relationship between glycemic status and bone remodeling was suggested recently.

282 ogical significance of OPG-HS interaction in bone remodeling, we created OPG knock-in mice (opg (AAA)

283 factor (NGF), administered when the pain and bone remodeling were first observed, blocks this ectopic

284 Genes associated with OA and bone remodeling were identified.

285 g pathways that impact both angiogenesis and bone remodeling were presented.

286 We show a role for Nbr1 in bone remodeling, where loss of function leads to perturb

287 receptor cascade as important regulators of bone remodeling, whereas its breakdown product, adenosin

288 or determinant of skeletal mass, governed by bone remodeling, which consists of bone resorption by os

289 The leptin regulation of bone remodeling, which has been documented through studi

290 acterial osteomyelitis triggers pathological bone remodeling, which in turn leads to sequestration of

291 ength throughout adult life requires ongoing bone remodeling, which involves coordinated activity bet

292 rder characterized by focal abnormalities of bone remodeling, which result in enlarged and deformed b

293 s indicating metabolic activity, hypoxia, or bone remodeling will be helpful for the characterization

294 en receptor modulators (SERMs) that suppress bone remodeling will change trabecular bone in ways such

295 bisphosphonate (BP) treatments that suppress bone remodeling will change trabecular bone in ways such

296 novel loading (4 N, 10 Hz, 5 min/d) altered bone remodeling with an increase in Wnt3a.

297 is the most exaggerated example of abnormal bone remodeling, with the primary cellular abnormality i

298 Coronal-load implants obviate resident bone remodeling without compromising local bone formatio

299 multifunctional protein with known roles in bone remodeling, wound healing, and normal and pathologi

300 Mechanical input is known to regulate bone remodeling, yet the molecular events involved in me