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

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

5 ed by osteolytic bone lesions with uncoupled bone remodeling.

6 with respect to the mathematical modeling of bone remodeling.

7 inking endothelium-dependent vasodilation to bone remodeling.

8 between chronic heart failure and catabolic bone remodeling.

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

10 normalities of postnatal skeletal growth and bone remodeling.

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

12 ntal ligaments may link mechanical strain to bone remodeling.

13 rder characterized by focal abnormalities of bone remodeling.

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

15 eir progenitors does not contribute to adult bone remodeling.

16 mits rapid exchange of factors important for bone remodeling.

17 ration of cells involved in osteogenesis and bone remodeling.

18 process on local bone formation and resident bone remodeling.

19 ability to suppress osseous angiogenesis and bone remodeling.

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

21 ce relevant bone formation but also resident bone remodeling.

22 ferent from those that affect later marginal bone remodeling.

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

24 vivo variable state of phosphorylation with bone remodeling.

25 essential for proper osteoblast activity and bone remodeling.

26 etion in osteoblasts only does not influence bone remodeling.

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

28 ofound inhibition of osteoclast function and bone remodeling.

29 appaB ligand stimulation to initiate greater bone remodeling.

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

31 99m)Tc-methylene diphosphonate (MDP) reflect bone remodeling.

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

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

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

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

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

37 mmation, immunity mediated by Th1 cells, and bone remodeling.

38 nzymatic activity did not affect normal long bone remodeling.

39 type IA receptor for BMP) in osteoblasts for bone remodeling.

40 like cells and have critical implications in bone remodeling.

41 OS and RANKL in a manner leading to positive bone remodeling.

42 development and activation of osteoclasts in bone remodeling.

43 roteinases are involved in the regulation of bone remodeling.

44 OPN as an osteoclast autocrine factor during bone remodeling.

45 of CaP growth in bone through inhibition of bone remodeling.

46 eptors (GPCRs) play a key role in regulating bone remodeling.

47 phenotype is expressed during the process of bone remodeling.

48 plays a critical role in bone resorption and bone remodeling.

49 feration and migration of osteoblasts during bone remodeling.

50 hesize that OCLs participate in pathological bone remodeling.

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

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

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

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

55 olytic functions in antigen presentation and bone remodeling.

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

57 regulators of osteoclast differentiation and bone remodeling.

58 hannels is detrimental to cell viability and bone remodeling.

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

60 formation, temporally and spatially coupling bone remodeling.

61 signaling for osteoclast differentiation and bone remodeling.

62 se findings are presumed to represent normal bone remodeling.

63 se mice substantially rescued the defects of bone remodeling.

64 Thus, bisphosphonate drastically inhibited bone remodeling.

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

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

67 hich the sympathetic nervous system controls bone remodeling.

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

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

70 Bone remodeling, a coupled process involving bone resorp

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

72 he role of the ADP-ribosyl cyclase, CD38, in bone remodeling, a process by which the skeleton is bein

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

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

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

76 acid (RGD) peptide, agents known to perturb bone remodeling, adjacent to maxillary molars in rats.

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

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

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

80 n of bone formation will cause a decrease in bone remodeling and a continued increased risk of fractu

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

82 e hormone functioning as a major mediator of bone remodeling and as an essential regulator of calcium

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

84 receptor) in osteoblastic cells to regulate bone remodeling and calcium homeostasis.

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

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

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

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

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

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

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 athyroid hormone (PTH) plays a major role in bone remodeling and has the ability to increase bone mas

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

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

98 L is highly expressed in areas of trabecular bone remodeling and inflammatory bone loss, is increased

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

100 Osteoclast activation is important for bone remodeling and is altered in multiple bone disorder

101 he major mediator of calcium homeostasis and bone remodeling and is now known to be an effective drug

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

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

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

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

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

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

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

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

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

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

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

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

128 and its receptor RANK are key regulators of bone remodeling, and they are essential for the developm

129 tion confers a unique osteogenic activity in bone remodeling, and this understanding may facilitate t

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

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

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

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

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

135 The ability to predict the amount of bone remodeling around implants is important for a stabl

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

137 te in patients that the magnitude of initial bone remodeling around these one-piece dental implants i

138 Transgenic mice demonstrated enhanced bone remodeling as well as enhanced urinary excretion of

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

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

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

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

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

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

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

146 ere they proliferate, and induce significant bone remodeling, bone destruction, and cancer pain.

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

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

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

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

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

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

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

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

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

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

157 Such bone remodeling caused disturbed bone mineralization and

158 A significant amount of bone remodeling compared to baseline occurred for all im

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

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

161 Bone remodeling compartments (BRCs) were recently recogn

162 Bone remodeling comprises balanced activities between os

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

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

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

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

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

168 Bone remodeling depends on the precise coordination of b

169 Bone remodeling depends upon proper osteoblast and osteo

170 Lingual bone remodeling did not reveal any significant differenc

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

198 Continuous bone remodeling in response to mechanical loading is cri

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

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

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

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

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

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

205 Changes in bone remodeling induced by pharmacological and genetic m

206 Bone remodeling involves the removal of old or damaged b

207 Healthy bone remodeling is a balanced and dynamic equation betwe

208 Bone remodeling is a balanced process between bone synth

209 Bone remodeling is a complex process that must be precis

210 Bone remodeling is a continuous process of osteoblastic

211 of mature lamellar bone formation and active bone remodeling is a relatively common and unexpected fi

212 Bone remodeling is age-dependently regulated and changes

213 Bone remodeling is characterized by tethering of the act

214 Bone remodeling is controlled by dual actions of osteocl

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

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

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

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

219 Buccal bone remodeling is significantly more extensive around i

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

221 Increased bone remodeling, leading to microarchitectural deteriora

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

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

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

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

226 We measured soluble RANKL (sRANKL), OPG, and bone remodeling markers in 121 patients with newly diagn

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

228 sRANK-Fc also reduced systemic bone remodeling markers, including serum osteocalcin and

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

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

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

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

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

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

235 formation of new bone during the process of bone remodeling occurs almost exclusively at sites of pr

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

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

238 It has been suggested that subchondral bone remodeling plays a role in the progression of osteo

239 Subchondral bone remodeling plays an important role in the pathogene

240 egulates osteogenesis during development and bone remodeling postnatally.

241 ement include anticipating future growth and bone remodeling potential, minimizing physeal injury, an

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

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

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

245 The bone remodeling process within the spine was assessed by

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

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

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

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

250 hese microstrains on the bone may affect the bone remodeling rate in a direct relationship.

251 Recent reports suggest that the bone remodeling rate next to an implant may be used to e

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

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

254 Bone remodeling remained stable with a slight increase,

255 Normal bone remodeling requires a tight coupling of bone resorp

256 Bone remodeling requires bone resorption by osteoclasts,

257 Bone remodeling requires osteoclasts to generate and mai

258 ontrols mineralized cartilage resorption and bone remodeling, respectively.

259 are in the mild overload zone, an increased bone remodeling response occurs, which results in a reac

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

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

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

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

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

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

266 del results corroborate all behaviors of the bone remodeling system that we have simulated, including

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

268 as to investigate the amount of radiographic bone remodeling that occurs over time using a one-piece

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 Exercise promotes positive bone remodeling through controlling cellular processes i

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

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

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

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

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

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

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

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 a process involving perturbations of normal bone remodeling, was tested.

283 To investigate the role of BMPs during bone remodeling, we generated a postnatal osteoblast-spe

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

285 Genes associated with OA and bone remodeling were identified.

286 bone with hematopoietic elements and active bone remodeling were present in 36 valves (13%) with dys

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

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

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

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

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

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

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

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

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

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

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