ライフサイエンスコーパス: osteocyte

1 our bones and accommodates a cell network of osteocytes.

2 n is suggested to induce RANKL expression in osteocytes.

3 e formation and Wnt/beta-catenin activity in osteocytes.

4 calized ACVR2A and ACVR2B to osteoblasts and osteocytes.

5 , becoming embedded in bone matrix as mature osteocytes.

6 dentified as novel markers of differentiated osteocytes.

7 ressive phase stimulates RANKL expression in osteocytes.

8 expression was recently found in osteoblasts/osteocytes.

9 creased loading was lost in mice depleted of osteocytes.

10 ion resulting from loss of WNT1 signaling in osteocytes.

11 come embedded in bone and differentiate into osteocytes.

12 ce to address the role of the GH/IGF axis in osteocytes.

13 of endoplasmic reticulum and mitochondria in osteocytes.

14 anied by positive effects on osteoblasts and osteocytes.

15 onic acid (ZOL), opened Cx43 hemichannels in osteocytes.

16 ion of CCL5 and matrix metalloproteinases in osteocytes.

17 vation was also obtained in isolated primary osteocytes.

18 ore than doubles this zone of dead and dying osteocytes.

19 sition, attenuates Saa3 expression in MLO-Y4 osteocytes.

20 which negatively regulates Wnt signaling in osteocytes.

21 required for constitutive Sost expression in osteocytes.

22 s expressed in osteoclasts, osteoblasts, and osteocytes.

23 ing in part by its action on osteoblasts and osteocytes.

24 rs, shouldering duties believed exclusive to osteocytes.

25 rentiating into adipocytes, chondrocytes, or osteocytes.

26 ation rich in osteoblasts and newly-embedded osteocytes.

27 nt to replicate the effects of fluid flow on osteocytes.

28 entiate further into chondrocytes and mature osteocytes.

29 of the cell (osteoblast, 12.68% vs. 13.68%; osteocyte, 15.74% vs. 5.37%).

30 live cell imaging to evaluate the effect of osteocytes, a mechanosensitive bone cell, on the migrato

31 ated by their capacity to differentiate into osteocytes, adipocytes, and chondrocytes.

32 The number of tibia cortical osteocytes also decreased, whereas serum SOST levels inc

33 Osteocytes also extend their influence beyond the local

34 or osteoclastogenesis, our data suggest that osteocytes also produce IFN-beta as an inhibitor of oste

35 n the number of activated caspase-3-positive osteocytes among groups and time points.

36 Osteocyte and osteocyte lacuna counts, percent bone matr

37 droxyapatite substrates, differentiated into osteocytes and applied a strain gradient to the samples.

38 real time and quantified Ca(2+) responses in osteocytes and bone surface cells in situ under controll

39 tors produce CD146(+), CD166(+) progenitors, osteocytes and CXCL12-producing stromal cells.

40 steocytes as assessed by RNA-seq in cultured osteocytes and following in vivo administration.

41 T gene, is produced postnatally primarily by osteocytes and is a negative regulator of bone formation

42 Female Tg mice had increased number of dying osteocytes and male Tg mice had a trend for more empty l

43 r of nuclear factor-kappaB ligand (RANKL) in osteocytes and mouse calvarial explants and preferential

44 Importantly, direct contact between osteocytes and multiple myeloma cells reciprocally activ

45 acterize the local mechanical environment of osteocytes and osteoblasts from healthy and osteoporotic

46 Apoptosis of osteocytes and osteoblasts precedes bone resorption and

47 sis of gene expression in mouse osteoblasts, osteocytes and osteoclasts.

48 volves osteoclastic bone resorption but also osteocytes and perilacunar resorption.

49 on induced by fluid shear stress in cultured osteocytes and stimulation of Piezo1 by a small molecule

50 gen control of B cell number is indirect via osteocytes and that the increase in bone marrow B cells

51 tinct roles of ATP and adenosine released by osteocytes and the activation of corresponding receptors

52 Neoteleost fish, however, lack osteocytes and yet are known to be capable of bone model

53 tion of mesenchymal stem cells, osteoblasts, osteocytes, and chondrocytes.

54 involves EphrinB2-RhoA-limited autophagy in osteocytes, and disruption leads to a bone fragility ind

55 subsets of these stromal cells, osteoblasts, osteocytes, and hypertrophic chondrocytes secrete a C-ty

56 ecular thinning, higher numbers of apoptotic osteocytes, and imbalanced metabolism, leading to defect

57 ess markers for osteoblasts, osteoclasts and osteocytes, and that bone matrix proteins are present in

58 nhibit resorption, prevented the increase in osteocyte apoptosis and osteocytic RANKL expression.

59 the importance of changes in osteoclast and osteocyte apoptosis in response to estrogen deficiency a

60 These results demonstrate that osteocyte apoptosis leads to increased osteocytic RANKL.

61 thickness was significantly associated with osteocyte apoptosis rates and osteoclasts numbers were i

62 Mechanistic studies revealed that osteocyte apoptosis was initiated by multiple myeloma ce

63 Sclerostin expression in osteocytes appeared to be reduced during periodontitis i

64 Osteocytes are an ancient cell, appearing in fossilized

65 Osteocytes are cells embedded in bone, able to modify th

66 Osteocytes are considered to be the major mechanosensory

67 s in individual osteoblasts, osteoclasts and osteocytes are limited and impair our ability to assess

68 Because osteocytes are major RANKL producers, we hypothesized th

69 Osteocytes are master orchestrators of bone remodeling;

70 Osteocytes are the most abundant but least understood ce

71 Osteocytes are the terminally differentiated cell type o

72 Living inhabitants of the hip bone (e.g. osteocytes) are visible in their local extracellular mat

73 Sclerostin and DKK1, both secreted mainly by osteocytes, are important Wnt inhibitors and as such can

74 lling tools created a zone of dead and dying osteocytes around the osteotomy.

75 tumor microenvironment, and they identified osteocytes as a critical mediator in the bone metastatic

76 this work identifies an anabolic function of osteocytes as a source of Wnt in bone development and ho

77 ibition mimics many of the effects of PTH in osteocytes as assessed by RNA-seq in cultured osteocytes

78 Despite progress in understanding osteocyte biology and function, much remains to be eluci

79 mRNA was expressed by odontoblasts (dentin), osteocytes (bone), and cementocytes (cellular cementum)

80 Osteocytes, but not surface cells, displayed repetitive

81 intracellular Ca(2+) responses of individual osteocytes by using a genetically encoded fluorescent Ca

82 It is known that osteocytes can sense changes in bone strain.

83 atigued ulnae had more severe disruptions of osteocyte canaliculi around linear microcracks.

84 osteocytic lacunae caused by bone-resorbing osteocytes cause the probe to fluoresce in vivo, thus al

85 Osteocyte cell adhesion supports FAK tyrosine phosphoryl

86 Conditioned media (CM) collected from MLO-Y4 osteocyte cells treated with bisphosphonates inhibited t

87 Osteocytes, cells ensconced within mineralized bone matr

88 Osteocytes, cells forming an elaborate network within th

89 sion of autophagy also reduced the amount of osteocyte cellular projections and led to retention of e

90 bone, alveolar bone, and cementum, including osteocyte/cementocyte marker dentin matrix protein 1 (Dm

91 Osteocytes communicate with osteoclasts and osteoblasts

92 Matrix-embedded osteocytes comprise more than 95% of bone cells and are

93 Tumor cells treated with MLO-A5 osteocyte-conditioned media (CM) decreased the tensile f

94 , late osteoblastic MLO-A5 cells, and MLO-Y4 osteocytes, consistent with findings using primary bone

95 The exact mechanisms by which osteocytes contribute to bone loss remain elusive.

96 Accumulation of senescent osteocytes contributes to deterioration of the periodont

97 nhibition of osteoclasts, demonstrating that osteocytes control osteoclasts differentiation through N

98 Hence, osteocytes coregulate bone and glucose homeostasis throu

99 cer cells were mediated by ATP released from osteocyte Cx43 hemichannels.

100 le was highly expressed at skeletal sites of osteocyte death and correlated with strong osteoclastic

101 data also suggest that reducing the zone of osteocyte death will improve osteotomy site viability, l

102 activation of osteoclasts after induction of osteocyte death, improved fracture repair, and attenuate

103 inflammation are characterized by excessive osteocyte death.

104 t activation and bone loss in the context of osteocyte death.

105 known about the regulation of osteoclasts by osteocyte death.

106 , including increased apoptosis of bystander osteocytes, decreased RANKL secretion, reduced osteoclas

107 Deletion of Tgif1 in osteoblasts and osteocytes decreases bone resorption due to an increased

108 tivation of the UPR in early differentiating osteocytes delays maturation, maintaining active bone sy

109 lactation and provides genetic evidence that osteocyte-derived Ctsk contributes not only to osteocyte

110 eloproliferation, suggesting that additional osteocyte-derived factors might be involved.

111 Elevated plasma levels of the osteocyte-derived hormone fibroblast growth factor 23 (F

112 Sclerostin is an osteocyte-derived inhibitor of osteoblast activity.

113 ontrol of bone-resorbing osteoclasts through osteocyte-derived RANKL is well defined, little is known

114 e expression and concomitant cleavage of the osteocyte-derived, phosphate-regulating hormone fibrobla

115 We hypothesized that alveolar bone osteocytes develop senescence characteristics in old age

116 However, Ca(2+) intensity within responding osteocytes did not change significantly with physiologic

117 tional hemichannels but not gap junctions in osteocytes did not display a significant difference.

118 aken together, the miR-23a cluster regulates osteocyte differentiation by modulating the TGF-beta sig

119 pproximately 24-2 (miR-23a cluster) promotes osteocyte differentiation.

120 EphrinB2-deficient osteocytes displayed more autophagosomes in vivo and in

121 timulatory subunit of G-protein (Gsalpha) in osteocytes (Dmp1-Gsalpha(KO) mice) have abnormal myelopo

122 Here, we find that suppression of osteocyte-driven perilacunar remodeling, a fundamental c

123 utonomous increase in Fgf23 secretion in Hyp osteocytes drives the accumulation of pyrophosphate thro

124 called perilacunar remodeling, bone-embedded osteocytes dynamically resorb and replace the surroundin

125 anotransduction phenomenon holds for in situ osteocytes embedded within a mineralized bone matrix und

126 ocytes, we prepared non-osteocytic cell-free osteocyte-enriched bone fragments (OEBFs).

127 Osteocyte-enriched fractions were used to characterize t

128 were significantly upregulated with aging in osteocyte-enriched samples.

129 g at the trabecular surfaces and in cortical osteocytes, epiphyseal chondrocytes, marrow adipocytes a

130 ucose variation would affect the function of osteocytes, essential regulators of bone homeostasis and

131 nt mechanism challenges current paradigms of osteocyte exclusivity in bone-modeling regulation, sugge

132 5 coreceptor specifically in osteoblasts and osteocytes exhibit the expected reductions in postnatal

133 In healthy bone tissue, osteocytes experience higher maximum strains (31,028 +/-

134 Osteocytes express genes required in osteoclasts for bon

135 Osteocytes express numerous G protein-coupled receptors

136 ting osteoporotic patients despite increased osteocyte-expressed RANKL.

137 to the morphological changes associated with osteocyte formation.

138 Sclerostin was expressed in osteocytes from bones from naive and myeloma-bearing mic

139 the factors that regulate differentiation of osteocytes from mature osteoblasts are poorly understood

140 c protein RANKL) in cultured osteoblasts and osteocytes from Notch2(tm1.1Ecan) mice.

141 mone both in vitro and in vivo, and protects osteocytes from oxidative stress.

142 Carbonic anhydrase III protects osteocytes from oxidative stress.

143 STZ) diabetic rat model and ex-vivo cultured osteocytes from these rats.

144 to examine the effects of glucose levels on osteocyte function and viability in vitro.

145 osteocalcin and Cobb angle indicate abnormal osteocyte function in adolescent idiopathic scoliosis.

146 s show that glucose levels directly regulate osteocyte function through sclerostin expression and sug

147 Recently, the role of osteocytes has been frequently addressed, with focus on

148 Osteocytes have a role in sensing and translating mechan

149 Osteocytes have emerged as key players in the developmen

150 ilt, stromal cells including fibroblasts and osteocytes have their own independent immunologic functi

151 /f) mice, in which SOCS3 has been ablated in osteocytes, have high trabecular bone volume and poorly

152 t group of specialized cells, also including osteocytes, hypertrophic chondrocytes, and odontoblasts.

153 cies (medaka), showing that although lacking osteocytes (i.e., internal mechanosensors), when loaded,

154 r in cementum in comparable fashion with the osteocyte in the skeleton, responding to changing tooth

155 Here, we report that osteocytes in a mouse model of human MM physically inter

156 y induced CCL7 may be to selectively protect osteocytes in an autocrine manner against glucocorticoid

157 ngs challenge the unique and primary role of osteocytes in bone remodeling, a basic tenet of bone bio

158 Furthermore, osteocytes in contact with multiple myeloma cells expres

159 r RANKL (TNFSF11) and sclerostin levels than osteocytes in control mice.

160 While long bone and alveolar bone osteocytes in Hyp mice overexpressed fibroblast growth f

161 e-derived bone cells to form osteoblasts and osteocytes in metaphyses.

162 y results in a narrow zone of dead and dying osteocytes in peri-implant bone that is not significantl

163 ne mineralizing activities of acid producing osteocytes in real time, thus allowing the study of thei

164 Finally, FGF23 is secreted by osteocytes in response to phosphate intake and binds to

165 CCL7 was increased in osteocytes in response to tooth movement in vivo.

166 uce measures of Wnt/beta-catenin activity in osteocytes in the loaded bone.

167 ble discoveries including the role played by osteocytes in the recruitment of immune cells, the invas

168 cal role of connexin (Cx) 43 hemichannels in osteocytes in the suppression of breast cancer bone meta

169 tiation of chondrocytes into osteoblasts and osteocytes in the TMJ.

170 nical stimulation has been widely studied in osteocytes in vitro and in bone explants, but has yet to

171 Mincle expression upon exposure to necrotic osteocytes in vitro and in vivo.

172 effect on MSCs induced to differentiate into osteocytes in vitro Our results indicate that CLCF1 bind

173 major mechanosensory cells of bone, but how osteocytes in vivo process, perceive, and respond to mec

174 lian SOST is expressed almost exclusively by osteocytes, in both medaka and zebrafish (a species with

175 In addition, Ctsk deletion in osteocytes increased bone Parathyroid Hormone related Pe

176 equencies examined, the number of responding osteocytes increased strongly with applied strain magnit

177 Here we reported that factors secreted by osteocytes increased the number of myeloid colonies and

178 his previously unrecognized, SOST-dependent, osteocyte-independent mechanism challenges current parad

179 to be capable of bone modeling, although no osteocyte-independent modeling regulatory mechanism has

180 igratory potential of tumor cells, and tumor-osteocyte interactions decrease the tension and motility

181 Therefore, a major arm of PTH signalling in osteocytes involves SIK inhibition, and small molecule S

182 ven in the context of nonskeletal cells, the osteocyte is perhaps among the least studied cells in al

183 Here, we examined whether RANKL produced by osteocytes is also required for the bone loss caused by

184 vator of NFkappaB ligand (RANKL) produced by osteocytes is essential for osteoclast formation in canc

185 Mechanistically, Saa3 produced by MLO-Y4 osteocytes is integrated into the extracellular matrix o

186 results demonstrate that RANKL expressed by osteocytes is required for the bone loss as well as the

187 we report that CAIII is highly expressed in osteocytes, is regulated by parathyroid hormone both in

188 ion of myeloid cells was further promoted by osteocytes lacking Gsalpha expression.

189 Osteocyte and osteocyte lacuna counts, percent bone matrix loss, and f

190 cro-CT analyses confirmed larger cementocyte/osteocyte lacunae and significantly reduced perilacunar

191 ized "halos" surrounding Hyp cementocyte and osteocyte lacunae.

192 tion in osteocytes prevented the increase in osteocyte lacunar area seen during lactation, as well as

193 demonstrated the potential link of abnormal osteocyte lacuno-canalicular network structure and funct

194 remodeling while causing degeneration of the osteocyte lacunocanalicular network, collagen disorganiz

195 cept for a sharp increase in osteoblasts and osteocytes, leading to a profound increase in bone volum

196 al deletion of Mbtps1 (cKO) protease in bone osteocytes leads to an age-related increase in mass (12%

197 sis, while its ablation by CRISPR/Cas9 in an osteocyte-like cell line (Ocy454) enhanced it.

198 Using an osteocyte-like cell line along with in vivo studies, we

199 st test this hypothesis, we used the IDG-SW3 osteocyte-like cell line to examine the effects of gluco

200 Osteocyte-like cells become embedded within the abnormal

201 Tnap expression is decreased in Hyp-derived osteocyte-like cells but not in Hyp-derived osteoblasts

202 d pyrophosphate concentration in Hyp-derived osteocyte-like cells in vitro.

203 In contrast, in Osmr(-/-) primary osteocyte-like cells stimulated with mOSM (therefore act

204 d enzyme enriched in primary cilia of MLO-Y4 osteocyte-like cells, may play a role in a primary ciliu

205 ctic myokine, was highly expressed in MLO-Y4 osteocyte-like cells.

206 is accelerated, indicating that EphrinB2 in osteocytes limits mineral accumulation.

207 s accompanied by decreased expression of the osteocyte marker and Wnt-signaling inhibitor sclerostin,

208 ll reduced, that of cyclin-dependent kinase, osteocyte marker, and pro-apoptotic genes were increased

209 AB volume between genotypes, but osteoblast/osteocyte markers were increased in all KOs, partially m

210 remarkably high bone turnover and defective osteocyte maturation that is accompanied by decreased ex

211 Whereas osteocytes may produce CCL2 in constitutively low levels

212 e in a primary cilium-dependent mechanism of osteocyte mechanotransduction in vitro.

213 rimary cilia and AC6 in a novel mechanism of osteocyte mechanotransduction.

214 Thus, osteocyte-mediated perilacunar remodeling maintains bone

215 and bone disease, suggesting that targeting osteocyte-multiple myeloma cell interactions through spe

216 Alveolar bone osteocytes negatively regulate Gli1+ PDLSCs activity thr

217 The interconnected osteocyte network within the bone matrix differentiates

218 d protein expression was reduced in cKO bone osteocytes, no differences in Mbtps1 or cre recombinase

219 tional deletion of Piezo1 in osteoblasts and osteocytes notably reduced bone mass and strength in mic

220 The vital canalicular networks required for osteocyte nourishment and communication, as well as the

221 ion rate were significantly reduced, whereas osteocyte number was increased.

222 ated with decreased osteoblast but increased osteocyte numbers.

223 or miR-27a, but not miR24-2, show decreased osteocyte numbers.

224 he role of the most common cell in bone, the osteocyte (OCy), in cancer biology.

225 We reported that osteocytes (Ocys) directly interact with MM cells to inc

226 e next proved that the pathologic changes in osteocytes (Ocys; changes from a spindle shape to round

227 mice rescued the suppressed TNAP activity in osteocytes of Hyp mice.

228 body weight activates a sensor dependent on osteocytes of the weight-bearing bones.

229 increased Sost/sclerostin expression in the osteocytes of these animals.

230 roles of ATP and adenosine released by bone osteocytes on breast cancers.

231 ce lacking Lrp4 in osteoblasts/osteocytes or osteocytes only.

232 e generated mice lacking Lrp4 in osteoblasts/osteocytes or osteocytes only.

233 e lacking these receptors in osteoblasts and osteocytes (osteocalcin-Cre).

234 Osteoclastogenesis is controlled by osteocytes; osteocytic osteoclastogenesis regulatory mol

235 Correlation between osteocytes per lacuna and age at death may reflect repor

236 teocyte-derived Ctsk contributes not only to osteocyte perilacunar remodeling, but also to the regula

237 osteocytes results in the loss of the mature osteocyte phenotype.

238 ith increased cellular maturation toward the osteocyte phenotype.

239 Osteocytes play an important role in bone metabolism and

240 together with disrupted trabeculae, loss of osteocytes, presence of calcified marrow, and elevated e

241 We show that Ctsk deletion in osteocytes prevented the increase in osteocyte lacunar a

242 , decreased osteoclast surfaces, and reduced osteocyte pro-inflammatory factors.

243 ta suggest that inhibitors of sclerostin, an osteocyte-produced Wnt signaling pathway antagonist, can

244 Osteocytes provide negative feedback to PDLSCs and inhib

245 Importantly, these osteocytes recapitulated the in vivo response to mechani

246 gamma expression in bone cells, particularly osteocytes, regulates energy metabolism remains unknown.

247 quired for osteoblasts to differentiate into osteocytes--remain a matter of conjecture with several h

248 Osteocytes reside in bone matrix, sense changes in mecha

249 This study provides direct evidence that osteocytes respond to in situ mechanical loading by Ca(2

250 How in situ osteocytes respond to mechanical stimuli is still unclea

251 Osteocyte responses are imaged by using multiphoton fluo

252 Deletion of Wnt1 in osteocytes resulted in low bone mass with spontaneous fr

253 sis and promote apoptosis of osteoblasts and osteocytes, resulting in decreased bone formation during

254 Depletion of Saa3 in MLO osteocytes results in the loss of the mature osteocyte p

255 steoblast differentiation requires EphrinB2, osteocytes retain its expression.

256 We hypothesized that osteocytes secrete Gsalpha-dependent factor(s) which reg

257 osteoclasts, therefore, we hypothesized that osteocyte-secreted factors might also regulate osteoclas

258 To identify osteocyte-secreted proteins, we used the osteocytic cell

259 Sclerostin is an osteocyte-secreted soluble antagonist of the Wnt/beta-ca

260 , vascular calcification, and stimulation of osteocyte secretion.

261 t) and Ocy454-Gsalpha(KO) ) to delineate the osteocyte "secretome" and its regulation by Gsalpha.

262 Osteocytes sense mechanical cues by changes in fluid flo

263 KL producers, we hypothesized that apoptotic osteocytes signal to neighboring osteocytes to increase

264 steoclast formation by knockout Rankl in the osteocytes significantly inhibits LSI-induced porosity o

265 Here, we show that mature osteoblast/osteocyte-specific ablation of PPARgamma in mice (Ocy-PP

266 th Cx43 osteocyte-specific knockout mice and osteocyte-specific Delta130-136 transgenic mice with imp

267 Furthermore, both Cx43 osteocyte-specific knockout mice and osteocyte-specific

268 heretofore unrecognized factors, such as the osteocyte-specific protein sclerostin, also regulate ren

269 Interestingly, assessment of the osteocyte-specific RANKL/OPG ratio showed that the stero

270 Sclerostin is an osteocyte-specific Wnt antagonist that inhibits bone for

271 m, we generated late-osteoblast-specific and osteocyte-specific WNT1 loss- and gain-of-function mouse

272 Conversely, Wnt1 overexpression from osteocytes stimulated bone formation by increasing osteo

273 " the osteocytes, where insights gained from osteocyte studies serve to inform the critical examinati

274 Here we report brittle bones in mice with osteocyte-targeted EphrinB2 deletion.

275 py (SEM) images of AIS demonstrated abnormal osteocytes that were more rounded and cobblestone-like i

276 Osteocytes, the bone cells embedded in the mineralized m

277 ion is under the control of WNT1 produced by osteocytes, the cells that reside deep in the bone matri

278 Application of pressure to osteocytes, the main mechanotransducing cells in bone, i

279 Osteocytes, the most abundant bone cells, were shown to

280 Thus, targeted osteocyte therapies could hold promise as novel osteopor

281 Despite lacking osteocytes, this tissue exhibits a striking resemblance

282 Furthermore, elevated osteocyte TNF-alpha, interleukin-6, RANKL, OPG, and scle

283 sed parathyroid hormone levels, we subjected osteocytes to an in vitro unloading environment achieved

284 kl/Opg (TNFRSF11B) ratio, and the ability of osteocytes to attract osteoclast precursors to induce lo

285 t apoptotic osteocytes signal to neighboring osteocytes to increase RANKL expression, which, in turn,

286 thyroid hormone (PTH) activates receptors on osteocytes to orchestrate bone formation and resorption.

287 We investigated the in vivo responses of osteocytes to strains ranging from 250 to 3,000 [Formula

288 ocally regulated with Saa3 at the osteoblast/osteocyte transition, attenuates Saa3 expression in MLO-

289 d that conditioned media (CM) collected from osteocytes treated with alendronate (AD), a bisphosphona

290 ed a ~70-fold up-regulation of Fgfr3 mRNA in osteocytes versus osteoblasts of Hyp mice.

291 ecular patterns (DAMPs) released by necrotic osteocytes via macrophage-inducible C-type lectin (Mincl

292 ntiation into chondrocytes, osteoblasts, and osteocytes via the BMP4-pSMAD5 and COX-2-PGE2 signaling

293 ss of strength, suggesting a contribution of osteocyte viability to strength independent of bone mass

294 loading plays a crucial role in maintaining osteocyte viability, CCL7 was tested for protective acti

295 ANKL) and osteoprotegerin (OPG) signaling in osteocytes was not studied in sheep.

296 factors up-regulated by mechanical strain in osteocytes, we discovered that chemokine (C-C motif) lig

297 To study primary osteocytes, we prepared non-osteocytic cell-free osteocy

298 Mice lacking RANKL in osteocytes were protected from the increase in osteoclas

299 mparing them to their closest "cousins," the osteocytes, where insights gained from osteocyte studies

300 expression were identified in alveolar bone osteocytes with aging.