ライフサイエンスコーパス: osteoclast

1 in many cell types including osteoblasts and osteoclasts.

2 grate to bone matrix, and differentiate into osteoclasts.

3 ropic effects on eBMD and gene expression in osteoclasts.

4 tivity of the nuclear envelope MTOC in human osteoclasts.

5 one lymphatics is impaired in mice that lack osteoclasts.

6 function of myelomonocytic cells, including osteoclasts.

7 ifferentiation of human CD14+ monocytes into osteoclasts.

8 ssed on human myeloid cells, including human osteoclasts.

9 5, which is essential for bone resorption by osteoclasts.

10 ancing the differentiation and maturation of osteoclasts.

11 inding Ig-like lectin, which is expressed on osteoclasts.

12 r lactose dehydrogenase production in mature osteoclasts.

13 gen species (ROS) for the differentiation of osteoclasts.

14 n and the differentiation of osteoblasts and osteoclasts.

15 own about Hdac3 activities in bone-resorbing osteoclasts.

16 early osteoclast progenitors, but not mature osteoclasts.

17 of cystinosin deficiency on osteoblasts and osteoclasts.

18 /macrophage lineage, including microglia and osteoclasts.

19 bers of bacteria were observed within mature osteoclasts.

20 (13) as a critical cytoskeletal regulator in osteoclasts.

21 TRAcP 5b were decreased as were tibial TRAP+ osteoclasts.

22 rease the bone-resorptive capacity of mature osteoclasts.

23 nearby exposed tumour cells, osteoblasts and osteoclasts.

24 bone forming osteoblasts and bone-resorbing osteoclasts.

25 on factor Foxp3 and are potent inhibitors of osteoclasts.

26 vestigated whether irisin directly regulates osteoclasts.

27 trix and triggers their differentiation into osteoclasts.

28 t apparatus, while facilitating formation of osteoclasts.

29 , consistent with a haematopoietic origin of osteoclasts(13,16,19) and studies that suggest that they

30 Here we utilize osteoclast ablation by denosumab (DMAb) and RNA-sequenci

31 In addition to macrophage ablation, osteoclast ablation occurred.

32 Osteoclasts act upon osteoblast lineage cells throughout

33 is a novel DAMP-mediated process that allows osteoclast activation and bone loss in the context of os

34 t-specific deletion of Slc7a5 in mice led to osteoclast activation and bone loss in vivo, and Slc7a5

35 Factors associated with osteoclast activation were affected by glucose, with Ran

36 ed with reduced soft tissue inflammation and osteoclast activation.

37 mice showed increased mRNA expression of the osteoclast activator-related gene, receptor activator of

38 oth injury, Smoc2(-/-) mutants had increased osteoclast activity and bone resorption surrounding the

39 genes, many of which were characteristic of osteoclast activity and differentiation, in particular m

40 The kinase Src promotes osteoclast activity and is activated in osteoclasts by t

41 theless, osteoporosis drugs that target only osteoclast activity are expected to preserve bone format

42 ve shared, non-redundant roles in regulating osteoclast activity during the formation of the adult sk

43 deficiency in osteopetrosis and to modulate osteoclast activity in vivo.

44 e compounds can inhibit both mouse and human osteoclast activity.

45 duced bone mass, mainly because of increased osteoclast activity.

46 a role for NO66 in tumor growth in bone and osteoclast activity.

47 itions, acting mainly through suppression of osteoclast activity.

48 steoporotic drugs targeting the mechanism of osteoclast adhesion onto the bone.

49 le for G-protein Galpha(13) in inhibition of osteoclast adhesion, fusion and bone resorptive function

50 n vivo effectively blocked the activation of osteoclasts after induction of osteocyte death, improved

51 estingly, treatment with E197 did not affect osteoclast and osteoblast numbers and hence did not impa

52 results identify the developmental origin of osteoclasts and a mechanism that controls their maintena

53 implant contact increased by 25-40%, and the osteoclasts and bone resorption were suppressed by 50% i

54 se from the caAcvr1-mutant mice formed large osteoclasts and demineralized pits, suggesting that BMP

55 ligand (Rankl) leads to ectopic formation of osteoclasts and excessive bone resorption, which can be

56 14 d, which correlated with decreased TRAP+ osteoclasts and F4/80+ macrophages.

57 ) and regulatory T cells (Treg) could affect osteoclasts and further bone formation.

58 ost exclusive Siglec-15 expression on murine osteoclasts and hardly any other expression on various o

59 The increased number of osteoclasts and higher expression of RANKL indicated inc

60 he palatal expansion procedure by regulating osteoclasts and implies the potential possibility for cl

61 derived macrophages were derived into mature osteoclasts and infected with B. abortus 2308, the vacci

62 ecrease and increase in the number of active osteoclasts and osteoblasts at the tumor-bone interface,

63 Osteocytes communicate with osteoclasts and osteoblasts via distinct signaling molec

64 eoporosis arises from imbalanced activity of osteoclasts and osteoblasts.

65 cifications express markers for osteoblasts, osteoclasts and osteocytes, and that bone matrix protein

66 bone, thereby inhibiting bone resorption by osteoclasts and stimulating bone formation by osteoblast

67 bone volume and cortical thickness, reduced osteoclasts and their bone marrow progenitors, and alter

68 ion of macrophages into multinucleated giant osteoclasts and their bone resorptive activity.

69 ence of EPO signaling in mature osteoblasts, osteoclasts, and adipocytes.

70 ment stromal cells including osteoblasts and osteoclasts, and effectively suppress both tumor and str

71 re no differences in numbers of osteoblasts, osteoclasts, and marrow adipocytes in Tg mice, suggestin

72 le nucleus, cell types such as trophoblasts, osteoclasts, and skeletal myofibers require multinucleat

73 ts followed by formation by osteoblasts, and osteoclasts are a source of bone formation-stimulating f

74 anges in the differentiation and activity of osteoclasts are accompanied by active metabolic reprogra

75 Osteoclasts are multinucleated cells of the monocyte/mac

76 These erythro-myeloid progenitor-derived osteoclasts are required for normal bone development and

77 Osteoclasts are specialised bone resorbing cells that co

78 ar factor of activated T-cells (NFATc1), and osteoclast-associated receptor (OSCAR).

79 ytic bone lesion area and reduced numbers of osteoclasts at the bone-tumor interface.

80 n, orchestrated T cells are able to regulate osteoclasts at the early stage of rapid palatal expansio

81 lpha play different but overlapping roles in osteoclast biology, highlighting the importance of the H

82 en learned about the molecular regulation of osteoclast biology, little is known about the metabolic

83 role(s) of the HIF-2alpha isoform of HIF in osteoclast biology.

84 g the importance of glycolytic metabolism in osteoclast biology.

85 s required for cardiomyocyte hypertrophy and osteoclast bone resorption activity.

86 also found that the postnatal maintenance of osteoclasts, bone mass and the bone marrow cavity involv

87 ned, little is known about the regulation of osteoclasts by osteocyte death.

88 otes osteoclast activity and is activated in osteoclasts by the receptor-type tyrosine phosphatase PT

89 bone marrow, CSF1R-FRed was also detected in osteoclasts, CD169(+) resident macrophages, and, consist

90 The osteoclast cell numbers (-32.45%, P = 0.01) and surface

91 In lysosomes and the ruffled border of osteoclasts, CLC-7 requires a beta-subunit, OSTM1, for s

92 P(+) osteoclasts (P < 0.01) in the Tregs/pre-osteoclast co-cultures.

93 its similar growth characteristics in mature osteoclasts compared to the primary target cell, the mac

94 ditions significantly impacted the number of osteoclasts compared with the periodontitis group.

95 ts, which revealed that mutant mice had more osteoclasts compared with WT mice, indicating that the p

96 These data suggest strategies to rescue osteoclast deficiency in osteopetrosis and to modulate o

97 Hdac3-deficient osteoclasts demonstrate increased K310 NF-kappaB acetyla

98 O) cells partially rescued the inhibition of osteoclasts, demonstrating that osteocytes control osteo

99 BBM exhibited the highest osteoclast density compared with the other materials gro

100 We surveyed a panel of osteoclast-derived coupling factors and found that Hdac3

101 LIF, CREG2, CST3, CCBE1, and DPP4 are likely osteoclast-derived coupling factors in humans.

102 veral coupling factors in humans and uncover osteoclast-derived DPP4 as a potential link between bone

103 Osteoclast-derived sphingosine-1-phosphate acts in parac

104 In bone homeostasis, it blocked osteoclast development by suppressing transcription fact

105 Deficiency of Siglec-15 leads to an impaired osteoclast development, resulting in a mild osteopetroti

106 th our in vitro studies, the total number of osteoclasts did not differ between the genotypes in vivo

107 Strikingly, osteoclasts differentiated from Nlrp3-deficient macropha

108 ty while siRNA targeting MMP9 also inhibited osteoclast differentiation although had little effect on

109 paB ligand (RANKL), which is responsible for osteoclast differentiation and activation.

110 ence of Nlrp3 and Caspase-1 in Rankl-induced osteoclast differentiation and activity and on LPS-induc

111 parib treatment or PARP1/2 deletion promotes osteoclast differentiation and bone loss.

112 elevated homocysteine, hypoxia, coagulation, Osteoclast differentiation and endochondral ossification

113 rapies calls for a holistic understanding of osteoclast differentiation and function.

114 a critical mechanism that limits TNF-induced osteoclast differentiation and inflammatory bone resorpt

115 irisin including upregulation of markers for osteoclast differentiation and resorption, as well as os

116 at CCR3 deficiency influences osteoblast and osteoclast differentiation and that it is associated wit

117 the DCSTAMP gene has an established role in osteoclast differentiation and the associations seen bet

118 ty, IL-6 must signal in osteoblasts to favor osteoclast differentiation and the release of bioactive

119 Knockdown of HIF-1alpha did not affect osteoclast differentiation but prevented the increase in

120 The alarmin S100A9 hampers osteoclast differentiation from human circulating precur

121 In vitro, irisin (2-10 ng/mL) increased osteoclast differentiation in C57BL/6J mouse bone marrow

122 nd examined the effects on bone modeling and osteoclast differentiation in mice.

123 promising OXPHOS, but nonetheless diminishes osteoclast differentiation in vitro.

124 ical inhibition of glycolysis did not affect osteoclast differentiation or viability, it efficiently

125 increased phagocytic activity, and a greater osteoclast differentiation potential at suboptimal RANK-

126 Here we show that the osteoclast differentiation receptor RANK(4,5) couples fe

127 oss significantly due to APR's inhibition on osteoclast differentiation shown in our in vitro studies

128 ncy causes trabecular bone loss by enhancing osteoclast differentiation through enhanced TNFalpha sig

129 the effectiveness of C-PC as an inhibitor of osteoclast differentiation, activity, and survival in vi

130 ed with inflammation, affects osteoblast and osteoclast differentiation, and may play a role in IRR.

131 one destruction not only relies on increased osteoclast differentiation, but also on the presence of

132 ur data show that S100A9 impedes monocyte-to-osteoclast differentiation, probably via a reduction in

133 to osteoblastic lesion formation by blocking osteoclast differentiation, while also contributing to o

134 predominant bioenergetic pathway to support osteoclast differentiation.

135 n cxcr3.2 prevent macrophage recruitment and osteoclast differentiation.

136 d positive regulators, NFATc1 and miR182, of osteoclast differentiation.

137 lasts, demonstrating that osteocytes control osteoclasts differentiation through Nrp-1 and Grn which

138 Osteoclast-directed Hdac3 deficiency decreased cortical

139 Here, Bmpr1a-disrupted osteoclasts displayed reduced phospho-SMAD1/5/9 (pSMAD1/

140 ferentiation of macrophages to TRAP-positive osteoclasts, distinctive osteoclast specific podosomal o

141 tween osteoblast-mediated bone formation and osteoclast-driven bone resorption.

142 growth medium derived from Phlpp1-deficient osteoclasts enhanced mineralization of ex vivo osteoblas

143 iated with formation of giant hypernucleated osteoclasts, enhanced bone resorption when cultured on b

144 oporosis risk variants among high-confidence osteoclast eQTL across multiple GWAS P value thresholds.

145 We detect co-localisation of eBMD GWAS and osteoclast eQTL association signals for 21 of the 69 loc

146 We utilise a unique osteoclast eQTL dataset to identify a number of potentia

147 Randomisation analysis of the eBMD GWAS and osteoclast eQTL datasets identifies significant associat

148 ciation results with those from our previous osteoclast expression quantitative trait locus (eQTL) da

149 Bone remodeling consists of resorption by osteoclasts followed by formation by osteoblasts, and os

150 monocytes were induced to differentiate into osteoclasts for 21 days in-vitro in the presence of macr

151 Osteocytes express genes required in osteoclasts for bone resorption, including cathepsin K (

152 olysis with 2-deoxy-D-glucose (2-DG) reduced osteoclast formation and activity under both basal and h

153 -deficient mice to study the role of CCR3 in osteoclast formation and activity.

154 osteoclastogenesis, but the role of CCR3 in osteoclast formation and bone remodeling in adult mice i

155 1 alpha (HIF-1alpha) transcription factor on osteoclast formation and bone resorption.

156 ective function might cause a more excessive osteoclast formation and contribute to greater osteolysi

157 These results suggest that Phlpp1 suppresses osteoclast formation and production of paracrine factors

158 ydroxamate-based MMP9 inhibitor reduced both osteoclast formation and resorption activity while siRNA

159 rthermore, AAV-sh-Ac45 significantly reduced osteoclast formation and the expression of proinflammato

160 alpha knockdown; HIF-2alpha siRNA increasing osteoclast formation in 3D.

161 dysfunction enhances phagocytic function and osteoclast formation in macrophages.

162 IL-37 exhibit a dose-dependent inhibition of osteoclast formation in vitro (~78.9% and 97.7% inhibiti

163 dicate that C-PC has the potential to reduce osteoclast formation via blocking the degradation of cyt

164 RSV notably inhibited the TNF-alpha-induced osteoclast formation, endothelial cell phenotypic change

165 ect bone resorption but moderately inhibited osteoclast formation.

166 using a unique gene footprint and to inhibit osteoclast formation.

167 sfunction, also showed higher propensity for osteoclast formation.

168 the PRF/BCP displayed an inhibitory role in osteoclasts formation and its molecular mechanism of act

169 t PRF membranes can inhibit the formation of osteoclasts from hematopoietic progenitors in bone marro

170 Osteoclasts from the Acvr1-floxed mice had reduced osteo

171 g that BMP signaling through ACVR1 regulates osteoclast fusion and activity.

172 ac3 is required for optimal bone healing and osteoclast fusion, potentially via its regulation of Pme

173 Thus, Siglec-15 on osteoclasts has a crucial function for bone erosion duri

174 Osteoporosis medications that inhibit osteoclasts have been associated with osteonecrosis, a c

175 show that bone resorption of differentiated osteoclasts heavily relies on increased aerobic glycolys

176 Growth of osteoclasts in 3D gels reversed the effect of HIF-2alpha

177 Csf1r or Flt3-to identify the precursors of osteoclasts in mice.

178 specificity in the roles of macrophages and osteoclasts in normal turnover and healing.

179 Here, we show that osteoclasts in pannus originate exclusively from circula

180 piratory chain deficiency in osteoblasts and osteoclasts in PolgA(mut/mut) mice compared with wild-ty

181 ve increase in the proportion of circulating osteoclasts in test group than control group (healthy in

182 cells results in long-term gene transfer in osteoclasts in the absence of haematopoietic-stem-cell c

183 urine arthritis models reduces the number of osteoclasts in the joints.

184 Whether the osteoclasts in these different tissue settings arise fro

185 without reducing resorptive activity, while osteoclasts infected with B. abortus S19 and S19vjbR wer

186 d, little is known about the consequences of osteoclast infection.

187 Lower osteoclasts infiltration is observed in chondroblastic,

188 he therapeutic potential of interfering with osteoclast-intrinsic metabolic pathways as possible stra

189 tions, the differentiation of bone-resorbing osteoclasts is delicately regulated by the balance betwe

190 Bone resorption by osteoclasts is essential for bone homeostasis.

191 Deficiency of Galpha(13) in myeloid osteoclast lineage (Galpha(13)(DeltaM/DeltaM) mice) lead

192 Hdac3 controls bone modeling by suppressing osteoclast lineage cell responsiveness to RANKL and coup

193 Hdac3-deficient osteoclast lineage cells were hyper-responsive to RANKL

194 of Foxo3 isoform2 specifically in macrophage/osteoclast lineage suppresses osteoclastogenesis and lea

195 membranes decreased expression levels of the osteoclast marker genes TRAP, Cathepsin K, dendritic cel

196 ted that AAV-sh-Ac45 simultaneously inhibits osteoclast-mediated bone resorption and attenuates dendr

197 Enhanced osteoclast-mediated bone resorption and diminished forma

198 Bone turnover, which is determined by osteoclast-mediated bone resorption and osteoblast-media

199 Mechanistically, tumors in the bone promote osteoclast-mediated bone resorption that releases TGF-be

200 ch causes bone destruction via activation of osteoclast-mediated osteolysis.

201 and host microenvironment cells and induces osteoclast-mediated osteolysis.

202 or principle underlying this process is that osteoclast-mediated resorption of a quantum of bone is f

203 AM-based calcium signaling pathways, skewing osteoclast metabolism toward oxidative phosphorylation.

204 unctionally conserved network that regulates osteoclast multinucleation and bone mass.

205 ects of MMnet genes on bone mass in mice and osteoclast multinucleation/resorption in humans with str

206 e from osteopetrotic syndromes indicate that osteoclasts not only resorb bone, but also provide signa

207 nsistently, boldine caused a decrease in the osteoclast number and RANKL/OPG ratio in periodontal les

208 ponsive to RANKL and showed elevated ex vivo osteoclast number and size and enhanced bone resorption

209 findings demonstrate that estrogens decrease osteoclast number by attenuating respiration, and thereb

210 stage of the experiment to downregulate the osteoclast number by inhibiting Th1 and Th17 cells, whic

211 eport that 17beta-estradiol (E(2)) decreased osteoclast number by promoting the apoptosis of early os

212 ise reduced and was accompanied by increased osteoclast number per trabecular bone surface.

213 gens protect against bone loss by decreasing osteoclast number through direct actions on cells of the

214 Bone resorption was measured by uCT and osteoclast number was determined by tartrate-resistant a

215 We revealed that the increased osteoclast number was downregulated at the end of the ea

216 mental periodontitis, osteonecrosis area and osteoclast number were significantly elevated in knock-i

217 e in empty lacunae, necrotic bone formation, osteoclast number, and surface area in antibiotic-treate

218 turbed bone micro-architecture and increased osteoclast number, highlighting a new biological pathway

219 cumference and increased cortical periosteal osteoclast number.

220 ony-stimulating factor, and 3-fold increased osteoclast numbers (P < 0.05) in Ddr1(-/-) versus WT per

221 uced obesity (DIO) diabetic mice, it reduced osteoclast numbers and alveolar bone loss significantly

222 lasts from the Acvr1-floxed mice had reduced osteoclast numbers and demineralization activity, wherea

223 deficiency enhances bone mass despite higher osteoclast numbers because it apparently disrupts PKCzet

224 histomorphometry analysis revealed decreased osteoclast numbers in Notch2 ASO-treated Notch2(tm1.1Eca

225 gnificant reduction in bone erosion area and osteoclast numbers in Siglec-15(-/-) mice, whereas the i

226 Moreover, reduced osteoclast numbers within the defect site are correlated

227 In summary, Phlpp1 critically regulates osteoclast numbers, and Phlpp1 deficiency enhances bone

228 eased interleukin-6 (IL-6) levels, increased osteoclast numbers, and significant trabecular bone loss

229 Casp1-KO mice had increased in osteoclast numbers, whereas the inflammatory infiltrate

230 ssociated with osteocyte apoptosis rates and osteoclasts numbers were increased in subchondral bone t

231 (PRF/BCP) on differentiation and survival of osteoclasts obtained from peripheral blood of CP patient

232 Further cellular studies show an increase of osteoclast (OC) differentiation in cocultures of bone ma

233 Osteoclasts (OC) originate from either bone marrow (BM)-

234 Bone-resorbing osteoclasts (OCLs) were recently identified as innate im

235 Osteoclasts (OCs) and much less dendritic cells (DCs) in

236 ors of monocytes (Mo's)/macrophages (MPhis), osteoclasts (OCs), and DCs.

237 The osteoclast offers a unique model for interrogating the c

238 NF-kappaB ligand protein (RANKL), numbers of osteoclasts on plastic, and pit formation and release of

239 dentified by the increased number of TRAP(+) osteoclasts (P < 0.01) in the Tregs/pre-osteoclast co-cu

240 These results suggest that osteoclasts play an important role in osteoarticular bru

241 d osteoblast population densities, increased osteoclast population densities, and mitochondrial respi

242 d an erythromyeloid progenitor (EMP)-derived osteoclast precursor population.

243 osteoclastogenic macrophages (AtoMs)) as the osteoclast precursor-containing population in the inflam

244 RNA-sequencing data showed that EMP-derived osteoclast precursors arose independently of the haemato

245 mprising a subset distinct from conventional osteoclast precursors in homeostatic bone remodeling.

246 Furthermore, EMPs gave rise to long-lasting osteoclast precursors that contributed to postnatal bone

247 Finally, infection of macrophages or osteoclast precursors with B. abortus 2308 resulted in g

248 g in mouse bone marrow macrophages, known as osteoclast precursors.

249 ibiting RANKL-induced NF-kappaB signaling in osteoclast precursors.

250 Increased osteoclasts' presence was observed in the beta-TCP group

251 ne decreased osteoclastogenesis by promoting osteoclast progenitor apoptosis via Bak/Bax.

252 a1 as a differentially expressed gene within osteoclast progenitor cells.

253 that ERalpha-mediated estrogen signaling in osteoclast progenitors decreases "oxidative phosphorylat

254 Genetic deletion of Glut1 in osteoclast progenitors reduces aerobic glycolysis withou

255 dy demonstrates that irisin acts directly on osteoclast progenitors to increase differentiation and p

256 t number by promoting the apoptosis of early osteoclast progenitors, but not mature osteoclasts.

257 oting mitochondrial apoptotic death of early osteoclast progenitors.

258 d massive bone loss and stimulation of mouse osteoclast-promoting genes, including Dickkopf1, Catheps

259 e cells showed a decreased production of the osteoclast-promoting protein TNF-alpha.

260 teocytes, decreased RANKL secretion, reduced osteoclast recruitment and bone resorption, and impaired

261 ntagonists AMG487 and NBI-74330 also reduced osteoclast recruitment and protected bone integrity agai

262 Here, we explore osteoclast regulation during skeletal development throug

263 d mineralised matrix formation and increased osteoclast resorption by PolgA(mut/mut) cells.

264 opsies from postmenopausal women to identify osteoclast-secreted factors suppressed by DMAb.

265 Herein we show that osteoclasts sense damage-associated molecular patterns (

266 Osteoclasts showed robust Mincle expression upon exposur

267 Also, it suppressed the expression of osteoclast specific markers, such as cathepsin K and int

268 es to TRAP-positive osteoclasts, distinctive osteoclast specific podosomal organization, and dentine

269 The osteoclast-specific deletion of Slc7a5 in mice led to os

270 We have recently constructed a unique osteoclast-specific eQTL resource using cells differenti

271 genitors leads to osteopetrosis due to fewer osteoclasts specifically in the female mice.

272 el, we show that PMMA particles abrogate the osteoclast suppressive function of T(REGS).

273 increased empty lacunae, necrotic bone, and osteoclast surface area in antibiotic- and zoledronic ac

274 OPG, and sclerostin corresponded with higher osteoclast surfaces and lower bone formation rate in DSS

275 lating blood monocytic cells with long-lived osteoclast syncytia.

276 macrophages of EMP origin produced neonatal osteoclasts that can create a space for postnatal bone m

277 bortus 2308 and S19 replicated inside mature osteoclasts, the attenuated mutants were progressively k

278 s targeting the differentiation or viability osteoclasts, the cells responsible for physiological and

279 and bone homeostasis by modulating NFATc1 in osteoclasts, thereby providing a molecular connection be

280 cells can differentiate into bone-resorbing osteoclasts, therefore, we hypothesized that osteocyte-s

281 Although the control of bone-resorbing osteoclasts through osteocyte-derived RANKL is well defi

282 bone-forming osteoblasts and bone-resorbing osteoclasts to orchestrate balanced progenitor cell recr

283 In contrast to classical bone-associated osteoclasts, VAOs are dispensable for cartilage resorpti

284 inhibited their differentiation into mature osteoclasts via a Gsalpha-dependent mechanism.

285 Interestingly, depletion of macrophages and osteoclasts via clodronate treatment had differential ef

286 with conditioned medium from Hdac3-deficient osteoclasts was markedly reduced.

287 bone marrow and can regulate osteoblasts and osteoclasts, we examined whether gut microbiome contribu

288 nted on hematoxylin-eosin-stained slides and osteoclasts were counted on tartrate-resistant acid phos

289 s reduced, and migration and adhesion of pre-osteoclasts were enhanced.

290 Bone loss and the number of osteoclasts were measured through radiographic and immun

291 Increased numbers of osteoclasts were present in regenerated AB of all KOs ve

292 Osteoclasts were quantified by histological identificati

293 ence staining were conducted to evaluate how osteoclasts were regulated by T cells during the bone re

294 t of rapamycin complex 1 (mTORC1) pathway in osteoclasts, whereas genetic activation of mTORC1 correc

295 Osteoclasts, which could be regulated by T cells and oth

296 Tartrate Resistant Acid Phosphatase-positive osteoclasts, which revealed that mutant mice had more os

297 ortus 2308 resulted in generation of smaller osteoclasts with decreased resorptive activity.

298 er spread morphology of multinucleated giant osteoclasts with elevated bone resorptive capacity, corr

299 Additional interactions of osteoclasts with osteoblast lineage cells, including int

300 ngly, B. abortus 2308 impaired the growth of osteoclasts without reducing resorptive activity, while