ライフサイエンスコーパス: osteoclast

1 activity rather than directly affecting the osteoclast.

2 ts; however, it does not induce multinuclear osteoclasts.

3 ession analysis in terminally differentiated osteoclasts.

4 ctions between tumor cells, osteoblasts, and osteoclasts.

5 bone forming osteoblasts and bone resorbing osteoclasts.

6 resorption, carried out by monocyte-derived osteoclasts.

7 -kappaB and phosphorylated IkappaB levels in osteoclasts.

8 uclear osteoclasts to fuse into multinuclear osteoclasts.

9 duced bone mass, with an increased number of osteoclasts.

10 impacts of loss of Bmpr1b on osteoblasts and osteoclasts.

11 ression in mouse osteoblasts, osteocytes and osteoclasts.

12 of miR-142-3p prevented their conversion to osteoclasts.

13 tor Wnt10b mRNA was increased in W(sh)/W(sh) osteoclasts.

14 native tissue, specifically osteoblasts and osteoclasts.

15 gand (RANKL)-stimulated differentiation into osteoclasts.

16 UAMS-1 and LAC cultures for osteoblasts and osteoclasts.

17 ere osteopenia owing to increased numbers of osteoclasts.

18 they differentiate from preosteoclasts into osteoclasts.

19 iltration, as well as an increased number of osteoclasts.

20 lis infection was able to differentiate into osteoclasts.

21 itical communication between osteoblasts and osteoclasts.

22 an essential cytokine for bone resorption by osteoclasts.

23 ironment, which involves the osteoblasts and osteoclasts.

24 icient in preventing actin ring formation in osteoclasts, a process required for bone resorption.

25 A slight reduction in the osteoclasts ability to migrate, as well as a reduction i

26 rabecular bone loss resulting from increased osteoclast activation and unbalanced coupling between re

27 al acidosis in the BM that in turn increases osteoclast activation through the modulation of TRPV1.

28 f insulin in correcting the pH variation and osteoclast activation.

29 e critical regulator of RANKL/RANK-dependent osteoclast activation.

30 SFN decreases the expression of the osteoclast activator receptor activator of nuclear facto

31 bone remodeling; they control osteoblast and osteoclast activities both directly via cell-to-cell com

32 coupling signals coordinating osteoblast and osteoclast activity and finely tuned expression of infla

33 indirectly on dentinogenesis by controlling osteoclast activity and the signaling network related to

34 inflammatory arthritis, the dysregulation of osteoclast activity by proinflammatory cytokines, includ

35 Activation of osteoclast activity by receptor activator of nuclear fac

36 Here, we demonstrate that sustained osteoclast activity is largely due to accumulation of NO

37 clast function, either by directly promoting osteoclast activity or by inhibiting osteoclast signalin

38 g that SMURF2 regulates osteoblast-dependent osteoclast activity rather than directly affecting the o

39 Finally, a significant increase of chondro-osteoclast activity was observed in the P3 MSC sheet-gra

40 Over the course of a week, osteoclast activity was responsible for resorbing the ne

41 ntly reduced inflammatory cell infiltration, osteoclast activity, and bone loss.

42 truction, cartilage prostaglandin depletion, osteoclast activity, and Th17 production.

43 bone interface exhibited microfractures and osteoclast activity.

44 n to regulate osteoblast differentiation and osteoclast activity.

45 uch role, we conditionally deleted Nemo from osteoclast and myeloid progenitors.

46 the increased myeloperoxidase activities and osteoclast and neutrophil densities in the EP, DM, and E

47 5% of bone cells and are major regulators of osteoclast and osteoblast activity, but their contributi

48 he effects of ticagrelor and dipyridamole on osteoclast and osteoblast differentiation whereas A2BR b

49 omorphometry revealed an increased number of osteoclasts and bone resorption, without a decrease in o

50 rlying cellular mechanisms in bone-resorbing osteoclasts and bone-forming osteoblasts in mice.

51 In PDCimG, the number of TRAP-positive osteoclasts and IL-6, MMP-1, and MMP-9-immunolabeled cel

52 lted in an increased number of alveolar bone osteoclasts and increased RANKL expression after P. ging

53 sorption and a marked reduction in number of osteoclasts and inflammatory cells.

54 tion and a marked reduction in the number of osteoclasts and inflammatory cells.

55 cated in the cell-cell communication between osteoclasts and osteoblasts and have been associated wit

56 to determine the individual contributions of osteoclasts and osteoblasts to HCS osteopenia, we create

57 ned that, at a cellular level, C57BL/6J mice osteoclasts and osteoblasts were less responsive to GC t

58 c-Kit was expressed in both osteoclasts and osteoblasts, and c-Kit expression was de

59 deling comprises balanced activities between osteoclasts and osteoblasts, which is regulated by vario

60 he interactions of metastatic BCa cells with osteoclasts and osteoblasts.

61 fractures associated with reduced numbers of osteoclasts and osteoblasts.

62 ial abnormalities in individual osteoblasts, osteoclasts and osteocytes are limited and impair our ab

63 w that MYC drives metabolic reprogramming in osteoclasts and that MYC induces estrogen receptor-relat

64 tor (TbetaRII) and p-Smad2 were expressed in osteoclasts and tumor cells, and were correlated with th

65 ell infiltration, numbers of osteoblasts and osteoclasts, and receptor activator of nuclear factor-ka

66 rescues hyper-activation of Gna13-deficient osteoclasts, and RhoA inhibition mimics the osteoclast h

67 T3A, through the canonical pathway, promoted osteoclast apoptosis and therefore attenuated the number

68 Osteoclasts are resorptive cells that are important for

69 Osteoclasts are the cells responsible for bone resorptio

70 Osteoclasts arise from the macrophage lineage, and their

71 solution structure of the collagen-activated osteoclast-associated receptor (OSCAR) bound to a collag

72 The osteoclast-associated receptor (OSCAR) is a collagen-bin

73 Osteoclast-associated receptor activator of NK-kappaB li

74 trate-resistant acid phosphatase (TRAP), and osteoclast-associated receptor increased significantly.

75 Osteoclasts begin as mononuclear cells that fuse to form

76 timulates osteoblast activity and diminishes osteoclast bone resorption, shifting the balance of bone

77 c-Kit expression was decreased in W(sh)/W(sh)osteoclasts, but not osteoblasts, suggesting an indirect

78 and suppressed development of bone-resorbing osteoclasts by downregulating NFATc1 through the elevati

79 fects of Wnt/betacatenin signaling in mature osteoclasts by generating mice lacking betacatenin in Ca

80 In BMMs committed to become osteoclasts by RANKL treatment, Saa3 expression peaked p

81 a novel target for the selective removal of osteoclasts by targeting of osteoclastogenic pathways.

82 We show that osteoblasts and osteoclasts can be differentiated from hiPSC-mesenchymal

83 the HCS mutation in osteoblasts, but not in osteoclasts, causes osteopenia.

84 We have previously shown that osteoclasts, cells that resorb bone, act as APCs.

85 Primary human osteoblast/osteoclast co-cultures were seeded onto Ti substrates wi

86 ormation, so we investigated the role of the osteoclast compartment.

87 EVs from mature osteoclasts contained receptor activator of nuclear fact

88 In addition, neutrophil and osteoclast densities and myeloperoxidase activities were

89 Osteoclast density and inflammatory cell infiltration in

90 ed inflammatory gene expression, and reduced osteoclast density.

91 steogenic differentiation, whereas Ppia(-/-) osteoclasts derived from the long bones showed increased

92 Furthermore, the osteoclast-derived coupling factor Wnt10b mRNA was incre

93 ion of RANK-rich EVs relieved the ability of osteoclast-derived EVs to inhibit osteoclast formation i

94 bone resorption with bone formation through osteoclast-derived Wnt 10 b.

95 d in correlation with an excessive number of osteoclasts, detected by TRAP staining and histomorphome

96 has indicated that melanocortin can control osteoclast development and function, but whether such pr

97 s subchondral bone remodeling by suppressing osteoclast development, and prevents degradation of cart

98 n, both of which are required to execute the osteoclast developmental program.

99 Osteoclasts differentiate from myeloid lineage cells.

100 RANKL is the osteoclast differentiating factor and diminishes BMD.

101 transgenic mice affects both osteoblast and osteoclast differentiation and activity.

102 ce with arthritis, a significant increase in osteoclast differentiation and bone resorption was obser

103 Forced expression of NUMBL inhibits osteoclast differentiation and function as evident by re

104 ti-resorptive properties, directly impairing osteoclast differentiation and function through a seroto

105 ng in maintaining bone quality by regulating osteoclast differentiation and function through cAMP/PKA

106 at MYC drives metabolic reprogramming during osteoclast differentiation and functions as a metabolic

107 Conversely, NUMBL-null BMMs, show increased osteoclast differentiation and mRNA expression of osteoc

108 logical or pathological functions, including osteoclast differentiation and osteoporosis.

109 We previously reported that IL-3 inhibits osteoclast differentiation and pathological bone loss.

110 , an alternative P2Y12 antagonist, inhibited osteoclast differentiation and promoted osteoblast diffe

111 Osteoclast differentiation and resorption activity was e

112 NF-kappaB signaling is essential for osteoclast differentiation and skeletal homeostasis.

113 he mechanisms that regulate all the steps of osteoclast differentiation are not entirely known.

114 the LTB4 pathway in bone loss, we performed osteoclast differentiation assays by stimulating with M-

115 strate that Gsalpha signaling also regulates osteoclast differentiation during bone modeling and remo

116 Histamine and Th17 cytokines induced the osteoclast differentiation from monocytes and JNJ7777120

117 MiRNA profiling of monocyte-to-osteoclast differentiation identified miR-142-3p as a mi

118 skolin treatment increased pCREB and rescued osteoclast differentiation in Gnas(+/p-) by reducing Nfa

119 a modulator of Ca(2+)-induced NFAT-dependent osteoclast differentiation in inflammatory bone loss.

120 of inflammatory cytokines and could increase osteoclast differentiation in vitro.

121 llular domain (ECD) binds RANKL and inhibits osteoclast differentiation in vivo.

122 H4R mediates RANKL expression and osteoclast differentiation induced by histamine and Th17

123 anism underlying IL-3-mediated inhibition of osteoclast differentiation is not fully understood.

124 Furthermore, IL-3 inhibited RANKL-induced osteoclast differentiation less effectively in the STAT5

125 ine- and chemokine-related pathways but also osteoclast differentiation may be involved in the effect

126 ation abilities of patDp/+ osteoblasts while osteoclast differentiation remained unchanged compared t

127 The c-Kit W(sh) mutation increased osteoclast differentiation, the number of committed oste

128 acting in concert to promote RANKL-dependent osteoclast differentiation, thereby creating an imbalanc

129 (ChIPac-seq) to an established cell model of osteoclast differentiation, we discovered that H3NT prot

130 ANs in osteoclast precursor cells attenuated osteoclast differentiation, while their overexpression i

131 axis to drive metabolic reprogramming during osteoclast differentiation.

132 AMPs for the NLRP3 inflammasome and regulate osteoclast differentiation.

133 ed that MYO10 is also expressed early during osteoclast differentiation.

134 nflammation, angiogenesis, tumor growth, and osteoclast differentiation.

135 ress from inflamed sites and is required for osteoclast differentiation.

136 the expression or activation of STAT5 during osteoclast differentiation.

137 role of STAT5 in IL-3-mediated inhibition of osteoclast differentiation.

138 d suppresses canonical RANK signaling during osteoclast differentiation.

139 aB ligand (RANKL), an essential cytokine for osteoclast differentiation.

140 on using antisense oligonucleotides, impeded osteoclast differentiation.

141 esis Irf8 by DNA methylation is required for osteoclast differentiation.

142 r LTB4R1 (BLT1) in synovial inflammation and osteoclast differentiation.

143 in whole mouse marrow cultures, and EVs from osteoclast-enriched cultures inhibited osteoclastogenesi

144 enriched in 1 in every 32 EVs isolated from osteoclast-enriched cultures.

145 which generated sealing zones; however these osteoclasts exhibited defective ruffled borders and were

146 We show that osteoclasts express the repulsive guidance factor Semaph

147 In addition, the in vivo importance of osteoclast-expressed MYC in physiological and pathologic

148 pecific genes (p < 0.05) alongside decreased osteoclast formation (p < 0.0001) in inflammatory (RANKL

149 hus, the impact of inflammatory cytokines on osteoclast formation and function was among the most imp

150 The RANKL/RANK pathway is critical for both osteoclast formation and function, and these effects are

151 ompared to wild-type controls due to reduced osteoclast formation and increased osteoblast numbers, r

152 differentiated into osteoclasts showed that osteoclast formation and resorptive activity were attenu

153 ss, may benefit from treatments that inhibit osteoclast formation and/or function.

154 -1(-/-) mice showed decreased multinucleated osteoclast formation compared with WT mice.

155 ability of osteoclast-derived EVs to inhibit osteoclast formation in 1,25-dihydroxyvitamin D3-stimula

156 NKL) produced by osteocytes is essential for osteoclast formation in cancellous bone under physiologi

157 Finally, osteoblast-derived VEGF stimulated osteoclast formation in the final remodeling phase of th

158 MM cell interactions strongly contributed to osteoclast formation in vitro, because osteoclastogenesi

159 promoted 1,25-dihydroxyvitamin D3-dependent osteoclast formation in whole mouse marrow cultures, and

160 , observed by micro-computed tomography, and osteoclast formation were decreased in Mk2(-/-) mice com

161 cluding monocyte and macrophage recruitment, osteoclast formation, bone resorption, and cortical and

162 sis, immune cell function and bone-resorbing osteoclast formation, the expression of TRAIL in human m

163 activation of pathways that are involved in osteoclast formation.

164 mechanistically linked to the inhibition of osteoclast formation.

165 rast to PTHrP1-36, PTHrP1-17 does not affect osteoclast formation/function in vitro or in vivo.

166 pe is the result of both the osteoblasts and osteoclasts from BgnFmod KO mice having higher different

167 subchondral bone and the differentiation of osteoclasts from bone marrow-derived cells were complete

168 Bone resorption of osteoclasts from subchondral bone and the differentiatio

169 associated with development and activity of osteoclasts from subchondral bone.

170 CD8(+) cell-derived IFN-gamma suppresses osteoclast function and may thus favor calcification in

171 which is associated with strongly increased osteoclast function and mildly reduced osteoblast functi

172 Ticagrelor regulates osteoblast and osteoclast function and promotes bone formation in vivo

173 stasis as they affect osteoclastogenesis and osteoclast function, either by directly promoting osteoc

174 kB ligand), two regulators of osteoblast and osteoclast function.

175 We found that osteoclast fusion required the dendrocyte-expressed seve

176 Conditioned medium from W(sh)/W(sh) osteoclasts had elevated Wnt10b protein levels and induc

177 steoclast numbers, although Smurf2-deficient osteoclasts have no intrinsic alterations in activity.

178 RANKL expression by IL-3 induces mononuclear osteoclasts; however, it does not induce multinuclear os

179 nal knockout mice of Lgr4 (Lgr4 CKO) exhibit osteoclast hyperactivation (including elevation of osteo

180 osteoclasts, and RhoA inhibition mimics the osteoclast hyperactivation resulting from Gna13-deficien

181 hat aberrant NOTCH2 signaling and consequent osteoclast hyperactivity are closely associated with the

182 Periodontal osteoclast impairment also occurs in Msx2 null mutant mi

183 e staining demonstrated a marked decrease in osteoclasts in anti-Netrin-1/anti-Unc5b-treated animals.

184 loss, correlating with decreased numbers of osteoclasts in bone tissue sections.

185 e-resistant acid phosphatase (TRAP)-positive osteoclasts in the alveolar process surface and number o

186 capacity of bone marrow macrophages to form osteoclasts in vitro In contrast, Notch2(COIN) inversion

187 nuated the number of M-CSF and RANKL-derived osteoclasts in vitro.

188 we have demonstrated that deletion of Myc in osteoclasts increases bone mass and protects mice from o

189 During bone remodelling, osteoclasts induce chemotaxis of osteoblasts and yet mai

190 hat are not only inflammomodulatory but also osteoclast-inhibitory or, rather, osteostimulative.

191 the role of IL-3 in regulation of osteoblast-osteoclast interactions and underlying mechanisms is not

192 dless of etiology and cellular contexts, the osteoclast is the bone-degrading cell.

193 ion of the differentiation of bone-resorbing osteoclasts is an effective strategy for the treatment o

194 Coordination between osteoblasts and osteoclasts is required for bone health and homeostasis.

195 Cross-presentation of Ags by osteoclasts leads to expression of CD25 and Foxp3, marke

196 e number and activity of bone marrow-derived osteoclast-like cells in vitro, suggesting that the rest

197 bone height and 4-fold increased numbers of osteoclast-like cells versus wild type at 24 wk, consist

198 ed their differentiation into multinucleated osteoclast-like cells.

199 ry M2 macrophages, could potentially display osteoclast-like functions.

200 However, the effect of this pathway on the osteoclast lineage has been less explored.

201 Overall, osteoclast lineage is the hyper responsiveness of knee l

202 atrix activate the NLRP3 inflammasome in the osteoclast lineage, and may represent a bone-restricted

203 receptor activator of NF-kappaB targeted in osteoclast lineage.

204 Osteoclast-lineage-specific Gna13 conditional knockout m

205 In osteoclasts, loss of CypA activates BtK (Bruton's tyrosi

206 ermore, osteoclast numbers and expression of osteoclast marker genes were increased in parallel with

207 clast differentiation and mRNA expression of osteoclast marker genes.

208 pression of the macrophage marker CD11b, the osteoclast marker tartrate-resistant acid phosphatase, o

209 eriodontal tissue regeneration by inhibiting osteoclast-mediated bone resorption and promoting osteob

210 The importance of osteoclast-mediated bone resorption in the process of os

211 t and homeostasis, but which is required for osteoclast-mediated inflammatory bone loss and hyper-mul

212 Osteoclast-mediated osteolysis has been regarded as the

213 and determined that MMP-13 directly enhances osteoclast multinucleation and bone-resorptive activity

214 noscale surface-adherent BMSCs increased the osteoclast number (P < 0.01).

215 ficiency triggers a drastic increase in both osteoclast number and activity (hyper-activation), mecha

216 ine decreases bone loss through reduction of osteoclast number and induces reduction of IL-6, MMP-1,

217 teocytes were protected from the increase in osteoclast number and the bone loss caused by ovariectom

218 last hyperactivation (including elevation of osteoclast number, surface area, and size) and increased

219 group, and melatonin significantly decreased osteoclast numbers (P <0.05) but had no effect on iNOS,

220 Furthermore, osteoclast numbers and expression of osteoclast marker g

221 amining the host response, colonization, and osteoclast numbers in aged versus young mice.

222 Osteoclast numbers in ligated group were significantly h

223 tibility, reflected by higher TNF levels and osteoclast numbers in the periodontium of aged versus yo

224 Osteoclast numbers in the XG + ozone group were higher t

225 -resistant acid phosphatase-positive (TRAP+) osteoclast numbers were also evaluated.

226 TRAP+ osteoclast numbers were the highest in the STZ+L group,

227 e is accompanied by a pronounced increase in osteoclast numbers, although Smurf2-deficient osteoclast

228 cluded that SR can reduce RANKL activity and osteoclast numbers, as well as ABL.

229 mice was associated with increased endosteal osteoclast numbers, with no significant effects on osteo

230 l molecule ERK5 pathway inhibitors increased osteoclast numbers.

231 y, reduced osteoblast numbers, and increased osteoclast numbers.

232 -STAMP) plays a key role in the induction of osteoclast (OC) cell fusion, as well as DC-mediated immu

233 demonstrated the importance of PLCgamma2 in osteoclast (OC) differentiation by modulating inositol 1

234 appoint mouse bone marrow (MBM) cells to the osteoclast (OC) lineage for osteoclastogenesis.

235 al bone thickness, associated with increased osteoclast (OC) numbers, but had no change in osteoblast

236 , which increase RANKL-mediated signaling in osteoclast (OC) precursor bone marrow macrophages (BMMs)

237 appaB ligand (RANKL) to its receptor RANK on osteoclast (OC) precursors up-regulates c-Fos and CCAAT/

238 ulture system (RCCS) enhanced bone resorbing osteoclast (OCL) differentiation.

239 Treatments that target osteoclasts (OCLs) block both pagetic bone resorption an

240 sis is well acknowledged whereas the role of osteoclasts (OCLs) is still unclear.

241 remodeling is controlled by dual actions of osteoclasts (OCs) and osteoblasts (OBs).

242 Excessive bone resorption by osteoclasts (OCs) can result in serious clinical outcome

243 s macrophages (MACs) and bone remodelling as osteoclasts (OCs).

244 functional balance of osteoblasts (OBs) and osteoclasts (OCs).

245 To activate Notch2 in osteoclasts or osteoblasts, Notch2(COIN) mice were bred

246 Overexpression of RCANs in osteoclast precursor cells attenuated osteoclast differe

247 Furthermore, adding either Bgn or Fmod to osteoclast precursor cultures significantly attenuated t

248 the lack of Wnt activation in osteoblast and osteoclast precursors and subsequently led to defective

249 Osteoclast precursors from Sirt3-/- mice underwent incre

250 Loss of MYO10 expression in osteoclast precursors inhibits the ability of mononuclea

251 However, EVs from osteoclast precursors promoted 1,25-dihydroxyvitamin D3-

252 also detected a change in the ability of the osteoclast precursors to form tunneling nanotubes (TNTs)

253 io, and the ability of osteocytes to attract osteoclast precursors to induce local bone resorption.

254 aintained when direct contact between M1 and osteoclast precursors was interrupted by cell culture in

255 using RAW264.7 cells or bone marrow cells as osteoclast precursors, addition of M1 macrophages signif

256 ciency hampered activation of IKK complex in osteoclast precursors, causing arrest of osteoclastogene

257 ely regulate Wnt signaling in osteoblast and osteoclast precursors, known to regulate bone homeostasi

258 ess that culminates in fusion of mononuclear osteoclast precursors.

259 ppressed by Wnt activation in osteoblast and osteoclast precursors.

260 xis in vivo, and RANKL-induced maturation of osteoclast-precursors in vitro, indicate the commensal m

261 aired osteoblast mineralization and enhanced osteoclast-progenitor survival, leading to increased ost

262 owever, the role of B cells is not to act as osteoclast progenitors but may be to act as osteoclast s

263 dies demonstrated that B cells do not act as osteoclast progenitors in estrogen-replete or estrogen-d

264 Functional analysis of osteoclast progenitors isolated from peripheral blood of

265 vating TRAF6-dependent signaling pathways in osteoclast progenitors.

266 The expression of prominent osteoclast-promoting factors tumor necrosis factor alpha

267 ea and suppressed the number and activity of osteoclasts, regardless of irradiation.

268 CAVD), activated T lymphocytes localize with osteoclast regions; however, the functional consequences

269 ency in BLT1 resulted in the upregulation of osteoclast-related genes and an increase in the formatio

270 steoblasts and bone formation rate while the osteoclasts remained relatively unaffected.

271 and CD86 increased in parallel with reduced osteoclast resorptive function, effects abrogated by neu

272 n and resorption mediated by osteoblasts and osteoclasts, respectively.

273 o experiments with cells differentiated into osteoclasts showed that osteoclast formation and resorpt

274 omoting osteoclast activity or by inhibiting osteoclast signaling intermediaries or through negative

275 Mice with osteoclast-specific Fbw7 ablation revealed osteoporotic

276 ment significantly reduced the expression of osteoclast-specific genes (p < 0.05) alongside decreased

277 aMKIV) induces transcriptional regulation of osteoclast-specific genes via NFATc1, which facilitate b

278 kappa B (NF-kappaB) ligand (RANKL), a potent osteoclast-stimulating factor, by human periodontal liga

279 is, whereas IL-12 increased the apoptosis of osteoclasts, suggesting molecular mechanisms underlying

280 osteoclast progenitors but may be to act as osteoclast support cells.

281 tively inhibiting the stimulation of RANK on osteoclast surfaces by RANKL similar to osteoprotegerin.

282 icantly less internalized by osteoblasts and osteoclasts than CC18 and CC28 C. acnes strains (p </= 0

283 Bone-resorbing multinucleated osteoclasts that play a central role in the maintenance

284 ecursors inhibits the ability of mononuclear osteoclasts to fuse into multinuclear osteoclasts.

285 myosin, has previously been shown in mature osteoclasts to play a role in attachment and podosome po

286 polarization lowers expression levels of the osteoclast transcriptional activator nuclear factor of a

287 virulence factors that limit osteoblast and osteoclast viability and that thereby promote bone destr

288 the plasticity of MDSC to differentiate into osteoclasts was assessed by staining for tartrate-resist

289 In vitro differentiation of Bmpr1b null osteoclasts was increased but resorption activity was de

290 es and the differentiation of bone marrow to osteoclasts was similar in TRAF6[L74H] and wild-type cel

291 Osteoclasts were absent in the allografts and there was

292 Osteoclasts were counted in tartrate-resistant acid phos

293 Osteoclasts were counted in TRAP-stained sections.

294 Osteoblasts and osteoclasts were cultured in the presence of elevated PA

295 Human osteoblasts and osteoclasts were infected by live C. acnes.

296 a robust formation of large, multinucleated osteoclasts which generated sealing zones; however these

297 erived MPs during their differentiation into osteoclasts, which increased their differentiation into

298 ficantly decreased the resorption ability of osteoclasts with a major impact by the CC36 strain (p </

299 Ctsk, and beta 3 integrin is reduced in the osteoclasts with reduced MYO10 expression.

300 ively regulated by the p38 MAPK-Creb axis in osteoclasts, with the promoters of PDGF-AA and BMP2 havi