ライフサイエンスコーパス: calvarial

1 cally significant osteogenic regeneration of calvarial and alveolar defects comparable to autogenous

2 mRNA level was highly elevated in Ank(KI/KI) calvarial and femoral bones.

3 In both primary rat calvarial and MC3T3E1 mouse calvarial osteoblasts, trans

4 accumulated on the endosteal surface in the calvarial and trabecular bone marrow.

5 Analysis of calvarial- and bone marrow-derived osteoblasts for miner

6 requirement is restricted to the developing calvarial aspect of the frontal bone, whereas the orbita

7 Using a calvarial bone defect model in rats, it was shown that P

8 phate/hydroxyapatite scaffold implanted in a calvarial bone defect, promoted significantly more bone

9 variety of pathological conditions in which calvarial bone development is compromised.

10 Runx2 is essential for calvarial bone development, as Runx2 haploinsufficiency

11 ction for both the CNC- and mesoderm-derived calvarial bone development.

12 precursor cells and the rate and pattern of calvarial bone development.

13 eoblast differentiation, mineralization, and calvarial bone development.

14 eased ALP activity and osteocalcin levels of calvarial bone extracts.

15 purified from conditioned medium stimulated calvarial bone formation and induced osteoblast differen

16 mvastatin has been shown to stimulate murine calvarial bone growth after multiple injections.

17 osteogenic fronts is the main mechanism for calvarial bone growth, but importantly, we show that sut

18 at suture mesenchyme cells can contribute to calvarial bone growth.

19 nitor cell population determines the rate of calvarial bone growth.

20 Mice lacking En1 exhibit generalized calvarial bone hypoplasia and persistent widening of the

21 microscopy to perform imaging studies of the calvarial bone marrow (BM) of xenografted mice, we show

22 current intravital imaging approaches in the calvarial bone marrow(3-5).

23 ription factor that controls ossification in calvarial bone of the developing skull.

24 We have utilized our unique live mouse calvarial bone organ culture models under conditions whi

25 e resorption model using live mouse neonatal calvarial bone organ cultures stimulated by parathyroid

26 nflammatory signal was found in meninges and calvarial bone overlying the occipital lobe in migraine

27 After 12 weeks, calvarial bone regeneration was evaluated radiographical

28 (TNF) activities only partially account for calvarial bone resorption induced by local application o

29 o, in a mouse model of P. gingivalis-induced calvarial bone resorption, injection of mmu-miR-155-5p o

30 r confirmed in osteoprogenitors close to the calvarial bone surface.

31 t-like MG-63 cell proliferation in vitro and calvarial bone thickness following in vivo administratio

32 These hypomorphic mice have altered calvarial bone volume, as observed by histology and micr

33 e intravital imaging studies using a chronic calvarial bone window showed that our QD-Ab conjugates d

34 athogen Porphyromonas gingivalis adjacent to calvarial bone with or without prior immunization agains

35 ties of the ITOP by fabricating mandible and calvarial bone, cartilage and skeletal muscle.

36 structures--such as the mandibular condyle, calvarial bone, cranial suture, and subcutaneous adipose

37 Furthermore, anomalies were restricted to calvarial bone, despite generalized, non-tissue-specific

38 2-arachidonoylglycerol, in the contralateral calvarial bone, whereas brain levels remained unchanged.

39 (P = 0.02) increase at the thickest point of calvarial bone, while MEM-SIM caused a highly significan

40 fferentiation and bone formation in cultured calvarial bone.

41 As the calvarial bones advance to envelop the brain, fibrous su

42 ellular mechanisms control the growth of the calvarial bones and conversely, what is the fate of the

43 rder that results in the premature fusion of calvarial bones and ensuing abnormalities in skull shape

44 blation of Tbx1 affected Runx2 expression in calvarial bones and overexpression of Tbx1 induced Runx2

45 n bone resorption in cultured neonatal mouse calvarial bones and their interaction with glucocorticoi

46 e fate of the sutural mesenchymal cells when calvarial bones approximate to form a suture.

47 testify that their headache feels as if the calvarial bones are deformed, crushed, or broken.

48 This has lead us to postulate that the calvarial bones are supplied by sensory fibers.

49 TNF administration over calvarial bones caused decreases in Smad1 and Runx2 prot

50 yer origins of the mesenchyme that forms the calvarial bones from inductive signaling that establishe

51 stimulated by ATRA was also blocked by GC in calvarial bones from mice with a GR mutation that blocks

52 raniosynostosis, the premature fusion of the calvarial bones of the skull, is a relatively common ped

53 s that serve as growth centers and allow the calvarial bones to expand as the brain enlarges.

54 Exposure of calvarial bones to GC inhibited the stimulatory effects

55 he broadly expressed CMV promoter causes the calvarial bones to invade the sagittal suture.

56 ostosis, the premature fusion of one or more calvarial bones with consequent abnormalities in skull s

57 alyses showed defective dentin, alveolar and calvarial bones, and sutures during development.

58 increased uptake were also detected in other calvarial bones, in several vertebras and in the proxima

59 mal spinal curvatures, and dysmorphic facial/calvarial bones, similar to the human phenotype.

60 inoic acid stimulated release of (45)Ca from calvarial bones.

61 tors (RARalpha/beta/gamma) were expressed in calvarial bones.

62 fferentiation of osteoblasts, which form the calvarial bones.

63 lastic cells in the osteogenic fronts of the calvarial bones.

64 defect characterized by premature fusion of calvarial bones.

65 cible Cre-ER-mediated ALK5-deficient primary calvarial cell cultures, we found that TGF-beta signalin

66 The spontaneously immortalized murine calvarial cell line MC3T3-E1 and its derivative subclone

67 Embryonic osteogenic calvarial cells (EOCCs) were isolated from fetuses at ge

68 Moreover, fetal rat osteogenic calvarial cells (FOCCs) from these obese dams have signi

69 Re-plating assays of primary RB1(-/-) calvarial cells after differentiation showed a clear adi

70 Using primary calvarial cells and explants, C3H10T1/2 cells, and C2C12

71 entiation after transfection into Runx2-null calvarial cells and mesenchymal cells.

72 GF expression was down-regulated in Osx-null calvarial cells and that osteoblast marker osteocalcin e

73 Calvarial cells but not embryonic fibroblasts from Runx2

74 Reintroduction of Runx2 into Runx2(-/-) calvarial cells by adenoviral delivery restores stringen

75 Consistently, Cpdm primary calvarial cells display reduced osteogenic capacity ex v

76 Finally, cultured Ku70 -/- calvarial cells exhibit a profound, selective deficiency

77 els of Runx2, Col1, and OPN identified using calvarial cells from DSPP-null and wild-type mice in an

78 ted in ex vivo cell culture of primary fetal calvarial cells from p47(phox-/-) mice.

79 was suppressed by ENPP1-specific shRNA, and calvarial cells isolated from Enpp1 knock-out mice show

80 First, in calvarial cells of embryonic day (E)18.5 Osx-null embryo

81 n both bone marrow stromal cells (BMSCs) and calvarial cells of mutant mice.

82 ivo overexpression of RCAS-Dlx5WT in BSP/TVA calvarial cells promoted, whereas that of RCAS-Dlx5RH in

83 man mesenchymal stem cells and primary mouse calvarial cells resulted in increased osteogenic capacit

84 n osteogenesis, and that in primary RB1(-/-) calvarial cells there is an increased osteoprogenitor po

85 When rat primary calvarial cells were cultured on the scaffolds in biorea

86 nicotine exposure increased proliferation in calvarial cells, an effect that was modified by receptor

87 Axin2 levels are elevated in Runx2(-/-) calvarial cells, and Runx2 represses transcription of Ax

88 c differentiation of C2C12 cells and primary calvarial cells, and suppression of this endogenous expr

89 asts accelerated in vitro differentiation of calvarial cells, as well as in vivo bone development, wh

90 in OC expression as compared with wild-type calvarial cells, confirming the biochemical data showing

91 dipogenic potential to immortalized RB1(+/+) calvarial cells, suggesting that these traits are not a

92 verexpression/knockdown studies in fetal rat calvarial cells, we show that thiazides increase the for

93 on in vitro differentiation of primary mouse calvarial cells.

94 1 endocytosis in pre-osteoblasts and primary calvarial cells.

95 LECT1, NGAL and PEDF are expressed by other calvarial cells.

96 Golgi and plasma membrane fractions of mouse calvarial cells.

97 lateral cerebellar atrophy, and compensatory calvarial changes.

98 Mass spectrometry analysis of Calvarial-CM identified 132 secreted factors.

99 Using live-cell imaging, we found that Calvarial-CM treatment increased cellular quiescence in

100 ding DKK3, BMP1, neogenin and vasorin in the Calvarial-CM.

101 yostatin deficiency altered fetal growth and calvarial collagen content of newborn mice and conferred

102 Type I calvarial collagen isolated from these mice showed reduc

103 The materials were placed into 8-mm calvarial critical-size defects (CSD).

104 treatment groups and anesthetized, and 8 mm calvarial critical-sized defects were created.

105 ed bone cell populations at days 7 and 17 of calvarial cultures revealed an increased specificity reg

106 In calvarial cultures we reduced osteoprogenitor cell proli

107 atic enhancement of bone formation in intact calvarial cultures.

108 profiles were evaluated in a critical-sized calvarial defect model in rats.

109 able of regenerating bone in a critical size calvarial defect model when transduced with BMP 2 or 4;

110 rogels in vivo with the critical-sized mouse calvarial defect model.

111 te bone formation in a murine critical-sized calvarial defect model.

112 bone regeneration utilizing a critical size calvarial defect model.

113 e-dimensional settings as well as in a mouse calvarial defect model.

114 y improved BMMSC-based bone regeneration and calvarial defect repair in C57BL/6 mice.

115 ibe the protocol for one such model, the rat calvarial defect.

116 wise to a silk scaffold and applied to a rat calvarial defect.

117 gates were implanted into rat critical-sized calvarial defects (CSD).

118 nsplants were introduced into critical-sized calvarial defects and contralateral control skull defect

119 cally enhanced the healing of critical-sized calvarial defects and increased both bone volume fractio

120 n transduced WT MDSCs when transplanted into calvarial defects created in CD-1 nude mice.

121 r transplanting MDSCs into the critical-size calvarial defects created in normal mice, we found that

122 alone or with endothelial cells into 8.5-mm calvarial defects created in nude rats.

123 to radio-opacity of microscopically ossified calvarial defects filled with fibroblast-free, BMP2-load

124 lly transduced BLK cells into critical-sized calvarial defects generated in C57BL6 mice.

125 To test this hypothesis, we created 40 calvarial defects in 20 12-week-old New Zealand White ra

126 phogenic protein 2 (BMP2) driving healing of calvarial defects in 4 weeks by a mechanism mediated in

127 were also investigated using critical-sized calvarial defects in mice repaired with noggin-suppresse

128 performed through standardized critical-size calvarial defects in rats treated with CEMP-1-p1 resulte

129 erimental) were implanted in two midsagittal calvarial defects in the parietal bone.

130 ted new bone formation to heal critical-size calvarial defects in vivo.

131 of the knee joints of experimental rats and calvarial defects of Jax mice.

132 ells; P = .02 and P = .04, respectively) and calvarial defects of recipient mice (mean, 21.7 msec vs

133 ell-1 protein-coated PLGA scaffolds into rat calvarial defects revealed the osteogenic potential of N

134 aseous ozone on bone healing in diabetic rat calvarial defects treated with xenografts.

135 Most Msx2-mutant phenotypes, including calvarial defects, are enhanced by genetic combination w

136 collagen-producing cells resulted in severe calvarial defects, decreased bone size, bone mineral den

137 into experimentally induced nonself healing calvarial defects, GW treatment substantially increased

138 ed MSCs (AT-MSCs) on the regeneration of rat calvarial defects.

139 dura mater cells to heal critical-size mouse calvarial defects.

140 but not adult, osteoblasts successfully heal calvarial defects.

141 n alloplast on the healing of critical-sized calvarial defects.

142 osteoblastic and keratinocyte cell lines and calvarial derived osteoblasts in which the expression of

143 rived adult stromal (ADAS) cells, BMS cells, calvarial-derived osteoblasts and dura mater cells to he

144 with bone marrow stromal cells and juvenile calvarial-derived osteoblasts.

145 ls having a better progenitor potential than calvarial-derived stromal cells.

146 , in an acute model of P. gingivalis-induced calvarial destruction, administration of Kava-205Me sign

147 panding and differentiating abilities during calvarial development and homeostastic maintenance.

148 Ps) correlated with key events in post-natal calvarial development and MC3T3 cell mineralization.

149 le-suture synostosis; by contrast, embryonic calvarial development appears mildly delayed.

150 s thus identify a novel mechanism underlying calvarial development in craniosynostosis.

151 he neural crest results in severe defects in calvarial development, although the cellular and molecul

152 have important regulatory roles in postnatal calvarial development.

153 s suggest that Msx genes have a dual role in calvarial development: They are required for the differe

154 d post-natal growth regulation of individual calvarial elements.

155 Finally, we measured brain and calvarial endocannabinoids levels post-mTBI.

156 appaB ligand (RANKL) in osteocytes and mouse calvarial explants and preferentially induces apoptosis

157 In the current study, cultured calvarial explants isolated from Nell-1 transgenic newbo

158 Osteoblasts from both stromal and calvarial explants showed delayed maturation in vitro as

159 We trace the origin of the calvarial foramen defect in Msx2 mutant mice to a group

160 defects of skull ossification and persistent calvarial foramen.

161 tations in MSX2 and TWIST are known to cause calvarial foramina in humans.

162 One such anomaly is familial calvarial foramina, persistent unossified areas within t

163 cts in craniofacial bones including impaired calvarial growth and frontal suture formation, cranial b

164 lations have a huge potential to predict the calvarial growth and optimise the management of this con

165 ha7, beta2, beta4 were identified within the calvarial growth sites (sutures) and centers (synchondro

166 Expansion of the brain is coupled with calvarial growth through a series of tissue interactions

167 Calvarial growth was simulated to predict the skull morp

168 s by combining their understanding of normal calvarial growth with a careful physical examination.

169 are able to recruit native cells and promote calvarial healing without delivery of additional therape

170 their ability to induce bone formation in a calvarial induction assay.

171 anial neural crest (CNC) and consists of the calvarial (lateral) aspect that covers the frontal lobe

172 Mineralization density was reduced in calvarial, maxillary, and mandibular alveolar bone follo

173 A reduction in calvarial membranous bone deposition and mineralization

174 sion pattern of FGF ligands and receptors of calvarial mesenchymal cells during their own osteogenic

175 ), and Bmp2 are expressed ectopically in the calvarial mesenchyme, which results in aberrant osteobla

176 s, including dental abnormalities, deficient calvarial mineralization, and reduced bone mass.

177 is was accomplished by the use of an in vivo calvarial model in mice with targeted deletion of TNF re

178 connective tissue, we used a well-documented calvarial model to study host-bacterium interactions.

179 Utilizing a murine calvarial model, Mk2(+/+) and Mk2(-/-) mice were treated

180 ure mesenchyme serves as a growth centre for calvarial morphogenesis and has been postulated to act a

181 eoprogenitors at the osteogenic front during calvarial morphogenesis, and closely resembles that asso

182 inite element method was used to predict the calvarial morphology of a patient based on its preoperat

183 del highlighted that a comparable pattern of calvarial morphology to the follow up CT data could be o

184 Calvarial OBs were cultured in the presence of MKs for v

185 Mouse calvarial organ culture revealed that EGF elevated the n

186 ith these data, addition of IL-7 to neonatal calvarial organ cultures blocked new bone formation, and

187 tion in both mesenchymal stem cell lines and calvarial organ cultures.

188 socket healing, AMC spheroids/FDBG promoted calvarial osseous defect regeneration, and the outcomes

189 h freeze-dried bone graft (FDBG) to fill rat calvarial osseous defects.

190 f immature animals to orchestrate successful calvarial ossification has been well described.

191 oreactors and 3D scaffolds for culturing rat calvarial osteoblast cells.

192 ssed during the proliferative phase of mouse calvarial osteoblast cultures but was preferentially dow

193 Primary calvarial osteoblast cultures demonstrated that the 2.5

194 Primary calvarial osteoblast cultures derived from 5- to 7-day-o

195 is of Amel- and Ambn-deficient calvariae and calvarial osteoblast cultures revealed a dramatic reduct

196 Primary mouse calvarial osteoblast cultures were established and inocu

197 way in the bone collar as well as in primary calvarial osteoblast cultures.

198 in the UMR cells, but was reduced in the rat calvarial osteoblast cultures.

199 The calvarial osteoblast development is significantly affect

200 In vitro, Nell-1 overexpression accelerated calvarial osteoblast differentiation and mineralization

201 study identifies EN1 as a novel modulator of calvarial osteoblast differentiation and proliferation,

202 , an autocrine canonical Wnt, during primary calvarial osteoblast differentiation revealed that scler

203 s total lipids and lipid fractions inhibited calvarial osteoblast gene expression and function in viv

204 h factors (FGFs) are important regulators of calvarial osteoblast growth and differentiation.

205 e effects of FGF treatment on primary murine calvarial osteoblast, and on OB1, a newly established os

206 th a more osteogenic differentiated state of calvarial osteoblast.

207 R 106-01 osteosarcoma cells, and primary rat calvarial osteoblastic cells also express another gap ju

208 reduced approximately 40-50% in fetal mouse calvarial osteoblastic cells exposed to 1% ethanol for 4

209 by FGF2 in phenotypically immature MC3T3-E1 calvarial osteoblastic cells.

210 eralization of bone nodules in primary mouse calvarial osteoblastic cultures was completely blocked b

211 Murine calvarial osteoblasts (MOBs) were grown in OST medium fo

212 However, when calvarial osteoblasts (OBs) were isolated from neonatal

213 high levels in testis and at lower levels in calvarial osteoblasts and brain.

214 velopment of the osteoblast phenotype in rat calvarial osteoblasts and in proliferating and growth-in

215 l studies, and ex vivo differentiation using calvarial osteoblasts and marrow stromal cells identifie

216 Ai mediated depletion of EMILIN-1 in primary calvarial osteoblasts and MC3T3-E1 cells only fibulin-4

217 OC expression in calvarial osteoblasts and odontoblasts is regulated in p

218 eletogenic mesenchyme, and, subsequently, to calvarial osteoblasts and osteoprogenitors.

219 ulation of Runx2 is also observed in primary calvarial osteoblasts and other osteoblastic cells with

220 uppression (luciferase reporter) in MC3T3-E1 calvarial osteoblasts as an assay.

221 wed increased mineral deposition by Enpp1-/- calvarial osteoblasts but decreased mineral deposition b

222 Using calvarial osteoblasts derived from wild-type and MN1 kno

223 ginning at the mineralization stage shown in calvarial osteoblasts ex vivo and supported by significa

224 Cultured RB1(-/-) calvarial osteoblasts fail to cease proliferation upon r

225 In calvarial osteoblasts from Col-luc transgenic mice carry

226 Calvarial osteoblasts from mice carrying floxed IGF-1R a

227 Calvarial osteoblasts from mice homozygous for the floxe

228 nd transcriptional activity were elevated in calvarial osteoblasts from TgMek-sp mice and reduced in

229 on in cocultures of spleen cells and primary calvarial osteoblasts from wild-type (WT) and IL-1R type

230 on of Runx2 to bone cell proliferation using calvarial osteoblasts from wild-type and Runx2-deficient

231 nthetic collagen peptide analog and cultured calvarial osteoblasts in conjunction with mass spectrome

232 gulates the expression of the OC promoter in calvarial osteoblasts in part by de-repression, antagoni

233 Sox2 is expressed in calvarial osteoblasts in vivo and we show that constitut

234 Expression of OST-PTP mRNA in primary rat calvarial osteoblasts is temporally regulated, and peak

235 In addition, primary mouse calvarial osteoblasts isolated from CCR3-deficient mice

236 Release of ATP in the primary calvarial osteoblasts occurred within 1 min of onset of

237 Calvarial osteoblasts prepared from c-Abl null mice show

238 Primary calvarial osteoblasts proliferated more quickly but had

239 Further, transplantation of primary rat calvarial osteoblasts revealed statistically significant

240 ling in TgFGF mice also induced apoptosis in calvarial osteoblasts that was not, however, corrected b

241 and analysis of differentiating primary rat calvarial osteoblasts verified that both IL-18 mRNA and

242 Treatment of fetal rat calvarial osteoblasts with a 70-kDa N-terminal fibronect

243 C3TC-E1 and RAW 264.7 cells), primary murine calvarial osteoblasts, and bone marrow-derived osteoclas

244 In MC3T3E1 calvarial osteoblasts, fibroblast growth factor receptor

245 To delete Cnb1 in vitro, primary calvarial osteoblasts, harvested from Cnb1(f/f) mice, we

246 Primary calvarial osteoblasts, isolated from 3-day-old NZO and c

247 both primary rat calvarial and MC3T3E1 mouse calvarial osteoblasts, transient expression of Dlx5 only

248 5 and Msx2 are both expressed by primary rat calvarial osteoblasts, we examined whether Msx2 and Dlx5

249 of Igfbp2(-/-) bone marrow stromal cells and calvarial osteoblasts.

250 g the appropriate maturation and function of calvarial osteoblasts.

251 nal resemblance to the others, or to primary calvarial osteoblasts.

252 is shows that EN1 regulates FGF signaling in calvarial osteoblasts.

253 th plate chondrocytes, as well as in primary calvarial osteoblasts.

254 ense orientations, on primary cultured chick calvarial osteoblasts.

255 regulated during differentiation of MC3T3E1 calvarial osteoblasts.

256 expression profile of subclone 4 and primary calvarial osteoblasts.

257 RAP74 that regulate OC promoter activity in calvarial osteoblasts.

258 expression by FGF and cyclic AMP in MC3T3-E1 calvarial osteoblasts.

259 and it showed no effect on OPG expression in calvarial osteoblasts.

260 ed reduced N-cadherin expression in RB1(-/-) calvarial osteoblasts.

261 Moreover, EN1 indirectly influences calvarial osteoclast recruitment and bone resorption by

262 s required for both early and late phases of calvarial osteogenesis.

263 s provides insight into normal mechanisms of calvarial osteogenesis.

264 Rat calvarial osteogenic cells were cultured on Ti disks wit

265 actor receptor 2 (Fgfr2) in regulating early calvarial osteogenic differentiation, and postulate that

266 n of activity in an MSX2-mediated pathway of calvarial osteogenic differentiation.

267 nium particle-induced osteoclastogenesis and calvarial osteolysis in vitro, ex vivo and in vivo.

268 ing/closed sutures in these animals revealed calvarial overgrowth and overlap along with increased os

269 In summary, Nell-1 overexpression induced calvarial overgrowth resulting in premature suture closu

270 Increased calvarial periosteal and tibial/femoral endosteal bone d

271 onses in affected (ie, where the head hurts) calvarial periosteum of (1) patients whose CMs are assoc

272 stitial collagenase mRNA was detected in the calvarial periosteum of PTH-treated, but not vehicle-tre

273 roinflammatory genes (eg, CCL8, TLR2) in the calvarial periosteum significantly increased in CM patie

274 the brain, fibrous sutures form between the calvarial plates.

275 ) completely abrogated the effect of mTBI on calvarial porosity and significantly reduced MCD, compar

276 over, elevated osteoclasts and intracortical/calvarial porosity is exacerbated by overexpressing Sost

277 Calvarial pre-osteoblasts from Bmpr1b mutant showed comp

278 Different from calvarial pre-osteoblasts, Bmpr1b mutant bone marrow mes

279 However when calvarial progenitor cells derived from the same transge

280 Calvarial reconstruction is the most common treatment op

281 only by P. gingivalis LPS and FimA in mouse calvarial scalp, further confirming the differences of c

282 ved cells (ADCs) to regenerate critical size calvarial (superior portion of the skull) defects in mic

283 Calcein labeling of calvarial surfaces was increased in Col1a1(r/r) relative

284 actyly syndrome in which premature fusion of calvarial suture (craniosynostosis) is an infrequent but

285 efect model ex vivo as well as its effect on calvarial suture closure.

286 Exposing murine calvarial suture derived cells and isotype cells to rele

287 That it may function in calvarial suture development and figure in the pathophys

288 suggest a novel role for Gli3 in regulating calvarial suture development by controlling canonical Bm

289 s that infiltrate the periosteum through the calvarial sutures may be positioned to mediate migraine

290 expressed during premature bone formation in calvarial sutures of craniosynostosis patients.

291 e-specific overexpression of Msx2 within the calvarial sutures to address the developmental mechanism

292 icantly increase premature bone formation in calvarial sutures.

293 Axin2 to prevent the untimely closure of the calvarial sutures.

294 A trend toward calvarial thickening was observed in patients with conco

295 regulated chemokines CCL3 and CCL4 in murine calvarial tissue.

296 tivation of p38 signaling in mutant skin and calvarial tissues.

297 In addition, calvarial uptake correlated linearly with the number of

298 PTH treatment increased calvarial uptake of 64Cu-CB-TE2A-c(RGDyK), compared with

299 TNFalpha injected over the calvarial vault caused a greater increase in osteoclast

300 aB ligand (RANKL) or PTHrP in vivo increased calvarial vessel density and osteoclast number.