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1  This suggests that FSH negatively regulates osteoblast number.
2 ing to increased mineral apposition rate and osteoblast number.
3 ar bone with thinner cortices, and decreased osteoblast number.
4 one volume and BFR as well as osteoclast and osteoblast numbers.
5 rsus non-Tg siblings, arising from increased osteoblast numbers.
6 tis, clopidogrel had little effect on MSC or osteoblasts numbers.
7 olume (32%), trabecular thickness (29%), and osteoblast numbers (68%) as well as a 40% decrease in os
8 ytes stimulated bone formation by increasing osteoblast number and activity, which was due in part to
9 -expressing cells resulted in an increase in osteoblast number and an increased rate of mineral appos
10  formation because no significant changes in osteoblast number and bone formation rate were observed.
11 in bone mass was due to an early increase in osteoblast number and bone formation rate, mediated by a
12 ading to, among other changes, a decrease in osteoblast number and bone formation.
13                                              Osteoblast number and bone resorption were not altered.
14  inhibition, or local P-SSC ablation reduces osteoblast number and delays bone healing.
15                   Effects of mobilization on osteoblast number and function depend on the function of
16 evere osteopenia due to a marked decrease in osteoblast number and function, although bone resorption
17    Hey2 transgenic females exhibited reduced osteoblast number and function, but no changes in bone r
18 last numbers, with no significant effects on osteoblast number and function.
19 icoid-induced bone loss, thanks to increased osteoblast number and function.
20 L-C reduces bone mineral density by reducing osteoblast number and function.
21 es (expressing Osterix1) exhibited increased osteoblast number and high bone mass that was maintained
22 dvancing age in mice is because of decreased osteoblast number and is associated with increased oxida
23 -R(-/-) bones exhibit a striking increase in osteoblast number and matrix accumulation.
24                                              Osteoblast number and mineral apposition rate were signi
25 reased bone mass was the result of increased osteoblast number and osteoblast activity with unaltered
26 s from a combination of Wnt-driven increased osteoblast number and resorption-dependent osteoblast ac
27                                 In contrast, osteoblast number and surface and bone formation rate in
28    OG2-DeltaFosB mice demonstrated increased osteoblast numbers and an osteosclerotic phenotype but n
29  the small molecule inhibitor R992 increases osteoblast numbers and bone formation in mice.
30 ment with anti-sclerostin antibody increased osteoblast numbers and bone formation rate but did not i
31 , PTH administration significantly increased osteoblast numbers and bone formation rate in both contr
32  uncovers a pivotal mechanism for increasing osteoblast numbers and bone formation, resulting in grea
33  showed significantly reduced osteoclast and osteoblast numbers and exhibited an osteopenic bone phen
34 ment with E197 did not affect osteoclast and osteoblast numbers and hence did not impair bone formati
35  deficient in PP5 phosphatase have increased osteoblast numbers and high bone formation, which result
36           This was associated with increased osteoblast numbers and osteoblast activity based on bone
37 necessary for the ability of PTH to increase osteoblast numbers and stimulate bone formation.
38 rden, mouse IL-6, and osteoclasts, increased osteoblast number, and inhibited bone destruction as mea
39 ed osteoblast function without a decrease in osteoblast numbers, and by increased bone resorption tha
40 emonstrate low bone mineral density, reduced osteoblast numbers, and increased osteoclast numbers.
41 , increased osteoclastogenesis and decreased osteoblast number, as quantified by histomorphometry and
42 revention was attributable to maintenance of osteoblast numbers because inhibition of serotonin recep
43 ate osteoblast apoptosis, thereby increasing osteoblast number, bone formation rate, and bone mass, b
44  were associated with low osteoclast number, osteoblast number, bone formation rate, and wall width i
45                                              Osteoblast number, bone volume, and trabecular thickness
46 and negatively correlated with BV/TV and the osteoblast number (both P < 0.01).
47 icantly reduced these changes; SCI decreased osteoblast numbers, but increased expression in these ce
48 ed greater bone volume by twofold and higher osteoblast number by threefold, compared with the contro
49                       Teriparatide increases osteoblast numbers by suppressing osteoblast apoptosis a
50                                 We show that osteoblast numbers decrease by 55% in myelodysplasia and
51 d significant increase in osteoid thickness, osteoblast number, erosion surface with osteoclasts, and
52                           Besides increasing osteoblast number in the trabecular bone, deletion of Bm
53  reduced bone formation because of decreased osteoblast numbers in response to ibandronate.
54  osteoblasts lining trabecular bone, whereas osteoblast numbers in similarly treated mice lacking the
55                                              Osteoblast numbers in SR625 group were significantly hig
56 of duodenal serotonin, a hormone suppressing osteoblast numbers, inhibited loss of osteoblasts.
57 ce have low bone mass accompanied by reduced osteoblast numbers, low bone formation rates, and increa
58      In vivo, MAGP1Delta mice exhibit normal osteoblast number, mineralized bone surface, and bone fo
59 varia in vivo model, cause a 50% decrease in osteoblast number (N.Ob-BS) and a 32% decrease in minera
60  were no differences in adipocyte number and osteoblast number or activity.
61 s and bone resorption, without a decrease in osteoblast number or bone formation.
62 steoclast (OC) numbers, but had no change in osteoblast numbers or bone formation rate.
63 position rates) and static (osteoid markers, osteoblast number) parameters of bone formation were dec
64  characterized by significant depressions in osteoblast number, perimeters, bone formation rates, and
65 o reduced osteoclast formation and increased osteoblast numbers, respectively.
66 of HBD peptide to Igfbp2(-/-) mice increased osteoblast number, suppressed marrow adipogenesis, resto
67  mice, which was due to a marked increase in osteoblast number that was likely to be driven by hyperp
68                                 In contrast, osteoblast number was increased 3-8-fold with PTH treatm
69                                              Osteoblast number was markedly decreased and osteogenic
70    Although CFU-fibroblast (CFU-F) and total osteoblast numbers were decreased, the bone formation ra
71 R625, and SR900 groups, significantly higher osteoblast numbers were detected than in control group (
72 contrast, new bone and osteoid formation and osteoblast numbers were increased significantly vs. untr
73                               Interestingly, osteoblast numbers were maintained despite the anti-reso
74 clast numbers and progressive bone loss, but osteoblast numbers were not coordinately increased, as i
75         Consistently, significantly elevated osteoblast numbers were noted.
76 ological approaches result in an increase in osteoblast number, which is linked to the expansion of t
77  found that the TIEG(-/-) mice had increased osteoblast numbers with no increased bone formation para
78 mr(-/-)) also had reduced bone formation and osteoblast number within the injury site.