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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  formation because no significant changes in osteoblast number and bone formation rate were observed.
10 in bone mass was due to an early increase in osteoblast number and bone formation rate, mediated by a
11 ading to, among other changes, a decrease in osteoblast number and bone formation.
12                                              Osteoblast number and bone resorption were not altered.
13                   Effects of mobilization on osteoblast number and function depend on the function of
14 evere osteopenia due to a marked decrease in osteoblast number and function, although bone resorption
15    Hey2 transgenic females exhibited reduced osteoblast number and function, but no changes in bone r
16 last numbers, with no significant effects on osteoblast number and function.
17 es (expressing Osterix1) exhibited increased osteoblast number and high bone mass that was maintained
18 dvancing age in mice is because of decreased osteoblast number and is associated with increased oxida
19 -R(-/-) bones exhibit a striking increase in osteoblast number and matrix accumulation.
20                                              Osteoblast number and mineral apposition rate were signi
21 reased bone mass was the result of increased osteoblast number and osteoblast activity with unaltered
22 s from a combination of Wnt-driven increased osteoblast number and resorption-dependent osteoblast ac
23                                 In contrast, osteoblast number and surface and bone formation rate in
24    OG2-DeltaFosB mice demonstrated increased osteoblast numbers and an osteosclerotic phenotype but n
25 ment with anti-sclerostin antibody increased osteoblast numbers and bone formation rate but did not i
26 , PTH administration significantly increased osteoblast numbers and bone formation rate in both contr
27  showed significantly reduced osteoclast and osteoblast numbers and exhibited an osteopenic bone phen
28  deficient in PP5 phosphatase have increased osteoblast numbers and high bone formation, which result
29           This was associated with increased osteoblast numbers and osteoblast activity based on bone
30 rden, mouse IL-6, and osteoclasts, increased osteoblast number, and inhibited bone destruction as mea
31 ed osteoblast function without a decrease in osteoblast numbers, and by increased bone resorption tha
32 emonstrate low bone mineral density, reduced osteoblast numbers, and increased osteoclast numbers.
33 , increased osteoclastogenesis and decreased osteoblast number, as quantified by histomorphometry and
34 revention was attributable to maintenance of osteoblast numbers because inhibition of serotonin recep
35 ate osteoblast apoptosis, thereby increasing osteoblast number, bone formation rate, and bone mass, b
36  were associated with low osteoclast number, osteoblast number, bone formation rate, and wall width i
37                                              Osteoblast number, bone volume, and trabecular thickness
38 icantly reduced these changes; SCI decreased osteoblast numbers, but increased expression in these ce
39 ed greater bone volume by twofold and higher osteoblast number by threefold, compared with the contro
40                       Teriparatide increases osteoblast numbers by suppressing osteoblast apoptosis a
41                                 We show that osteoblast numbers decrease by 55% in myelodysplasia and
42 d significant increase in osteoid thickness, osteoblast number, erosion surface with osteoclasts, and
43                           Besides increasing osteoblast number in the trabecular bone, deletion of Bm
44  reduced bone formation because of decreased osteoblast numbers in response to ibandronate.
45  osteoblasts lining trabecular bone, whereas osteoblast numbers in similarly treated mice lacking the
46                                              Osteoblast numbers in SR625 group were significantly hig
47 of duodenal serotonin, a hormone suppressing osteoblast numbers, inhibited loss of osteoblasts.
48 ce have low bone mass accompanied by reduced osteoblast numbers, low bone formation rates, and increa
49      In vivo, MAGP1Delta mice exhibit normal osteoblast number, mineralized bone surface, and bone fo
50 varia in vivo model, cause a 50% decrease in osteoblast number (N.Ob-BS) and a 32% decrease in minera
51  were no differences in adipocyte number and osteoblast number or activity.
52 s and bone resorption, without a decrease in osteoblast number or bone formation.
53 steoclast (OC) numbers, but had no change in osteoblast numbers or bone formation rate.
54 position rates) and static (osteoid markers, osteoblast number) parameters of bone formation were dec
55  characterized by significant depressions in osteoblast number, perimeters, bone formation rates, and
56 o reduced osteoclast formation and increased osteoblast numbers, respectively.
57 of HBD peptide to Igfbp2(-/-) mice increased osteoblast number, suppressed marrow adipogenesis, resto
58  mice, which was due to a marked increase in osteoblast number that was likely to be driven by hyperp
59                                              Osteoblast number was markedly decreased and osteogenic
60    Although CFU-fibroblast (CFU-F) and total osteoblast numbers were decreased, the bone formation ra
61 R625, and SR900 groups, significantly higher osteoblast numbers were detected than in control group (
62 contrast, new bone and osteoid formation and osteoblast numbers were increased significantly vs. untr
63                               Interestingly, osteoblast numbers were maintained despite the anti-reso
64 clast numbers and progressive bone loss, but osteoblast numbers were not coordinately increased, as i
65         Consistently, significantly elevated osteoblast numbers were noted.
66  found that the TIEG(-/-) mice had increased osteoblast numbers with no increased bone formation para
67 mr(-/-)) also had reduced bone formation and osteoblast number within the injury site.

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