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1 cancer cells that are involved in increasing osteoclast activity.
2 rly adulthood, show increased osteoblast and osteoclast activity.
3                    Other fractions inhibited osteoclast activity.
4 amate is less important in regulating mature osteoclast activity.
5 day 7 of culture was ineffective in reducing osteoclast activity.
6 factors produced by osteoclasts that inhibit osteoclast activity.
7 used appeared to be the strongest inducer of osteoclast activity.
8 nt of osteoporosis associated with increased osteoclast activity.
9 her with subchondral bone loss and increased osteoclast activity.
10 ited bone loss and resorption by suppressing osteoclast activity.
11 neral density, consistent with inhibition of osteoclast activity.
12 mpared with WT controls due to a decrease in osteoclast activity.
13 rosine kinase also mediates RANKL-stimulated osteoclast activity.
14 ivity and bone formation, and an increase in osteoclast activity.
15 dral bone are likely attributed to increased osteoclast activity.
16 ls, indicating that Hh signaling is vital to osteoclast activity.
17 ing formation were measured as indicators of osteoclast activity.
18  functions as an autocrine factor regulating osteoclast activity.
19  bone interface exhibited microfractures and osteoclast activity.
20 esence of necrotic bone tissue and increased osteoclast activity.
21 eoporosis reflects a relative enhancement of osteoclast activity.
22 er than RANKL may mediate the cancer-induced osteoclast activity.
23 ating that mu-calpain is required for normal osteoclast activity.
24 ncy osteolytic bone metastases, and enhanced osteoclast activity.
25 opause by the balance between osteoblast and osteoclast activity.
26 ANKL) promotes resorption through regulating osteoclast activity.
27 n to regulate osteoblast differentiation and osteoclast activity.
28 sions in PC-3 implanted tibias by inhibiting osteoclast activity.
29 inavir (LPV) and amprenavir did not increase osteoclast activity.
30 t LPA1 is essential for in vitro and in vivo osteoclast activities.
31 decreased calcium efflux, medium PGE(2), and osteoclast activity; Acid led to an increase in all thre
32 n, a secreted 'decoy' receptor that inhibits osteoclast activity, also blocks behaviors indicative of
33 ha deficiency with respect to stimulation of osteoclast activity and also augments osteoblast prolife
34  increased bone mass caused by inhibition of osteoclast activity and also the strongly reduced bone f
35  osteoclast precursors, leading to increased osteoclast activity and an overall TMJ subchondral trabe
36              However, the effects of CypA on osteoclast activity and bone maintenance are entirely un
37 nuria, and hypoglycemia leading to increased osteoclast activity and bone resorption.
38 coupling signals coordinating osteoblast and osteoclast activity and finely tuned expression of infla
39                                  It inhibits osteoclast activity and is thought to result in a net in
40            DUSP-1 is a critical regulator of osteoclast activity and limits bone destruction in an ex
41  roles for ASC as an antioxidant suppressing osteoclast activity and number as well as a cofactor pro
42                       Zol markedly inhibited osteoclast activity and recruitment, promoting osteogeni
43 us delivery of these miRNAs in vivo inhibits osteoclast activity and reduces osteolytic bone metastas
44 that calpain activity is required for normal osteoclast activity and suggest that calcitonin inhibits
45 idate to inhibit multiple myeloma growth and osteoclast activity and that it should receive attention
46  indirectly on dentinogenesis by controlling osteoclast activity and the signaling network related to
47 of the galectins family, exhibit accelerated osteoclasts activity and bone turnover, which culminates
48 y plays a critical role in the regulation of osteoclast activity, and activation of the pathway is de
49 ression, a reduction in RANKL expression and osteoclast activity, and an increase in alveolar bone fo
50 KL and TNF-alpha promote osteoclastogenesis, osteoclast activity, and bone loss, WP9QY prevented the
51 ntly reduced inflammatory cell infiltration, osteoclast activity, and bone loss.
52           This agent acts as an inhibitor of osteoclast activity, and is thought to result in more ne
53                      Bisphosphonates inhibit osteoclast activity, and previous studies showed that th
54 an Igs, high blood calcium levels, increased osteoclast activity, and severe resorption of the human
55 truction, cartilage prostaglandin depletion, osteoclast activity, and Th17 production.
56 dihydroxyvitamin D(3), as well as markers of osteoclast activity, and the number of resorption lacuna
57                     Bisphosphonates suppress osteoclast activity, and their intravenous use has been
58 n in advanced stages of bone cancer, ongoing osteoclast activity appears to be involved in the genera
59                          Blockade of ongoing osteoclast activity appears to have the potential to red
60         Although the mechanisms of increased osteoclast activity are partially understood, comparativ
61 mercially available DFDBA samples on porcine osteoclast activity as measured by resorption on calcium
62 bone remodeling; they control osteoblast and osteoclast activities both directly via cell-to-cell com
63 eoprotegerin (OPG), bisphosphonates suppress osteoclast activity but not osteoclast numbers.
64 -CSF)-induced signaling, c-Src is central to osteoclast activity, but not differentiation.
65           We also showed that stimulation of osteoclast activity by parathyroid hormone is dependent
66 inflammatory arthritis, the dysregulation of osteoclast activity by proinflammatory cytokines, includ
67                                Activation of osteoclast activity by receptor activator of nuclear fac
68                           In these diseases, osteoclast activity causes bone loss that leads to pain,
69             Serum N-telopeptide, a marker of osteoclast activity, decreased significantly after zoled
70 he increases in Arf(-/-) ribosome output and osteoclast activity, demonstrating that these gains requ
71       Zoledronic acid, a potent inhibitor of osteoclast activity, differentiation, and survival, decr
72 mod(-/-) TMJs, including 5 genes involved in osteoclast activity/differentiation.
73 n bone obtained from patients with increased osteoclast activity exhibited increased NOX4 expression.
74 n tumor-bearing mice, OPG treatments reduced osteoclast activity from approximately 2-fold above norm
75 determinants of bone remodelling that affect osteoclast activity have been characterized, but the mol
76 ays that require c-Src expression for normal osteoclast activity have not been elucidated.
77           Cortical porosity is the result of osteoclast activity; however, the etiology of marrow fib
78 sely, alendronate treatment, which restricts osteoclast activity, improved bone quality but not aneur
79 s and bone mineral density without affecting osteoclast activities in young mice.
80 fically inhibit bone resorption, the lack of osteoclast activity in c-fos-/- mice, and a new transgen
81 formation provides a rationale for increased osteoclast activity in the anabolic effects of PTH in ad
82 increased osteoblast activity and diminished osteoclast activity in the HMWKO.
83 last-activating factors but rather stimulate osteoclast activity in the presence of human bone marrow
84 se (TRAP)-positive cell number, and enhanced osteoclast activity in TMJ subchondral trabecular bone o
85 ide of type I collagen, suggesting decreased osteoclast activity in vivo.
86          Here, we demonstrate that sustained osteoclast activity is largely due to accumulation of NO
87                                    Increased osteoclast activity is responsible for the enhanced bone
88 cal bone remodeling, but localized excessive osteoclast activity is responsible for the periarticular
89 iodontal disease, and osteoporosis, elevated osteoclast activity leads to bone destruction.
90                 A balance of osteoblasts and osteoclasts activities maintains bone homeostasis.
91                   These results suggest that osteoclast activity may not be critical for the developm
92                                              Osteoclast activity, measured using a rat neonatal calva
93 clast function, either by directly promoting osteoclast activity or by inhibiting osteoclast signalin
94 zoledronic acid (Zol), a potent inhibitor of osteoclast activity/osteoclastogenesis and promoter of o
95 ator of nuclear factor-kappaB ligand-induced osteoclast activity over concentration ranges that repre
96 (P <0.05), alveolar bone loss (P <0.05), and osteoclast activity (P <0.05) throughout the experimenta
97 se results emphasize the important role that osteoclast activity plays in the establishment of CaP sk
98 bits multiple myeloma cell proliferation and osteoclast activity, potentially by controlling NF-kappa
99 tifying the molecular pathways that regulate osteoclast activity provides a key to understanding the
100 tifying the molecular pathways that regulate osteoclast activity provides a key to understanding the
101 sive crises (VOCs), increased bone turnover, osteoclast activity (RankL), and osteoclast recruitment
102 togenesis (Runx2, Sparc), and increased both osteoclast activity (RankL, Cathepsin k) and osteoclast
103 g that SMURF2 regulates osteoblast-dependent osteoclast activity rather than directly affecting the o
104 the mechanism that uncouples osteoblast from osteoclast activities remains unexplained.
105 ated to osteoblast impairment, and increased osteoclast activity resulted from local hypoxia, oxidati
106 tyrosine phosphatase (PTP-oc), essential for osteoclast activity, shows sequence identity with the in
107 es was accompanied by increased staining for osteoclast activity, suggesting that there was a sex-spe
108 t lower LPS doses, other pathways leading to osteoclast activity that are independent of TNF and IL-1
109 ltiple myeloma is characterized by increased osteoclast activity that results in bone destruction and
110 hypothesis that breast cancer cells modulate osteoclast activity using multiple regulatory factors th
111 f remodeling-based bone formation coupled to osteoclast activity versus modeling-based bone formation
112 tein 6 (TRIP6) in sealing zone formation and osteoclast activity was examined.
113      Accordingly, direct evidence of reduced osteoclast activity was found in transgenic mouse skulls
114   Finally, a significant increase of chondro-osteoclast activity was observed in the P3 MSC sheet-gra
115                                          The osteoclast activity was positively correlated with OARSI
116                   Over the course of a week, osteoclast activity was responsible for resorbing the ne
117     Epithelial downgrowth, inflammation, and osteoclast activity were evaluated; alveolar bone loss w
118    Immunohistochemical staining of RANKL and osteoclast activity were significantly lower in the Mel-
119                      Bisphosphonates inhibit osteoclast activity, which is central to the development
120 eogenic markers, coupled with an increase in osteoclast activity, which resulted in a slight increase
121          Such bidirectional signaling limits osteoclast activity while stimulating osteoblast differe

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