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1 e multinucleated monocyte lineage cells with resorptive abilities, forming the bone marrow cavity dur
2 Ca(2+)](o) in bone milieu as a result of the resorptive action of osteoclasts are implicated in promo
3 o assess the role of collagenase in the bone resorptive actions of PTH, we used mice homozygous (r/r)
4 l regulatory component of bone formative and resorptive activities, and the pathway inhibitor DKK1 is
5  the proliferating capability and activating resorptive activities.
6 sponse was reversed as osteoclasts recovered resorptive activity after inhibitors were removed.
7 ]) directly stimulate osteoclastogenesis and resorptive activity and to explore the mechanisms underl
8 e cells was produced without DFDBA; however, resorptive activity appears to be significantly increase
9  porcine osteoclasts show significantly more resorptive activity as measured on calcium phosphate-coa
10 enhances osteoclast multinucleation and bone-resorptive activity by triggering upregulation of the ce
11  showed a approximately 2.5-fold increase in resorptive activity compared with wild-type cells.
12  and bone mineral density and decreased bone resorptive activity in vivo.
13 tro, and transgenic osteoblasts enhanced the resorptive activity of co-cultured osteoclast precursors
14 ne phosphatase expression and suppressed the resorptive activity of co-cultured osteoclast precursors
15         Our results demonstrate an anti-bone-resorptive activity of muscle contraction by ES that dev
16                                     The anti-resorptive activity of NE10790 is thus likely due to dis
17  nucleotides can stimulate the formation and resorptive activity of osteoclasts (bone-destroying cell
18 on of cytoskeletal structures and functional resorptive activity of osteoclasts.
19   Extracellular ADP enhanced OC adhesion and resorptive activity of WT, but not P2ry12-/-, OCs.
20 on organization, polarization, spreading and resorptive activity resulting from impaired signaling do
21 rom p91 knockout mice, explaining the normal resorptive activity seen in the osteoclasts where no p91
22  functional analyses whereby osteoclast bone resorptive activity was determined.
23 oclasts showed that osteoclast formation and resorptive activity were attenuated after treatment with
24                  Consistent with accelerated resorptive activity, 3D trabecular volume fraction, trab
25 nger inflammation, attenuated and persistent resorptive activity, and weaker proliferating potential
26 lagenases arm fibroblasts with potent matrix-resorptive activity, only MT1-MMP confers the focal coll
27 ne if this complication reflects accelerated resorptive activity, we studied the impact of two common
28  macrophages are involved in osteoclast bone resorptive activity, whereas osteoblasts promote osteocl
29 d the growth of osteoclasts without reducing resorptive activity, while osteoclasts infected with B.
30 tures, impaired maturation, and reduced bone resorptive activity.
31 s of immature OCs that exhibit impaired bone resorptive activity.
32  upwards of 100 nuclei, and exhibit enhanced resorptive activity.
33 dly decreasing bone density due to excessive resorptive activity.
34 d number of cell fusion events - have higher resorptive activity.
35 lasts, where La promotes multinucleation and resorptive activity.
36 e MMP-13-enhanced osteoclast fusion and bone-resorptive activity.
37 tinucleated giant osteoclasts and their bone resorptive activity.
38 ast numbers were maintained despite the anti-resorptive activity.
39 ta in regulating osteoclast cytoskeleton and resorptive activity.
40 ust induction of osteoclastogenesis and bone-resorptive activity.
41 ration of smaller osteoclasts with decreased resorptive activity.
42 pendently increased osteoclast formation and resorptive activity.
43 n overall decrease in osteoclastogenesis and resorptive activity.
44 s derived from mkp-1(-/-) mice had increased resorptive activity.
45 tic growth factor, VEGF-C, to increase their resorptive activity.
46 3 gene significantly abrogates TRAP and bone-resorptive activity; and (iii) inflammation-induced TRAP
47 isphosphonate risedronate and is a weak anti-resorptive agent.
48 ween the GC dexamethasone (DEX) and the bone resorptive agents 1,25(OH)(2)-vitamin D(3) (D3) and para
49 ose was to determine the effects of the anti-resorptive agents alone and in combination with intermit
50 onal studies have noted that the use of anti-resorptive agents following hip fracture, during rheumat
51                                When the anti-resorptive agents were combined with intermittent PTH, m
52                                         Anti-resorptive agents--including estrogen (E), calcitonin (C
53 ate that targeting these cells has both anti-resorptive and anabolic effects on bone.
54                                 Current anti-resorptive and anabolic therapies are insufficient for t
55 the model predicts that combinations of anti-resorptive and anabolic therapies provide significant be
56 y evaluated the antihyperglycemic, anti-bone-resorptive, and anti-inflammatory efficacy of the probio
57 actor produced more TRAP(+) MNCs and greater resorptive area.
58 ing live-cell imaging, we monitored the bone resorptive behaviour of OCs during dose-dependent inhibi
59      Alpha-halogenated analogues of the anti-resorptive bisphosphonate risedronate (5, Ris) and its p
60 th hypercalciuria and increased BTMs (mainly resorptive), but also up to 30% have hypocitraturia and
61 d enhanced osteoclast number, size, and bone resorptive capacity in BMM cultures.
62 their cytoskeleton, and, as such, their bone-resorptive capacity is arrested.
63 tion and has been shown to increase the bone-resorptive capacity of mature osteoclasts.
64 n irreversible manner and also inhibited the resorptive capacity of mature osteoclasts.
65 ter than wild type, thereby accelerating the resorptive capacity of the cell.
66 ormalize the cytoskeleton of DKO OCs and the resorptive capacity of the cells.
67  able to impair the maturation and alter the resorptive capacity of these cells.
68 e, c-Fos expression increases the number and resorptive capacity of wild-type osteoclasts induced by
69 cleated giant osteoclasts with elevated bone resorptive capacity, corroborated with an osteoporotic b
70 s reduced by retarding osteoclast functional resorptive capacity, rather than differentiation.
71 bsence of PIP5KIgamma would compromise their resorptive capacity.
72 s with increased Cdc42 activity had enhanced resorptive capacity.
73 ast fusion, sealing zone perimeter, and bone resorptive capacity.
74 n that regulates sealing dimensions and bone resorptive capacity.
75 perimeter, along with decreased motility and resorptive capacity.
76  it plays a positive role in osteoclast bone resorptive capacity.
77  with larger sealing zones and enhanced bone resorptive capacity.
78                       Thus, this unique bone resorptive cell is a prominent therapeutic target.
79 c agents that either directly block the bone-resorptive cell or do so indirectly via cytokine arrest.
80 most likely due to a dysfunction of the bone resorptive cell, the osteoclast.
81 lved in controlling the activity of the bone-resorptive cell.
82 requires intimacy between the matrix and the resorptive cell.
83 nction of the osteoclast, the exclusive bone resorptive cell.
84 gand, possibly accounting for the paucity of resorptive cells and the dominance of mineral in atheros
85 gesting that this growth factor may regulate resorptive cells either directly or indirectly.
86 s are multinucleated cells and the principal resorptive cells of bone.
87                              Osteoclasts are resorptive cells that are important for homeostatic bone
88 l ligament (PDL), followed by recruitment of resorptive cells that remove root structure.
89   To define the direct impact of GCs on bone-resorptive cells, we compared the effects of dexamethaso
90 rly, arresting their development into mature resorptive cells.
91 rved when WASp-null animals are exposed to a resorptive challenge.
92 e preservation would prevent post-extraction resorptive changes as assessed by clinical and histologi
93        The tooth most frequently affected by resorptive changes was the right central upper incisor.
94                                        These resorptive changes, when compared between treatment grou
95           Moreover, both the osteoclast bone-resorptive compartment environment and PAC traffic from
96 contribute to mechanisms that result in bone-resorptive cytokine production in periapical lesion.
97  and interleukin-1beta (IL-1), a potent bone-resorptive cytokine, have been associated with periodont
98 and interleukin 1-beta (IL-1), a potent bone-resorptive cytokine, have both been associated with peri
99 talk upregulates other inflammatory and bone-resorptive cytokines (IL-1beta, IL-6, and TNF-alpha).
100                   The expression of the bone-resorptive cytokines IL-1 alpha and TNF-alpha was also i
101  as well as with elevated expression of bone-resorptive cytokines IL-1alpha and IL-1beta, in periapic
102 rrelated with reduced expression of the bone resorptive cytokines interleukin 1alpha (IL-1alpha) (P <
103 ress high levels of pro-inflammatory and pro-resorptive cytokines.
104 givalis immune evasion and induction of bone-resorptive cytokines.
105                                          The resorptive defect in beta3-deficient osteoclasts may ref
106 ing alveolar bone extended into the existing resorptive defects, but without clinical evidence of ank
107 sion may be a viable strategy to combat bone resorptive disorders such as osteoporosis or arthritis.
108 sharing without membrane breaching in highly resorptive Drosophila rectal papillae.
109 es, concerns about rare side-effects of anti-resorptive drugs, particularly bisphosphonates, and the
110                                          The resorptive effect of ATRA was characterized by mRNA expr
111 on sufficiently to counteract its local anti-resorptive effect, thus leading to a net effect of impai
112 e that it is possible to dissociate the bone-resorptive effects of GM-CSF, to reduce metastatic risk,
113 py is indicated to attenuate the physiologic resorptive events that occur as a consequence of tooth e
114 hanced TNF-alpha increases the expression of resorptive factors in chondrocytes through a process tha
115 keletal tissues, PKA activation induces bone resorptive factors in the vasculature and that aortic SM
116 rtically disposed alternating depository and resorptive fields in relation to anterior dental roots a
117 ay a fundamental role in modulating both the resorptive function and formation of mammalian osteoclas
118 ver, the mechanisms that restrain osteoclast resorptive function are not fully understood.
119  show that GSLs are essential for enterocyte resorptive function but are primarily not for polarizati
120 s suggests that ouabain also inhibits an ion resorptive function of Na/K-ATPase in the type I acini.
121 acini, is followed by a dopamine-independent resorptive function of Na/K-ATPase in type I acini locat
122       Thus, talin1 and Rap1 are critical for resorptive function, and their selective inhibition in m
123                    In keeping with inhibited resorptive function, CtsK-VCL and LysM-VCL mice exhibit
124 ncreased in parallel with reduced osteoclast resorptive function, effects abrogated by neutralizing a
125 er of osteoclasts and activation of the bone resorptive function.
126 tact differentiation markers, but diminished resorptive function.
127 tion of osteoclast adhesion, fusion and bone resorptive function.
128 1 year without symptoms or recurrence of the resorptive lesion and the affected tooth remained vital.
129     A similar condition, feline osteoclastic resorptive lesions (FORL), affects up to 70% of domestic
130 ify the cellular source of RANKL in the bone resorptive lesions of periodontal disease.
131                                          The resorptive lesions were asymptomatic, unassociated with
132                                    Infrabony resorptive lesions were induced by surgical pulp exposur
133                         Histologically, many resorptive lesions were noted along the cementum surface
134                                          The resorptive lesions were progressive in nature, with addi
135  alveolar bone, including radiolucencies and resorptive lesions, osteoid accumulation on the alveolar
136 epithelium that functions as a high capacity resorptive machine.
137 ical improvements and GCF levels of the bone resorptive marker ICTP were significantly reduced.
138 ium stone formers have serum beta-crosslaps (resorptive marker) greater than 0.311 ng/ml, serum osteo
139                          Serum formation and resorptive markers P1NP and TRAcP 5b were decreased as w
140                                         Anti-resorptive medication inhibits bone break down and pread
141  plasmalemma results in acidification of the resorptive microenvironment and release of CatK to diges
142 tion and formation of an isolated, acidified resorptive microenvironment.
143  these data suggests that BE is a novel anti-resorptive molecule that is active both in vitro and in
144                        Oxylipids also induce resorptive osteoclastic cells within the bone environmen
145 environment, raising the question of whether resorptive osteoclasts can be harnessed in the vascular
146 is resulting from increased numbers of hyper-resorptive osteoclasts.
147 prolonged hyponatremia, thereby leading to a resorptive osteoporosis in patients with SIADH.
148 their leading edges, whereas during the bone resorptive phase multiple podosomes are densely aggregat
149 bone marrow mononuclear cells acquire a bone resorptive phenotype in vitro.
150 -76 is the dominant SLP family member in the resorptive process.
151 ing maxillary anterior teeth may be prone to resorptive processes after extraction and immediate impl
152  in managing bone diseases due to their anti-resorptive properties but are linked to medication-relat
153 rleukin 1 beta (IL-1 beta) also possess bone-resorptive properties, and are generally considered to p
154                   Peripherally, Flx has anti-resorptive properties, directly impairing osteoclast dif
155 w that BT-GSI has dual anti-myeloma and anti-resorptive properties, supporting the therapeutic approa
156 entin and root biomodification may limit the resorptive response following connective tissue graft pr
157 osteoclastogenesis and the inflammatory bone-resorptive response possibly explaining the acro-osteoly
158 ation of genes classically associated with a resorptive response.
159 y cilia are required for osteogenic and bone resorptive responses to dynamic fluid flow.
160 orption in vivo and that Caspase-1 has a pro-resorptive role in experimental periodontal disease.
161 , however, it demonstrates osteichthyan-like resorptive shedding of scale odontodes (dermal teeth) an
162  as bone mesenchymal stem cells, to the bone resorptive sites and that this process is mediated throu
163 oclast bone resorption recruits MSCs to bone-resorptive sites.
164  a fall of NTX and a shift from the dominant resorptive state, which we postulate involves full recov
165  examined the bone phenotype and response to resorptive stimuli of PAR1-deficient (knockout [KO]) mic
166 tic origin, is an attractive target for anti-resorptive therapeutics.
167                 Our model confirms that anti-resorptive therapies are unable to partially restore bon
168                These data indicate that anti-resorptive therapies may provide the most effective bone
169                                   Thus, anti-resorptive therapy could be used to prevent bone loss in
170 th calcimimetics or introducing earlier anti-resorptive treatment with bone active pharmacologic agen
171  multiple proinflammatory cytokines and bone resorptive/turnover markers.
172 hibits bone break down and preadmission anti-resorptive use is associated with superior survival amon
173 mbrane-anchored collagenases during collagen-resorptive versus collagen-invasive events.

 
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