ライフサイエンスコーパス: resorptive

1 Ca(2+)](o) in bone milieu as a result of the resorptive action of osteoclasts are implicated in promo

2 o assess the role of collagenase in the bone resorptive actions of PTH, we used mice homozygous (r/r)

3 l regulatory component of bone formative and resorptive activities, and the pathway inhibitor DKK1 is

4 the proliferating capability and activating resorptive activities.

5 sponse was reversed as osteoclasts recovered resorptive activity after inhibitors were removed.

6 ]) directly stimulate osteoclastogenesis and resorptive activity and to explore the mechanisms underl

7 e cells was produced without DFDBA; however, resorptive activity appears to be significantly increase

8 porcine osteoclasts show significantly more resorptive activity as measured on calcium phosphate-coa

9 enhances osteoclast multinucleation and bone-resorptive activity by triggering upregulation of the ce

10 showed a approximately 2.5-fold increase in resorptive activity compared with wild-type cells.

11 and bone mineral density and decreased bone resorptive activity in vivo.

12 tro, and transgenic osteoblasts enhanced the resorptive activity of co-cultured osteoclast precursors

13 ne phosphatase expression and suppressed the resorptive activity of co-cultured osteoclast precursors

14 Our results demonstrate an anti-bone-resorptive activity of muscle contraction by ES that dev

15 The anti-resorptive activity of NE10790 is thus likely due to dis

16 nucleotides can stimulate the formation and resorptive activity of osteoclasts (bone-destroying cell

17 on of cytoskeletal structures and functional resorptive activity of osteoclasts.

18 Extracellular ADP enhanced OC adhesion and resorptive activity of WT, but not P2ry12-/-, OCs.

19 on organization, polarization, spreading and resorptive activity resulting from impaired signaling do

20 rom p91 knockout mice, explaining the normal resorptive activity seen in the osteoclasts where no p91

21 functional analyses whereby osteoclast bone resorptive activity was determined.

22 oclasts showed that osteoclast formation and resorptive activity were attenuated after treatment with

23 Consistent with accelerated resorptive activity, 3D trabecular volume fraction, trab

24 nger inflammation, attenuated and persistent resorptive activity, and weaker proliferating potential

25 lagenases arm fibroblasts with potent matrix-resorptive activity, only MT1-MMP confers the focal coll

26 ne if this complication reflects accelerated resorptive activity, we studied the impact of two common

27 s of immature OCs that exhibit impaired bone resorptive activity.

28 upwards of 100 nuclei, and exhibit enhanced resorptive activity.

29 ast numbers were maintained despite the anti-resorptive activity.

30 ta in regulating osteoclast cytoskeleton and resorptive activity.

31 ust induction of osteoclastogenesis and bone-resorptive activity.

32 pendently increased osteoclast formation and resorptive activity.

33 n overall decrease in osteoclastogenesis and resorptive activity.

34 s derived from mkp-1(-/-) mice had increased resorptive activity.

35 tic growth factor, VEGF-C, to increase their resorptive activity.

36 tures, impaired maturation, and reduced bone resorptive activity.

37 3 gene significantly abrogates TRAP and bone-resorptive activity; and (iii) inflammation-induced TRAP

38 isphosphonate risedronate and is a weak anti-resorptive agent.

39 ose was to determine the effects of the anti-resorptive agents alone and in combination with intermit

40 When the anti-resorptive agents were combined with intermittent PTH, m

41 Anti-resorptive agents--including estrogen (E), calcitonin (C

42 ate that targeting these cells has both anti-resorptive and anabolic effects on bone.

43 the model predicts that combinations of anti-resorptive and anabolic therapies provide significant be

44 actor produced more TRAP(+) MNCs and greater resorptive area.

45 Alpha-halogenated analogues of the anti-resorptive bisphosphonate risedronate (5, Ris) and its p

46 th hypercalciuria and increased BTMs (mainly resorptive), but also up to 30% have hypocitraturia and

47 their cytoskeleton, and, as such, their bone-resorptive capacity is arrested.

48 n irreversible manner and also inhibited the resorptive capacity of mature osteoclasts.

49 ter than wild type, thereby accelerating the resorptive capacity of the cell.

50 ormalize the cytoskeleton of DKO OCs and the resorptive capacity of the cells.

51 e, c-Fos expression increases the number and resorptive capacity of wild-type osteoclasts induced by

52 bsence of PIP5KIgamma would compromise their resorptive capacity.

53 s with increased Cdc42 activity had enhanced resorptive capacity.

54 ast fusion, sealing zone perimeter, and bone resorptive capacity.

55 n that regulates sealing dimensions and bone resorptive capacity.

56 perimeter, along with decreased motility and resorptive capacity.

57 it plays a positive role in osteoclast bone resorptive capacity.

58 with larger sealing zones and enhanced bone resorptive capacity.

59 Thus, this unique bone resorptive cell is a prominent therapeutic target.

60 c agents that either directly block the bone-resorptive cell or do so indirectly via cytokine arrest.

61 most likely due to a dysfunction of the bone resorptive cell, the osteoclast.

62 lved in controlling the activity of the bone-resorptive cell.

63 requires intimacy between the matrix and the resorptive cell.

64 nction of the osteoclast, the exclusive bone resorptive cell.

65 gand, possibly accounting for the paucity of resorptive cells and the dominance of mineral in atheros

66 gesting that this growth factor may regulate resorptive cells either directly or indirectly.

67 s are multinucleated cells and the principal resorptive cells of bone.

68 Osteoclasts are resorptive cells that are important for homeostatic bone

69 l ligament (PDL), followed by recruitment of resorptive cells that remove root structure.

70 To define the direct impact of GCs on bone-resorptive cells, we compared the effects of dexamethaso

71 rly, arresting their development into mature resorptive cells.

72 rved when WASp-null animals are exposed to a resorptive challenge.

73 e preservation would prevent post-extraction resorptive changes as assessed by clinical and histologi

74 These resorptive changes, when compared between treatment grou

75 contribute to mechanisms that result in bone-resorptive cytokine production in periapical lesion.

76 and interleukin-1beta (IL-1), a potent bone-resorptive cytokine, have been associated with periodont

77 and interleukin 1-beta (IL-1), a potent bone-resorptive cytokine, have both been associated with peri

78 talk upregulates other inflammatory and bone-resorptive cytokines (IL-1beta, IL-6, and TNF-alpha).

79 The expression of the bone-resorptive cytokines IL-1 alpha and TNF-alpha was also i

80 as well as with elevated expression of bone-resorptive cytokines IL-1alpha and IL-1beta, in periapic

81 rrelated with reduced expression of the bone resorptive cytokines interleukin 1alpha (IL-1alpha) (P <

82 givalis immune evasion and induction of bone-resorptive cytokines.

83 The resorptive defect in beta3-deficient osteoclasts may ref

84 ing alveolar bone extended into the existing resorptive defects, but without clinical evidence of ank

85 es, concerns about rare side-effects of anti-resorptive drugs, particularly bisphosphonates, and the

86 The resorptive effect of ATRA was characterized by mRNA expr

87 on sufficiently to counteract its local anti-resorptive effect, thus leading to a net effect of impai

88 e that it is possible to dissociate the bone-resorptive effects of GM-CSF, to reduce metastatic risk,

89 hanced TNF-alpha increases the expression of resorptive factors in chondrocytes through a process tha

90 keletal tissues, PKA activation induces bone resorptive factors in the vasculature and that aortic SM

91 rtically disposed alternating depository and resorptive fields in relation to anterior dental roots a

92 ay a fundamental role in modulating both the resorptive function and formation of mammalian osteoclas

93 show that GSLs are essential for enterocyte resorptive function but are primarily not for polarizati

94 s suggests that ouabain also inhibits an ion resorptive function of Na/K-ATPase in the type I acini.

95 acini, is followed by a dopamine-independent resorptive function of Na/K-ATPase in type I acini locat

96 Thus, talin1 and Rap1 are critical for resorptive function, and their selective inhibition in m

97 In keeping with inhibited resorptive function, CtsK-VCL and LysM-VCL mice exhibit

98 ncreased in parallel with reduced osteoclast resorptive function, effects abrogated by neutralizing a

99 tact differentiation markers, but diminished resorptive function.

100 er of osteoclasts and activation of the bone resorptive function.

101 1 year without symptoms or recurrence of the resorptive lesion and the affected tooth remained vital.

102 A similar condition, feline osteoclastic resorptive lesions (FORL), affects up to 70% of domestic

103 ify the cellular source of RANKL in the bone resorptive lesions of periodontal disease.

104 The resorptive lesions were asymptomatic, unassociated with

105 Infrabony resorptive lesions were induced by surgical pulp exposur

106 Histologically, many resorptive lesions were noted along the cementum surface

107 The resorptive lesions were progressive in nature, with addi

108 alveolar bone, including radiolucencies and resorptive lesions, osteoid accumulation on the alveolar

109 ical improvements and GCF levels of the bone resorptive marker ICTP were significantly reduced.

110 ium stone formers have serum beta-crosslaps (resorptive marker) greater than 0.311 ng/ml, serum osteo

111 Anti-resorptive medication inhibits bone break down and pread

112 plasmalemma results in acidification of the resorptive microenvironment and release of CatK to diges

113 tion and formation of an isolated, acidified resorptive microenvironment.

114 these data suggests that BE is a novel anti-resorptive molecule that is active both in vitro and in

115 Oxylipids also induce resorptive osteoclastic cells within the bone environmen

116 environment, raising the question of whether resorptive osteoclasts can be harnessed in the vascular

117 is resulting from increased numbers of hyper-resorptive osteoclasts.

118 prolonged hyponatremia, thereby leading to a resorptive osteoporosis in patients with SIADH.

119 their leading edges, whereas during the bone resorptive phase multiple podosomes are densely aggregat

120 bone marrow mononuclear cells acquire a bone resorptive phenotype in vitro.

121 -76 is the dominant SLP family member in the resorptive process.

122 ing maxillary anterior teeth may be prone to resorptive processes after extraction and immediate impl

123 rleukin 1 beta (IL-1 beta) also possess bone-resorptive properties, and are generally considered to p

124 Peripherally, Flx has anti-resorptive properties, directly impairing osteoclast dif

125 entin and root biomodification may limit the resorptive response following connective tissue graft pr

126 ation of genes classically associated with a resorptive response.

127 y cilia are required for osteogenic and bone resorptive responses to dynamic fluid flow.

128 as bone mesenchymal stem cells, to the bone resorptive sites and that this process is mediated throu

129 oclast bone resorption recruits MSCs to bone-resorptive sites.

130 a fall of NTX and a shift from the dominant resorptive state, which we postulate involves full recov

131 tic origin, is an attractive target for anti-resorptive therapeutics.

132 Our model confirms that anti-resorptive therapies are unable to partially restore bon

133 These data indicate that anti-resorptive therapies may provide the most effective bone

134 Thus, anti-resorptive therapy could be used to prevent bone loss in

135 multiple proinflammatory cytokines and bone resorptive/turnover markers.

136 hibits bone break down and preadmission anti-resorptive use is associated with superior survival amon

137 mbrane-anchored collagenases during collagen-resorptive versus collagen-invasive events.