ライフサイエンスコーパス: subchondral bone

1 omprising calcified cartilage and underlying subchondral bone.

2 leads to degeneration of both cartilage and subchondral bone.

3 lamination of the cartilage with exposure of subchondral bone.

4 r cartilage, talar dome cartilage, and talar subchondral bone.

5 s in synovial fluid, with no supply from the subchondral bone.

6 articular cartilage and MMP-9 expression in subchondral bone.

7 increased BMD, BV/TV, and decreased Tb.Sp in subchondral bone.

8 s, an indirect consequence of protecting the subchondral bone.

9 from intermediate to late stage of OA in the subchondral bone.

10 issue functioning to cushion and protect the subchondral bone.

11 development and activity of osteoclasts from subchondral bone.

12 regulate the crosstalk between cartilage and subchondral bone.

13 artilage degeneration through crosstalk with subchondral bone.

14 partially regulated by norepinephrine within subchondral bone.

15 sed invasive marrow cavities, and suboptimal subchondral bone.

16 pression of pSMAD158 and VEGF in the MCC and subchondral bone.

17 ced type I collagen in bgn(-/0)fmod(-/-) TMJ subchondral bone.

18 tive disease that affects both cartilage and subchondral bone.

19 he UCC, without a definite contribution from subchondral bone.

20 ry to altered architecture of the underlying subchondral bone.

21 rocytes contributed to ~80% of bone cells in subchondral bone, ~70% in a somewhat more inferior regio

22 This might explain why increased subchondral bone activity can predict cartilage loss.

23 focal bone resorption can be detected in the subchondral bone adjacent to the bone marrow space into

24 and from both the articular surface and the subchondral bone after intravenous injection.

25 th a concave curve that was highest near the subchondral bone and articular surfaces.

26 matory changes in the region of soft tissue, subchondral bone and bone marrow.

27 dividual chondrocytes at the boundary of the subchondral bone and calcified cartilage.

28 DNA methylation changes occurred earlier in subchondral bone and identified different methylation pa

29 ith OA and blocked osteoclast recruitment to subchondral bone and osteophytes.

30 Comparison of DMGs identified in subchondral bone and site-matched cartilage indicated th

31 Subchondral bone and synovium may be responsible for noc

32 Immunohistochemical analysis of subchondral bone and synovium revealed RANK-positive per

33 by growth factors produced by chondrocytes, subchondral bone and synovium.

34 Bone resorption of osteoclasts from subchondral bone and the differentiation of osteoclasts

35 trimental effects on articular cartilage and subchondral bone, and may subsequently influence the dev

36 mensional histology for calcified cartilage, subchondral bone, and subchondral bone plate thickness a

37 of the joint, including cartilage, meniscus, subchondral bone, and the joint capsule with synovium.

38 n the architecture and composition of hip OA subchondral bone, and to examine the pathological role o

39 n hip OA patients is associated with altered subchondral bone architecture and type I collagen compos

40 egradation, osteophyte formation, changes to subchondral bone architecture, and eventual progression

41 Changes of cartilage and subchondral bone are associated with development and act

42 osteopenia and focal erosion of marginal and subchondral bone are commonly seen.

43 issue defects in young bgn(-/0)fmod(-/-) TMJ subchondral bone are likely attributed to increased oste

44 Tibial and weight-bearing femoral condylar subchondral bone area and cartilage surface were segment

45 ve remodelling in the condylar cartilage and subchondral bone, as revealed by increased cartilage thi

46 , whereas inhibition of TGF-beta activity in subchondral bone attenuated the degeneration of articula

47 By magnetic resonance imaging (MRI), subchondral bone attrition (SBA) can be seen in early os

48 use were associated with significantly less subchondral bone attrition and bone marrow edema-like ab

49 The only established system to grade subchondral bone attrition in knee osteoarthritis (OA) h

50 age [UCC] only, calcified cartilage [CC] and subchondral bone [bone] [CC/bone], bone only; and UCC, C

51 rrageenan, osteoclasts formed transiently in subchondral bone, but regressed 7 days after disease ons

52 est the hypothesis that abnormalities of the subchondral bone can result in osteoarthritis (OA).

53 ith varying degrees of osteophyte formation, subchondral bone change, and synovitis.

54 y investigates how age affects cartilage and subchondral bone changes in mouse joints following DMM.

55 Cortical and trabecular subchondral bone changes were documented by microfocal c

56 Femoral osteophytes, superolateral JSN, and subchondral bone changes were independent predictors of

57 iosteum next to the synovial membrane and in subchondral bone channels.

58 of disk, uncalcified CEP, calcified CEP, and subchondral bone components and were imaged with proton

59 Mutant subchondral bone contained numerous Catepsin K- expressi

60 ) and osteochondral (n = 5, 3-4 mm deep into subchondral bone) defects were created in the intercarpa

61 morbid factors that are involved in condylar subchondral bone degradation that is regulated by the sy

62 le of cathepsin K in articular cartilage and subchondral bone erosion was further corroborated by the

63 of AIA but, in particular, failed to develop subchondral bone erosions and were completely protected

64 MSCs from experimental condylar subchondral bone expressed higher levels of beta2-AR and

65 sfully obtained from calcified cartilage and subchondral bone for the first time.

66 TGF-beta1 concentrations are also high in subchondral bone from humans with osteoarthritis.

67 Subchondral bone from over-weight/obese hip OA patients

68 g microarray analysis of articular cartilage/subchondral bone from the tibial plateaus of STR/Ort mic

69 the genome-wide DNA methylation profiles of subchondral bone from three regions on tibial plateau re

70 t of osteoarthritis, however, epigenetics of subchondral bone has not been extensively studied.

71 associated with osteoarthritic cartilage and subchondral bone histopathology and severity of degenera

72 rabecular number and reduced separation) and subchondral bone (i.e., increased plate thickness), the

73 cunae in areas of calcified cartilage and in subchondral bone immediately adjacent to calcified carti

74 ncentration from the synovial surface to the subchondral bone in articular cartilage.

75 Two case studies, in subchondral bone in osteoarthritis and in Pax5 in acute

76 wth factor beta1 (TGF-beta1) is activated in subchondral bone in response to altered mechanical loadi

77 glycan and fibromodulin are critical for TMJ subchondral bone integrity and reveal a potential role f

78 alone, the matrix seems to develop from the subchondral bone interface as compared to the normal car

79 (-/0)fmod(-/-) TMJs with an intact cartilage/subchondral bone interface.

80 mandibular condylar cartilage (MCC) and its subchondral bone is an important but understudied topic

81 ntly decreased prevalence of knee OA-related subchondral bone lesions compared with those reporting n

82 CIS and UAC synergistically promote condylar subchondral bone loss and cartilage degradation; such pr

83 Sympathectomy simultaneously prevented subchondral bone loss and decreased bone norepinephrine

84 ral bone of experimental rats, together with subchondral bone loss and increased osteoclast activity.

85 Subchondral bone loss and increased subchondral bone nor

86 beta-antagonist (propranolol) suppressed subchondral bone loss and osteoclast hyperfunction while

87 m into a reliable tool for the assessment of subchondral bone loss in knee OA.

88 cells and reversed cartilage degradation and subchondral bone loss in mice with OA of the TMJ.

89 t is concluded that beta2-AR signal-mediated subchondral bone loss in TMJ osteoarthritisis associated

90 Combined CIS + UAC produced more severe subchondral bone loss, higher bone norepinephrine level,

91 ts, together with cartilage degeneration and subchondral bone loss.

92 Subchondral bone marrow abnormalities, graded in the med

93 The mean depth and cross-sectional area of subchondral bone marrow edema increased with increasing

94 Subchondral bone marrow edema was also seen beneath four

95 Subchondral bone marrow edema was seen beneath 105 (19%)

96 ere used to correlate MR imaging findings of subchondral bone marrow edema with the arthroscopic grad

97 o determine the size, depth, and location of subchondral bone marrow edema without knowledge of the a

98 iliac joints is indicated by the presence of subchondral bone marrow edema, synovitis, bursitis, or e

99 nd greater depth and cross-sectional area of subchondral bone marrow edema.

100 strongly correlated with the total volume of subchondral bone marrow lesions (BMLs) (beta=0.22, P=0.0

101 y assessed, evaluating cartilage morphology, subchondral bone marrow lesions, meniscal morphology/ext

102 ltrastructure of the articular cartilage and subchondral bone matrix.

103 Supply from the subchondral bone may be of particular importance.

104 Cartilage degeneration, subchondral bone microarchitecture and the expression of

105 n of degeneration of articular cartilage and subchondral bone microarchitecture associated with OA.

106 the degeneration of articular cartilage and subchondral bone microarchitecture in a mouse model of h

107 eared as either a multiloculated cyst in the subchondral bone mimicking a subchondral cyst (six patie

108 le delivery of IGF-1 showed higher scores in subchondral bone morphology as well as chondrocyte and g

109 ired leptin signaling induced alterations in subchondral bone morphology without increasing the incid

110 Subchondral bone loss and increased subchondral bone norepinephrine level were observed in t

111 Degenerative changes of condylar subchondral bone occur frequently in temporomandibular d

112 -AR expression were observed in the condylar subchondral bone of experimental rats, together with sub

113 gh signal intensity in deep zone adjacent to subchondral bone of femoral condyle (in zero, zero, and

114 age thickness, and influx of oxygen from the subchondral bone on the oxygen profile in the tissue was

115 teration of the osteochondral tissue and its subchondral bone plate component.

116 conductance of the osteochondral tissue and subchondral bone plate could have deleterious biomechani

117 These results support a relationship between subchondral bone plate exposure and prevalent and incide

118 ulic conductance of osteochondral tissue and subchondral bone plate increases with structural changes

119 ndicated by less cartilage degradation, less subchondral bone plate sclerosis and smaller osteophytes

120 histology scores and muCT quantification of subchondral bone plate thickness and osteophyte formatio

121 r calcified cartilage, subchondral bone, and subchondral bone plate thickness and vascular canal dens

122 Subchondral bone plate vascularity was altered with incr

123 nductance of native osteochondral tissue and subchondral bone plate was higher (2,700-fold and 3-fold

124 tal articular cartilage), but increased SBP (subchondral bone plate) and B.Ar/T.Ar (trabecular bone a

125 of articular cartilage and remodeling of the subchondral bone plate, comprising calcified cartilage a

126 Full-thickness cartilage defects expose the subchondral bone plate.

127 eveloped more cartilage erosions and thicker subchondral bone plates after DMM than 4 M males.

128 Subchondral bone plays a key role in the development of

129 This article reviews evidence that subchondral bone plays a role in the degeneration of car

130 nt structural changes in joint cartilage and subchondral bone post-DMM, facilitating more thoughtful

131 we hypothesized that knee loading regulates subchondral bone remodeling by suppressing osteoclast de

132 e by aberrant joint loading elicits abnormal subchondral bone remodeling in temporomandibular joint (

133 It has been suggested that subchondral bone remodeling plays a role in the progress

134 Subchondral bone remodeling plays an important role in t

135 articular cartilage at the joint margins and subchondral bone resorption associated with bone-derived

136 ALN suppressed subchondral bone resorption, which was markedly increase

137 teoclastogenesis at the erosion front and in subchondral bone, resulting in a bidirectional assault o

138 res (osteophytes, joint space narrowing, and subchondral bone sclerosis) in each compartment.

139 ature most strongly associated with pain was subchondral bone sclerosis.

140 , high concentrations of active TGF-beta1 in subchondral bone seem to initiate the pathological chang

141 ibe the separation of an articular cartilage subchondral bone segment from the remaining articular su

142 ilage, proteoglycan loss, and alterations of subchondral bone structure.

143 ed by loss of trabecular bone and erosion of subchondral bone surface.

144 as avascular and integrated with regenerated subchondral bone that had well defined blood vessels.

145 tion of abnormal vascularity in synovium and subchondral bone that have not been apparent with conven

146 eptin impairment was associated with reduced subchondral bone thickness and increased relative trabec

147 rofocal computed tomography bone morphology, subchondral bone thickness evaluation, and histologic ev

148 ce had a decrease in bone density, increased subchondral bone thickness, and increased cartilage dege

149 RL/MpJ mice, no differences in bone density, subchondral bone thickness, or histologic grading of car

150 ear of life, enabling serial measurements of subchondral bone thickness, subchondral pseudocysts, and

151 illed across the joint traversing the tibial subchondral bone, tibial articular cartilage, talar dome

152 howed that, aside from the joint pannus, the subchondral bone tissue constitutes an essential element

153 the greater activity was associated with the subchondral bone tissue.

154 ntegrity and reveal a potential role for TMJ subchondral bone turnover during the initial early stage

155 everal studies have suggested that increased subchondral bone turnover is a determinant of progressio

156 ombined to characterize articular cartilage, subchondral bone, vascularization, and ROS, providing un

157 Subchondral bone volume and osteophyte area were measure

158 The factor representing subchondral bone was significantly higher, but the numbe

159 investigate the role of I-PTH on the MCC and subchondral bone, we carried out our studies using 4 to

160 Changes in articular cartilage and subchondral bone were analyzed by histology and micro-co

161 contents in the subjects' serum and condylar subchondral bone were detected by ELISA; bone and cartil

162 Structural parameters of subchondral bone were determined by MicroCT and type I c

163 arameters and related gene expression in the subchondral bone were examined.

164 s) and remodeling parameters in the condylar subchondral bone were investigated.

165 and the area and thickness of cartilage and subchondral bone were measured.

166 ars) containing cartilaginous end plates and subchondral bone were prepared.

167 Mesenchymal stem cells (MSCs) from condylar subchondral bones were harvested for comparison of their

168 onents (i.e., cartilage, synovium, meniscus, subchondral bone) were examined by histologic and immuno

169 Cs that migrate to the inflamed synovium and subchondral bone, where they are exposed to unopposed RA

170 ficant increase in trabecular spacing in the subchondral bone, whereas 0.25 N of forced mouth opening