ライフサイエンスコーパス: subchondral bone

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

2 tive disease that affects both cartilage and subchondral bone.

3 umbers per cartilage area, and thickening of subchondral bone.

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

5 ry to altered architecture of the underlying subchondral bone.

6 omprising calcified cartilage and underlying subchondral bone.

7 ges in both the cartilage and the underlying subchondral bone.

8 arly changes in aging and OA-affected murine subchondral bone.

9 lamination of the cartilage with exposure of subchondral bone.

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

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

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

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

14 issue functioning to cushion and protect the subchondral bone.

15 cartilage damage and abnormal remodeling of subchondral bone.

16 nd affects both cartilage and the underlying subchondral bone.

17 strated incomplete healing and damage of the subchondral bone.

18 depth-wise zones of articular cartilage and subchondral bone.

19 n of the synovial lining, and changes to the subchondral bone.

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

21 leads to degeneration of both cartilage and subchondral bone.

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

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

24 development and activity of osteoclasts from subchondral bone.

25 regulate the crosstalk between cartilage and subchondral bone.

26 artilage degeneration through crosstalk with subchondral bone.

27 partially regulated by norepinephrine within subchondral bone.

28 sed invasive marrow cavities, and suboptimal subchondral bone.

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

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

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

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

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

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

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

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

37 w BGJ398 treatment rescued the OA changes in subchondral bone and knee articular cartilage of HMWTgFG

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

39 resorption as exemplified by a reduction in subchondral bone and osteophytes.

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

41 Subchondral bone and synovium may be responsible for noc

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

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

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

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

46 collagen fibers in the articular cartilage, subchondral bone, and menisci using complementary techni

47 ient tissues (including articular cartilage, subchondral bone, and osteophytic cartilage) and identif

48 ed local immune inflammatory response in the subchondral bone, and reduced degeneration of the articu

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

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

51 innervation of the periosteum, synovium and subchondral bone, and the pathological innervation of ar

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

68 age damage, whereas ALN primarily attenuated subchondral bone changes associated with OA progression.

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

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

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

72 es, and spatial relationship between CLS and subchondral bone changes.

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

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

75 Mutant subchondral bone contained numerous Catepsin K- expressi

76 monstrate that Gli1(+) cells residing in the subchondral bone contribute to bone formation and homeos

77 al blood vessels in immature joints leads to subchondral bone defects and limits cartilage repair aft

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

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

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

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

82 s were detected in the deeper regions of the subchondral bone except for increased Col I fiber thickn

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

84 oarthritis tissues, miR-126-3p is highest in subchondral bone, fat pad and synovium, and lowest in ca

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

86 ivated piezoelectric hydrogel show increased subchondral bone formation, improved hyaline-cartilage s

87 is a disorder where articular cartilage and subchondral bone fragments come loose from the articular

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

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

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

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

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

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

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

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

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

97 topathological scoring system for changes in subchondral bone in murine models of knee osteoarthritis

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

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

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

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

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

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

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

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

106 Sympathectomy simultaneously prevented subchondral bone loss and decreased bone norepinephrine

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

108 Subchondral bone loss and increased subchondral bone nor

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

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

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

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

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

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

115 Subchondral bone marrow abnormalities, graded in the med

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

117 Subchondral bone marrow edema was also seen beneath four

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

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

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

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

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

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

124 der with symptomatic knee osteoarthritis and subchondral bone marrow lesions detected by magnetic res

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

126 ltrastructure of the articular cartilage and subchondral bone matrix.

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

128 r with a reduced OARSI histopathology score, subchondral bone, menisci score and synovitis compared t

129 Cartilage degeneration, subchondral bone microarchitecture and the expression of

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

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

132 Our findings suggest that impairment of subchondral bone microstructure in early stage of OA is

133 +) osteogenic progenitors result in improved subchondral bone microstructure, attenuated local immune

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

135 ll, our results demonstrate the potential of subchondral bone-modifying therapies to slow the progres

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

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

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

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

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

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

142 ral changes may be identified throughout the subchondral bone of the human femoral head.

143 Subchondral bone of wild-type (WT) and Fas-knockout (Fas

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

145 (OR 1.04, 95%CI 0.89-1.24, p = 0.697) or the subchondral bone phenotype (OR 1.13, 95%CI 0.95-1.36, p

146 e osteoarthritis (OA), three key parameters, subchondral bone plate (Subcho.BP) consisting of the com

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

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

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

150 lar to the normal cartilage and protects the subchondral bone plate from early bone loss.

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

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

153 d surgery-induced OA cartilage degeneration, subchondral bone plate sclerosis, and joint pain.

154 At the late disease stages, subchondral bone plate thickened concomitant with increa

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

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

157 At the early disease stage, subchondral bone plate thinning and reduced subchondral

158 Subchondral bone plate vascularity was altered with incr

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

160 The subchondral bone plate was virtually isolated to evaluat

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

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

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

164 layer, displaying only a thin, highly porous subchondral bone plate.

165 y reduced bone mineral density of the tibial subchondral bone-plate associated with increased osteocl

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

167 Subchondral bone plays a key role in the development of

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

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

170 Here, we examined the contributions of the subchondral bone properties to OA development.

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

172 disease, characterized by cartilage loss and subchondral bone remodeling in response to abnormal mech

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

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

175 Subchondral bone remodeling plays an important role in t

176 he subchondral bone, which leads to abnormal subchondral bone remodeling via Hedgehog (Hh) signaling

177 Knee loading restores OPOA by regulating subchondral bone remodeling, and may provide an effectiv

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

179 ALN suppressed subchondral bone resorption, which was markedly increase

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

181 uted tomography analyses of the distal femur subchondral bone revealed significant reductions in trab

182 The functional relationship between subchondral bone (SB) and articular cartilage (AC) is un

183 joints that includes cartilage degeneration, subchondral bone (SCB) sclerosis, and meniscal damage.

184 repeated compressive stresses, resulting in subchondral bone (SCB) sclerosis, fatigue microcracks, a

185 ion of hyaline articular cartilage (HAC) and subchondral bone (SCB), and their involvement in the pat

186 In late disease stages, subchondral bone sclerosis has been linked to heightened

187 CD271+CD56+ BMSC subset and implicates it in subchondral bone sclerosis in hip OA.

188 signaling without improving PTOA-associated subchondral bone sclerosis or chondrocyte apoptosis.

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

190 profound synovitis, cartilage degeneration, subchondral bone sclerosis, and pain after joint injury.

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

192 Notably, subchondral bone score was dramatically higher in SAMP8

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

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

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

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

197 d center of closest contact location between subchondral bone surfaces were analyzed over 0-30% stanc

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

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

200 s ER stress to promote chondrocyte death and subchondral bone thickening, which could be relieved by

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

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

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

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

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

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

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

208 ration was evaluated histologically, and the subchondral bone tissue microarrays (TMAs) were subseque

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

210 es and osteoclasts numbers were increased in subchondral bone tissues.

211 ed (FFPE) KOA osteochondral (i.e., cartilage-subchondral bone) tissues.

212 he KOA tibial plateau and the feasibility of subchondral bone TMA construction for N-glycan MALDI-MSI

213 ondrial DNA mutations predispose to elevated subchondral bone turnover and hypertrophy in calcified c

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

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

216 Subchondral bone underwent abnormal remodeling, the diff

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

218 Subchondral bone volume and osteophyte area were measure

219 subchondral bone plate thinning and reduced subchondral bone volume fraction (B.Ar/T.Ar) were observ

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

221 ly prevented, and the abnormal remodeling of subchondral bone was significantly inhibited.

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

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

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

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

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

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

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

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

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

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

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

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

234 ibution of osteogenic differentiation in the subchondral bone, which leads to abnormal subchondral bo