ライフサイエンスコーパス: subchondral

1 ected cartilage from degradation and blocked subchondral and periosteal bone erosion in inflamed join

2 l computed tomography (muCT), and changes in subchondral and trabecular bone were assessed by standar

3 Maximum values of each subchondral area (patellofemoral or medial and lateral f

4 difference (P < .001) in PF in the immediate subchondral area was found between TBMES and osteonecros

5 Osteonecrosis joints showed a subchondral area with low or no detectable PF and MTT ad

6 ated with a high K/L score, while markers of subchondral BMD formed a completely separate group.

7 eophytes compared with those associated with subchondral BMD raise the possibility that these 2 proce

8 rt the idea that Wnt5a/Ror2 signaling in TMJ subchondral BMSCs enhanced by UAC promoted BMSCs to incr

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

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

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

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

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

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

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

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

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

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

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

20 Subchondral bone and synovium may be responsible for noc

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

41 Mutant subchondral bone contained numerous Catepsin K- expressi

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

63 Sympathectomy simultaneously prevented subchondral bone loss and decreased bone norepinephrine

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

65 Subchondral bone loss and increased subchondral bone nor

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

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

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

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

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

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

72 Subchondral bone marrow abnormalities, graded in the med

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

74 Subchondral bone marrow edema was also seen beneath four

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

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

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

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

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

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

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

82 ltrastructure of the articular cartilage and subchondral bone matrix.

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

84 Cartilage degeneration, subchondral bone microarchitecture and the expression of

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

102 Subchondral bone plate vascularity was altered with incr

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

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

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

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

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

108 Subchondral bone plays a key role in the development of

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

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

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

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

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

114 Subchondral bone remodeling plays an important role in t

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

116 ALN suppressed subchondral bone resorption, which was markedly increase

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

134 Subchondral bone volume and osteophyte area were measure

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

159 tive disease that affects both cartilage and subchondral bone.

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

161 ry to altered architecture of the underlying subchondral bone.

162 omprising calcified cartilage and underlying subchondral bone.

163 leads to degeneration of both cartilage and subchondral bone.

164 lamination of the cartilage with exposure of subchondral bone.

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

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

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

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

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

170 issue functioning to cushion and protect the subchondral bone.

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

172 development and activity of osteoclasts from subchondral bone.

173 regulate the crosstalk between cartilage and subchondral bone.

174 artilage degeneration through crosstalk with subchondral bone.

175 partially regulated by norepinephrine within subchondral bone.

176 sed invasive marrow cavities, and suboptimal subchondral bone.

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

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

179 No subchondral changes were found around the SAF.

180 , >50% defect; and grade 4, grade three plus subchondral changes) and measured in two dimensions.

181 articular cartilage thickness decreased, and subchondral cortical bone thickness increased in the pos

182 ted cyst in the subchondral bone mimicking a subchondral cyst (six patients) or a single osteochondra

183 For subchondral cyst detection, the sensitivity of tomosynth

184 4.2-6.4; P = .001-.011) and medially located subchondral cysts (odds ratio, 6.7-17.8; P = .004-.03) w

185 al intestinal inflammation (mean diameter of subchondral cysts [2.9 vs. 1.2 mm; P = 0.026] and blurri

186 presence of osteophytes, bone sclerosis, and subchondral cysts and the absence of inflammatory featur

187 space narrowing, subchondral sclerosis, and subchondral cysts for the detection of articular cartila

188 space narrowing, subchondral sclerosis, and subchondral cysts for the detection of articular cartila

189 Presence of osteophytes and subchondral cysts in four locations of tibiofemoral join

190 Tomosynthesis depicted more osteophytes and subchondral cysts than did radiography.

191 space narrowing, subchondral sclerosis, and subchondral cysts were less sensitive radiographic featu

192 with tomosynthesis-depicted osteophytes and subchondral cysts were more likely to feel pain than tho

193 Subchondral cysts were seen almost exclusively in noninf

194 eoarthritis, Bankart and Hill-Sachs lesions, subchondral cysts), and evidence of prior surgery were g

195 hin rim enhancement of effusion, presence of subchondral cysts, or intraarticular bodies indicate abs

196 CT, MR imaging, or both demonstrated subchondral cysts, osseous erosions, or a type 2 odontoi

197 ralabral cysts, articular cartilage lesions, subchondral cysts, osteophytes, and synovial herniation

198 meniscal tears (P = .001); and osteophytes, subchondral cysts, sclerosis, joint effusion, and synovi

199 ilage, bone marrow edema (BME), osteophytes, subchondral cysts, sclerosis, meniscal and/or ligamentou

200 space narrowing, subchondral sclerosis, and subchondral cysts.

201 MR imaging depicted 171 osteophytes and 51 subchondral cysts.

202 TBMES joints showed a subchondral elongated area of high PF and low MTT that w

203 tribute to better understanding of cartilage-subchondral interactions in arthropathies.

204 uality of tissue repair in both chondral and subchondral layers was analyzed based on quantitative hi

205 The relative SNR in the subchondral plate with SWIFT (0.91) was more than four t

206 as aggressive osteoclastic resorption of the subchondral plate.

207 otype in which there is complete loss of the subchondral plate.

208 measurements of subchondral bone thickness, subchondral pseudocysts, and osteophytes.

209 AF on MR arthrograms (10.5%), the absence of subchondral reaction, and the absence of cartilage defec

210 R arthrograms showing SAF were evaluated for subchondral reactions.

211 The extent of subchondral sclerosis and the development of marginal os

212 esence of cartilage lesions, osteophytes and subchondral sclerosis were not observed in GH/IGF-1-defi

213 cular cartilage, osteophytic remodeling, and subchondral sclerosis were reduced in cell-treated joint

214 pidemiologic studies clearly show increasing subchondral sclerosis with disease progression.

215 gnificant progression of lytic bone lesions, subchondral sclerosis, and osteophyte size over periods

216 ge area, fibrillation, clefting, eburnation, subchondral sclerosis, and osteophytes.

217 marginal osteophytes, joint space narrowing, subchondral sclerosis, and subchondral cysts for the det

218 marginal osteophytes, joint space narrowing, subchondral sclerosis, and subchondral cysts for the det

219 Joint space narrowing, subchondral sclerosis, and subchondral cysts were less s

220 marginal osteophytes, joint space narrowing, subchondral sclerosis, and subchondral cysts.

221 ncluding articular cartilage degradation and subchondral sclerosis, while the defects were significan

222 al, but not genetic, clustering was seen for subchondral sclerosis.

223 actal signature analysis (FSA) of the medial subchondral tibial plateau was performed on fixed flexio

224 trates specific architectural changes in the subchondral trabecular bone in osteoarthrosis that are c

225 eased osteoclast activity and an overall TMJ subchondral trabecular bone loss in the UAC-treated rats

226 mporomandibular joints (TMJs), displaying as subchondral trabecular bone loss.

227 the osteoblast activity in the tissue of TMJ subchondral trabecular bone of these UAC-treated rats wa

228 ber, and enhanced osteoclast activity in TMJ subchondral trabecular bone of UAC-treated rats.

229 Increased subchondral trabecular bone turnover due to imbalanced b

230 rocyte maturation markers and an increase in subchondral trabecular spacing.

231 omineralization of deposited collagen in the subchondral zone of osteoarthritic femoral heads, suppor

232 th the greatest changes occurring within the subchondral zone.