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 otal volumes (TVs) and bone volumes (BVs) of subchondral and ramus bone of Ddr1(-/-) versus WT condyl

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

24 Subchondral bone and synovium may be responsible for noc

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

46 Mutant subchondral bone contained numerous Catepsin K- expressi

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

73 Sympathectomy simultaneously prevented subchondral bone loss and decreased bone norepinephrine

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

75 Subchondral bone loss and increased subchondral bone nor

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

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

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

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

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

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

82 Subchondral bone marrow abnormalities, graded in the med

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

84 Subchondral bone marrow edema was also seen beneath four

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

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

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

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

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

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

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

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

93 ltrastructure of the articular cartilage and subchondral bone matrix.

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

95 Cartilage degeneration, subchondral bone microarchitecture and the expression of

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

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

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

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

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

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

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

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

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

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

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

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

108 (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

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

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

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

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

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

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

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

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

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

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

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

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

121 Subchondral bone plate vascularity was altered with incr

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

123 The subchondral bone plate was virtually isolated to evaluat

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

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

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

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

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

136 Subchondral bone remodeling plays an important role in t

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

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

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

140 ALN suppressed subchondral bone resorption, which was markedly increase

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

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

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

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

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

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

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

148 Notably, subchondral bone score was dramatically higher in SAMP8

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

167 Subchondral bone underwent abnormal remodeling, the diff

168 Subchondral bone volume and osteophyte area were measure

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

198 sed invasive marrow cavities, and suboptimal subchondral bone.

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

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

201 tive disease that affects both cartilage and subchondral bone.

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

203 ry to altered architecture of the underlying subchondral bone.

204 omprising calcified cartilage and underlying subchondral bone.

205 lamination of the cartilage with exposure of subchondral bone.

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

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

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

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

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

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

212 issue functioning to cushion and protect the subchondral bone.

213 nd affects both cartilage and the underlying subchondral bone.

214 strated incomplete healing and damage of the subchondral bone.

215 cartilage damage and abnormal remodeling of subchondral bone.

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

217 leads to degeneration of both cartilage and subchondral bone.

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

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

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

221 development and activity of osteoclasts from subchondral bone.

222 regulate the crosstalk between cartilage and subchondral bone.

223 artilage degeneration through crosstalk with subchondral bone.

224 partially regulated by norepinephrine within subchondral bone.

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

226 No subchondral changes were found around the SAF.

227 , >50% defect; and grade 4, grade three plus subchondral changes) and measured in two dimensions.

228 , highlighting effects of OA in the superior subchondral cortical and trabecular bone.

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

230 osteopenia of epiphyseal trabecular bone and subchondral cortical plate.

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

232 For subchondral cyst detection, the sensitivity of tomosynth

233 4.2-6.4; P = .001-.011) and medially located subchondral cysts (odds ratio, 6.7-17.8; P = .004-.03) w

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

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

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

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

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

239 hondral sclerosis, and 91.3% (95 of 104) for subchondral cysts in the external test set.

240 dral sclerosis, and 97.6% (1501 of 1538) for subchondral cysts in the internal test set, and 82.7% (8

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

242 Subchondral sclerosis and subchondral cysts were graded as present or absent.

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

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

245 Subchondral cysts were seen almost exclusively in noninf

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

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

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

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

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

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

252 MR imaging depicted 171 osteophytes and 51 subchondral cysts.

253 space narrowing, subchondral sclerosis, and subchondral cysts.

254 tly higher number of disrupted microvessels, subchondral edema, and angiogenesis compared to mature c

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

256 IACS injections: accelerated OA progression, subchondral insufficiency fracture, complications of ost

257 tcomes including accelerated OA progression, subchondral insufficiency fracture, complications of pre

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

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

260 of regenerative tissues in both chondral and subchondral layers was significantly improved in dual de

261 These data indicate subchondral MSCs may be involved in OA progression by pa

262 everity (CLS) and microstructural changes in subchondral plate and trabecular bone remain elusive.

263 ereas clear differences were identifiable in subchondral plate architecture.

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

265 as aggressive osteoclastic resorption of the subchondral plate.

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

267 kness, and greater BS/BV and porosity in the subchondral plate; and with thinner, less separated trab

268 In almost all subchondral plates, especially the medial femur and tibi

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

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

271 R arthrograms showing SAF were evaluated for subchondral reactions.

272 postero-lateral quadrants extending from the subchondral region into the mid trabecular region.

273 Subchondral sclerosis and subchondral cysts were graded

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

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

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

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

278 % (84 of 104) for JSN, 88.5% (92 of 104) for subchondral sclerosis, and 91.3% (95 of 104) for subchon

279 7 of 1538) for JSN, 95.8% (1473 of 1538) for subchondral sclerosis, and 97.6% (1501 of 1538) for subc

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

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

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

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

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

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

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

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

288 novial hyperplasia, osteophyte outgrowth and subchondral sclerosis.

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

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

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

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

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

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

295 Increased subchondral trabecular bone turnover due to imbalanced b

296 However, molecular changes in KOA subchondral trabecular bone, when exposed to different j

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

298 te, leading to Modic changes (non-neoplastic subchondral vertebral bone marrow lesions) and the gener

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

300 th the greatest changes occurring within the subchondral zone.