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1 lasts display polarised behaviour to deposit osteoid.
2 y of the bone in which spindle cells produce osteoid.
3 ding to adipose (4 kPa), muscle (13 kPa) and osteoid (30 kPa) tissues respectively by exposing them t
6 uding radiolucencies and resorptive lesions, osteoid accumulation on the alveolar bone crest, and sig
8 biopsy specimens revealed numerous areas of osteoid and bone formation around FDBA particles, with n
10 ed with decreased trabecular bone volume and osteoid and osteoblast surfaces in postmenopausal osteop
11 nd length of trabecular surface covered with osteoid and up-regulates bone marker gene (OPN, Cbfa1, C
12 ing CMF bone matrix also had an abundance of osteoid, and in locations where compact lamellar bone ty
13 expanded alveolar bone with accumulation of osteoid, and micro-CT confirmed decreased bone volume fr
14 there was no significant difference in total osteoid between the two samples, suggesting that increas
15 lastic bone resorption with simultaneous new osteoid/bone formation in the absence of ascorbate (vita
17 sed as the osteoblast differentiates into an osteoid cell or osteocyte, first appearing on the formin
18 bone porosity (pore water and total water), osteoid density (bound water [BW]), morphologic structur
19 , morphologic structure, mineralization, and osteoid density are affected in postmenopausal osteoporo
28 tly, osteoblast development and synthesis of osteoid in the nascent bone collar was uncoupled from th
31 SC) clusters, leading to formation of marrow osteoid islets accompanied by high levels of angiogenesi
33 ates, adjusted apposition rates) and static (osteoid markers, osteoblast number) parameters of bone f
34 the splenic nodules revealed the presence of osteoid matrices and osteocytes trapped within mineraliz
35 rate significantly increased regeneration of osteoid matrix (32 +/- 7% of total tissue area; mean +/-
36 tion, shown by accumulation of unmineralized osteoid matrix and interglobular patterns of protein dep
38 trengthened by observations showing that the osteoid matrix that is responsible for implant osseointe
39 the presence of transformed cells producing osteoid matrix, even if these cells comprise a minority
43 the primary spongiosa with reduced immature osteoid (new bone formation) and overall length, which l
44 the block specimens exhibited no evidence of osteoid or active bone formation, but large marrow space
48 ndings that were diagnostic for nonvertebral osteoid osteoma and no contraindications to MR imaging-g
50 ef and the other experienced a recurrence of osteoid osteoma at 11 months, which was successfully tre
51 ale; mean age, 21 years) with a diagnosis of osteoid osteoma based on clinical and imaging findings.
52 CT-guided cryoablation for the treatment of osteoid osteoma between January 2013 and June 2019 in a
53 at MR-guided focused ultrasound treatment of osteoid osteoma can be performed safely with a high rate
55 olinium-enhanced MR imaging demonstrated the osteoid osteoma equally well in eight of 11 patients and
56 ing, the edema and hyperemia associated with osteoid osteoma gradually disappeared in all lesions.
59 monstrate secondary radiological findings of osteoid osteoma in both paediatric and adult patients.
62 bone location, bone segment, location of the osteoid osteoma in relation to the native cortex, nidus
63 ) of 11 patients had peak enhancement of the osteoid osteoma in the arterial phase with early partial
68 ve and should become the method of choice in osteoid osteoma treatment because of its minimal invasiv
75 y ablation is now the standard treatment for osteoid osteoma, as the procedure can be performed with
76 wever, in the 10 patients with biopsy-proved osteoid osteoma, puncture of the tumor caused the mean c
77 CT-guided cryoablation for the treatment of osteoid osteoma, with a 96% (48 of 50 patients) overall
85 dolinium-enhanced MR images demonstrated the osteoid osteomas significantly better than the nonenhanc
89 es of 11 patients with pathologically proven osteoid osteomas who underwent nonenhanced MR imaging, d
90 six patients with histopathologically proven osteoid osteomas, complete clinical files, and CT data w
91 compass enchondromas, aneurysmal bone cysts, osteoid osteomas, giant-cell lesions of bone, bone sarco
96 radiographic mineralization and histological osteoid production, the differentiation state of tumors
98 s significantly increased; as a consequence, osteoid seams were evident throughout the facial skeleto
99 O bones were hypo-mineralized with prominent osteoid seams, analogous to the phenotypes of mice with
102 d mineralization lag time, as well as higher osteoid surface, osteoblastic surface, resorption surfac
105 ng decrease in the rate of mineralization of osteoid that occurred despite an unexpected osteoblast a
106 hat Dkk2-null mice have increased numbers of osteoids, these data indicate that Dkk2 has a role in la
108 one at 6 wk revealed significant increase in osteoid thickness, osteoblast number, erosion surface wi
111 Risedronate did associate with increased osteoid volume and trabecular thickness in male particip
112 ysis demonstrates a significant reduction in osteoid volume to bone volume and osteoid surface to bon
113 increased in all KOs, partially mineralized osteoid volume was increased in dKO versus controls at P
114 with ADPKD demonstrated significantly lower osteoid volume/bone volume (0.61 vs. 1.21%) and bone for
116 collagen type I is the main component of the osteoid, we hypothesized that the bone vasculature guide