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1 ncy and heparin administration as a cause of extraskeletal 99mTc bone tracer accumulation.
2                                There were no extraskeletal abnormalities and no relationship between
3 epiction, location, and characterization and extraskeletal abnormalities were evaluated.
4                                   Pathologic extraskeletal bone formation, or heterotopic ossificatio
5  (FOP) is a rare but devastating disorder of extraskeletal bone formation.
6 pamycin significantly decreased or inhibited extraskeletal bone formation.
7                                              Extraskeletal bone forms through an endochondral process
8 ic ossification, the pathologic formation of extraskeletal bone, occurs as a common complication of t
9 ising target to prevent and treat pathologic extraskeletal bone.
10 Secondary hyperparathyroidism contributes to extraskeletal calcification and is associated with all-c
11 mic patients are prone to widespread ectopic extraskeletal calcification resulting from an imbalance
12 nisms are etiological agents of pathological extraskeletal calcification.
13 moral (0% to 12%; P=0.13) artery plaques and extraskeletal calcifications (34.4% to 65.6%; P=0.006) i
14 vitamin D deficiency is associated with many extraskeletal chronic disorders, including the autoimmun
15 Secondary hyperparathyroidism contributes to extraskeletal complications in chronic kidney disease.
16 at is essential for modeling of skeletal and extraskeletal connective tissues.
17 ntegrate therapies for both the skeletal and extraskeletal consequences with a view toward improving
18 ical setting and result in both skeletal and extraskeletal consequences.
19 oid CS is pathogenetically distinct from its extraskeletal counterpart.
20 (18)F-FDG PET/CT and whole-body MRI detected extraskeletal disease that may change the management of
21  develop hypocalcemia, rickets, and possibly extraskeletal disorders (e.g., type 1 diabetes).
22 ssiva, a disorder characterized by extensive extraskeletal endochondral bone formation, share a recur
23 rimary renal primitive neuroectodermal tumor/extraskeletal Ewing's sarcoma (PNET/EES) is a very rare
24 matopoietic abnormalities do not result from extraskeletal expression of endogenous collagen X or the
25 provided evidence for a role of vitamin D in extraskeletal health.
26 rimary tumor was bone in 57% of patients and extraskeletal in 43% of patients.
27 parathyroidism, are thought to contribute to extraskeletal (including vascular) calcification among p
28             The (18)F(-)/(18)F-FDG uptake in extraskeletal lesions showed no significant difference w
29 to-background ratio of (18)F(-)/(18)F-FDG in extraskeletal lesions showed no significant difference w
30                                          For extraskeletal lesions, (18)F-NaF/(18)F-FDG PET/CT and wh
31                                              Extraskeletal manifestations have not been reported in P
32 haracterized by brittle bones, fractures and extraskeletal manifestations.
33 fic antigen or radiological), baseline pain, extraskeletal metastases, and bisphosphonate use, were r
34 ny metastasis, even in the presence of other extraskeletal metastases, is not recommended.
35      Molecular studies have established that extraskeletal myxoid chondrosarcoma is a unique entity d
36                              A proportion of extraskeletal myxoid chondrosarcomas (EMC) have been sho
37 c and molecular genetic findings, except for extraskeletal myxoid chondrosarcomas.
38  molecular genetic changes are diagnostic of extraskeletal myxoid chondrosarcomas.
39                          Notably, 2 cases of extraskeletal myxoid CS showed neither an EWS/CHN fusion
40                                              Extraskeletal myxoid CS thus represents yet another sarc
41 ent, suggesting genetic heterogeneity within extraskeletal myxoid CS.
42 , has been recognized in CS, specifically in extraskeletal myxoid CS.
43 en characterized in only a limited number of extraskeletal myxoid CSs and its presence in other types
44 he EWS/CHN gene fusion was present in 6 of 8 extraskeletal myxoid CSs and was not detected in any of
45                 We studied 46 cases of CS (8 extraskeletal myxoid, 4 skeletal myxoid, 4 mesenchymal,
46                                              Extraskeletal new bone formation, as seen in myositis os
47 er of skeletal malformations and progressive extraskeletal ossification.
48 ormation, as seen in myositis ossificans and extraskeletal osteosarcoma, represents an exception wher
49       It remains unclear whether skeletal or extraskeletal problems will develop postnatally from exp
50 ites during development, suggesting possible extraskeletal roles for these proteins.
51 s to prevent or treat development of bone in extraskeletal sites.
52 eletal health, and might also have a role in extraskeletal tissues.
53                                 Mice bearing extraskeletal tumors show significantly elevated levels
54                          There was, however, extraskeletal uptake of the 99mTc bone tracer in the ant

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