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1  and bone regeneration, resulting in delayed fracture healing.
2 role of Scx in cortical bone development and fracture healing.
3 e role of Scx in cortical bone mechanics and fracture healing.
4 n-situ strain sensors to objectively measure fracture healing.
5 oth chondrocytes and osteoblasts during bone fracture healing.
6 in order to investigate the effect of TBI on fracture healing.
7 sis, decreased adipogenesis, and accelerated fracture healing.
8 ng aging, reduced bone strength, and delayed fracture healing.
9 otential for clinical management of impaired fracture healing.
10 injuries, in part through inhibition of bone fracture healing.
11 es in cortical bone, as well as asymmetry in fracture healing.
12  play important roles in bone remodeling and fracture healing.
13 udied in context of skeletal development and fracture healing.
14 us places and at various times during normal fracture healing.
15 oxide production from arginine during normal fracture healing.
16  of injury, supplying new osteoblasts during fracture healing.
17 ant component of bone homeostasis as well as fracture healing.
18 progenitor cells, which may be important for fracture healing.
19 ilage callus maturation at an early stage of fracture healing.
20 igated the expression of all LOX isoforms in fracture healing.
21 in compensation for the lack of COX-2 during fracture healing.
22 ulated during osteoblast differentiation and fracture healing.
23 ne formation and remodeling, and at sites of fracture healing.
24 lay a role in the periosteal response during fracture healing.
25 and earlier return to activity with reliable fracture healing.
26 E2 is an unacceptable therapeutic option for fracture healing.
27 emporal profile of all isolated cDNAs during fracture healing.
28                               To investigate fracture healing, 12-week-old C57BL/6J mice underwent a
29 flammatory phase was demonstrated to improve fracture healing after severe injury.
30 e substantive and prolonged contributions to fracture healing and can be targeted as a therapeutic ap
31                                              Fracture healing and distraction osteogenesis have impor
32                Resident MSC are critical for fracture healing and function as a source of TGF-beta1 i
33  administration in craniofacial bones and in fracture healing and implant integration.
34 ential for regenerative applications such as fracture healing and osseous defects of the oral cavity.
35 eptidyl molecule with the ability to promote fracture healing and prevent malunions.
36 the development of new approaches to improve fracture healing and to treat osteoporosis by increasing
37 sis of many conditions such as osteoporosis, fracture healing, and loosening of orthopedic implants.
38 keletal development, tissue differentiation, fracture healing, and mechanotransduction.
39 rstanding normal bone formation, remodeling, fracture healing, and skeletal tissue repair.
40 vels or deleted in mice at the late stage of fracture healing, and the effects on healing quality wer
41 anisms responsible for the effect of EtOH on fracture healing are still incompletely understood, and
42 lles' therapeutic efficacy in promoting bone fracture healing as demonstrated by micro-CT and histolo
43 jured patients frequently suffer compromised fracture healing because of systemic post-traumatic infl
44  and endothelial cells that is essential for fracture healing, bone remodeling, and osteogenesis.
45              Both strains exhibited impaired fracture healing, disturbed osteoclastogenesis and delay
46 ndral ossification and that its loss impairs fracture healing, due to inhibition of compensatory mech
47                  However, the role of Scx in fracture healing has not yet been explored.
48                                         Bone fracture healing impairment related to systemic diseases
49 fore, we investigated mechanisms of impaired fracture healing in a model of multiple low-dose strepto
50 on of EP4, but not EP2 rescued impaired bone fracture healing in COX-2(-/-) mice.
51 ignaling in the remodeling phase during bone fracture healing is currently unknown.
52  essential role of cyclooxygenase (COX)-2 in fracture healing is known, the targeted genes and molecu
53                This temporo-spatial model of fracture healing is the first model to consider the effe
54             Use of a transplant system and a fracture healing model revealed that expression of Wnt-i
55                                         In a fracture-healing model, COX-2(-/-) mice showed delayed i
56                                       During fracture healing, multipotential stem cells differentiat
57                  Importance: Failure of bone fracture healing occurs in 5% to 10% of all patients.
58 o assess bone morphometry and the effects of fracture healing on Scx localization and gene expression
59 thods do not provide an objective measure of fracture healing or weight bearing for lower extremity f
60 , infection, cardiovascular disease, delayed fracture healing, or hypocalcemia, and there were no cas
61 mice showed no significant difference in the fracture healing process compared to control mice.
62                Postnatal bone remodeling and fracture healing provide evidence that an osteochondropr
63          These effects lead to improved bone fracture healing quality compared with wildtype mice.
64                                              Fracture healing recapitulates aspects of endochondral b
65 lammation via anti-TNFalpha treatment during fracture healing reduced these changes in Sdc4(-/-) mice
66 g mechanisms by which these implants improve fracture healing remain elusive.
67 d mortality associated with impaired/delayed fracture healing remain high.
68 s with TBI, the relationship between TBI and fracture healing remains poorly understood, with clinica
69 re FDA approved to promote spinal fusion and fracture healing, respectively, and the first FDA-approv
70 g], and conditional knock-out of Sox2 during fracture healing results in reduction of the fracture ca
71 in bones lacking BMP2, the earliest steps of fracture healing seem to be blocked.
72 Furthermore, by targeting distinct facets of fracture healing, the bispecific antibody shows superior
73 ted with increased fracture risk and delayed fracture healing; the underlying mechanism, however, rem
74 tly activated level during the late stage of fracture healing to ensure better bone fracture repair.
75 L2 expression with the chondrogenic phase of fracture healing was found, prompting more detailed anal
76 2 gene in chondrocytes and in osteoblasts in fracture healing was investigated by generation and anal
77               In contrast, among adult mice, fracture healing was markedly delayed in Sdc4(-/-) anima
78 nt mouse, we showed that angiogenesis during fracture healing was significantly higher in MATN-1(-/-)
79     To elucidate the role of beta-catenin in fracture healing, we used a surgically induced tibial fr
80 , we found that in an in vivo mouse model of fracture healing where muscle progenitor cells were line

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