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1 expected for Zn alloys when considering bone fracture healing.
2 tion of Itm2a+ P-SSCs resulted in defects in fracture healing.
3 e expressed in human osteoblasts and mediate fracture healing.
4  to alleviate skeletal aging, did not affect fracture healing.
5 ture and an increased occurrence of impaired fracture healing.
6 significantly accelerated the time course of fracture healing.
7 ole of this transient IIFC population during fracture healing.
8 bsets of chondrocytes and osteoblasts during fracture healing.
9 ry phenotype (SASP) markers increased during fracture healing.
10 tic efficiency of Wnt targeted therapies for fracture healing.
11 optimal strain behaviour conducive to callus fracture healing.
12  significantly promotes bone regeneration in fracture healing.
13 tially benefit the prediction of complicated fracture healing.
14 ent novel therapeutic strategies to optimize fracture healing.
15 e ectopic bone formation, defect repair, and fracture healing.
16 ; thus, enhancing angiogenesis could improve fracture healing.
17 learance does not impair but rather improves fracture healing.
18 s within the fracture callus and accelerated fracture healing.
19 gest their critical involvement during human fracture healing.
20 tem/progenitor cells that contribute to bone fracture healing.
21 eum is the major source of cells involved in fracture healing.
22 which is a key value in bone remodelling and fracture healing.
23  neuroinflammatory state to accelerate early fracture healing.
24 st inflammatory response that resembles bone fracture healing.
25 tionally important for bone formation during fracture healing.
26 out the mechanical behavior of a bone during fracture healing.
27 tribute to mature lineages during periosteal fracture healing.
28  biomarkers increased markedly during murine fracture healing.
29 genitor cells and their contribution to bone fracture healing.
30      Wnt signaling is critically involved in fracture healing.
31 is, and provide a new therapeutic avenue for fracture healing.
32 ng stimulated bone formation and accelerated fracture healing.
33  beta-AR signaling, accompanied by disturbed fracture healing.
34  and bone regeneration, resulting in delayed fracture healing.
35 role of Scx in cortical bone development and fracture healing.
36 es in cortical bone, as well as asymmetry in fracture healing.
37  the long noncoding RNA (lncRNA) KCNQ1OT1 in fracture healing.
38 lay a role in the periosteal response during fracture healing.
39 e role of Scx in cortical bone mechanics and fracture healing.
40 n-situ strain sensors to objectively measure fracture healing.
41 oth chondrocytes and osteoblasts during bone fracture healing.
42 in order to investigate the effect of TBI on fracture healing.
43 sis, decreased adipogenesis, and accelerated fracture healing.
44 ng aging, reduced bone strength, and delayed fracture healing.
45 otential for clinical management of impaired fracture healing.
46 injuries, in part through inhibition of bone fracture healing.
47  play important roles in bone remodeling and fracture healing.
48 udied in context of skeletal development and fracture healing.
49 us places and at various times during normal fracture healing.
50 oxide production from arginine during normal fracture healing.
51  of injury, supplying new osteoblasts during fracture healing.
52 cquire the ability to continuously stimulate fracture healing.
53 ant component of bone homeostasis as well as fracture healing.
54 progenitor cells, which may be important for fracture healing.
55 ilage callus maturation at an early stage of fracture healing.
56 igated the expression of all LOX isoforms in fracture healing.
57 in compensation for the lack of COX-2 during fracture healing.
58 ulated during osteoblast differentiation and fracture healing.
59 fter fracture and, consequently, compromises fracture healing.
60 ne formation and remodeling, and at sites of fracture healing.
61 and earlier return to activity with reliable fracture healing.
62 E2 is an unacceptable therapeutic option for fracture healing.
63 emporal profile of all isolated cDNAs during fracture healing.
64                               To investigate fracture healing, 12-week-old C57BL/6J mice underwent a
65 flammatory phase was demonstrated to improve fracture healing after severe injury.
66 e substantive and prolonged contributions to fracture healing and can be targeted as a therapeutic ap
67                                              Fracture healing and distraction osteogenesis have impor
68 -1 (DKK1) levels in patients with respect to fracture healing and explore its association to sclerost
69                Resident MSC are critical for fracture healing and function as a source of TGF-beta1 i
70  administration in craniofacial bones and in fracture healing and implant integration.
71 jury has been associated with decreased bone fracture healing and increased rates of nonunion in elde
72 ential for regenerative applications such as fracture healing and osseous defects of the oral cavity.
73 eptidyl molecule with the ability to promote fracture healing and prevent malunions.
74 e temporal topography of the early stages of fracture healing and the dynamic response of periosteal
75 the development of new approaches to improve fracture healing and to treat osteoporosis by increasing
76 sis of many conditions such as osteoporosis, fracture healing, and loosening of orthopedic implants.
77 keletal development, tissue differentiation, fracture healing, and mechanotransduction.
78 rstanding normal bone formation, remodeling, fracture healing, and skeletal tissue repair.
79 vels or deleted in mice at the late stage of fracture healing, and the effects on healing quality wer
80  in aging owing to improved angiogenesis and fracture healing, and the lack of side effects associate
81 n, skeletal patterning, osteoblast activity, fracture healing, angiogenesis, and key signaling pathwa
82 anisms responsible for the effect of EtOH on fracture healing are still incompletely understood, and
83 re tissue-lytic features of blood vessels in fracture healing, arthritis and cancer.
84 lles' therapeutic efficacy in promoting bone fracture healing as demonstrated by micro-CT and histolo
85 jured patients frequently suffer compromised fracture healing because of systemic post-traumatic infl
86  and endothelial cells that is essential for fracture healing, bone remodeling, and osteogenesis.
87 ever, senescence in these cell types impedes fracture healing by unknown mechanisms.
88 ondary outcome was unplanned reoperation for fracture-healing complications.
89                            At late stages of fracture healing, CSC mice were characterized by decreas
90 e currently no pharmacological approaches in fracture healing designed to therapeutically stimulate e
91              Both strains exhibited impaired fracture healing, disturbed osteoclastogenesis and delay
92 ndral ossification and that its loss impairs fracture healing, due to inhibition of compensatory mech
93 ) are increasingly used to treat complicated fracture healing e.g., non-union.
94 latter group was divided into the successful fracture healing group (n = 30; bracing group) and the s
95 er, the potential role of senescent cells in fracture healing has not been defined.
96                  However, the role of Scx in fracture healing has not yet been explored.
97                                         Bone fracture healing impairment related to systemic diseases
98 fore, we investigated mechanisms of impaired fracture healing in a model of multiple low-dose strepto
99 d similar deficiencies in nerve regrowth and fracture healing in a mouse model of peripheral neuropat
100 rve as an alternative treatment to BMP-2 for fracture healing in aging owing to improved angiogenesis
101 on of EP4, but not EP2 rescued impaired bone fracture healing in COX-2(-/-) mice.
102 ase after fracture, as well as a compromised fracture healing in CSC mice.
103 c platelet thrombolysis also benefits senile fracture healing in female mice.
104 hoid sinus and LVs, causes LDI, and inhibits fracture healing in male mice, which can be rescued by a
105    Sufficient lymphatic drainage facilitates fracture healing in male mice.
106 elevated in the regenerative response during fracture healing in mice and has a critical role in chon
107 utrophil subpopulation, intrinsically impair fracture healing in mice irrespective of age.
108 levels of beta-catenin in the early phase of fracture healing in old animals slows osteogenesis, and
109  natural callus development to simulate bone fracture healing in rodents.
110                                         Bone fracture healing is a complex process with distinct phas
111 ignaling in the remodeling phase during bone fracture healing is currently unknown.
112  essential role of cyclooxygenase (COX)-2 in fracture healing is known, the targeted genes and molecu
113  the detrimental effects of hyperglycemia on fracture healing is still inadequate.
114                This temporo-spatial model of fracture healing is the first model to consider the effe
115 poiesis, however, whether LVs in bone affect fracture healing is unclear.
116                                          The fracture healing is usually impaired in diabetics, and o
117             Use of a transplant system and a fracture healing model revealed that expression of Wnt-i
118                                         In a fracture-healing model, COX-2(-/-) mice showed delayed i
119                                       During fracture healing, multipotential stem cells differentiat
120                  Importance: Failure of bone fracture healing occurs in 5% to 10% of all patients.
121 o assess bone morphometry and the effects of fracture healing on Scx localization and gene expression
122 thods do not provide an objective measure of fracture healing or weight bearing for lower extremity f
123 , infection, cardiovascular disease, delayed fracture healing, or hypocalcemia, and there were no cas
124                                              Fracture healing outcome was not different between analg
125 ects on experimental readout, and effects on fracture healing outcomes in male and female C57BL/6N mi
126  successfully while one-third may experience fracture healing problems that require secondary surgery
127 nd the secondary surgery group (n = 14) with fracture healing problems.
128 mice showed no significant difference in the fracture healing process compared to control mice.
129 eed for non-invasive therapies to aid in the fracture healing process.
130       A more rigorous method for determining fracture healing progression could significantly improve
131                Postnatal bone remodeling and fracture healing provide evidence that an osteochondropr
132          These effects lead to improved bone fracture healing quality compared with wildtype mice.
133                                              Fracture healing recapitulates aspects of endochondral b
134 lammation via anti-TNFalpha treatment during fracture healing reduced these changes in Sdc4(-/-) mice
135 g mechanisms by which these implants improve fracture healing remain elusive.
136 d mortality associated with impaired/delayed fracture healing remain high.
137 s with TBI, the relationship between TBI and fracture healing remains poorly understood, with clinica
138               Clinical determination of bone fracture healing remains qualitative, typically determin
139 re FDA approved to promote spinal fusion and fracture healing, respectively, and the first FDA-approv
140 e absence of Ksr2, bone strength, as well as fracture healing response, remains compromised in these
141 dual-action mechanism significantly enhances fracture healing, resulting in a 27.8% improvement in fl
142 g], and conditional knock-out of Sox2 during fracture healing results in reduction of the fracture ca
143 in bones lacking BMP2, the earliest steps of fracture healing seem to be blocked.
144                                  The pace of fracture healing slows with age, associated with a trans
145 ccur each year in the US, methods to promote fracture healing still rely primarily on fracture stabil
146    Clinical translatability is shown through fracture healing studies that demonstrate biomarkers of
147 pplying our method to microarray data from a fracture healing study revealed distinct temporal patter
148 Furthermore, by targeting distinct facets of fracture healing, the bispecific antibody shows superior
149 ted with increased fracture risk and delayed fracture healing; the underlying mechanism, however, rem
150          This allowed our sensor to indicate fracture healing through radiography in load scenarios g
151 is targeted delivery results in reduction of fracture healing times to <1/2 while creating repaired b
152 tly activated level during the late stage of fracture healing to ensure better bone fracture repair.
153 L2 expression with the chondrogenic phase of fracture healing was found, prompting more detailed anal
154 2 gene in chondrocytes and in osteoblasts in fracture healing was investigated by generation and anal
155               In contrast, among adult mice, fracture healing was markedly delayed in Sdc4(-/-) anima
156 nt mouse, we showed that angiogenesis during fracture healing was significantly higher in MATN-1(-/-)
157        To assess the impacts of metformin on fracture healing, we compared the healing process of clo
158     To elucidate the role of beta-catenin in fracture healing, we used a surgically induced tibial fr
159 fractures of which six patients had impaired fracture healing were included in this study.
160 , we found that in an in vivo mouse model of fracture healing where muscle progenitor cells were line
161 c ablation of p21-positive cells accelerated fracture healing, while removal of a different senescent
162     Conceptually, this view of senescence in fracture healing with a spotlight on osteoimmune cross-t
163 rently no standardized methods for assessing fracture healing, with physicians relying on X-rays whic
164 vation has long held that TBI can accelerate fracture healing, yet the complexity and heterogeneity o

 
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