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1 bone (resorption) and the laying down of new bone (formation).
2 rs that promote bone resorption and suppress bone formation.
3 r, reduces bone resorption while maintaining bone formation.
4 d by increased bone resorption and decreased bone formation.
5 rix deposited provides a scaffold for future bone formation.
6 entiation and activity, leading to a reduced bone formation.
7 ne resorption, but elevated serum markers of bone formation.
8 ZOL significantly (P < 0.0001) increased new bone formation.
9  Increased glycolysis mediates Wnt7b-induced bone formation.
10         Pannexin 3 (Panx3) is a regulator of bone formation.
11 by inhibiting bone destruction and promoting bone formation.
12 by promoting bone destruction and inhibiting bone formation.
13 s underlying the role of FCSCs in regulating bone formation.
14 eocyte-specific Wnt antagonist that inhibits bone formation.
15  are essential for FCSC-derived vascularized bone formation.
16 rging on shared nuclear targets that promote bone formation.
17 ved and non-conserved features in vertebrate bone formation.
18 iocompatibility and the potential to support bone formation.
19 cytes undergo programmed cell death prior to bone formation.
20  these cells as a source for loading-induced bone formation.
21 ning the balance between bone resorption and bone formation.
22 e a key group of growth factors that enhance bone formation.
23 helial cell interactions during vascularized bone formation.
24 ing an imbalance between bone resorption and bone formation.
25 eted and sustained delivery of E2 to promote bone formation.
26 -threatening cervical swelling and cyst-like bone formation.
27  is required to achieve maximal load-induced bone formation.
28  for osteoporosis that increases the rate of bone formation.
29  osteoclastic bone resorption and suppressed bone formation.
30  or function may also interfere with coupled bone formation.
31 nitors" (MMPs), are essential for cancellous bone formation.
32 previous study shows Nrf2 deletion decreases bone formation.
33 ing, neurotransmission, lipid transport, and bone formation.
34 s, suggesting an indirect effect of c-Kit on bone formation.
35 contrast, decreases serum IGF-1 and inhibits bone formation.
36  functions of FGF signaling during postnatal bone formation.
37 ts in cartilage development and endochondral bone formation.
38 Msx1 and Msx2 play a major role in tooth and bone formation.
39  osteoblast numbers and hence did not impair bone formation.
40 rb bone, but also provide signals to promote bone formation.
41  (encoded by Sost) expression stimulates new bone formation.
42 cell responsiveness to RANKL and coupling to bone formation.
43 resorption, and impaired osteoblast-mediated bone formation.
44 osine (Ade) has been identified to stimulate bone formation.
45 red for loading-induced Sost suppression and bone formation.
46 n without interfering with the amount of new bone formation.
47 g Th1 and Th17 cells, which governed the new bone formation.
48 c3 regulates coupling of bone resorption and bone formation.
49 erefore provides a functional marker for new bone formation.
50 nce of the vascular pedicle further enhanced bone formation.
51  DBBM exhibited similar effectiveness in new bone formation.
52  CD8+ T cells, which activated Wnt-dependent bone formation.
53 ated with inflammation, vascularization, and bone formation.
54  (Treg) could affect osteoclasts and further bone formation.
55 stosis characterized by asymmetric exuberant bone formation.
56 amellar formation and is essential for woven bone formation.
57 to increase osteoblast numbers and stimulate bone formation.
58 rized by impaired osteoid mineralization and bone formation.
59 e cells and more fuel for osteoblasts during bone formation.
60 and inducing an osteogenic response with new bone formation.
61  by inhibiting bone resorption and enhancing bone formation.
62 ocesses ranging from cell differentiation to bone formation.
63 enic activity in vivo and BMP10 also induces bone-formation.
64  sclerostin protein, a negative regulator of bone formation(5000-fold), compared to cells in control
65 till survive and actively participate in new bone formation 8 weeks after implantation.
66  membrane exposure and a noteworthy, ectopic bone formation above the mesh in 72% of sites.
67 s neither due to the changes in osteoblastic bone formation activity nor osteoclastic bone resorption
68                   All groups showed a spongy bone formation after 30 days.
69 s two separate processes during endochondral bone formation after birth, recent studies have demonstr
70                          To evaluate the new bone formation after grafting with a synthetic biphasic
71                            Next, we assessed bone formation after loading to low (7N) and high (11N)
72                   Our results show increased bone formation after TBI when injuries occur contralater
73 s emerged as a major mechanism for promoting bone formation and a target pathway for developing bone
74 ks showed that mechanical loading stimulated bone formation and accelerated fracture healing.
75 t 6 weeks of age, resulting in a decrease in bone formation and an increase in bone resorption.
76 h absorbed into bone from circulation during bone formation and are used to monitor mineralization in
77 riguing questions about potential effects on bone formation and bone health.
78 et gene and PTH treatment failed to increase bone formation and bone mass in Tgif1-deficient mice.
79  molecule SIK inhibitor YKL-05-099 increases bone formation and bone mass.
80 r of skeletal development that promotes both bone formation and bone resorption.
81 etabolic rewiring during osteoblast-mediated bone formation and bone-turnover.
82 on of osteogenic markers and intramembranous bone formation and by decreased expression of osteoclast
83  It also significantly reduced both reactive bone formation and cortical bone destruction by CM from
84 tein diet fed mice showed decreased in vitro bone formation and decreased osteogenic marker gene expr
85 estored trabecular bone volume by increasing bone formation and decreasing bone resorption.
86  and prevent bone loss but fail to influence bone formation and do not replace lost bone, so patients
87 elop early onset osteoporosis due to reduced bone formation and enhanced bone destruction.
88 e therapeutic strategies employed to enhance bone formation and fracture repair, but the mechanisms e
89 ymal progenitors responsible for both normal bone formation and fracture repair.
90 t then contributes in a major way to overall bone formation and growth.
91  in multiple whole-body processes, including bone formation and immune response.
92 microbiota was required for PTH to stimulate bone formation and increase bone mass.
93 ated with decreased periosteal and endosteal bone formation and increased endocortical resorption.
94  hormone (PTH) activates osteoblast-mediated bone formation and is used in patients with severe osteo
95  altered hematological parameters, increased bone formation and lipid accumulation in metabolically c
96                                     Skeletal bone formation and maintenance requires coordinate funct
97 isorder resulting in variable alterations of bone formation and mineralization that are caused by mut
98              Histologically, an enhanced new bone formation and more significant periodontal attachme
99 ned by a balance between osteoblast-mediated bone formation and osteoclast-driven bone resorption.
100 an efficient and facile method for promoting bone formation and osteointegration in bone repair.
101 V), are known to be associated with alveolar bone formation and periodontal improvements.
102 lucose, fatty acids and amino acids) to fuel bone formation and promote osteoblast differentiation.
103  SBC with saline significantly increased new bone formation and reduced connective tissue volume afte
104 yeloid lineage cells are required for proper bone formation and regeneration, in this study we examin
105 mplex effects on bone, including stimulating bone formation and regulating the hematopoietic stem cel
106 inhibition during the repair phase disturbed bone formation and remodeling.
107 roduction, particularly during states of new bone formation and remodelling.
108 ational potential of coimplantation to speed bone formation and repair.
109         HU MAT- mice had elevated cancellous bone formation and resorption compared to other treatmen
110                   Uncoupled and disorganized bone formation and resorption continued for the duration
111 are required to achieve coordination between bone formation and resorption during bone remodeling.
112 ation and maintenance of the balance between bone formation and resorption factors.
113 ergoes continuous remodeling due to balanced bone formation and resorption mediated by osteoblasts an
114 de of type I collagen (CTX-I) are markers of bone formation and resorption, respectively, that are re
115    25(OH)D3 deficiency results in failure in bone formation and skeletal deformation.
116 tion of beta-catenin significantly increased bone formation and slightly hindered bone resorption.
117 K signaling results in abnormal endochondral bone formation and subsequent severe scoliosis.
118 ned with ovariectomy recapitulates decreased bone formation and substandard matrix mineralization in
119 n platelet activation during blood clotting, bone formation and T cell activation.
120 ion between denervation-induced reduction of bone formation and TGF-beta gene expression, we measured
121 iR-874-3p expression during weaning enhances bone formation and that this miRNA may become a therapeu
122  p38alpha ablation resulted in a decrease in bone formation and the number of bone marrow mesenchymal
123 ve deubiquitination of RUNX2 is required for bone formation and this CK2/HAUSP deubiquitination pathw
124                                          New bone formation and tissue remodeling are the major chall
125 found to significantly increase load-induced bone formation and Wnt/beta-catenin activity in osteocyt
126  binds to and inhibits sclerostin, increases bone formation, and decreases bone resorption.
127 s in bone mass, impaired osteoblast-mediated bone formation, and enhanced bone marrow fat accumulatio
128 oma (MM) induces bone destruction, decreases bone formation, and increases marrow angiogenesis in pat
129 om the imbalance between bone resorption and bone formation, and restoring the normal balance of bone
130 d by increased bone resorption and decreased bone formation, and significantly decreased bone strengt
131 eeks, DOX (61.11%) also had the highest mean bone formation, and statistical differences were observe
132 steoclastogenesis, increases osteoblasts and bone formation, and suppresses bone marrow sclerostin le
133 active WNT signaling and enhanced periosteal bone formation, and the combined outcome is generalized
134     Consequently, tumour growth and abnormal bone formation are inhibited by these direct effects and
135 implicated in osteoblast differentiation and bone formation are involved in vascular calcification.
136 eotomy site viability, leading to faster new bone formation around implants.
137 nanorods on their surface to promote the new bone formation around the implants.
138  the patients, there was reactive periosteal bone formation around the nidus.
139 maintained (trabecular) or higher (cortical) bone formation as compared to vehicle-treated mice.
140 anscription factor 2 (RUNX2) is critical for bone formation as well as chondrocyte maturation.
141 M demonstrated the highest percentage of new bone formation at 4 weeks.
142                                Regarding new bone formation, at the end of 8 weeks, DOX (61.11%) also
143 phometry showed no differences in trabecular bone formation between WT and Col6alpha2-KO mice based o
144  well tolerated and resulted in increases in bone formation biomarkers and bone mineral density, sugg
145    Peri-nidus sclerosis, periosteal reactive bone formation, bone marrow and soft tissue oedema, pres
146  compounds increase mineral apposition rate, bone formation, bone mass, and bone strength, as well as
147 ween the groups for mean percentage of vital bone formation (bovine = 36.21%, porcine = 31.27%, P = 0
148 ascular invasion was apparent at the time of bone formation but not earlier.
149                        Knee loading promotes bone formation, but its effects on OA have not been well
150 influence osteoblastogenesis or endochondral bone formation, but notably enhanced osteoclastogenesis.
151 n 1-mo-old mice for 1 wk markedly stimulated bone formation, but the effect was essentially abolished
152       Finally, miR-101 also promotes in vivo bone formation by hBMSCs.
153 t1 overexpression from osteocytes stimulated bone formation by increasing osteoblast number and activ
154 ceptor 4 (EP4) in sensory nerves to regulate bone formation by inhibiting sympathetic activity throug
155 neage cells increases bone mass by elevating bone formation by OBs and reducing bone resorption by OC
156 ding, such as caused by exercise, stimulates bone formation by osteoblasts and increases bone strengt
157 osteoclast activity are expected to preserve bone formation by osteoblasts in contrast to current tre
158 ne resorption by osteoclasts and stimulating bone formation by osteoblasts, respectively.
159 one resorption by osteoclasts and stimulates bone formation by osteoblasts, respectively.
160 hanical load, and produce signals that alter bone formation by osteoblasts.
161 t is mainly due to defective intramembranous bone formation by osteoblasts.
162 n share their receptors in the regulation of bone formation by osteoblasts.
163 ne mass is determined by the balance between bone formation, carried out by mesenchymal stem cell-der
164 th BM-MSCs and AT-MSCs resulted in increased bone formation compared to that in Control and with simi
165 e curves increasingly over time as vertebral bone formation compresses the notochord asymmetrically,
166  of Piezo1 in intestinal epithelium promotes bone formation, decreases peristalsis, and protects from
167 lasts and osteocytes, resulting in decreased bone formation during long-term use.
168 pid palatal expansion and further facilitate bone formation during retention.
169  hypoplasia, but the biological mechanism of bone formation during this procedure is largely unknown.
170 etic disorder of heterotopic (extraskeletal) bone formation fibrodysplasia ossificans progressiva.
171  to examine the efficacy of blood vessel and bone formation following transfection with VEGF RNA or d
172 also enhances osteoblast differentiation and bone formation from mesenchymal stem cells.
173 nsity, structure, and strength by uncoupling bone formation from resorption.
174 wever, targeting tumor-derived modulators of bone formation has had limited success.
175 oach to improving bone quality by increasing bone formation, have been approved.
176 d mineralization, both essential for regular bone formation, however, remain incompletely understood.
177    The implication of WNT1 in the control of bone formation identifies a potential new target for the
178 nding tissues over time and to influence new bone formation in a 3 mm femur osteoporotic defect model
179 his study establishes a key role for Osx for bone formation in a non-mammalian species, and reveals c
180 is, posture-gait deterioration, and reactive bone formation in a patient with continuous pain that is
181 entation by providing a larger volume of new bone formation in a shorter time.
182 R-195 stimulates CD31(hi)Emcn(hi) vessel and bone formation in aged mice.
183                               Thus, abnormal bone formation in areas of subarticular ossification may
184  potential mechanism underlying the impaired bone formation in arthritis, so their preservation may r
185 tions of hyaluronic acid (HA) to improve new bone formation in critical-size calvaria defect (CSD) wh
186    Dietary factors during early life program bone formation in female rats.
187  collagen membrane on the quality of the new bone formation in guided bone regeneration (GBR) procedu
188                                              Bone formation in mammals requires continuous production
189 TrkA signaling is essential for load-induced bone formation in mice.
190 inically relevant dose of ZOL can induce new bone formation in microenvironments enriched for perivas
191 opose a new model that contrasts the mode of bone formation in much of the mandibular ramus (chondroc
192                         Thus, Wnt7b promotes bone formation in part through stimulating glucose metab
193  than micro-HA or mixed-HA bone graft in new bone formation in standardized surgically created defect
194 rable degrees of osteolysis and reactive new bone formation in the acute phase of osteomyelitis.
195 t mice, which exhibit dwarfism and defective bone formation in the axial, appendicular, and cranial s
196 he defect bridging but left little space for bone formation in the defect site.
197  microcomputed tomography analysis, more new bone formation in the DPSC and DPSC + THSG groups was ob
198  the cleft site with diminished capacity for bone formation in the expanded palate, more than 80% of
199 atic brain injury (mTBI) transiently induced bone formation in the femur via the cannabinoid-1 (CB1)
200  of MSC-laden microcarriers supports ectopic bone formation in the rat model.
201 teoblastogenesis from MSCs, thus suppressing bone formation in vitro and in vivo.
202  to reduced cell proliferation and deficient bone formation in vitro, as evidenced by reduced mineral
203 s not have any effect on osteoblast-mediated bone formation in vitro.
204 tion of parathyroid hormone (PTH) stimulates bone formation in vivo and also suppresses the volume of
205 oth drugs were found to enhance osteoblastic bone formation in vivo using a unique gene footprint and
206 eoblast and osteoclast function and promotes bone formation in vivo via an adenosine-dependent mechan
207 ow stromal cells (BMSCs), can induce ectopic bone formation in vivo.
208 administration of PTHrP1-17 augments ectopic bone formation in vivo.
209 hows that silencing SMS also reduces ectopic bone formation in vivo.
210 of osteoblasts, and reduced serum markers of bone formation, including osteocalcin and procollagen ty
211 ns, via rapid demineralization and decreased bone formation, independent of weight loss or Ca2+/vitam
212  or without rMSC aggregates resulted in less bone formation, indicating a prominent role of DA in eff
213 Gq/11 (D/D mice), PTH significantly enhanced bone formation, indicating that phospholipase C activati
214  was found to greatly attenuate load-induced bone formation induced by axial forelimb compression.
215                            Remarkably, woven bone formation induced by high-force loading was blocked
216  the effect of spinal loading on stimulating bone formation, inhibiting bone resorption, and promotin
217        These findings reveal that suppressed bone formation is a direct consequence of myeloma-MSC co
218                           The suppression of bone formation is a hallmark of multiple myeloma.
219 thesis that denervation-induced reduction of bone formation is a result of inhibition of TGF-beta gen
220 ortance of glucose metabolism in Wnt-induced bone formation is lacking.
221               Excessive bone resorption over bone formation is the root cause for bone loss leading t
222 e JCI, Joeng and colleagues demonstrate that bone formation is under the control of WNT1 produced by
223 fication, an important process in vertebrate bone formation, is highly dependent on correct functioni
224  has demonstrated extraordinary potential in bone formation, its clinical applications require suprap
225 scular calcification is a process similar to bone formation leading to an inappropriate deposition of
226 assessment evidenced marked endochondral new bone formation leading to joint ankylosis over time.
227 nses in addition to promoting an increase in bone formation markers and transcription factors.
228 hypertrophic, hypertrophic, and subsequently bone formation markers in a sequential manner in euthyro
229                   Transient increases in the bone formation markers procollagen type-I N-terminal pro
230 uggest that denervation-induced reduction of bone formation may be regulated by glucocorticoids via i
231 ing, which is amenable to subsequent dynamic bone formation measurements.
232 obtain mineralized bone sections for dynamic bone formation measures.
233 to quantify the vertical distribution of new bone formation (nBF) in MSFA and to characterize the ver
234 s plasma biomarkers and mediators of growth, bone formation, neurodevelopment, and immune function in
235                    While the majority of new bone formation occurred around the HCCS-PDA particulates
236 s (chondrocyte-derived) with intramembranous bone formation of the mandibular body (non-chondrocyte-d
237 ment analysis incorrectly predicts preferred bone formation on the periosteal surface, we demonstrate
238  with autologous bone tissue did not improve bone formation or defect bridging compared to the empty
239 nstrating no significant difference in vital bone formation or dimensional changes among 50%/50% cort
240 ficant difference in empty lacunae, necrotic bone formation, osteoclast number, and surface area in a
241                                 Analogous to bone formation, osteogenic cells are thought to be recru
242 ments revealed that both bone resorption and bone formation parameters were increased in male Erk5 (f
243 sorption, the peak of which is followed by a bone formation phase, leading ultimately to an accelerat
244   The current concept regarding endochondral bone formation postulates that most hypertrophic chondro
245 l telopeptides of type I collagen (CTX)) and bone formation (procollagen type I amino-terminal peptid
246 Keap1 Ht mice showed significant increase in bone formation rate (+30.7%, P = 0.0029), but did not ch
247 in antibody increased osteoblast numbers and bone formation rate but did not inhibit bone resorption
248 gnificantly increased osteoblast numbers and bone formation rate in both control and P-Gsalpha(OsxKO)
249 ed with higher osteoclast surfaces and lower bone formation rate in DSS animals as well as lower ulti
250 gh (11N) forces and observed that periosteal bone formation rate in experimental mice was reduced by
251  new bone volume generated and increased the bone formation rate more than the DBBM controls.
252 tion rate and higher trabecular and cortical bone formation rate was displayed in CCR3-deficient mice
253  a decrease in the number of osteoblasts and bone formation rate while the osteoclasts remained relat
254 mice based on the mineral appositional rate, bone formation rate, and mineralizing perimeter.
255 hanical properties; however, irisin elevated bone formation rate, decreased osteoclast surfaces, and
256 oss is associated with significantly reduced bone formation rate, reduced osteoblast population densi
257                                At 24 months, bone formation rate, trabecular thickness, and bone volu
258 , but had no change in osteoblast numbers or bone formation rate.
259 d previously unknown Chd7 targets, including bone formation regulators Osterix (also known as Sp7) an
260       In tibial bone, the mRNA expression of bone formation related genes such as Osx and Bmp2 was el
261                                          The bone formation-related proteins such as BMP2, COL1a1 and
262 rtebrate lineages, its role in non-mammalian bone formation remains elusive.
263 ated bone resorption and osteoblast-mediated bone formation, represents a highly energy consuming pro
264                    Cell-based approaches for bone formation require instructional cues from the surro
265  if there is a significant difference in new bone formation, residual graft material, and connective
266  allowing for continued teriparatide-induced bone formation, resulting in larger increases in hip and
267 Cs) must be tightly regulated, as inadequate bone formation results in low bone mass and skeletal fra
268 ere additionally present in the areas of new bone formation rich in osteoblasts and newly-embedded os
269 etween the two groups for mean percent vital bone formation (short-term = 18.17%, long-term = 40.32%,
270 y shown to play key roles in normal alveolar bone formation), significant loss in alveolar bone mass
271  factor during development and essential for bone formation, skeletal growth and postnatal homeostasi
272  the rate of bone resorption exceeds that of bone formation, so we investigated the role of the osteo
273 durations from hours to beyond 4 days, where bone formation starts.
274 osteoblasts, and osteoclasts are a source of bone formation-stimulating factors.
275 y inhibit bone resorption but also stimulate bone formation, such as potentially inhibitors of 17beta
276 6 conjugated drugs showed significantly more bone formation than DBBM control at 2 and 4 weeks.
277 lveolar bone lineage differentiation and new bone formation through WNT, bone morphogenetic protein,
278                                  Stimulating bone formation to increase bone mass and fracture resist
279 modest but persistent programming effects on bone formation to prevent OVX-induced bone loss in adult
280 modest but persistent programming effects on bone formation to prevent OVX-induced bone loss in adult
281  multiple mechanisms mediate the coupling of bone formation to resorption in remodeling.
282 l and central actions of PDE5A inhibitors on bone formation together with their antiresorptive action
283 lator of inflammation in RA, but its role in bone formation under arthritic conditions is not complet
284 on-osteogenic C4-2b PCa cells led to ectopic bone formation under subcutaneous implantation.
285  (rAAV9-amiR-shn3) in mice markedly enhanced bone formation via augmented osteoblast activity.
286                     Loading-induced lamellar bone formation was diminished but not prevented in exper
287 e, the inflammatory response was altered and bone formation was disturbed, which negatively affected
288      The expression of genes associated with bone formation was higher in the newly formed bone induc
289 e concluded that the material resorption and bone formation was highly impacted by the particle-speci
290                                              Bone formation was limited 7 days after the extraction p
291                    In the NC and TCN groups, bone formation was limited to the margins of the defects
292                                      Ectopic bone formation was monitored by micro-computed tomograph
293 ermine the underlying mechanism for impaired bone formation, we modelled the disease by silencing SMS
294 se PGE2 level locally, significantly boostes bone formation, whereas the effect is obstructed in EP4
295  The nHA-LC (38% HA content) paste supported bone formation with a high defect bridging-rate.
296 lecular phenamil synergized osteogenesis and bone formation with BMP2 in a rat critical size mandibul
297 asome inhibitors exert an anabolic effect on bone formation with elevated levels of osteoblast marker
298 that integrate the metabolic requirements of bone formation with global energy balance through the re
299 eointegration, translating to highly regular bone formation with minimal fibrous tissue and increased
300 ), producing a scaffold that induces ectopic bone formation with or without BMSCs.

 
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