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Results: 5

1.
FIG. 4.

FIG. 4. From: Fgf-18 Is Required for Osteogenesis But Not Angiogenesis During Long Bone Repair.

Osteoclastogenesis is impaired in Fgf-18+/− tibia. Tartrate resistant acid phosphatase (TRAP) staining of Fgf-18+/− and WT tibial defects at 7 day postoperatively revealed a marked decrease in staining in Fgf-18+/− tibial defects. Scale bar: 200 μm. Dotted lines indicate the bony edges of the defects. Color images available online at www.liebertonline.com/tea

Björn Behr, et al. Tissue Eng Part A. 2011 August;17(15-16):2061-2069.
2.
FIG. 1.

FIG. 1. From: Fgf-18 Is Required for Osteogenesis But Not Angiogenesis During Long Bone Repair.

No apparent differences in Fgf-18+/− and WT tibia. (A) Computed tomography scans of uninjured Fgf-18+/− and WT tibia revealed no obvious differences in shape. (B) Measurement of bone mineral density revealed no significant difference between Fgf-18+/− and WT tibia. (C) Quantitative real-time PCR analysis did not show differences in the gene expression profile for osteogenic, proliferative, and vascular markers. BMD, bone mineral density; Oc, osteocalcin; PCR, polymerase chain reaction; WT, wild type. Color images available online at www.liebertonline.com/tea

Björn Behr, et al. Tissue Eng Part A. 2011 August;17(15-16):2061-2069.
3.
FIG. 5.

FIG. 5. From: Fgf-18 Is Required for Osteogenesis But Not Angiogenesis During Long Bone Repair.

Rescue of Fgf-18+/− tibial defects by application of FGF-18 but not VEGF. (A) Aniline blue staining of Fgf-18+/− tibial defects treated with phosphate-buffered saline (PBS), 2 μg VEGFA, or 2 μg FGF-18 7 days postoperatively. The injury site is segregated to the right column. Scale bar: 200 μm. (B) Histomorphometry revealed rescue of Fgf-18+/− tibial defects with FGF-18 protein but not with PBS or VEGFA, ***p<0.0005. (C) Histomorphometry of untreated WT defects or WT defects treated with PBS or 2 μg FGF-18 revealed a significant increase of healing with FGF-18 treatment as compared with PBS control at 7 day postoperatively. Moreover, there was a trend to increased healing with FGF-18 as compared with untreated WT defects; however, this was not significant, *p<0.05. Color images available online at www.liebertonline.com/tea

Björn Behr, et al. Tissue Eng Part A. 2011 August;17(15-16):2061-2069.
4.
FIG. 3.

FIG. 3. From: Fgf-18 Is Required for Osteogenesis But Not Angiogenesis During Long Bone Repair.

Angiogenesis is not impaired in Fgf-18+/− tibia. (A) At day 3 immunohistochemistry for PECAM-1 and vascular endothelial growth factor A (VEGFA) did not reveal differences between Fgf-18+/− and WT tibia. (B) Quantification of vessel numbers as indicated by PECAM staining revealed no statistical differences between Fgf-18+/− and WT defects. (C) Microcomputed tomography-angiography of Fgf-18+/− and WT tibial defects at 7 day postoperatively. (D) Quantification of the vessel volume and (E) vessel surface area in the defects of Fgf-18+/− and WT mice did not reveal significant differences between the two groups. Scale bars: (A) 50 μm, (C) 200 μm. Dotted lines indicate the bony edges of the defects. PECAM, platelet endothelial cell adhesion molecule. Color images available online at www.liebertonline.com/tea

Björn Behr, et al. Tissue Eng Part A. 2011 August;17(15-16):2061-2069.
5.

FIG. 2. From: Fgf-18 Is Required for Osteogenesis But Not Angiogenesis During Long Bone Repair.

Bone regeneration is impaired in Fgf-18+/− tibia. (A) Aniline blue staining of unicortical tibial defects revealed markedly impaired bone regeneration in Fgf-18+/− as compared with WT tibia at days 5 and 7 (upper panels). Histomorphometry performed on aniline blue-stained slides revealed a marked impairment of bone regeneration in Fgf-18+/− mice at both time points. ***p<0.0005. (B) Hematoxylin and eosin staining of adjacent defects of Fgf-18+/− and WT tibia at days 5 and 7 paralleled these findings. (C) real-time-PCR (RT-PCR) analysis time course of Runx2, Osteocalcin, and Vegfa harvested from defects of Fgf-18+/− and WT tibia. (D) Quantitative RT-PCR analysis of Fgf-2, -9, and -18 and Bmp2. *p<0.05 and **p<0.005. (E) Immunohistochemistry for PCNA, Runx2, and Osteocalcin in Fgf-18+/− and WT mice. No differences were observed in staining for PCNA; however, reduced immunoreactivity for Runx2 and Osteocalcin were observed in defects of Fgf-18+/− tibia. (F) Quantification of PCNA-positive cells revealed no statistical differences in proliferation between Fgf-18+/− and WT defects. Scale bars: (A, B) 200 μm, (E) 50 μm. PCNA, proliferative cell nuclear antigen. Color images available online at www.liebertonline.com/tea

Björn Behr, et al. Tissue Eng Part A. 2011 August;17(15-16):2061-2069.

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