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Fig. 6 | Stem Cell Research & Therapy

Fig. 6

From: Aspirin inhibits RANKL-induced osteoclast differentiation in dendritic cells by suppressing NF-κB and NFATc1 activation

Fig. 6

Aspirin treatment promotes HA/TCP-mediated new bone formation in the rat mandibular defect model. a Two months after surgery, new bone and blood vessels were observed in the control group. HA/TCP was also detected in the mineralized tissues. (Black lines show the margins of the bone defect generated during surgery. Blue lines show the area of new bone formation.) b The area of a green rectangle in a shows new bone around HA/TCP particles under a high-magnification microscope, and new blood vessels can be seen between the bone. c Large volumes of connective tissues remain at the edge of the bone defect, which surround the HA/TCP particles. (The area enclosed with a yellow rectangle in a.) d New bone formation almost completely repaired the bone defect in the aspirin group after 2 months. (Black lines show the margins of the bone defect generated during surgery. Blue lines show the area of new bone formation.) e The area in a green rectangle of d shows new bone formation and a large number of new surrounding blood vessels. f Higher magnification of the area in a yellow rectangle in d shows osteoblasts surrounding the surface of HA/TCP particles, with new bone formation still being active. g Two months later, aspirin treatment accelerated bone regeneration compared to the control group (P < 0.05). HA = HA/TCP particles, CT = connective tissue, BV = blood vessel, NB = new bone. Scale bar = 200 μm in a, d and scale bar = 50 μm in b, c, e, f

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