Moreover, the bone defects of sildenafil-treated animals contained more tartrate-resistant acid phosphatase (TRAP)-positive osteoclasts and CD68-positive macrophages and exhibited a higher expression of the pro-angiogenic and pro-osteogenic markers cysteine rich protein (CYR)61 and vascular endothelial growth factor (VEGF) when compared to controls.

This was associated with a higher bending stiffness as well as an increased number of CD31-positive microvessels and a higher oxygen saturation within the callus tissue. Bone formation was markedly improved in defects of sildenafil-treated mice when compared to controls. The animals were treated daily with either 5 mg/kg body weight sildenafil (n = 35) or saline (control n = 35) per os. Bone regeneration was analyzed by means of X-ray, biomechanics, photoacoustic and micro-computed tomography (♜T) imaging as well as histological, immunohistochemical and Western blot analyses at 2, 5 and 10 weeks after surgery. After creation of a 1.8 mm segmental defect, mice femora were stabilized by pin-clip fixation. Therefore, the aim of the present study was to analyze the impact of sildenafil in an atrophic non-union model in mice. The phosphodiesterase-5 (PDE-5) inhibitor sildenafil has been shown to exert pro-angiogenic and pro-osteogenic effects in vitro and in vivo. Non-union formation represents a major complication in trauma and orthopedic surgery.

Actin western blot size