Shock wave application enhances pertussis toxin protein-sensitive bone formation of segmental femoral defect in XXXX .

@entity361 @entity174 @entity9356 @entity1810 @entity2095 @entity35 @entity460 @entity2096
Extracorporeal shock waves (ESWs) elicit a dose-dependent effect on the @entity2096 in @entity35 . After ESW treatment, the segmental defect underwent progressive @entity361 , endochondral ossification, and hard callus formation. Along with the intensive bone formation, there was a persistent increase in @entity1810 and @entity2095 expression. Pretreatment with pertussis toxin reduced ESW-promoted callus formation and gap healing, which presumably suggests that Gi proteins mediate osteogenic signaling. INTRODUCTION: Extracorporeal shock waves (ESWs) have previously been used to promote bone repair. In our previous report, we found that ESWs promoted osteogenic differentiation of mesenchymal cells through membrane perturbation and activation of Ras protein. In this report, we show that ESWs elicit a dose-dependent effect on the healing of segmental defects and that Gi proteins play an important role in mediating ESW stimulation. MATERIALS AND METHODS: @entity35 with @entity2096 were subjected to ESW treatment at different energy flux densities (EFD) and impulses. Bone mass (mineral density and @entity460 content), osteogenic activities (bone alkaline phosphatase activity and @entity9356 content), and immunohistochemistry were assessed. RESULTS: An optimal ESW energy (500 impulses at 0.16 mJ/mm2 EFD) stimulated complete bone healing without complications. ESW-augmented healing was characterized by significant increases (p < 0.01) in callus size, bone mineral density, and bone tissue formation. With exposure to ESW, alkaline phosphatase activity and @entity9356 production in calluses were found to be significantly enhanced (p < 0.05). After ESW treatment, the histological changes we noted included progressive @entity361 , endochondral ossification, and hard callus formation. Intensive bone formation was associated with a persistent increase in @entity1810 ( @entity1810 ) and @entity2095 ( @entity2095 ) expression, suggesting both growth factors were active in ESW-promoted bone formation. We also found that pertussis toxin, an inhibitor of membrane-bound Gi proteins, significantly reduced (p < 0.01) ESW promotion of callus formation and @entity174 healing. CONCLUSION: ESW treatments enhanced bone formation and the @entity2096 in @entity35 . It also seems likely that @entity1810 and @entity2095 are important osteogenic factors for ESW promotion of @entity174 healing, presumably through Gi protein-mediated osteogenic signaling.
