Objective: To establish the model of swan-like memory compressive connector(SMC)treating experimental humeral fracture in rabbits, and apply following techniquesas: biomechanics, microangiography, radioactive microsphere fluometry, bioelectricpotential, bone mineral density, scan electroscope, reverse transcriptase polyerase chainreaction(RT-PCR), immunohistofluorescence dying, and elucidate following questionsabout humeral fractures fixed by SMC: (1)Radiographic and the biomechanicalcharacteristic in fracture healing of humerus treated by SMC, stress shielding ratio(SSR)of SMC. (2) Bioelectrical potential development and its correlationship with fracturehealing under light microscopic examination. (3)The perfusion changes and microvesselcompromise and revascularization of cortical bone during fracture healing. (4)Bone mineraldensity changes , dynamical evolvement of collagen architecture and remodel of corticalbone. (5) Modulation of the osteopontin(OSP) and osteonectin(OSN) mRNA expression invariety of time intervals. (6) Development of Oncogene c-fos expression during fracturehealing. Eventually to make clear the mechanism of SMC promoting bone healing in gross,cell and molecular level, and supply sufficient academic foundation for SMC clinicalspreading. Methods: The humerus shafts of new Zealand rabbits were osteotomied by linesawas fracture models treated with internal fixation. One humerus was randomly fixed by SMC,the contrallateral fixed by 4-hole dynamic compressive plate (DCP) as contral. (1) The SSR,anti-torsion biomechnics and geometrical conformation of bone fixed by SMC and DCPwere explored , the radiographic characteristic of fixed fractures was observed during bonehealing. (2) The bioelectric potential of fracture site were determined using modifiedFriedenberg's technique, the humerus were harvested for HE sections at various intervalpostoperatively. (3) The microangiography of cortical bone using Shanghai ink infusionand radioactive microsphere measuring blood flow were performed at intervals after 4ç¬¬äºŒå†›åŒ»å¤§å¦ è‹±æ–‡æ‘˜è¦ åšå£«å¦ä½è®ºæ–‡operation, to explore the influence of SMC on perfusion of long bone fracture. (4) The bonemineral density of fixed bones were examined using dual energy radiographyabsorptiometry (DRA), the collagen architecture in cortical bones beneath internal fixationwere harvested for scanning electroscopic obervation. (5) The spatial and temporalexpression patterns of OSP and OSN mRNA in fracture site were observed by RT-PCRtechnique. (6) Expression of oncogene c-fos during bone healing was examined usingimmunohistofluorescence dying . Results: (1) The fracture healing fixed by SMC presents primary healing. Neitherexternal callus nor osteoporosis beneath the SMC-body was found, the SSR in SMC groupwere significantly lower than that of DCP. (2) The bioelectric potential of fracture site ofexperimental group remained negative invariable all the time, fracture healing mainlydepended of endochondral osteogenesis, but the osteogenesis synchronized with bonematrix remodeling , and chondral bone was mineralized earlier than that in DCP group. (3)SMC had advantage on material characteristic and geometric contour, which not onlycomprised perfusion of cortical bone less than DCP, but also contributed to the recovery ofrevasculariation earlier. (4) Bone mineral depositing in SMC group was faster and more.No regional osteoporosis and collagen disorganization were found in SMC group duringthe whole experimental process. (5) SMC started up the OSP and OSN mRNA to expressearlier than DCP, and rapidly upregulated the expression to highest value at the earliertime of healing. (6) c-fos gene in SMC group was activated earlier than that in DCP andexpressed shortly, but expression was acutely upregulated to the peak, then attenuated atlater time point. Conclusion...
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