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[骨质疏松症损害大鼠骨质疏松模型中胫骨的骨折愈合]

[Osteoporosis impairs fracture healing of tibia in a rat osteoporotic model].

作者信息

Xu Shao-wen, Wang Jian-wei, Li Wei, Wang Yun, Zhao Guang-feng

机构信息

Department of Orthopaedics, Second Affiliated Hospital, Medical College of Zhejiang University, Hangzhou 310009, China.

出版信息

Zhonghua Yi Xue Za Zhi. 2004 Jul 17;84(14):1205-9.

Abstract

OBJECTIVE

To evaluate the influence of osteoporosis on fracture healing.

METHODS

Eighty-four 4 months old female Sprague-Dawley rats were randomly divided into osteoporosis (OP) group and sham operation (SO) group, 42 in each. Rats in OP group were performed ovariectomy operation while those in SO group with sham operation. When osteoporosis formed 10 weeks after ovariectomy, midshaft tibia fracture model was established. Tibias were harvested 2 weeks (2 rats per group), 4 weeks (9 rats per group), 6 weeks (9 rats per group), 12 weeks (9 rats per group) and 18 weeks (7 rats per group) after fracture for bone mineral density (BMD), histomorphological and biomechanical evaluation.

RESULTS

Compared with the SO group: (1) Callus BMD was significantly lower about 12.8%, 18.0%, 17.0% in OP group 6, 12, 18 weeks after fracture, respectively (P < 0.05). (2) Callus failure load was significantly lower about 24.3%, 31.5%, 26.6%, 28.8% in OP group, and callus failure stress was also significantly lower about 23.9%, 33.6%, 19.1%, 24.9% in OP group 4, 6, 12, 18 weeks after fracture, respectively (P < 0.05). (3) In OP group, endochondral bone formation was delayed, more osteoclast cell could be seen around the trabecula, and the new bone trabecula arranged loosely and irregularly.

CONCLUSION

Osteoporosis influences the middle and late periods of fracture healing in the rat osteoporostic model. The impairment is considered to be the result of the combined effects of the prolonged endochondral calcification, high activated osteoclast cell and the deceleration of the increase in bone mineral density.

摘要

目的

评估骨质疏松对骨折愈合的影响。

方法

将84只4月龄雌性Sprague-Dawley大鼠随机分为骨质疏松(OP)组和假手术(SO)组,每组42只。OP组大鼠行卵巢切除术,SO组大鼠行假手术。卵巢切除术后10周骨质疏松形成时,建立胫骨中段骨折模型。骨折后2周(每组2只大鼠)、4周(每组9只大鼠)、6周(每组9只大鼠)、12周(每组9只大鼠)和18周(每组7只大鼠)处死大鼠,采集胫骨进行骨密度(BMD)、组织形态学和生物力学评估。

结果

与SO组相比:(1)OP组骨折后6周、12周、18周骨痂BMD分别显著降低约12.8%、18.0%、17.0%(P<0.05)。(2)OP组骨痂破坏载荷分别显著降低约24.3%、31.5%、26.6%、28.8%,骨痂破坏应力在骨折后4周、6周、12周、18周也分别显著降低约23.9%、33.6%、19.1%、24.9%(P<0.05)。(3)OP组软骨内成骨延迟,小梁周围可见更多破骨细胞,新生骨小梁排列疏松、不规则。

结论

在大鼠骨质疏松模型中,骨质疏松影响骨折愈合的中晚期。这种损害被认为是软骨内钙化延长、破骨细胞高活性和骨密度增加减速共同作用的结果。

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