These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


PUBMED FOR HANDHELDS

Search MEDLINE/PubMed


  • Title: [Osteoporosis impairs fracture healing of tibia in a rat osteoporotic model].
    Author: Xu SW, Wang JW, Li W, Wang Y, Zhao GF.
    Journal: Zhonghua Yi Xue Za Zhi; 2004 Jul 17; 84(14):1205-9. PubMed ID: 15387984.
    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.
    [Abstract] [Full Text] [Related] [New Search]