Osteoporosis influences the middle and late periods of fracture healing in a rat osteoporotic model.
- Author:
Jian-wei WANG
1
;
Wei LI
;
Shao-wen XU
;
Di-sheng YANG
;
Yun WANG
;
Min LIN
;
Guang-feng ZHAO
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Biomechanical Phenomena; Body Weight; Bone Density; Disease Models, Animal; Female; Fracture Healing; Osteoporosis; complications; pathology; physiopathology; Ovariectomy; Rats; Rats, Sprague-Dawley; Reference Values; Tibial Fractures; etiology; pathology; physiopathology
- From: Chinese Journal of Traumatology 2005;8(2):111-116
- CountryChina
- Language:English
-
Abstract:
OBJECTIVETo evaluate the influence of osteoporosis on the middle and late periods of fracture healing process through observing the histomorphological changes, bone mineral density and biomechanical properties in ovariectomized rats.
METHODSEighty-four female SD rats of 4 months old were randomly divided into osteoporosis group and sham operation group, 42 in each. Rats in osteoporosis group were performed ovariectomy operation while those in sham operation group were given sham operation. A midshaft tibia fracture model was established 10 weeks after ovariectomy. Tibias were harvested 2, 4, 6, 12, 18 weeks after fracture for bone mineral density, histomorphological and biomechanical evaluation.
RESULTSCompared with the sham operation group, callus bone mineral density was 12.8%, 18.0%, 17.0% lower in osteoporosis group 6, 12, 18 weeks after fracture, respectively (P<0.05); callus failure load was 24.3%, 31.5%, 26.6%, 28.8% lower in osteoporosis group, and callus failure stress was 23.9%, 33.6%, 19.1%, 24.9% lower in osteoporosis group 4, 6, 12, 18 weeks after fracture, respectively (P<0.05). In osteoporosis group, endochondral bone formation was delayed, more osteoclast cells could be seen around the trabecula, and the new bone trabecula arranged loosely and irregularly.
CONCLUSIONSOsteoporosis influences the middle and late periods of fracture healing in the rat osteoporotic model. The impairment is considered to be the result of combined effects of prolonged endochondral calcification, high activated osteoclast cell and the deceleration of the increase in bone mineral density.