Objective: Primary osteoporosis (OP) is a systemic metabolic skeletal disease characterized by low bone mass and microarchitectural deterioration of bone tissue. These characters result in an increase on the bone fragility and the risk of fracture. The aged, especially postmenopausal women, often suffer from OP. With standard of living rising and population aging, OP and the fracture caused by it have been global Medical care problems and social problems, as they severely threaten health of the aged. It is urgent to explore the possible pathogenesis of OP to provide the experimental base for preventing and treating the OP.OP is a complex syndrome. Up to now, its mechanism is not very clear. It was found that the incidence rate of OP is high in postmenopausal women, so that the effect of decrease in estrogen level on bone mineral density in postmenopausal women was paid more attention to. Though some achievements have been obtained, it can not be explained reasonably why there is individual difference in the occurrence of OP in different people on the same physiological enviroment. In other words, OP is a commom disease, but not all Postmenopausal women suffer from it and there is individual difference in time or degree. Obviously, OP is not caused by the single hormone disturbance, but is a result of multiple factors. Primary osteoporosis is a polygenic disease. It was reported that heritability of BMD reaches to 60% ~ 80%. Is genetic factor an important reason for individual difference in the occurrence of OP in different people ? Molecular biology developing speedily provides a possibility for explaining individual difference in OP. The role of genetic factor on the occurrence of OP is thought more and more highly of.In this experiment, the purpose was to explore the pathogenesis of OP. On one hand we studied the relationship between the changes of hormone level which affect bone metabolism and BMD (bone mineral density), on the other hand we also explored relationship between vitamine D receptor gene polymorphism and Calcitonin receptor gene polymorphism and BMD. These will help to understand further OP which is very harmful to the health and provide theoretic base for preventing and treating OP.1. Effect of Postmenopausal Endocrine disturbance on bone mineral density of the woman of the Han nationality in Hebei.Method: 60 women of the Han nationality were divided into three groups: (1) premenopause group: 15 women; (2) menopause less than 10 years group: 27 women; (3) menopause more than 10 years group: 18 women. Detect the values of E2, PTH, CT, calcium, Phosphorus and ALP in serum ; BMD was measured at the L1-4 , Neck, Troch and Wards, of femur by dual energy X ray absorptiometry. We explored the pathogenesis of postmenopausal OP by comparing these bone metabolic hormones and these biochemical markers among three groups and analyzing the relationship between the changes of these markers and BMD.ResultsThe change of BMD in postmenopausal women: results show that BMD at the L1-4 and the Wards, decreased significantly after menopause (P<0.05). At the Neck and the Trouch, there is no obvious difference in BMD between premenopause group and less than 10 years group(P>0.05). But bone mass loss aggravated while aging and there is obvious difference in BMD at both sites between premenopause group and more than 10 years group (P<0.05). Except Trouch, there is obvious difference in BMD at all sites in more than 10 years group, compared with less than 10 years group (P<0.05). These suggested bone mass loss happened mainly at the L1-4 and the Wards, after menopause, thereafter bone mass loss continues aggravating with aging. The change of E2, PTH and CT in postmenopausal women: the results show that E2 in serum decreased significantly after menopause(P<0.05). Decrease on E2 in menopause less than 10 years group is the most significant. After then, there is a tendency for increase ,but there is no statistical significance(P>0.1); After menopause, PTH in serum increased... |