EPIDEMIOLOGY OF AGE RELATED BONE LOSS & FRACTURE

骨质疏松症是一个巨大的公共卫生问题， 在美国，每例骨折的成本高达100亿美元 年 我们的具体目标是试图填补知识上的空白， 设计和实施有效的控制方案。 1)年龄- 分层，随机抽样的262罗切斯特，明尼苏达州的妇女谁已被跟踪 连续测量骨矿物质密度（BMD）长达8年， 进行了广泛的基线研究，这是一种独特的资源。 获得 长期数据的模式和原因的骨流失和骨折，我们 2）骨的新生化指标 骨密度测量的新技术已经开发 这将大大提高骨折风险的定义。 利用 评估其预测价值，并开发和测试模型 为了描述人群中的骨丢失和骨折，我们将招募 并前瞻性地跟踪一个新的随机样本的罗切斯特妇女。 第三章 虽然他们占了相当大的比例， 骨折，没有系统的研究，对骨丢失的原因 和男性骨折。 因此，我们将招募并前瞻性地随访 随机抽取罗切斯特的男性样本，以获得这些信息，并将比较 并与女性的结果进行对比。 4)众所周知， 强大的遗传成分。 我们将寻找遗传标记， 可以用来预测未来骨质疏松症的风险， 白细胞DNA限制性片段长度多态性与皮肤 成纤维细胞中1型前胶原基因之一的突变。 第五章） 虽然雌激素替代疗法（ERT），开始于绝经期，是 最有效的方法来预防骨质疏松症的妇女，这是不知道的 它是否必须无限期地持续下去以获得长期利益。 我们将 试图通过比较一个国家的BMD值来解决这个重要问题。 一群切除卵巢的罗切斯特妇女，其中一些人，但不是其他人， 接受ERT治疗的时间间隔不同。 在所有这些研究中，我们将 继续严重依赖罗切斯特流行病学项目，一个独特的 进行基于人群的流行病学研究的资源。 我们会委聘 使用双能X射线吸收测定法来评估 骨丢失（包括全身和局部骨骼以及侧位扫描） 脊椎扫描）和估计瘦体重（用于研究 肌肉质量和骨量之间的关系），新的生化标志物 (for评估骨转换）和分子生物学技术（用于 评估骨质疏松症的遗传易感性）。 这项研究将 使我们能够识别和量化骨质流失的决定因素， 骨折在一般人群中，以便更好地认识那些 有骨质疏松症风险的人，然后可以针对他们进行 预防性干预。

Osteoporosis is an enormous public health problem causing at least 1.3 million fractures and costing up to $10 billion in the United States each year. Our specific aims attempt to fill gaps in knowledge that impede the design and implementation of an effective control program. 1) The age- stratified, random sample of 262 Rochester, MN women who have been followed for up to 8 yrs with serial measurements of bone mineral density (BMD) and having had extensive baseline studies fare a unique resource. To obtain long-term data on the patterns and causes of bone loss and fractures, we will extend their followup to 12 yrs. 2) Novel biochemical indices of bone turnover and new technologies for measurement of BMD have been developed that should greatly enhance the definition of fracture risk. To exploit these and evaluate their prognostic value and to develop and test models for describing bone loss and fractures in the population, we will enroll and follow prospectively a new random sample of Rochester women. 3) Although they account for a substantial proportion of age-related fractures, there have been no systematic studies on the causes of bone loss and fractures in men. Thus, we will enroll and follow prospectively a random sample of Rochester men to obtain this information and will compare and contrast results with those in women. 4) Bone mass is known to have strong hereditary component. We will search for genetic markers that might be used to predict future risk for osteoporosis by analyzing leucocyte DNA for restriction fragment length polymorphisms and skin fibroblasts for mutations in one of the genes for type 1 procollagen. 5) Although estrogen replacement therapy (ERT), begun at menopause, is the most effective way to prevent osteoporosis in women, it is not known whether it must be continued indefinitely for long-term benefit. We will attempt to resolve this important question by comparing values for BMD in a cohort of oophorectomized Rochester women, of whom some, but not others, received ERT for variable intervals. In all of these studies, we will continue to rely heavily on the Rochester Epidemiology Project, a unique resource for making population-based epidemiologic studies. We will employ state-of-the-art methods using dual energy x-ray absorptiometry to assess bone loss (including scans of the total and regional skeleton and lateral scans of the vertebrae) and to estimate lean body mass (for studying the relationship between muscle mass and bone mass), new biochemical markers (for assessing bone turnover), and molecular biology techniques (for assessing genetic predisposition to osteoporosis). This research will allow us to identify and quantify the determinants of bone loss and fractures in the general population so as to recognize better those individuals at risk for osteoporosis, who could then be targeted for preventive intervention.