EFFECT OF MINOCYCLINE IN POSTMENOPAUSAL OSTEOPOROSIS

骨质疏松症是中国女性和男性的主要公共健康问题 美国。随着人口的增加，骨质疏松症的问题也在增加 年龄。目前治疗骨质疏松症的方法，如膳食钙 补充，雌激素替代疗法，双磷酸盐和降钙素， 很大程度上是为了降低骨吸收的速度。骨 在使用抗吸收疗法期间，形成最终受到限制。 由于成骨细胞/破骨细胞偶联。没有一种主要作用于 增加骨形成，如氟化物或人类甲状旁腺激素， 可以接受治疗。四环素和四环素衍生物是 已知与骨骼中的矿化前沿结合，并被识别为 抑制破骨细胞活性。四环素类药物，包括米诺环素，也 抑制哺乳动物胶原酶活性和抑制甲状旁腺 组织培养中激素诱导的骨吸收。活体内 对啮齿动物的组织形态计量学研究表明，米诺环素也可以 增加骨形成速度，同时降低骨形成速度 吸收导致骨量的净增加。要确定是否 米诺环素对成骨细胞功能有直接影响，我们将评估 米诺环素对人骨骼基质蛋白合成的影响 体外培养成骨细胞。我们假设美国政府 米诺环素治疗绝经后骨质疏松症一年 每天200毫克，最低钙摄入量为每天800毫克，维他命400U D，将诱导骨密度增加，毒性最小。 这是一项安慰剂对照的掩蔽第二阶段研究，将扩大 如果在一年后观察到对骨密度有积极影响 治疗。

Osteoporosis is a major public health problem for women and men in the United States. The problem of osteoporosis increases as the population ages. Current treatments for osteoporosis, such as dietary calcium supplements, estrogen replacement therapy, bisphosphonates and calcitonin, are largely aimed at decreasing the rate of bone resorption. Bone formation is eventually limited during the use of antiresorptive therapies due to osteoblast/osteoclast coupling. No agent with a primary effect of increasing bone formation, such as fluoride or human parathyroid hormone, is available for therapy. Tetracycline and tetracycline derivatives are known to bind to the mineralization front in bone and are recognized to inhibit osteoclast activity. Tetracyclines, including minocycline, also inhibit the activity of mammalian collagenase and inhibit parathyroid hormone-induced bone resorption in tissue culture. In vivo histomorphometric studies in rodents indicate that minocycline may also increase the rate of bone formation, as well as decrease the rate of bone resorption leading to a net increase in bone mass. To determine if minocycline has direct effects on osteoblast function, we will assess the minocycline effect on the synthesis of skeletal matrix proteins by human osteoblastic cells in vitro. We hypothesize that the administration of minocycline for one year to osteoporotic postmenopausal women at a dose of 200 mg/day with a minimum calcium intake of 800 mg/day and 400 U vitamin D, will induce an increase in bone mineral density with minimal toxicity. This is a placebo-controlled, masked Phase II study that will be expanded if a positive effect on bone density is observed after one year of treatment.