Ambrus J L, Ambrus J L, Robin J C, Ambrus C M, Kahn E A
J Med. 1984;15(4):295-309.
Etiologic and pathologic factors in clinical osteoporosis are reviewed. Techniques were developed to determine total skeletal calcium content with in vivo neutron activation analysis and to induce osteoporosis (in about three months) with low calcium diet, corticosteroid or heparin treatment in experimental animals. Genetic influence was demonstrated: C3H/St (Ha) mice were more susceptible to osteoporosis by all three modalities than C57B1/6 (J) mice. Fluoride was ineffective in preventing osteoporosis induced by either of these three modalities. Heparin induced osteoporosis was prevented by conjugated estrogens, progestins or their combinations. Progestins were shown in other studies to inhibit estrogen induced metaplasia and neoplasia. Combining estrogens with progestin may result in an increased therapeutic index for the prevention of postmenopausal osteoporosis. Human and salmon calcitonin, Deca - Durabolin, an anabolic steroid, Mopidamole, a pyrimidopyrimidine derivative, Trental, a methylxanthine derivative, certain 2-thiophene carboxylic acid derivatives and imidazoquinazolines exhibited anti-osteoporotic effects.
本文综述了临床骨质疏松症的病因和病理因素。已开发出相关技术，可通过体内中子活化分析来测定骨骼总钙含量，并在实验动物中通过低钙饮食、皮质类固醇或肝素治疗诱导骨质疏松症（约三个月）。研究表明存在遗传影响：与C57B1/6（J）小鼠相比，C3H/St（Ha）小鼠对这三种诱导方式导致的骨质疏松症更敏感。氟化物对预防这三种方式诱导的骨质疏松症均无效。共轭雌激素、孕激素或其组合可预防肝素诱导的骨质疏松症。其他研究表明，孕激素可抑制雌激素诱导的化生和肿瘤形成。将雌激素与孕激素联合使用可能会提高预防绝经后骨质疏松症的治疗指数。人降钙素和鲑鱼降钙素、癸酸诺龙（一种合成代谢类固醇）、潘生丁（一种嘧啶并嘧啶衍生物）、己酮可可碱（一种甲基黄嘌呤衍生物）、某些2-噻吩羧酸衍生物和咪唑喹唑啉具有抗骨质疏松作用。
