Manzke E, Gruber H E, Hiness R W, Baylink D J
Metabolism. 1982 Jan;31(1):25-32.
This study of two cases documents increased bone mass in a 30-yr old man and osteopetrosis in a 38-yr-old woman and examines the patients in terms of radiologic features, bone photon absorptiometry and bone biopsy analyses which include tetracycline kinetics. Both patients had elevated bone mass based on quantitative bone histology of iliac crest biopsies normal, or low PTH, and normal calcitonin values. However, they differed markedly from each other in other respects: One patient possessed significantly increased rates of bone formation and mineralization, had elevated serum alkaline phosphatase, increased total hydroxyproline over a 24 hour urine collection but displayed a normal amount of bone surface involved in resorption. The other subject had normal bone formation parameters, but had elevated serum acid phosphatase and a significantly elevated resorbing (crenated) surface. Although most theories ascribe and cause of osteopetrosis to decreased resorption, our study shows that increased bone formation, even when accompanied by normal resorption, can lead to the abnormal accumulation of bone mass. In this respect, the resorptive response of this patient was abnormal; the normal coupled relationship between bone formation and bone resorption, which ensures proper control of endosteal bone volume, had been lost.
本研究通过两个病例记录了一名30岁男性的骨量增加以及一名38岁女性的骨质石化症，并从放射学特征、骨光子吸收测定法以及包括四环素动力学的骨活检分析等方面对患者进行了检查。基于髂嵴活检的定量骨组织学检查，两名患者的骨量均升高，甲状旁腺激素正常或偏低，降钙素值正常。然而，他们在其他方面存在显著差异：一名患者的骨形成和矿化速率显著增加，血清碱性磷酸酶升高，24小时尿总羟脯氨酸增加，但参与吸收的骨表面量正常。另一名受试者的骨形成参数正常，但血清酸性磷酸酶升高，吸收（锯齿状）表面显著升高。尽管大多数理论将骨质石化症的病因归因于吸收减少，但我们的研究表明，即使在伴有正常吸收的情况下，骨形成增加也会导致骨量异常积累。在这方面，该患者的吸收反应异常；确保骨内膜骨量得到适当控制的骨形成与骨吸收之间的正常耦合关系已经丧失。
