骨重建
骨量减少
骨质疏松症
代谢性骨病
医学
骨重建期
骨量
骨吸收
小梁骨
骨病
病态的
还原(数学)
病理
解剖
内分泌学
内科学
破骨细胞
骨矿物
受体
几何学
数学
出处
期刊:Endocrine Reviews
[Oxford University Press]
日期:1986-11-01
卷期号:7 (4): 379-408
被引量:603
摘要
THE INTRODUCTION of the quantum concept for bone remodeling and in vivo tetracycline labeling by Frost in 1964 (1–3) has had a profound impact on histological studies of metabolic bone diseases over the last two decades. The quantum concept implies that changes in bone mass result from an imbalance between the amount of bone resorbed and formed, leading to either loss or gain of bone during the continuous remodeling of adult bone (1–3). Recently, a new dimension to the theories on bone loss emphasizing the importance of trabecular perforations in the development of osteopenia has been introduced by Parfitt (4). This theory explains the profound disintegration of the trabecular network occurring in certain disease states characterized by high bone turnover and increased resorptive activity (e.g. postmenopausal osteoporotic women with spontaneous vertebral fractures) and may also explain part of the bone loss that occurs with increasing age.
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