骨组织形态学在原发性和继发性骨质疏松的病理生理评价和各种治疗方式。

APMIS. Supplementum Pub Date : 1995-01-01
T Steiniche
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引用次数: 0

摘要

在正常人中,骨量在25-35岁达到峰值,此后随着年龄的增长,男女骨量都有所下降。绝经期的正常女性骨质流失加速。由于骨量峰值较低或随着年龄增长或绝经期骨质流失更明显,一些人达到骨量的骨折阈值并发生自发性骨折。为了理解与年龄相关的骨质流失背后的机制,我们必须认识到,成人的骨骼是通过内部重组不断更新的,通过局部破骨细胞吸收,然后是成骨细胞形成(重塑)。吸收期和形成期的完全重建可以通过应用于髂骨活检的组织形态学方法进行,从而给出吸收期和形成期事件的详细描述。在骨重建过程中,骨可通过3种机制获得或丢失:1。可逆性骨损失取决于重建空间的大小,即在重建过程中骨被吸收但尚未重建的量。2. 由于重塑部位的负平衡导致骨小梁不可逆变薄。3.由深吸收腔隙穿穿小梁板引起的整个小梁单元的不可逆损失。尽管与正常对照相比,绝经后骨质疏松伴椎体骨折患者骨量明显减少20-30%,但存在大量重叠。我们的研究和其他几项研究表明,除了骨小梁体积的轻微减少外,骨质疏松症患者与正常对照组之间的微观结构存在显著差异。这些结构变化可能是小梁板穿孔的结果。虽然骨质疏松症患者在骨重建(骨转换)方面是一个非常异质性的群体,患者的骨转换低、正常甚至增加,但在我们的研究中没有发现正在进行的骨重建过程中出现的迹象可以解释为什么这些患者会出现骨质减少和小梁结构的变化。患者的骨平衡略呈阴性,但与正常对照组的平衡没有区别。因此,骨质疏松症的原因可能是发生在生命早期的因素,可能早于疾病的表现。任何年龄的骨量都是两个变量的结果——生长过程中获得的骨质量和随后的骨质流失速度。成熟时的骨量峰值可能对确定出现症状性骨质疏松症的风险具有重要意义。(摘要删节为400字)
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Bone histomorphometry in the pathophysiological evaluation of primary and secondary osteoporosis and various treatment modalities.

In normal individuals, peak bone mass is reached at 25-35 years of age and thereafter a decrease with age occurs in both sexes. An acceleration in the bone loss is observed in normal women at menopause. Because of either a low peak bone mass or a more pronounced bone loss with age or during menopause, some individuals reach the fracture threshold for bone mass and suffer spontaneous fractures. To understand the mechanism behind age related bone loss, one must recognize that bone in adults is continually renewed through internal reorganization by which bone is turned over by localized osteoclastic resorption followed by osteoblastic formation (remodelling). A total reconstruction of the resorptive and formative phase can be performed by histomorphometric methods applied on iliac crest bone biopsies and thereby give a detailed description of resorptive and formative events. By the remodelling process bone may be gained or lost by 3 mechanisms: 1. Reversible bone loss depending on the magnitude of the remodelling space, which is the amount of bone resorbed and not yet reformed during the remodelling sequence. 2. Irreversible thinning of the trabeculae due to a negative balance at the remodelling site. 3. Irreversible loss of whole trabecular elements caused by deep resorption lacunae perforating the trabecular plates. Although the bone mass is significantly reduced by 20-30% in postmenopausal osteoporotic patients with vertebral fractures compared with normal controls a substantial overlap exists. Our study and several other studies have shown that beside the slight reduction in trabecular bone volume significant differences in microstructure exist between osteoporotic patients and normal controls. These changes in structure are probably a consequence of trabecular plate perforations. Although osteoporotic patients in term of remodelling (bone turnover) are a very heterogeneous group, with patients having a low, normal and even increased bone turnover, no signs in the ongoing remodelling process was found in our study that could explain why these patients had developed osteopenia and changes in the trabecular structure. The bone balance was in the patients slightly negative but no different from the balance found in normal controls. The cause of osteoporosis may therefore be factors occurring earlier in life, maybe long before the manifestation of the disease. Bone mass at any age is the result of two variables--the amount of bone achieved during growth and the subsequent rate of bone loss. Peak bone mass at maturity may be of great importance in determining the risk of developing symptomatic osteoporosis.(ABSTRACT TRUNCATED AT 400 WORDS)

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