IMPLICATIONS OF ARCHITECTURE FOR THE PATHOGENESIS AND PREVENTION OF VERTEBRAL FRACTURE
IMPLICATIONS OF ARCHITECTURE FOR THE PATHOGENESIS AND PREVENTION OF VERTEBRAL FRACTURE
复制标题
DOI：
10.1016/8756-3282(92)90196-4
复制
发表时间：
1992-01-01
期刊：
影响因子：
4.1
通讯作者：
PARFITT, AM
中科院分区：
文献类型：
--
作者：
PARFITT, AM
绝经后松质骨的快速丢失是通过一种机制发生的，该机制完全去除了一些结构元素，留下那些保持更广泛分离和更少连接的结构元素。松质骨的缓慢流失通过减少在快速流失的初始阶段存活的结构元件的厚度的机制而继续。骨质疏松所致椎体压缩性骨折患者的这两个过程都比同龄健康受试者进展得更快;这是否是因为它们开始得更早、进展得更快或持续时间更长尚不清楚。这一总体概念是在大约十年前首次提出的，现在已经被各种不同的方法所证实，包括节点-支柱分析、星星体积和曲率随剖面膨胀的变化。由于非侵入性密度测定方法可获得结构对抗压强度的部分贡献，并且皮质骨对抗压强度的贡献很大，因此很难通过体外比较结构测量与生物力学测试来证明骨脆性的独立结构成分。然而，三项独立的临床研究，比较了有和没有椎骨骨折的受试者，都强烈地表明了骨折风险的独立结构贡献。小梁板的局灶性穿孔可导致结构成分的完全清除，但穿孔的机制仍有争议。骨小梁厚度的普遍或局灶性减少、吸收深度和骨小梁厚度的频率分布之间的随机关系以及较薄骨小梁上重塑激活的优先发生都可能起作用，但基于间接推理，不可能仅通过这些机制解释观察到的事实，这意味着在绝经后的最初几年内，吸收深度的实质性增加是必要的。这一过程很少在人类受试者中观察到，但已在三种不同的动物物种-猴子，大鼠和小型猪中独立证明，后两者是雌激素缺乏的结果。结构对于预防以及对于椎骨骨折的发病机制具有重要意义，因为增加现有小梁的厚度对连接性的影响很小。由于失去的骨小梁不能被替代，一旦骨骼被破坏，很可能没有药物干预对剩余骨的强度有很大影响。因此，必须更加重视预防，通过雌激素或雌激素的某些替代品，也将减少再吸收深度以及重塑激活的速率。
Rapid loss of cancellous bone after menopause occurs by a mechanism that removes some structural elements completely, leaving those that remain more widely separated and less well connected. Slow loss of cancellous bone continues by a mechanism that reduces the thickness of the structural elements that survive the initial phase of rapid loss. Both processes have advanced further in patients with vertebral compression fracture due to osteoporosis, than in healthy subjects of similar age; whether this is because they began sooner, proceeded more rapidly or continued for longer is unknown. This overall concept, first developed about ten years ago, has now been confirmed by a variety of different methods including node-strut analysis, star volume and the change in curvature with profile dilation. Because part of the architectural contribution to compressive strength is captured by non-invasive densitometric methods, and the contribution of cortical bone to compressive strength is significant, it has been difficult to demonstrate an independent architectural component of bone fragility by in vitro comparison of structural measurements with biomechanical testing. Nevertheless, three independent clinical studies, comparing subjects with and without vertebral fracture, have each strongly suggested an independent architectural contribution to fracture risk. Complete removal of structural elements is initiated by focal perforation of trabecular plates, but the mechanism of perforation remains controversial. Generalised or focal reductions in trabecular thickness, a stochastic relationship between the frequency distributions of resorption depth and trabecular thickness, and preferential occurrence of remodelling activation on thinner trabeculae may all contribute, but based on indirect reasoning, it is impossible to account for the observed facts by these mechanisms alone, implying the necessity during the first few years after menopause for a substantial increase in resorption depth. This process has rarely been observed in human subjects, but has been independently demonstrated in three different animal species - monkeys, rats and minipigs, in the latter two as a consequence of oestrogen deficiency. Architecture has important implications for the prevention as well as for the pathogenesis of vertebral fracture, since increasing the thickness of existing trabeculae has only minimal effect on connectivity. Because lost trabeculae cannot be replaced, once destruction of the skeleton has been allowed to proceed, it is likely that no pharmacologic intervention will have much effect on the strength of the bone that remains. Consequently, more emphasis must be given to prevention, either by oestrogen, or by some substitute for oestrogen that will also reduce resorption depth as well as the rate of remodelling activation.