Department of Medicine, The University of Melbourne, Austin Health, Melbourne, Australia.
Department of Endocrinology, Level 2 Centaur Wing, Austin Health Repatriation Campus, 300 Waterdale Road, Heidelberg Heights, Melbourne, Victoria, 3081, Australia.
Curr Osteoporos Rep. 2018 Oct;16(5):561-572. doi: 10.1007/s11914-018-0478-0.
Bone densitometry provides a two-dimensional projected areal apparent bone mineral density that fails to capture the heterogeneity of bone's material composition and macro-, micro-, and nano-structures critical to its material and structural strength. Assessment of the structural basis of bone fragility has focused largely on trabecular bone based on the common occurrence of fragility fractures at sites with substantial amounts of trabecular bone. This review focuses on the contribution of cortical bone to bone fragility throughout life.
Accurately differentiating cortical and trabecular bone loss has important implications in quantifying bone fragility as these compartments have differing effects on bone strength. Recent advances in imaging methodology have improved distinction of these two compartments by (i) recognition of a cortico-trabecular transitional zone and (ii) quantifying bone microstructure in a region of interest that is a percentage of bone length rather than a fixed point. Additionally, non-invasive three-dimensional imaging methods allow more accurate quantification of changes in the cortical, trabecular, and cortico-trabecular compartments during growth, aging, disease, and treatment. Over 75% of the skeleton is assembled as cortical bone. Of all fragility fractures, ~ 80% are appendicular and involve regions rich in cortical bone and ~ 70% of all age-related appendicular bone loss is cortical and is mainly due to unbalanced intracortical remodeling which increases cortical porosity. The failure to achieve the optimal peak bone microstructure during growth due to disease and the deterioration in cortical and trabecular bone produced by bone loss compromise bone strength. The loss of strength produced by microstructural deterioration is disproportionate to the bone loss producing this deterioration. The reason for this is that the loss of strength increases as a 7th power function of the rise in cortical porosity and a 3rd power function of the fall in trabecular density (Schaffler and Burr in J Biomech. 21(1):13-6, 1988), hence the need to quantify bone microstructure.
骨密度测量提供了二维投影面积表观骨矿物质密度,但未能捕捉到对其物质和结构强度至关重要的骨的材料组成和宏观、微观及纳米结构的异质性。评估骨骼脆弱性的结构基础主要集中在基于大量松质骨存在的脆性骨折常见部位的松质骨上。本综述重点关注皮质骨对整个生命周期中骨骼脆弱性的贡献。
准确区分皮质骨和松质骨丢失对于量化骨骼脆弱性具有重要意义,因为这些部位对骨骼强度有不同的影响。成像方法的最新进展通过(i)识别皮质-松质过渡区和(ii)在感兴趣区域内量化骨微结构,该区域为骨长度的百分比而不是固定点,从而改善了这两个部位的区分。此外,非侵入性三维成像方法可更准确地量化生长、衰老、疾病和治疗过程中皮质骨、松质骨和皮质-松质骨的变化。超过 75%的骨骼是由皮质骨构成的。所有脆性骨折中,约 80%为四肢骨折,涉及富含皮质骨的区域,约 70%的所有与年龄相关的四肢骨丢失为皮质骨,主要是由于不平衡的皮质内重塑导致皮质骨多孔性增加。由于疾病导致的生长期间未能达到最佳峰值骨微结构以及由骨丢失引起的皮质骨和松质骨的恶化会损害骨骼强度。由微观结构恶化引起的强度损失与产生这种恶化的骨丢失不成比例。其原因在于,随着皮质骨孔隙率升高的 7 次幂函数和松质骨密度降低的 3 次幂函数,强度损失增加(Schaffler 和 Burr,J Biomech. 21(1):13-6, 1988),因此需要定量骨微结构。