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arXiv 1206.6071q-bio.TOphysics.med-ph
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骨质疏松症中皮质内骨丢失:骨表面可用性的作用

Endocortical bone loss in osteoporosis: The role of bone surface availability

Pascal R. Buenzli, C. David L. Thomas, John G. Clement, Peter Pivonka

摘要:

绝经后骨质疏松症和绝经后骨质疏松症是骨重建的疾病,其中骨重建比再吸收少。然而,这种骨重建的失调并不是在所有的骨区域都同样发生。骨丢失在内皮质附近和处更明显,导致皮质壁变薄和髓腔扩张,这一过程有时被称为“小梁化”或“取消”。皮质壁变薄是骨质疏松症的主要问题,因为它与骨机械性能的强烈恶化有关。在本文中,我们研究的可能性,微观骨表面可用性的不均匀性可以解释骨质疏松症的骨丢失的不均匀性。我们使用骨重建的计算模型,其中微观骨表面可用性影响骨转换率,并模拟长骨中段骨体积分数分布的演变。我们发现,骨丢失是加速附近的内皮层壁的比表面是最高的。随着时间的推移,这导致骨内膜的皮质壁厚度显著减少。髓腔的相关扩张可以与墨尔本股骨标本集的实验观察横截面数据相匹配。最后,我们计算了在这个不断发展的骨结构的机械应力的重新分布,并表明,机械负荷成为关键转移到骨膜皮质骨。

英文摘要:

Age-related bone loss and postmenopausal osteoporosis are disorders of bone remodelling, in which less bone is reformed than resorbed. Yet, this dysregulation of bone remodelling does not occur equally in all bone regions. Loss of bone is more pronounced near and at the endocortex, leading to cortical wall thinning and medullary cavity expansion, a process sometimes referred to as "trabecularisation" or "cancellisation". Cortical wall thinning is of primary concern in osteoporosis due to the strong deterioration of bone mechanical properties that it is associated with. In this paper, we examine the possibility that the non-uniformity of microscopic bone surface availability could explain the non-uniformity of bone loss in osteoporosis. We use a computational model of bone remodelling in which microscopic bone surface availability influences bone turnover rate and simulate the evolution of the bone volume fraction profile across the midshaft of a long bone. We find that bone loss is accelerated near the endocortical wall where the specific surface is highest. Over time, this leads to a substantial reduction of cortical wall thickness from the endosteum. The associated expansion of the medullary cavity can be made to match experimentally observed cross-sectional data from the Melbourne Femur Collection. Finally, we calculate the redistribution of the mechanical stresses in this evolving bone structure and show that mechanical load becomes critically transferred to the periosteal cortical bone.

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