Department of Biomedical Engineering, Boston University, Boston, Massachusetts, USA.
PLoS Comput Biol. 2011 Apr;7(4):e1001125. doi: 10.1371/journal.pcbi.1001125. Epub 2011 Apr 21.
Pulmonary emphysema is a connective tissue disease characterized by the progressive destruction of alveolar walls leading to airspace enlargement and decreased elastic recoil of the lung. However, the relationship between microscopic tissue structure and decline in stiffness of the lung is not well understood. In this study, we developed a 3D computational model of lung tissue in which a pre-strained cuboidal block of tissue was represented by a tessellation of space filling polyhedra, with each polyhedral unit-cell representing an alveolus. Destruction of alveolar walls was mimicked by eliminating faces that separate two polyhedral either randomly or in a spatially correlated manner, in which the highest force bearing walls were removed at each step. Simulations were carried out to establish a link between the geometries that emerged and the rate of decline in bulk modulus of the tissue block. The spatially correlated process set up by the force-based destruction lead to a significantly faster rate of decline in bulk modulus accompanied by highly heterogeneous structures than the random destruction pattern. Using the Karhunen-Loève transformation, an estimator of the change in bulk modulus from the first four moments of airspace cell volumes was setup. Simulations were then obtained for tissue destruction with different idealized alveolar geometry, levels of pre-strain, linear and nonlinear elasticity assumptions for alveolar walls and also mixed destruction patterns where both random and force-based destruction occurs simultaneously. In all these cases, the change in bulk modulus from cell volumes was accurately estimated. We conclude that microscopic structural changes in emphysema and the associated decline in tissue stiffness are linked by the spatial pattern of the destruction process.
肺气肿是一种结缔组织疾病，其特征是肺泡壁的进行性破坏导致气腔扩大和肺弹性回缩力降低。然而，微观组织结构与肺僵硬度下降之间的关系尚不清楚。在这项研究中，我们开发了一种肺组织的三维计算模型，其中预应变的立方块组织由空间填充多面体的细分表示，每个多面体单元代表一个肺泡。通过随机或空间相关的方式消除分离两个多面体的面来模拟肺泡壁的破坏，其中在每个步骤中去除承载最高力的壁。进行了模拟以建立出现的几何形状与组织块体模量下降率之间的联系。基于力的破坏建立的空间相关过程导致体模量下降率显著加快，并且结构高度不均匀，而随机破坏模式则不然。使用 Karhunen-Loève 变换，建立了从气腔单元体积的前四个矩估计体模量变化的估计器。然后，针对具有不同理想化肺泡几何形状、预应变水平、肺泡壁线性和非线性弹性假设以及同时发生随机和基于力的破坏的混合破坏模式进行了组织破坏的模拟。在所有这些情况下，细胞体积的体模量变化都得到了准确估计。我们得出结论，肺气肿中的微观结构变化和组织僵硬度的相关下降与破坏过程的空间模式有关。
