Fortunato R N, Robertson A M, Sang C, Duan X, Maiti S
Department of Mechanical Engineering and Materials Science, University of Pittsburgh Pittsburgh, USA.
Department of Bioengineering, University of Pittsburgh Pittsburgh, USA.
Exp Mech. 2021 Jan;61(1):5-18. doi: 10.1007/s11340-020-00657-7. Epub 2020 Sep 25.
Calcification was recently found to be present in the majority of cerebral aneurysms, though how calcification and the presence or absence of co-localized lipid pools affect failure properties is still unknown.
The primary objective is to quantify the biomechanical effect of a macro-calcification with surrounding Near-Calcification Region (NCR) of varying mechanical properties on tissue failure behavior.
We utilized a structurally informed finite element model to simulate pre-failure and failure behavior of a human cerebral tissue specimen modeled as a composite containing a macro-calcification and surrounding NCR, embedded in a fiber matrix composite. Data from multiple imaging modalities was combined to quantify the collagen organization and calcification geometry. An idealized parametric model utilizing the calibrated model was used to explore the impact of NCR properties on tissue failure.
Compared to tissue without calcification, peak stress was reduced by 82% and 49% for low modulus (representing lipid pool) and high modulus (simulating increase in calcification size) of the NCR, respectively. Failure process strongly depended on NCR properties with lipid pools blunting the onset of complete failure. When the NCR was calcified, the sample was able to sustain larger overall stress, however the failure process was abrupt with nearly simultaneous failure of the loaded fibers.
Failure of calcified vascular tissue is strongly influenced by the ultrastructure in the vicinity of the calcification. Computational modeling of failure in fibrous soft tissues can be used to understand how pathological changes impact the tissue failure process, with potentially important clinical implications.
最近发现大多数脑动脉瘤中存在钙化，然而钙化以及是否存在共定位脂质池如何影响失效特性仍不清楚。
主要目的是量化具有不同力学性能的大钙化及其周围近钙化区域（NCR）对组织失效行为的生物力学影响。
我们利用一个结构信息有限元模型来模拟一个人类脑组织标本的失效前和失效行为，该标本被建模为一个包含大钙化和周围NCR的复合材料，嵌入纤维基质复合材料中。结合来自多种成像模态的数据来量化胶原组织和钙化几何形状。利用校准模型的理想化参数模型来探索NCR特性对组织失效的影响。
与无钙化组织相比，对于低模量（代表脂质池）和高模量（模拟钙化尺寸增加）的NCR，峰值应力分别降低了82%和49%。失效过程强烈依赖于NCR特性，脂质池使完全失效的起始变钝。当NCR钙化时，样本能够承受更大的整体应力，然而失效过程是突然的，加载的纤维几乎同时失效。
钙化血管组织的失效受到钙化附近超微结构的强烈影响。纤维软组织失效的计算建模可用于理解病理变化如何影响组织失效过程，具有潜在重要的临床意义。
