Computational study on the effect of loading alteration caused by disc degeneration on the trabecular architecture in human lumbar spine.
A thorough understanding of age-related phenomena on the trabecular architecture in the human lumbar spine can help the diagnosis and prognosis of age-related architectural changes, and provide an insight into the corresponding clinical assessments. In this paper we considered the different loading conditions of the young and old lumbar spines mainly caused by disc degeneration and studied the effect of loading alteration on trabecular architecture in lumbar spines. A two-dimensional muFE models with a 40mum pixel resolution were built to represent the full trabecular architecture in the human lumbar spine, and a topology optimization with the aid of finite element method was conducted to numerically investigate the trabecular morphological changes. Topology optimization iteratively distributes material in a design domain producing optimal layout or configuration, and it has been widely and successfully used for the study of bone remodeling. As a result of adaptive response of bone remodeling due to different loading conditions, we obtained two distinctively different trabecular architectures for the young and old lumbar spines, and we observed a strong correlation between our numerical results and the actual trabecular architecture in the literature. The proposed numerical framework and results demonstrated the potential use of the topology optimization-based numerical tool for putative treatments in advance of actual clinical procedures for the patients.
Jang
In Gwun
IG
Department of Ocean Systems Engineering, Korea Advanced Institute of Science and Technology, 373-1 Guseong-dong, Yuseong-gu, Daejon, Republic of Korea 305-701. jangin0407@kaist.ac.kr
Kim
Il Yong
IY
D000375:Aging / Q000473:pathology*; D003198:Computer Simulation; D006801:Humans; D007405:Intervertebral Disc Displacement / Q000473:pathology* / Q000503:physiopathology*; D008159:Lumbar Vertebrae / Q000473:pathology* / Q000503:physiopathology*; D008953:Models, Anatomic; D008954:Models, Biological; D016474:Weight-Bearing