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  3. Influence of metastatic bone lesion type and tumor origin on human vertebral bone architecture, matrix quality, and mechanical properties.

Influence of metastatic bone lesion type and tumor origin on human vertebral bone architecture, matrix quality, and mechanical properties.

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DOI
10.48350/166745
Publisher DOI
10.1002/jbmr.4539
PubMed ID
35253282
Abstract
Metastatic spine disease is incurable, causing increased vertebral fracture risk and severe patient morbidity. Here, we demonstrate that osteolytic, osteosclerotic, and mixed bone metastasis uniquely modify human vertebral bone architecture and quality, affecting vertebral strength and stiffness. Multivariable analysis showed bone metastasis type dominates vertebral strength and stiffness changes, with neither age nor gender having an independent effect. In osteolytic vertebrae, bone architecture rarefaction, lower tissue mineral content and connectivity, and accumulation of advanced glycation end-products (AGEs) affected low vertebral strength and stiffness. In osteosclerotic vertebrae, high trabecular number and thickness but low AGEs, suggesting a high degree of bone remodeling, yielded high vertebral strength. Our study found that bone metastasis from prostate and breast primary cancers differentially impacted the osteosclerotic bone microenvironment, yielding altered bone architecture and accumulation of AGEs. These findings indicate that therapeutic approaches should target the restoration of bone structural integrity. This article is protected by copyright. All rights reserved.
Date Issued
2022-05
Publication Type
Article
Subjects
Advanced Enzymatic glycation Bone architecture Human vertebrae Metastatic bone lesions Vertebral mechanical properties
Language(s)
en
Author(s)
Bailey, Stacyann
Stadelmann, Marc André  
ARTORG Center - Biomechanics  
Zysset, Philippe  orcid-logo
ARTORG Center - Biomechanics  
Vashishth, Deepak
Alkalay, Ron N
Additional Credits
ARTORG Center - Biomechanics  
Journal
Journal of bone and mineral research
Publisher
Wiley-Blackwell
ISSN
0884-0431
Access(Rights)
open.access
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