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Cancellous bone microdamage in the proximal femur: influence of age and osteoarthritis on damage morphology and regional distribution.

Authors
  • Fazzalari, N L
  • Kuliwaba, J S
  • Forwood, M R
Type
Published Article
Journal
Bone
Publisher
Elsevier
Publication Date
Dec 01, 2002
Volume
31
Issue
6
Pages
697–702
Identifiers
PMID: 12531564
Source
Medline
License
Unknown

Abstract

This study describes the in vivo distribution of cancellous bone microdamage in the proximal femur of an autopsy control sample. In addition, in vivo microdamage in the region medial to the greater trochanter of the proximal femur is compared between patients with severe osteoarthritis and controls. Taken at autopsy, the control group comprised normal right proximal femora that were then cut in the coronal plane with an Exakt saw (n = 12; aged 20-83 years). Cancellous bone samples were taken from the subchondral principal compressive region, the medial principal compressive region, and medial to the greater trochanter. A cancellous bone core biopsy was taken of the region medial to the greater trochanter (of the proximal femur) from patients with primary osteoarthritis undergoing total hip replacement surgery (n = 33; aged 37-85 years). Samples were embedded in resin, and in vivo microdamage identified in 70-microm-thick sections using the basic fuchsin en bloc staining technique. Microdamage was similar in all proximal femur sites in controls, except in the subchondral principal compressive region, where a significantly smaller crack length (microm) was identified (p < 0.05). In the region medial to the greater trochanter, osteoarthritic vs. control group comparisons showed that the crack density (#/mm(2)) and crack surface density (mm/mm(2)) were not significantly different, but crack length was significantly less (p < 0.03) and damage volume fraction was significantly increased for osteoarthritics (p < 0.005). The osteoarthritic and control data for crack density, and the osteoarthritic data for damage volume fraction, showed a nonlinear increase with age. Furthermore, crack length was not dependent on damage volume fraction or age for either the osteoarthritic or control group. This study identified differences in microdamage between osteoarthritic and autopsy control cases. We hypothesize that these results are consistent with the reported bone material property differences for osteoarthritis. In addition, the relatively uniform distribution of microdamage in the control group suggests that the principal components of the femoral cancellous bone network are equally exposed to deformations resulting in microdamage. Further study into the factors that influence the accumulation and skeletal distribution of microdamage is fundamental to understanding skeletal health.

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