Abstract
Changes in trabecular micro-architecture are key to our understanding of osteoporosis. Previous work focusing on structure model index (SMI) measurements have concluded that disease progression entails a shift from plates to rods in trabecular bone, but SMI is heavily biased by bone volume fraction. As an alternative to SMI, we proposed the ellipsoid factor (EF) as a continuous measure of local trabecular shape between plate-like and rod-like extremes. We investigated the relationship between EF distributions, SMI and bone volume fraction of the trabecular geometry in a murine model of disuse osteoporosis as well as from human vertebrae of differing bone volume fraction. We observed a moderate shift in EF median (at later disease stages in mouse tibia) and EF mode (in the vertebral samples with low bone volume fraction) towards a more rod-like geometry, but not in EF maximum and minimum. These results support the notion that the plate to rod transition does not coincide with the onset of bone loss and is considerably more moderate, when it does occur, than SMI suggests. A variety of local shapes not straightforward to categorize as rod or plate exist in all our trabecular bone samples.
Highlights
The metabolic bone disease osteoporosis is a major health concern associated with high mortality rates and considerable economic costs [1,2], likely to be exacerbated by the increase in the proportion of elderly people in future demographics
Because such osteoporosis-related changes to the trabecular bone micro-architecture form a link between the bonemodelling balance at a tissue level and the mechanical performance of the bone organ, they are key to our understanding of the disease
We report mean and maximum trabecular thickness (Tb.Th) in these samples, in order to be able to gauge whether a change in ellipsoid factor (EF) might be attributed to badly resolved trabeculae in samples with e.g. low bone volume fraction
Summary
The metabolic bone disease osteoporosis is a major health concern associated with high mortality rates and considerable economic costs [1,2], likely to be exacerbated by the increase in the proportion of elderly people in future demographics. In this disease, imbalance between osteoblastic (bone-forming) and osteoclastic (bone-resorbing) cell activity is thought to lead to lower bone turnover and relatively higher resorption than royalsocietypublishing.org/journal/rsos R. Because such osteoporosis-related changes to the trabecular bone micro-architecture form a link between the bone (re)modelling balance at a tissue level and the mechanical performance of the bone organ, they are key to our understanding of the disease
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