Altered tissue properties induce changes in cancellous bone architecture in aging and diseases
Journal of Biomechanics , Volume 37 - Issue 3 p. 367- 374
The mechanical properties of cancellous bone depend on its architecture and the tissue properties of the mineralized matrix. The architecture is continuously adapted to external loads. In this paper, it was assumed that changes in tissue properties leading to changes in tissue deformation can induce adaptation of the architecture. We asked whether changes in cancellous bone architecture with aging and in e.g. early osteoarthrosis can be explained from changes in tissue properties.This was investigated using computer models in which the cancellous architecture was adapted to external loads. Bone tissue with deformations below a certain threshold was resorbed, deformations above another threshold induced formation. Deformations between these two boundaries, in the 'lazy zone', did not induce bone adaptation. The effects of changes in bone tissue stiffness on bone mass, global stiffness and architecture were investigated. The bone gain (40-60%) resulting from a 50% decrease in tissue stiffness (simulating diseased tissue) was much larger than the bone loss (2-30%) resulting from a 50% increase in tissue stiffness (simulating highly mineralized, old tissue). The adaptation induced by a decrease in tissue stiffness resulted in an almost constant stiffness in the main load bearing direction, but the transversal stiffness decreased. An increased tissue stiffness resulted in a higher stiffness in the main direction and overcompensation in the transversal directions: the global stiffness could become even smaller than the stiffness of the original model. Concluding, we showed that changes in trabecular bone in aging and diseases can be partly explained from changes in tissue properties.
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|Journal of Biomechanics|
|Organisation||Erasmus MC: University Medical Center Rotterdam|
van der Linden, J.C, Day, J.S, Verhaar, J.A.N, & Weinans, H.H. (2004). Altered tissue properties induce changes in cancellous bone architecture in aging and diseases. Journal of Biomechanics, 37(3), 367–374. doi:10.1016/S0021-9290(03)00266-5