Modelling age-related and post-menopausal bone loss in the human spine
Osteoporosis is the decrease of bone mass density (BMD) and commonly seen in elderly people. Bone loss occurs in two main phases in human life: a slow age-related phase of bone loss that begins around the age of 40 and an accelerated postmenopausal phase of bone loss due to estrogen deficiency. The underlying cellular cause is a disbalance in bone turnover, the continuous process of resorption and formation of bone.
The first objective of this project was to perform a literature study on the cellular behaviour, related to mechanical factors and aging. Secondly, it was aimed to implement the found age-related and postmenopausal changes in bone cell biology into a macro bone adaptation model. Subsequently, this macro bone adaptation model was used to simulate the effect of these cellular changes on the apparent density of a (macro scale) Finite Element model of the spine. The aim of the macro bone adaptation model in combination with the spinal FE model was to simulate a realistic development of bone loss in the spine during aging.
Methods, results and conclusions
The disbalance in bone turnover was implemented into a macro bone adaptation model which is based on the strain adaptive macro model of Weinans et al. In a Sensitivity study, several simulations were done with a single vertebra FE model. The appropriate parameters to simulate a realistic decrease in density due to aging and the menopause were identified. Different parameters have been tested and compared with densitometry studies to determine two functions which account for both aging and the postmenopausal period.
These two determined functions were used to simulate bone loss in the spinal FE model. The simulated decreases in density of a whole vertebral body, due to age-related and postmenopausal cellular behaviour, were comparable with values that were found in densitometric studies. Additional simulation of degenerated intervertebral discs, another main aspect of the aging spine, resulted in a relatively high rate of bone loss in the core of the vertebra in comparison with surrounding regions. This is in agreement with literature.
The increase in microdamage is another effect seen in aging bone, besides the decrease in density. A first approach in modelling of microdamage was made. The influence of age-related bone loss on the damage formation rate, the accumulated damage, and the damage-related decrease of stiffness corresponded with our preliminary expectations.
To conclude, a successful first step was made in the modelling of the disbalance in bone turnover in the spine that occurs as a result of aging and estrogen deficiency.