A dynamic simulation model for long term bone mass homeostasis and osteoporosis

Abstract

Osteoporosis is a skeletal disorder related to low bone mass and increased risk of fracture. Although it is seen in both sexes, the disease is more prevalent among women after menopause. Decreased estrogen level, altered physical activity and insufficient dietary calcium supplementation are the basic causes of the disease. A considerable percent of postmenopausal and women aged over 80 are affected by osteoporosis. There is an increasing mortality and morbidity rate related to osteoporotic fractures. The goal of this thesis is to construct a dynamic simulation model that can realistically reproduce long term behaviour of postmenopausal bone loss. For this purpose, a system dynamics model is built which focuses on bone’s mechanical properties and its interactions with calcium homeostasis system in blood. Comparisons with available data indicate that the model realistically reproduces the behaviour of bone loss for both menopausal and nonmenopausal causes in women. Experiments with the model demonstrate that keeping peak strains above disuse threshold is essential in bone health. Both medical and nonmedical interventions work for treating bone loss after menopause, but drug therapies are most influential in treating osteoporosis. For avoiding non-menopausal losses, simulation experiments show that calcium supplementation is essential in pre and post-menopausal years.