A theoretical framework for strain-related trabecular bone maintenance and adaptation.
It is assumed that density and morphology of trabecular bone is partially controlled by mechanical forces. How these effects are expressed in the local metabolic functions of osteoclast resorption and osteoblast formation is not known. In order to investigate possible mechano-biological pathways for these mechanisms we have proposed a mathematical theory (Nature 405 (2000) 704). This theory is based on hypothetical osteocyte stimulation of osteoblast bone formation, as an effect of elevated strain in the bone matrix, and a role for microcracks and disuse in promoting osteoclast resorption. Applied in a 2-D Finite Element Analysis model, the theory explained the formation of trabecular patterns. In this article we present a 3-D FEA model based on the same theory and investigated its potential morphological predictability of metabolic reactions to mechanical loads. The computations simulated the development of trabecular morphological details during growth, relative to measurements in growing pigs, reasonably realistic. They confirmed that the proposed mechanisms also inherently lead to optimal stress transfer. Alternative loading directions produced new trabecular orientations. Reduction of load reduced trabecular thickness, connectivity and mass in the simulation, as is seen in disuse osteoporosis. Simulating the effects of estrogen deficiency through increased osteoclast resorption frequencies produced osteoporotic morphologies as well, as seen in post-menopausal osteoporosis. We conclude that the theory provides a suitable computational framework to investigate hypothetical relationships between bone loading and metabolic expressions.
Ruimerman
R
R
Department of Biomedical Engineering, Eindhoven University of Technology, P.O. Box 513, WH 4.131, 5600 MB Eindhoven, The Netherlands.
Hilbers
P
P
van Rietbergen
B
B
Huiskes
R
R
D000222:Adaptation, Physiological; D001862:Bone Resorption; D001842:Bone and Bones / Q000166:cytology / Q000502:physiology*; D004967:Estrogens / Q000172:deficiency; D020342:Finite Element Analysis; D006801:Humans; D021621:Imaging, Three-Dimensional; D008954:Models, Biological; D008962:Models, Theoretical; D010010:Osteoclasts / Q000502:physiology; D010012:Osteogenesis; D010024:Osteoporosis; D013180:Sprains and Strains; D013314:Stress, Mechanical; D016474:Weight-Bearing
D004967:Estrogens