Publication: Modeling of bone formation and resorption mediated by parathyroid hormone: Response to estrogen/PTH therapy
Issued Date
2003-01-01
Resource Type
ISSN
03032647
Other identifier(s)
2-s2.0-0038738223
Rights
Mahidol University
Rights Holder(s)
SCOPUS
Bibliographic Citation
BioSystems. Vol.70, No.1 (2003), 55-72
Suggested Citation
Chontita Rattanakul, Yongwimon Lenbury, Nateetip Krishnamara, David J. Wollkind Modeling of bone formation and resorption mediated by parathyroid hormone: Response to estrogen/PTH therapy. BioSystems. Vol.70, No.1 (2003), 55-72. doi:10.1016/S0303-2647(03)00040-6 Retrieved from: https://repository.li.mahidol.ac.th/handle/123456789/20779
Research Projects
Organizational Units
Authors
Journal Issue
Thesis
Title
Modeling of bone formation and resorption mediated by parathyroid hormone: Response to estrogen/PTH therapy
Other Contributor(s)
Abstract
Bone, a major reservoir of body calcium, is under the hormonal control of the parathyroid hormone (PTH). Several aspects of its growth, turnover, and mechanism, occur in the absence of gonadal hormones. Sex steroids such as estrogen, nonetheless, play an important role in bone physiology, and are extremely essential to maintain bone balance in adults. In order to provide a basis for understanding the underlying mechanisms of bone remodeling as it is mediated by PTH, we propose here a mathematical model of the process. The nonlinear system model is then utilized to study the temporal effect of PTH as well as the action of estrogen replacement therapy on bone turnover. Analysis of the model is done on the assumption, supported by reported clinical evidence, that the process is characterized by highly diversified dynamics, which warrants the use of singular perturbation arguments. The model is shown to exhibit limit cycle behavior, which can develop into chaotic dynamics for certain ranges of the system's parametric values. Effects of estrogen and PTH administrations are then investigated by extending on the core model. Analysis of the model seems to indicate that the paradoxical observation that intermittent PTH administration causes net bone deposition while continuous administration causes net bone loss, and certain other reported phenomena may be attributed to the highly diversified dynamics which characterizes this nonlinear remodeling process. © 2003 Elsevier Science Ireland Ltd. All rights reserved.