On the role of bone damage in calcium homeostasis.
Bone serves as the reservoir of some minerals including calcium. If calcium is needed anywhere in the body, it can be removed from the bone matrix by resorption and put back into the blood flow. During bone remodelling the resorbed tissue is replaced by osteoid which gets mineralized very slowly. Then, calcium homeostasis is controlled by bone remodelling, among other processes: the more intense is the remodelling activity, the lower is the mineral content of bone matrix. Bone remodelling is initiated by the presence of microstructural damage. Some experimental evidences show that the fatigue properties of bone are degraded and more microdamage is accumulated due to the external load as the mineral content increases. That damage initiates bone remodelling and the mineral content is so reduced. Therefore, this process prevents the mineral content of bone matrix to reach very high (non-physiological) values. A bone remodelling model has been used to simulate this regulatory process. In this model, damage is an initiation factor for bone remodelling and is estimated through a fatigue algorithm, depending on the macroscopic strain level. Mineral content depends on bone remodelling and mineralization rate. Finally, the bone fatigue properties are defined as dependent on the mineral content, closing the interconnection between damage and mineral content. The remodelling model was applied to a simplified example consisting of a bar under tension with an initially heterogeneous mineral distribution. Considering the fatigue properties as dependent on the mineral content, the mineral distribution tends to be homogeneous with an ash fraction within the physiological range. If such dependance is not considered and fatigue properties are assumed constant, the homogenization is not always achieved and the mineral content may rise up to high non-physiological values. Thus, the interconnection between mineral content and fatigue properties is essential for the maintenance of bone's structural integrity as well as for the calcium homeostasis.
Martínez-Reina
J
J
Department of Mechanical Engineering, University of Seville, Escuela Superior de Ingenieros, Camino de los Descubrimientos s/n, E-41092 Sevilla, Spain. jmreina@us.es
García-Aznar
J M
JM
Domínguez
J
J
Doblaré
M
M
D015519:Bone Density / Q000502:physiology; D016723:Bone Remodeling / Q000502:physiology; D001842:Bone and Bones / Q000378:metabolism*; D002113:Calcification, Physiologic / Q000502:physiology; D002118:Calcium / Q000378:metabolism* / Q000502:physiology; D015775:Fractures, Stress / Q000378:metabolism / Q000503:physiopathology*; D006706:Homeostasis / Q000502:physiology; D006801:Humans; D008954:Models, Biological; D013314:Stress, Mechanical
D002118:Calcium