Autor: |
Cointry GR; Center for P-Ca Metabolism Studies (CEMFoC), National University of Rosario (UNR), Rosario, Argentina., Capozza RF, Chiappe MA, Feldman S, Meta MD, Daniele SM, Fracalossi NM, Reina P, Ferretti JL |
Jazyk: |
angličtina |
Zdroj: |
Journal of bone and mineral metabolism [J Bone Miner Metab] 2005; Vol. 23 Suppl, pp. 30-5. |
DOI: |
10.1007/BF03026320 |
Abstrakt: |
In this article, we summarize the results of six different tomographic/biomechanical rat studies involving hypophysectomy (Hx), ovariectomy, treatment with rhGH, olpadronate, alendronate, and toxic doses of aluminum and the development of a genetic diabetes in the eSS strain. All these conditions induced some interesting and rarely reported effects on postyield bone strength. These effects were generally related neither to the degree of mineralization or the elastic modulus of the bone tissue nor to the preyield behavior of the bones. In two particular cases (Hx, eSS), the elastic modulus of bone tissue varied independently of its degree of mineralization. These results suggest the involvement of some microstructural factor(s) of bone tissue resistance to crack progression (a postyield feature of bone behavior), rather than to crack initiation (the yield-determining factor) in the corresponding mechanism. Changes in collagen or crystal structure may play that role. These changes are relevant to the mechanism of fracture production during plastic deformation, a feature of bone strength that might be independent from mineralization. Therefore, these changes might help to explain some effects of novel treatments on bone strength unrelated to bone mineralization. This questions the belief that the remaining bone mass in metabolic osteopenias is biologically and mechanically normal. |
Databáze: |
MEDLINE |
Externí odkaz: |
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