Author
Listed:
- Diego Alexander Garzón-Alvarado
- Liliana Mabel Peinado Cortés
- Rosy Paola Cárdenas Sandoval
Abstract
The role of cartilage canals is to transport nutrients and biological factors that cause the appearance of the secondary ossification centre (SOC). The SOC appears in the centre of the epiphysis of long bones. The canal development is a complex interaction between mechanical and biological factors that guide its expansion into the centre of the epiphysis. This article introduces the ‘Hypothesis on the growth of cartilage canals’. Here, we have considered that the development of these canals is an essential event for the appearance of SOC. Moreover, it is also considered to be important for the transport of molecular factors (RUNX2 and MMP9) at the ends of such canals. Once the canals are merged in the centre of the epiphysis, these factors are released causing hypertrophy of adjacent cells. This RUNX2 and MMP9 release occurs due to the action of mechanical loads that supports the epiphysis. In order to test this hypothesis, we use a hybrid approach using the finite element method to simulate the mechanical stresses present in the epiphysis and the cellular automata to simulate the expansion of the canals and the hypertrophy factors pathway. By using this hybrid approach, we have obtained as a result the spatial–temporal patterns for the growth of cartilage canals and hypertrophy factors within the epiphysis. The model is in qualitative agreement with experimental results previously reported by other authors. Thus, we conclude that this model may be used as a methodological basis to present a complete mathematical model of the processes involved in epiphyseal development.
Suggested Citation
Diego Alexander Garzón-Alvarado & Liliana Mabel Peinado Cortés & Rosy Paola Cárdenas Sandoval, 2010.
"A mathematical model of epiphyseal development: hypothesis on the cartilage canals growth,"
Computer Methods in Biomechanics and Biomedical Engineering, Taylor & Francis Journals, vol. 13(6), pages 765-772.
Handle:
RePEc:taf:gcmbxx:v:13:y:2010:i:6:p:765-772
DOI: 10.1080/10255841003606116
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