A1 Refereed original research article in a scientific journal
Microdamage detection and repair in bone: fracture mechanics, histology, cell biology
Authors: Hazenberg JG, Hentunen TA, Heino TJ, Kurata K, Lee TC, Taylor D
Publication year: 2009
Journal: Technology and Health Care
Journal name in source: Technology and health care : official journal of the European Society for Engineering and Medicine
Journal acronym: Technol Health Care
Volume: 17
Issue: 1
First page : 67
Last page: 75
ISSN: 0928-7329
DOI: https://doi.org/10.3233/THC-2009-0536
Abstract
Bone is an elementary component in the human skeleton. It protects vital organs, regulates calcium levels and allows mobility. As a result of daily activities, bones are cyclically strained causing microdamage. This damage, in the form of numerous microcracks, can cause bones to fracture and therefore poses a threat to mechanical integrity. Bone is able to repair the microcracks through a process called remodelling which is tightly regulated by bone forming and resorbing cells. However, the manner by which microcracks are detected, and repair initiated, has not been elucidated until now. Here we show that microcrack accumulation causes damage to the network of cellular processes, resulting in the release of RANKL which stimulates the differentiation of cells specialising in repair.
Bone is an elementary component in the human skeleton. It protects vital organs, regulates calcium levels and allows mobility. As a result of daily activities, bones are cyclically strained causing microdamage. This damage, in the form of numerous microcracks, can cause bones to fracture and therefore poses a threat to mechanical integrity. Bone is able to repair the microcracks through a process called remodelling which is tightly regulated by bone forming and resorbing cells. However, the manner by which microcracks are detected, and repair initiated, has not been elucidated until now. Here we show that microcrack accumulation causes damage to the network of cellular processes, resulting in the release of RANKL which stimulates the differentiation of cells specialising in repair.
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