Affiliations: [a] Department of Anatomy, Royal College of Surgeons in Ireland, Dublin, Ireland | [b] Department of Anatomy, Institute of Biomedicine, University of Turku, Turku, Finland | [c] Department of Biorobotics, Faculty of Engineering, Kyushu Sangyo University, Fukuoka, Japan | [d] Trinity Centre for Bioengineering, Trinity College, Dublin, Ireland
Correspondence:
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Address for correspondence: Jan G. Hazenberg, Department of Anatomy, Royal College of Surgeons, St. Stephen's Green, Dublin 2, Ireland. E-mail: [email protected].
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.
