eCM (Eur Cell Mater / e Cells & Materials) Not-for-profit Open Access
Created by Scientists, for Scientists
 ISSN:1473-2262         NLM:100973416 (link)         DOI:10.22203/eCM

2003   Volume No 6 - pages 46-56

Title: Bone microdamage and cell apoptosis

Authors: B Noble

Address: Musculo-Skeletal Research Unit, University of Edinburgh Medical School, Edinburgh, Scotland, U.K.

E-mail: Brendon.Noble at ed.ac.uk

Key Words: Osteocyte, apoptosis, microdamage, bone, osteoclast, signaling, targeted bone resorption.

Publication date: December 21st 2003

Abstract: Accumulation of microdamage in bone leads to the reduced strength of our skeleton. In health, bone adapts to the prevailing mechanical needs of the organism and is also capable of self-repair, sensing, removing and replacing damaged or mechanically insufficient volumes of bone. In disease and old age these characteristics are reduced. In order to undertake both of the processes of functional adaptation and repair the bone resorbing and forming cells must be very accurately targeted to areas of physiological need. The mechanism by which cells are precisely targeted to areas requiring repair is both clinically relevant and poorly understood. The osteocyte has been assumed to play a role in sensing damage and signaling for its removal, due largely to its abundance throughout the mineralized bone matrix. However, until recently there has been little evidence that osteocyte function is modified in the vicinity of the microdamage. Here I outline the possibility that the targeted removal of bone containing microcracks might involve signals derived from the apoptotic death of the osteocyte. I shall discuss data that support or refute this view and will consider the possible molecular mechanisms by which controlled cell death might contribute to the signals for repair in the light of work involving cells in bone and other tissue systems.

Article download: Pages 46-56. (PDF file)
DOI: 10.22203/eCM.v006a05