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5 - Local regulators of bone turnover

Published online by Cambridge University Press:  01 June 2011

Janet E. Henderson
Affiliation:
McGill University, Montréal
David Goltzman
Affiliation:
McGill University, Montréal
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Summary

Introduction

To attempt to understand a disease such as osteoporosis, we must come to a complete elucidation of the nature or pathology of the disorder, the cellular mechanisms whereby the pathology develops and, lastly, what caused the cellular machinery to go awry in the first place (e.g., control by genes, hormones, growth factors, vitamins, minerals, etc.). While many investigators may still disagree on a unified definition of osteoporosis which fully describes its pathology, for a number of years now we have fairly well understood the nature of the disease, and to describe the gross cellular mechanisms which do go awry. That is to say that we can all agree that the end result of undermineralized bone is due to a chronic imbalance of skeletal turnover whereby more mineral is removed than is incorporated into the matrix. It is only recently, however, that we have been able to tackle why the cellular machinery goes wrong, and that has resulted from a clearer understanding of the role(s) of growth factors and cytokines in the skeletal microenvironment. Both bone itself and the bone marrow compartment produce, store, and are influenced by a plethora of cytokines, stem factors and growth factors. However, in this brief chapter we will concentrate on those factors which are known to be both produced and stored within the matrix of bone itself; these are the insulin-like growth factors (IGFs), fibroblast growth factors (FGFs), transforming growth factor-β (TGF-β), and the bone morphogenic proteins (BMPs).

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Publisher: Cambridge University Press
Print publication year: 2000

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