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Clinical Chemistry and Laboratory Medicine (CCLM)

Published in Association with the European Federation of Clinical Chemistry and Laboratory Medicine (EFLM)

Editor-in-Chief: Plebani, Mario

Ed. by Gillery, Philippe / Lackner, Karl J. / Lippi, Giuseppe / Melichar, Bohuslav / Schlattmann, Peter / Tate, Jillian R.


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Oxidative stress, free radicals and bone remodeling

Giuseppe Banfi1 / Eugenio L. Iorio2 / Massimiliano M. Corsi3

1Laboratory of Cell Culture and Molecular Biology, IRCCS Istituto Ortopedico Galeazzi, Milan, Italy and Department of Health Technology, University of Milan, Milan, Italy

2International Observatory of Oxidative Stress, Salerno, Italy

3Institute of General Pathology, Laboratory of Clinical Pathology, University of Milan, Milan, Italy and Laboratory of Biotechnological Applications, IRCCS Istituto Ortopedico Galeazzi, Milan, Italy

Corresponding author: Prof. Massimiliano M. Corsi, MD, PhD, Institute of General Pathology, Laboratory of Clinical Pathology, Medical Faculty, University of Milan, 20133, Milan, Italy

Citation Information: Clinical Chemistry and Laboratory Medicine. Volume 46, Issue 11, Pages 1550–1555, ISSN (Online) 1437-4331, ISSN (Print) 1434-6621, DOI: 10.1515/CCLM.2008.302, October 2008

Publication History

Received:
2008-05-09
Accepted:
2008-06-26
Published Online:
2008-10-10

Abstract

Reactive oxygen species (ROS) are widely considered to be a causal factor in aging and in a number of pathological conditions, such as atherosclerosis, carcinogenesis and infarction. Their role in bone metabolism is dual, considering their effects under physiological or pathological conditions. Under physiological conditions, the production of ROS by osteoclasts helps accelerate destruction of calcified tissue, thus assisting in bone remodeling. In pathological conditions, when a bone fractures, e.g., radical generation is remarkably high. However, though the increases in osteoclastic activity and ROS production are linked in many skeletal pathologies, it remains to be clarified whether increased ROS production overwhelms antioxidant defenses, leaving the individual open to hyperoxidant stress.

Clin Chem Lab Med 2008;46:1550–5.

Keywords: bone metabolism; ethanol (EtOH); NADPH oxidase (Nox); nitric oxide (NO); osteoporosis; oxidized low-density lipoprotein (OxLDL); reactive oxygen species (ROS); tartrate-resistant acid phosphatase (TRACP)

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