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Biomed Rep. 2013 Jan;1(1):85-88. doi: 10.3892/br.2012.6. Epub 2012 Aug 28.

Excess iron undermined bone load-bearing capacity through tumor necrosis factor-α-dependent osteoclastic activation in mice.

Biomedical reports

Junping Li, Yanli Hou, Shuping Zhang, Hong Ji, Haiqin Rong, Guangbo Qu, Sijin Liu

Affiliations

  1. Shandong Institute of Endocrine and Metabolic Diseases, Jinan 250062; ; State Key Laboratory of Environmental Chemistry and Ecotoxicology, Research Center for Eco-Environmental Sciences, Chinese Academy of Sciences, Beijing 100085, P.R. China.
  2. State Key Laboratory of Environmental Chemistry and Ecotoxicology, Research Center for Eco-Environmental Sciences, Chinese Academy of Sciences, Beijing 100085, P.R. China.
  3. Shandong Institute of Endocrine and Metabolic Diseases, Jinan 250062;

PMID: 24648899 PMCID: PMC3956768 DOI: 10.3892/br.2012.6

Abstract

Iron overload has been associated with bone mass loss. To elucidate the effects of excess iron on bone metabolism, an iron-overloading mouse model was established by administering iron-dextran at 250 mg/kg to female BALB/c mice. After 4 weeks, the mice were sacrificed and the biomechanical properties of the femurs were examined. The results suggested a notable decrease of the maximal bending stress and the modulus of bending elasticity in the femurs obtained from the excess iron-treated mice compared to the control mice. The levels of the serum osteocalcin, C-telopeptide of type I collagen (CTX-1) and tumor necrosis factor-α (TNF-α) were measured in order to investigate the underlying mechanism responsible for the excess iron-induced bone strength reduction. Overall, the results suggested that iron overload resulted in a marked reduction of bone load-bearing capacity through a TNF-triggered osteoclast differentiation and resorption mechanism.

Keywords: bone mass; bone resorption; bone strength; iron overload

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