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The role of homocysteine in bone remodeling

Thomas P Vacek1, Anuradha Kalani, Michael J Voor

  • 1Department of Physiology and Biophysics, University of Louisville School of Medicine Louisville, Louisville, KY 40202, USA.

Clinical Chemistry and Laboratory Medicine
|March 2, 2013
PubMed

Insights

High homocysteine (Hcy) levels impact bone remodeling by affecting osteoblasts and osteoclasts. This study proposes a mitochondrial mechanism involving reactive oxygen species (ROS) and matrix metalloproteinases (MMPs) in Hcy-induced bone changes.

Area of Science:

  • Biochemistry
  • Bone Biology
  • Mitochondrial Medicine

Background:

  • Homocysteine (Hcy) significantly influences bone remodeling through mechanisms like altered osteoblast/osteoclast activity and direct matrix interaction.
  • Elevated Hcy (hyperhomocysteinemia, HHcy) is linked to decreased bone blood flow and increased matrix metalloproteinases (MMPs), potentially weakening bone structure.
  • Mitochondria play a key role in reactive oxygen species (ROS) generation, and mitochondrial abnormalities are observed in HHcy, suggesting a role in Hcy's bone effects.

Purpose of the Study:

  • To elucidate the largely unknown mitochondrial mechanism by which Hcy induces alterations in bone properties.
  • To investigate the role of ROS and MMPs in Hcy-mediated bone matrix degradation via a mitochondrial pathway.

Main Methods:

  • The study proposes a hypothetical mitochondrial pathway for Hcy's effects on bone.
  • It discusses the role of ROS generated by mitochondria in activating MMPs.
  • It considers bone turnover markers like hydroxyproline and N-terminal collagen 1 telopeptides in the context of HHcy.

Main Results:

  • Hcy may induce bone alterations through mitochondrial ROS generation, leading to MMP activation and subsequent bone matrix degradation.
  • Contrasting reports exist regarding Hcy's effect on bone density.
  • Previous studies indicate altered bone biomechanical properties in HHcy and deficiencies in vitamins B12 and folate.

Conclusions:

  • A mitochondrial mechanism involving ROS and MMPs is proposed for Hcy's detrimental effects on bone.
  • Folate and vitamin therapy may act through both Hcy-dependent and independent pathways.
  • Further research is essential to fully clarify the mechanistic role of Hcy in bone diseases.

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