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Related Experiment Videos

AZT enhances osteoclastogenesis and bone loss.

George Pan1, Xiaojun Wu, Margaret A McKenna

  • 1The Department of Pathology, The University of Alabama at Birmingham, 35294-0007,USA.

AIDS Research and Human Retroviruses
|July 10, 2004
PubMed
Summary

Zidovudine (AZT) increases bone-resorbing osteoclast activity, leading to osteopenia. This finding explains a key mechanism behind bone loss associated with highly active antiretroviral therapy (HAART).

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Area of Science:

  • Bone Biology
  • Pharmacology
  • Immunology

Background:

  • Highly active antiretroviral therapy (HAART) is linked to metabolic complications like osteopenia and osteoporosis.
  • Zidovudine (AZT) is a common nucleoside reverse transcriptase inhibitor used in HAART.

Purpose of the Study:

  • To investigate the effects of zidovudine (AZT) on osteoclastogenesis.
  • To determine the impact of AZT on bone mineral density and identify mechanisms of HAART-induced osteopenia.

Main Methods:

  • Cultured mouse macrophage preosteoclast cell line (RAW264.7) and primary bone marrow precursors were used.
  • Osteoclastogenesis, tartrate-resistant acid phosphatase (TRAP) promoter activity, and NF-kappaB binding were assessed.
  • Bone mineral density (BMD) was measured in AZT-treated mice.

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Main Results:

  • AZT significantly increased osteoclastogenesis in a dose-dependent manner.
  • AZT enhanced TRAP promoter activity and NF-kappaB binding and function.
  • AZT-treated mice exhibited decreased BMD and marked osteopenia.

Conclusions:

  • AZT stimulates osteoclastogenesis, partly by enhancing RANKL-mediated pathways.
  • AZT-induced osteoclastogenesis is a significant contributor to HAART-associated osteopenia.