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Related Experiment Video

Updated: Jul 2, 2025

ATAC-Seq Library Preparation of Murine Bone Marrow-Derived Neutrophils
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Neutrophils in Inflammatory Bone Diseases.

Carmelo Carmona-Rivera1, Mariana J Kaplan2, Liam J O'Neil3

  • 1Systemic Autoimmunity Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD, 20892, USA. carmelo.carmona-rivera@nih.gov.

Current Osteoporosis Reports
|February 28, 2024
PubMed
Summary

Neutrophils contribute to bone damage in inflammatory diseases like rheumatoid arthritis. Neutrophil extracellular traps (NETs) promote osteoclast activity, worsening bone erosion and homeostasis imbalance.

Keywords:
CarbamylationCitrullinationHistonesNETsNeutrophilsOsteoclastPeriodontitisRheumatoid arthritis

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Area of Science:

  • Immunology
  • Bone Biology
  • Rheumatology

Background:

  • Neutrophil infiltration is characteristic of inflammatory bone diseases, including rheumatoid arthritis (RA) and periodontitis disease (PD).
  • These conditions involve a disruption of bone homeostasis, leading to bone degradation and erosion.
  • Osteoclasts are key cells responsible for bone turnover and damage in these diseases.

Purpose of the Study:

  • To review current evidence on the role of neutrophils in bone damage.
  • To explore the mechanisms by which neutrophils and neutrophil extracellular traps (NETs) exacerbate osteoclast function.

Main Methods:

  • Literature review of current evidence on neutrophil involvement in bone diseases.
  • Analysis of recent findings on NET proteins and their impact on osteoclastogenesis.
  • Examination of post-translational modifications of proteins in the context of RA autoantigens.

Main Results:

  • Neutrophils and NETs can enhance osteoclast activity through direct and indirect pathways.
  • NET proteins, such as histones and elastase, can induce non-canonical inflammatory osteoclasts.
  • Post-translational modifications like citrullination and carbamylation mediate NET-induced osteoclastogenesis and act as autoantigens in RA.

Conclusions:

  • NETs, autoantibodies, modified proteins, cytokines, and osteoclasts collectively contribute to bone damage in RA and PD.
  • Further research is necessary to fully elucidate the complex role of neutrophils in inflammatory bone diseases.