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Inflammatory mediators as essential elements in bone remodeling.

S R Goldring1

  • 1Beth Israel Deaconess Medical Center, Harvard Medical School, New England Baptist Bone and Joint Institute. Harvard Institutes of Medicine, Boston, MA, USA. sgoldrin@caregroup.harvard.edu

Calcified Tissue International
|October 21, 2003
PubMed
Summary

Inflammatory disorders like rheumatoid arthritis trigger bone loss by activating osteoclasts, similar to normal bone remodeling. Understanding these shared pathways is key for developing new therapies to prevent skeletal damage.

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Area of Science:

  • Skeletal biology
  • Immunology
  • Rheumatology

Background:

  • Inflammatory disorders, such as rheumatoid arthritis (RA), significantly impact skeletal homeostasis.
  • Pathologic bone remodeling in RA differs from physiologic remodeling by inflammatory cell recruitment and local cytokine action.

Purpose of the Study:

  • To investigate the mechanisms of bone remodeling in inflammatory conditions like RA.
  • To compare cellular and molecular pathways in physiologic versus pathologic bone remodeling.
  • To identify therapeutic targets for preventing bone loss in inflammatory diseases.

Main Methods:

  • Comparative analysis of cellular recruitment in physiologic and RA-induced bone remodeling.
  • Examination of osteoclastogenic cytokine involvement in both remodeling processes.

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  • Review of existing literature on skeletal homeostasis and inflammatory mediators.

    • Main Results:

    • Osteoclasts are the primary cell type responsible for bone resorption in both physiologic and pathologic remodeling.
    • Macrophage lineage cells and local cytokines initiate bone remodeling in RA.
    • Shared cytokines and mediators are implicated in both normal and disease-related bone remodeling.

    Conclusions:

    • The mechanisms of bone remodeling in RA share similarities with physiologic processes, particularly involving osteoclasts.
    • Understanding these common pathways offers potential for developing targeted therapies to mitigate bone loss in inflammatory conditions.