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Terminal N-acetylglucosamine in chronic synovitis
M Sharif1, G Rook, L S Wilkinson
1Department of Microbiology, University College and Middlesex Hospital, School of Medicine.
British Journal of Rheumatology
|February 1, 1990
Summary
Rheumatoid arthritis synovium shows abnormal N-acetylglucosamine (GlcNAc) deposits, unlike normal tissue or osteoarthritis. These deposits may trigger inflammation in rheumatoid arthritis by acting as an antigen or interacting with macrophage receptors.
Area of Science:
- Immunology
- Histopathology
- Biochemistry
Background:
- Terminal N-acetylglucosamine (GlcNAc) residues are present on various cell surfaces.
- Their distribution in synovial tissue, particularly in rheumatoid arthritis, is not well understood.
Purpose of the Study:
- To investigate the distribution of terminal GlcNAc in normal and rheumatoid arthritis synovial tissue.
- To explore the potential role of GlcNAc deposits in rheumatoid arthritis pathogenesis.
Main Methods:
- Utilized a mouse monoclonal antibody (mAb) specific for terminal GlcNAc.
- Examined synovial tissue samples from patients with rheumatoid arthritis and osteoarthritis, as well as normal human connective tissue and epithelial tissues.
Main Results:
- Normal synovium and connective tissue lacked terminal GlcNAc staining.
- Synovium from rheumatoid arthritis patients exhibited dense granular staining of macrophages and reticular extracellular staining.
- Extracellular GlcNAc deposition was absent in osteoarthritis synovium.
Conclusions:
- Abnormal deposition of terminal GlcNAc occurs in the synovium of rheumatoid arthritis patients.
- These extracellular GlcNAc deposits may contribute to rheumatoid arthritis pathogenesis by acting as inflammatory stimuli.
- Potential mechanisms include antigenicity or interaction with macrophage receptors, mimicking microbial presence.