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Software-Assisted Quantitative Measurement of Osteoarthritic Subchondral Bone Thickness
Published on: March 18, 2022
S100A8 and S100A9 in experimental osteoarthritis
Hala Zreiqat1, Daniele Belluoccio, Margaret M Smith
1Tissue Engineering and Biomaterials Research Unit, School of AMME J07, Faculty of Engineering, Bosch Institute, University of Sydney, Corner of Shepherd and Cleavland Street, New South Wales 2006, Australia. hzreiqat@usyd.edu.au
Arthritis Research & Therapy
|January 29, 2010
Summary
S100A8 and S100A9 proteins drive early cartilage damage in osteoarthritis (OA) by upregulating matrix-degrading enzymes. Their expression decreases in late-stage OA, suggesting a limited role in ongoing cartilage destruction in this condition.
Area of Science:
- Biochemistry
- Molecular Biology
- Immunology
Background:
- Osteoarthritis (OA) and inflammatory arthritis are distinct joint diseases.
- S100A8 and S100A9 proteins are implicated in inflammatory processes.
Purpose of the Study:
- To investigate the differential roles of S100A8, S100A9, and their complex in cartilage during osteoarthritis versus inflammatory arthritis.
- To understand the impact of these proteins on cartilage matrix gene expression.
Main Methods:
- Analyzed S100A8 and S100A9 protein localization in mouse models of inflammatory arthritis and surgically-induced OA.
- Utilized cartilage explant cultures stimulated with IL-1.
- Performed microarray expression profiling of S100 proteins.
- Assessed the effect of S100A8/S100A9 on chondrocyte gene expression of matrix components and degradative enzymes using qRT-PCR.
Main Results:
- Interleukin-1 (IL-1) stimulation increased S100A8 and S100A9 mRNA and protein in chondrocytes.
- S100A8 and S100A9 mRNA expression was elevated in early mouse OA but decreased in late stages.
- Unlike in inflammatory arthritis, S100A8 staining was lost in late-stage OA chondrocytes.
- Homodimeric S100A8 and S100A9 upregulated genes for matrix metalloproteinases (MMPs) and aggrecanases, while decreasing collagen II and aggrecan expression.
Conclusions:
- Chondrocyte-derived S100A8 and S100A9 may play a sustained role in cartilage degradation in inflammatory arthritis.
- In osteoarthritis, these proteins might initiate early cartilage degradation by upregulating MMPs and aggrecanases.
- Reduced expression in late-stage OA suggests S100A8 and S100A9 do not have an ongoing role in cartilage destruction in this non-inflammatory condition.
