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Sclerostin in the development of osteoarthritis: A mini review
K Y Chin1, S O Ekeuku2, K L Pang3
1Universiti Kebangsaan Malaysia, Faculty of Medicine, Department of Pharmacology, Kuala Lumpur, Malaysia. chinkokyong@ppukm.ukm.edu.my.
Abstract:
Wnt signalling plays an important role in bone and cartilage metabolism. Activation of Wnt signalling promotes bone formation but cartilage degradation. Sclerostin (SOST) can inhibit Wnt signalling. It is expressed by chondrocytes in the articular cartilage and osteocytes in the subchondral bone. Since osteoarthritis (OA) is a joint degenerative disease involving both bone and joint compartments, SOST may have a role in mediating the progression of this disease. This review examined the current literature on the role of SOST in the pathogenesis of OA and its usefulness as a biomarker of OA. Most studies agree that SOST is upregulated as a rescue mechanism in OA to prevent further degenerative changes of the joint. It antagonises inflammation-induced cartilage catabolism while preserving chondrocyte anabolic activities. It also prevents abnormal bone mineralisation and osteophyte formation. However, studies on the performance of SOST as a biomarker to detect and stage OA are limited. Further studies are required to determine whether SOST can be a biomarker or therapeutic target for OA.
Insights
Sclerostin (SOST) acts as a protective factor in osteoarthritis (OA), inhibiting Wnt signaling to prevent cartilage and bone damage. Further research is needed to confirm SOST
Area of Science:
- Biochemistry
- Orthopedics
- Rheumatology
Background:
- Wnt signaling influences bone and cartilage metabolism, with activation promoting bone formation but cartilage degradation.
- Sclerostin (SOST), an inhibitor of Wnt signaling, is expressed in articular cartilage and subchondral bone.
- Osteoarthritis (OA) is a degenerative joint disease affecting both bone and cartilage compartments.
Purpose of the Study:
- To review the current literature on the role of SOST in osteoarthritis (OA) pathogenesis.
- To evaluate the potential of SOST as a biomarker for OA detection and staging.
Main Methods:
- Literature review of studies investigating SOST in OA.
- Analysis of SOST expression and function in OA models and patient samples.
Main Results:
- SOST is generally upregulated in OA as a protective mechanism, counteracting inflammation-induced cartilage breakdown.
- SOST preserves chondrocyte anabolic activity and inhibits abnormal bone mineralization and osteophyte formation.
- Limited studies exist on SOST's performance as an OA biomarker for detection and staging.
Conclusions:
- SOST plays a significant role in OA pathogenesis, acting to mitigate degenerative changes in the joint.
- Further investigation is required to establish SOST as a reliable biomarker or therapeutic target for OA.
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