Osteoarthritis Pathophysiology and Treatment Approaches
Summary
Osteoarthritis is a chronic degenerative joint disease characterised by progressive cartilage erosion, subchondral bone remodelling and low‐grade synovial inflammation. Mechanical stress, biochemical mediators and genetic predisposition converge to drive imbalance between anabolic and catabolic processes in the articular cartilage extracellular matrix. Chondrocyte dysfunction leads to depletion of critical matrix components such as type II collagen and proteoglycans, while subchondral bone undergoes sclerosis and osteophyte formation alters joint biomechanics. Synovial lining cells contribute pro-inflammatory cytokines, amplifying matrix degradation and pain. Current management focuses on symptom relief through physiotherapy, weight management and analgesics, with intra-articular injections of corticosteroids or hyaluronic acid as adjuncts. Emerging strategies aim to modify disease progression by targeting inflammatory signalling pathways, promoting cartilage repair via cell-based or gene therapies, and developing disease-modifying osteoarthritis drugs (DMOADs). Integrative approaches combining tailored exercise regimens, nutraceuticals and novel pharmacological agents hold promise for preserving joint structure and function.
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Osteoarthritis Pathophysiology and Treatment Approaches publication trend
The graph below shows the total number of articles in osteoarthritis pathophysiology and treatment approaches across all publications each year (not limited to Nature Index journals).
Technical terms
Chondrocyte: The specialised cell responsible for producing and maintaining the cartilage extracellular matrix.
Synoviocyte: A cell in the synovial membrane that secretes lubricating fluid and mediates inflammatory responses in the joint.
Extracellular matrix: The network of proteins and proteoglycans that provides structural integrity to cartilage tissue.
Osteophyte: A bony projection that forms at joint margins in osteoarthritis, contributing to pain and stiffness.
DMOAD: Disease-modifying osteoarthritis drug, designed to slow or reverse structural joint damage rather than just relieve symptoms.
NF-κB: A transcription factor that controls expression of inflammatory genes in chondrocytes and synovial cells.
References
- Short-term response of primary human meniscus cells to simulated microgravity. Cell Communication and Signaling (2024).
- Moderate Physical Activity as a Prevention Method for Knee Osteoarthritis and the Role of Synoviocytes as Biological Key. International Journal of Molecular Sciences (2019).
- Role of Physical Exercise and Nutraceuticals in Modulating Molecular Pathways of Osteoarthritis. International Journal of Molecular Sciences (2021).
- Update on novel pharmacological therapies for osteoarthritis. Therapeutic Advances in Musculoskeletal Disease (2019).
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