Osteoarthritis is a chronic joint disease characterized by the progressive breakdown of articular cartilage, changes in the underlying bone and inflammation of the joint lining. It most commonly affects knees, hips, hands and the spine and is strongly associated with aging, obesity, joint injury and genetic susceptibility.

Modern research has reframed osteoarthritis from a simple “wear and tear” condition to a whole joint disease. Cartilage degradation is driven by an imbalance between breakdown and repair. Enzymes such as matrix metalloproteinases and aggrecanases are upregulated and destroy cartilage components like collagen and proteoglycans. Inflammatory mediators, including cytokines released by the synovium and subchondral bone, amplify this destructive process and contribute to pain.

Genetic studies have identified multiple risk loci that influence cartilage structure, bone remodeling and inflammatory pathways. Mechanical factors such as malalignment and overloading of joints accelerate local damage. Obesity contributes both by increasing joint load and by releasing inflammatory mediators from adipose tissue.

Current treatment focuses on symptom relief and maintaining function through exercise, weight management, physical therapy and analgesic or anti inflammatory drugs. Intra articular injections and joint replacement are used in more advanced disease. Research is actively exploring disease modifying therapies that can slow or reverse structural damage. Approaches under investigation include inhibitors of cartilage degrading enzymes, anabolic growth factors to stimulate repair, targeting inflammatory pathways and using cell based or tissue engineered cartilage implants. Advances in imaging and biomarkers aim to detect early disease and monitor progression more precisely, supporting the development of more effective and personalized interventions.