Osteoarthritis is a degenerative joint disease characterized by progressive breakdown of articular cartilage, changes in subchondral bone and inflammation of the synovial membrane. It most commonly affects the knees, hips, hands and spine and is a leading cause of pain and disability in older adults. Mechanical overload, aging, obesity, joint injury and genetic susceptibility contribute to its onset and progression.

Research shows that cartilage degeneration is driven by an imbalance between anabolic and catabolic processes in chondrocytes. Pro inflammatory cytokines such as interleukin 1 beta and tumor necrosis factor alpha, along with matrix metalloproteinases and aggrecanases, accelerate breakdown of the extracellular matrix. Subchondral bone becomes thickened and sclerotic, with formation of osteophytes, while synovial inflammation further amplifies joint damage.

Biomarker studies in blood, urine and synovial fluid aim to detect early disease, monitor progression and guide therapy. Imaging advances including high resolution MRI and quantitative cartilage assessment provide detailed evaluation beyond conventional radiography.

Current treatment focuses on symptom relief and functional preservation through weight loss, exercise therapy, physical aids, analgesics and nonsteroidal anti inflammatory drugs. Intra articular corticosteroids and hyaluronic acid are used selectively. Joint replacement remains the definitive option for end stage disease.

Emerging therapies target molecular pathways involved in cartilage catabolism, inflammation and subchondral bone remodeling. These include inhibitors of catabolic enzymes, biologic agents against inflammatory cytokines, disease modifying osteoarthritis drugs and experimental cell based strategies such as mesenchymal stem cell therapy and tissue engineering. Research is also exploring personalized approaches based on phenotypes and endotypes to better match patients with specific therapeutic strategies.