Osteoarthritis is a chronic arthropathy characterized by disruption and potential loss of joint cartilage along with other joint changes, including bone hypertrophy (osteophyte formation),subchondral sclerosis and subchondral cysts formation .
Osteoarthritis begins with tissue damage from mechanical injury (eg, torn meniscus), transmission of inflammatory mediators from the synovium into cartilage, or defects in cartilage metabolism. The tissue damage stimulates chondrocytes to attempt repair, which increases production of proteoglycans and collagen. However, efforts at repair also stimulate the enzymes that degrade cartilage, as well as inflammatory cytokines, which are normally present in small amounts. Inflammatory mediators trigger an inflammatory cycle that further stimulates the chondrocytes and synovial lining cells, eventually breaking down the cartilage. Chondrocytes undergo programmed cell death (apoptosis). Once cartilage is destroyed, exposed bone becomes eburnated and sclerotic.
Articular as welll as the periarticular tissues are involved in OA. Subchondral bone stiffens, then undergoes infarction, and develops subchondral cysts. Attempts at bony repair cause subchondral sclerosis and osteophytes at the joint margins. The osteophytes seem to develop in an attempt to stabilize the joint. The synovium becomes inflamed and thickened and produces synovial fluid with less viscosity and greater volume. Periarticular tendons and ligaments become stressed, resulting in tendinitis and contractures. As the joint becomes less mobile, surrounding muscles thin and become less supportive. Menisci fissure and may fragment.