Pathophysiology of Osteoarthritis
Osteoarthritis (OA) is primarily a disease of cartilage. Cartilage is a tissue with viscoelastic and compressive properties. It is predominantly composed of type II collagen and proteoglycans. In a normal condition the extracellular matrix undergoes a dynamic remodeling process in which low levels of degradative and synthetic enzyme activities are balanced. When OA is present, the matrix degrading enzymes will become overexpressed. This results in loss of collagen and proteoglycans from the matrix (Ling & Bathon, 2012). Once the articular cartilage breaks down, the progressive formation of osteophytes (bone spurs) protrude into the joint space decreasing joint movement. Some factors that may cause OA may include mechanical injury, genetic and hormonal factors or previous joint damage. Risk factors may include older age, sex, obesity, and bone deformities.
Clinical manifestations of OA usually consist of pain, stiffness and functional impairment. Movement or exercise may aggravate the joint pain. The affected joint may have a decreased range of motion and may appear enlarged. OA often occurs in weight-bearing joints such as hips, knees, cervical and lumbar spine although the interphalangeal and distal interphalangeal joints may also be involved.