Synovial fluid nourishes the chondrocytes and lubricates the joint. Hyaline cartilage has no blood supply, significantly limiting its reparative, restorative capacity. OA affects the degradation–synthesis cycle of the chondrocytes, as well as of the extracellular matrix and the subchondral bone, which in turn leads to softening, fibrillation, ulceration, and loss of cartilage. OA bony changes include fractures of subchondral trabecular (spongy) bone, marginal osteophytes (bone spurs), and subchondral cysts. Hyaline cartilage has no nerves, and the pain that accompanies OA arises from the subchondral trabecular bone, the joint capsule, and the periarticular tissues. Synovial inflammation may be present, in part because of cartilage debris, which may result in joint effusion (swelling). Periarticular structures, especially the muscles, are also affected.2
While any diarthrodial joint can be involved in OA, the distal and proximal interphalangeal joints of the hands are the most commonly affected, followed by the knees and the hips.3, 5 A diagnosis of OA is determined by joint symptoms, including pain and functional impairment or joint pathoanatomic changes, or both. A significant problem in addressing risk and progression of OA is the wide spectrum of clinical features that depend in part on demographic factors and the joint affected. Although epidemiologically OA is often described by a single joint region, in reality patients often have OA in multiple joints.