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Osteoarthritis and Joint Pain

Last updated: Sun, Jun 25, 2017

Osteoarthritis (OA) is a common source of pain in hand, knee, and foot joints. About 25 million Americans older than 25 are estimated to have what is called “radiographic osteoarthritis,” which means they have radiographic signs of OA whether or not they have pain and stiffness. Painful hand OA is present in 7% of Americans over age 26 but in 26% of women and 13% of men over age 70. Painful knee OA has been found in 7% or 17% of the population over age 45, depending on the study. Painful hip OA was found in about 10% of the population over age 45 in one study.1 Radiographic signs of OA are present in many symptom-free people, and symptoms are common in people without positive radiographic signs. Persistent knee pain, for example, has been reported to occur in about 25% of people over age 55, only half of whom have radiographic OA.2

OA is a disease of gradual joint degeneration. It is marked by damage to and loss of joint cartilage, growth of bone spurs around the joint, bone loss under the cartilage, damage to areas of bone marrow beneath the cartilage, inflammation of the synovial fluid, and seepage of synovial fluid. Symptoms include pain, stiffness, and decreased range of motion. Pain usually occurs initially only when the joint is used, but can be present even at rest in later stages. Since joint cartilage is only sparsely innervated, it is believed that much of the pain of OA is from nerves in the soft tissues, especially the ligaments of the joint capsule. Bone spurs may cause pain by stretching the sensitive “skin” of the bone, the periosteum.

The occurrence and progress of OA are thought to be the combined result of damage, use, and vulnerability. Knee injury, for example, increases the risk of developing OA in the knee by four times.3 Body weight is an important risk factor. One study showed that a two-unit decrease in body mass index cut in half the risk of developing symptomatic knee arthritis in women. There is a strong heritability component to OA, and several of the genes involved have been identified.4