Classic physical exam findings in hand OA include Heberden’s nodes (posterolateral swellings of DIP joints), Bouchard’s nodes (posterolateral swellings of PIP joints), and “squaring” at the base of the thumb (first CMC joints).Ī thorough history and physical exam (with a focused musculoskeletal exam) should be performed on all patients, with some findings summarized above. Tenderness may be present at joint lines, and there may be pain upon passive motion. Typical exam findings in OA include bony enlargement, crepitus, effusions (non-inflammatory), and a limited range of motions. Joints can be at different stages of disease progression. OA can be monoarticular or polyarticular in the presentation. OA typically affects proximal and distal interphalangeal joints, first carpometacarpal (CMC) joints, hips, knees, first metatarsophalangeal joints, and joints of the lower cervical and lumbar spine. Patients may also experience bony swelling, joint deformity, and instability (patients complain that the joint is “giving way” or “buckling,” a sign of muscle weakness). In those patients in whom the disease progresses, pain is more continuous and begins to affect activities of daily living, eventually causing severe limitations in function. Pain is typically related to activity and resolves with rest. Patients can also present with muscle weakness and balance issues.

The triad of symptoms of OA is joint pain, stiffness, and locomotor restriction. The presentation and progression of OA vary greatly from person to person. Their role is unclear, but they are thought to contribute to synovial inflammation. In end-stage OA, both calcium phosphate and calcium pyrophosphate dihydrate crystals are present. Soft-tissue structures (ligaments, joint capsule, menisci) are also affected. There is also some degree of synovial inflammation and hypertrophy, although this is not the inciting factor as is the case with inflammatory arthritis. Even rarer, bony erosions appear in erosive OA. Improperly mineralized collagen causes subchondral bone thickening in advanced disease, bone cysts infrequently occur. As more of the collagen matrix is damaged, chondrocytes undergo apoptosis. A phenotypic change to hypertrophic chondrocyte occurs, causing cartilage outgrowths that ossify and form osteophytes. On a microscopic level, after cartilage injury, the collagen matrix is damaged, causing chondrocytes to proliferate and form clusters. These erosions eventually extend down to the bone and continually expand to involve more of the joint surface. Usually, the earliest changes that occur in OA are at the level of the articular cartilage that develops surface fibrillation, irregularity, and focal erosions. The complete pathway that leads to the destruction of the entire joint is unknown. The combination leads to pro-inflammatory markers and proteases that eventually mediate joint destruction. The cause of OA is an interplay of risk factors (mentioned above), mechanical stress, and abnormal joint mechanics. OA is a disease of the entire joint sparing no tissues.

Hip osteoarthritis xray vs normal hip