musculoskeletal and connective tissue disorders
Osteoarthritis (OA)
Pathophysiology of Osteoarthritis
Normal joints have little friction with movement and do not wear out with typical use, overuse, or most trauma. Hyaline cartilage is avascular, aneural, and alymphatic. It is 95% water and extracellular cartilage matrix and only 5% chondrocytes. Chondrocytes have the longest cell cycle in the body (similar to central nervous system and muscle cells). Cartilage health and function depend on compression and release of weight bearing and use (ie, compression pumps fluid from the cartilage into the joint space and into capillaries and venules, whereas release allows the cartilage to reexpand, hyperhydrate, and absorb necessary electrolytes and nutrients). The trigger of osteoarthritis is most often unknown, but osteoarthritis sometimes begins with tissue damage from mechanical injury (eg, torn meniscus), transmission of inflammatory mediators from the synovium into cartilage, or defects in cartilage metabolism. Obesity triggers some of these defects in cartilage metabolism, leading to cartilage matrix damage and subchondral bone remodel­ing mediated by adipokines, such as leptin and adipsin, and compounded by mechanical factors due to excess weight. 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. All articular and some periarticular tissues can become involved in osteoarthritis. 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 mildly 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 weaken and become less supportive. Knee menisci, which are partially innervated, fissure and may fragment and contribute to the pain. Osteoarthritis of the spine can, at the disk level, cause marked thickening and proliferation of the posterior longitudinal ligaments, which are posterior to the vertebral body but anterior to the spinal cord. The result can be transverse bars that encroach on the anterior spinal cord. Hypertrophy and hyperplasia of the ligamenta flava, which are posterior to the spinal cord, often compress the posterior canal, causing Symptoms and Signs . In contrast, the anterior and posterior nerve roots, ganglia, and common spinal nerve are relatively well protected in the intervertebral foramina, where they occupy only 25% of the available and well-cushioned space. 