Pathogenesis of osteoarthritis

  Articular cartilage is an aggregation of 1-2mm thick collagen fibers, glycoproteins, and hyaluronates, which when hydrated acts as a cushion-like layer to absorb and disperse the weight bearing and mechanical forces applied. Under physiological conditions, articular cartilage relies on periarticular and thermal contraction and the subchondral bone to perform the above tasks completely. The contraction of the muscles, in addition to driving joint movement, also acts as a rubber band, absorbing a large amount of incoming impulse and protecting the joint. When an accident occurs (such as a fall), because the muscles do not have a timely protective response to this sudden shock and make the joints heavier, which can cause damage to the joints, so the muscles do not have a timely protective response to this sudden shock and make the joints heavier, which can cause damage to the joints. In addition, muscle aging, peripheral neuropathy, muscle energy absorption function is also greatly reduced. Another factor that helps cartilage to bear weight is the bone mass under the cartilage that presents a reticular distribution, whose texture is softer than the cartilage, but softer than the bone cortex, so it has a high degree of elasticity and is conducive to bearing pressure.  Osteoarthritis can be seen in the following two situations: first, when there are abnormalities in the articular cartilage, subchondral cortex and periarticular muscles, such as senile degeneration, osteoporosis, inflammation, metabolic diseases, etc.; second, when the articular cartilage, subchondral bone mass and periarticular muscles are normal but are subjected to excessive pressure, such as obesity and trauma.  Pathology: The deformation of articular cartilage occurs earliest and has characteristic lesions. When the cartilage matrix loses glycoprotein, the cartilage on the surface of the joint softens and fractures at the site of pressure, leaving the cartilage surface in the form of a fine filamentous material. Later, the cartilage is gradually shed in sheets and the cartilage layer becomes thin or even disappears. Small fractures and necrosis of the subchondral bone occur, and the osteophytes in and around the joint surface constitute osteosclerosis and bone arthrosis and bone cystic changes on X-ray. The synovial membrane of the joint may show mild proliferative changes including proliferation of synovial cells and infiltration of lymphocytes due to destruction of cartilage and bone and shedding of metabolites such as the joint cavity, which is much less pronounced than in rheumatoid arthritis. In severe osteoarthritis, there is fibrosis of the joint capsule wall and damage to the surrounding tendons.