Osteoarthritis and rheumatoid arthritis: Nursing pathophysiology

Osteoarthritis, or OA, and rheumatoid arthritis, or RA, are diseases that affect the synovial joints. OA is mostly a degenerative disease, while RA is a systemic autoimmune disease that can also impact other organs like the heart and lungs.

Joints, or the places where bones meet, can be classified into three main groups based on their structure and range of movement. Fibrous joints, like those between the bones of the skull in young children, are composed of a thin layer of fibrous tissue that allows for some movement to accommodate a child’s growing brain; by adulthood, the fibrous tissue is replaced by bone. On the other hand, cartilaginous joints, like the joints of the spine, contain a pad of fibrocartilage, allowing for some movement. Lastly, synovial or diarthrodial joints, like those of the wrist, shoulders, hips, and knees, are freely movable.

Okay, let’s take a closer look at synovial joints, which consist of two bones, each with its own layer of articular cartilage, a type of connective tissue that provides cushioning and allows the bones to glide against each other without friction. The cartilage has high tensile strength, which helps weight-bearing joints like the knees to distribute weight so the underlying bone absorbs the shock and weight. An important component of the articular cartilage are special cells called chondrocytes, which are essential for the maintenance and repair of the cartilage.

Surrounding the joint is an outer fibrous joint capsule that forms an inner space called the joint cavity, which is filled with synovial fluid. The inner surface of the joint capsule is lined with a synovial membrane, or synovium, which is mostly composed of connective tissue, elastic fibers, blood, and lymphatic vessels. It also contains macrophages that remove bacteria and debris, and fibroblasts that produce a viscous substance called hyaluronate, which is the main component of the synovial fluid, that lubricates the articular surfaces.

Now, OA is caused by damage to the synovial joints and can be categorized as primary or secondary. Primary, or idiopathic, OA occurs due to risk factors such as being biologically female; advanced age; obesity; joint trauma; and occupations that involve heavy lifting, prolonged standing, or repetitive motion. In contrast, secondary OA occurs when there’s a preexisting joint abnormality that can initiate biomechanical stress on the joint, like Marfan syndrome.

On the other hand, the exact cause of RA is unknown, though it likely involves genetic, epigenetic, and environmental factors that give rise to an autoimmune response. Triggers thought to initiate this response include environmental agents, like exposure to cigarette smoke, and certain bacteria or viruses. Additionally, individuals with mutations in genes that play a role in the immune system, like the HLA-DRB1 gene, are at an increased risk of RA. And like OA, biological females are more likely to develop RA, and risk increases with age.

Okay so, OA occurs due to degradation, inadequate repair, and loss of articular cartilage. Chondrocytes, that usually repair injured articular cartilage, lose their ability function. This leads to a gradual degradation of the articular cartilage over time, which means eventually there’s not much cartilage separating the two bones anymore, so now there’s a significant amount of friction between them. As the cartilage deteriorates, cracks and pits develop, along with osteophyte formation, which are bony growths on the articular surface. As a result, chronic low-level inflammation is generated, which contributes to the progression of the disease.

On the flip side, the autoimmunity process of RA is mediated by autoantibodies against self-antigens and activation of immune cells. Within the joints, immune cells release inflammatory mediators that cause inflammation and tissue injury. The inflammation eventually creates a pannus, which is a thickened synovial membrane consisting of inflammatory cells and granulation tissue.