Rheumatic diseases often cause joint pain and have different patterns of joint involvement. These can be used to differentiate the different types of disorders. For example, rheumatoid arthritis usually affects multiple smaller joints, whereas reactive arthritis involves fewer, yet larger joints. On the other hand, the most commonly affected joint in gout is the metatarsophalangeal joint. Each condition demonstrates a characteristic pattern of joint involvement. Needless to say, the presentation of this pattern can sometimes vary. This leads us to the aim of this series on rheumatic disease: to recognize these patterns. We’ll focus on joint pain, so let’s start by looking at the structure of a joint. The function of a joint is to connect two bones to enable motion. A joint is surrounded by a joint capsule, which is lined internally by a synovial membrane.
The synovial membrane produces synovial fluid, or joint fluid, which is secreted into the joint cavity. In addition, the synovial membrane is responsible for the resorption of synovial fluid. The bone is covered with cartilage, which helps to reduce pressure between bones. Muscles are attached to the bone and help move the joint. At the end of the muscle is the tendon, which inserts into the bone. The tendon is surrounded by a tendon sheath, a synovial membrane layer that allows the tendon to stretch. Some synovial joints also have at least one bursa that acts as a cushion, reducing the friction between bones and muscles. Now, all of the structures mentioned represent potential starting points leading to disease processes, so let’s look at them individually. One of these conditions is inflammation of the synovial membrane, termed synovitis, which is often caused by autoimmune processes. Bacterial infection of the joint is known as septic arthritis, also called infectious arthritis. Another condition is crystal-induced arthropathy, a form of inflammation that occurs as a result of the accumulation of crystal deposits in the joint cavity. The most well-known example of a crystal-induced arthropathy is gout, which is caused by uric acid build-up that crystallizes and deposits in the joint cavity. In addition, the tissue surrounding the joint can become inflamed. Let’s focus initially on the tendons.
There are two ways in which tendons become inflamed. First, the site where the tendon inserts into the bone can become inflamed. This condition is termed enthesitis. The word “enthesitis” is derived from ancient Greek and means insertion. Second, the tendon sheath can become inflamed and is called tenosynovitis.
It’s important to note that tenosynovitis and enthesitis manifest in two completely different diseases. Whereas tenosynovitis is characteristic of rheumatoid arthritis, enthesitis is a central feature of spondyloarthritis. Another condition is myositis, which is characterized by muscle inflammation. Myositis can be caused by, for example, autoimmune diseases or drugs such as statins. Inflammation of the bursa is termed bursitis, which is usually caused by repetitive strain placed on the bursa. Okay, let’s quickly summarize this information. Up until now, we’ve learned that many different structures inside or in the close vicinity of a joint can become inflamed. These inflammatory processes can be caused by bacteria, mechanical irritation, crystal deposits, or by autoimmune diseases. However, degenerative processes need to be clearly differentiated from inflammatory processes, which are collectively termed arthritides. These degenerative changes refer to the deterioration of cartilage and bone. It’s caused by overuse and is referred to as osteoarthritis.