In the main lesson, we went over the general aspects of several common forms of arthritis. Here, we will dig deeper into the mechanisms of each disease, starting with osteoarthritis. Joint injuries, particularly a torn anterior cruciate ligament (ACL) increase your likelihood of developing osteoarthritis (OA). This is because the ACL is responsible for stabilizing knee movement. When this ligament is torn, the joint becomes unstable. This changes the distribution of pressure and friction on your cartilage during movement, which leads to cartilage breakdown. Numerous small injuries can also lead to OA over time by increasing inflammation in the knee joint. After inflammatory immune cells come into your knee joint, they increase the presence of certain enzymes that can further degrade cartilage. These factors lead to cartilage degeneration and can also contribute to pain. Another common feature of OA is the formation of bone spurs – which are bony outgrowths called osteophytes. Osteophytes develop through your body’s attempt to stabilize the knee joint or to strengthen weak bones. If you would like to read more on OA, here is a helpful review: “Osteoarthritis Pathogenesis: A Review of Molecular Mechanisms.”
The next most common form of arthritis is rheumatoid arthritis. RA also causes cartilage degradation and joint pain, but the cause of RA is very different from osteoarthritis. As discussed in the main lesson, RA is an autoimmune disease. This means that the body attacks itself with the help of auto-antibodies. In healthy individuals, antibodies help tag foreign objects, such as bacteria, for destruction by immune cells. In autoimmune diseases, auto-antibodies mistakenly target our own proteins. While the exact mechanism by which a person develops RA is unclear, most people have a genetic variant which makes their immune cells more likely to mistakenly recognize one’s own proteins, especially if those proteins are damaged. The auto-antibodies that are formed in this process lead the body to eat away at cartilage, thinking that it is a foreign object that must be removed. Doctors can usually diagnose if you have RA by the presence of these specific auto-antibodies in your blood. If you want to know more about the immunology involved in rheumatoid arthritis, please watch this video made by Nature. If you would like to read more on RA, here is a review article: “Rheumatoid arthritis: pathological mechanisms and modern pharmacologic therapies.”

Whereas rheumatoid arthritis is an auto-immune disease, spondyloarthritis is considered an auto-inflammatory disease. This means that there is immune dysfunction and inflammation, but no auto-antibodies are formed-that we know of. One of the main features of spondyloarthritis – or SpA-- is the formation of new bone -- similar to bone spurs that form in OA, but do not form in RA. People with SpA will also develop enthesitis, which is inflammation of the sites where tendons or ligaments insert into the bone – known as entheses. This inflammation can also occur in OA and RA but is less likely. You can take NSAIDs like acetaminophen or TNF-alpha blocking therapy to help ameliorate your SpA, but unfortunately, these treatments do not cure SpA. If you would like to read more on SpA, here is a review article: Spondyloarthritis: update on pathogenesis and management.”

Many forms of arthritis require pharmaceuticals to reduce the disease progression, however none of them have cures. As discussed in the main lesson, a more effective way to make sure you don’t suffer from one of these diseases is abstaining from smoking and maintaining a healthy weight- excess weight puts more stress on your joints. Regular moderate exercise is also good for your joints. There is evidence that cartilage can start thinning and osteoporosis can quicken with a sedentary lifestyle.

Most people with severe arthritis end up needing a total knee replacement after they have lost all their cartilage. However, researchers are working on therapies to delay the need for knee replacement. Since the 1990s, doctors have tried to promote our body’s natural healing process through a procedure called microfracture. This is where surgeons create small holes in the bone under the cartilage to allow bone marrow stem cells to leak out and create new cartilage. However, this new cartilage is not like the original cartilage, it is known as “fibrocartilage” and only lasts for 1 to 2 years. Using new techniques, scientists have developed a promising new method termed “MACI”- or matrix-induced autologous chondrocyte implant. This involves harvesting chondrocytes -- the cells from a small piece of your cartilage
- and growing these cells on a sheet of collagen before implanting into the area where cartilage has degraded. This procedure improves cartilage healing and reduces pain compared to microfracture. Here is a video of a seasoned ultramarathon runner who had MACI performed after damaging cartilage in her knee.

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