Inflammation is an important part of the arthritic process.
In Greek, “arthro-” means “combined as at a joint” and the suffix “itis” means “a disease process especially involving inflammation” so “arthritis” literally translates to "arthritis of a joint”.
There are several forms of arthritis. They all involve some level of inflammatory process. For the purposes of this article, we’ll be mainly referring to the two most common forms of arthritis: osteoarthritis (OA) and rheumatoid arthritis (RA).
When inflammation is not useful for the body
Inflammation is a very necessary process the body uses to heal itself. Without inflammation, cuts would never heal, bones would never knit together and viruses and other microbial foreign invaders would never be killed and expelled from our system.
Like most things though, inflammation can turn from a useful process into a dysfunctional disease process if not utilized by our bodies in appropriate moderation.
Inflammation in rheumatoid arthritis
In the case of RA, inflammation is used in a mistaken attempt to destroy cells that our immune systems, for some currently unknown reason, have identified as foreign invaders.
This is why RA is known as an autoimmune disorder. For whatever reason, our bodies target the linings of our joints and release cells called “inflammatory cytokines” that cause breakdown of bony portions of our joints and swelling of the synovial lining around the joints. Additionally, cells called “fibroblasts” start thickening the soft tissues in the area in an attempt to fix the damage that our own bodies are causing.
That’s why arthritic joints look swollen and feel stiff and painful.
Inflammation in osteoarthritis
Traditionally, OA has actually been classified as “non-inflammatory”, but the more that we learn about the process of the joint breakdown, the clearer it becomes that inflammation definitely plays a role.
The occurrence of synovitis in OA is actually similar to RA, but there are some fundamental differences, starting with the root cause of OA to begin with. OA is caused by an injury to or breakdown of the protective lining of the joint. In this regard, OA is a result of a biomechanical problem rather than an autoimmune problem.
There can definitely be a genetic component to all this, in that people that inherit hypermobile joints with lax ligamentous support and/or an overactive inflammatory system will be more prone to the development of OA. That being said, the whole process is started because the lining of the joint has undergone some sort of physical trauma or repetitive irritation.
At first, the joint will be mildly achy and perhaps a bit swollen as the ligaments are uncomfortably stretched and pressure increases on surfaces of the joint in ways they are not well-adapted to tolerate. At this point, the cells that make up the cartilage and synovial lining of the joint begin producing inflammatory cells. Because of the increased fluid and tissue swelling that accompany inflammation, this can have a bit of a “snowball” effect on the joint since decreased joint space and abnormal joint surfaces can increase the rate of tissue irritation and break-down.
Difference in treatment
For the above reasons, osteoarthritis is treated primarily with splinting, exercise and then, if needed, surgical intervention to change the biomechanical issues that lead to OA in the first place, while medication and diet changes are regarded as more of a secondary intervention to reduce pain and slow down the process that might be exacerbated by swelling and changes to the joint surfaces.
On the other hand, intervention for rheumatoid and other autoimmune-based arthritis usually is treated with medication and dietary changes to regulate the inflammatory response while splinting and surgeries are regarded as secondary albeit critical interventions to reduce pain, reduce joint deformation and improve function.
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