Osteoarthritis Is Inflammatory

OA is considered a non-communicable chronic disease; that is, you can’t ‘catch’ OA. OA is basically a disease of damaged cartilage.

Articular (joint) cartilage is made of a very specialized connective tissue. It is comprised of collagen, chondrocytes, an extracellular matrix, smaller proteins like aggrecan, proteoglycan, cartilage oligomatrix protein, glycoproteins, water and fibronectin. There are also biologically active enzymes and cytokines present. Some enzymes function to degrade cartilage, some function in matrix turnover, some will stimulate the chondrocytes to make more cartilage and others manage the inflammatory environment of the joint itself. OA is a disease of the entire joint; it affects the bone, synovium, ligaments, fascia and the cartilage.

enes associated with tissue metabolism are active for cartilage. Changes in the genes will trigger changes that lead to disorders in the cellular functional pathways. For example, the initiation and progression of OA can cause changes in the nf-kB pathway. This pathway is one of the primary drivers of chronic and low-grade inflammation. Different abnormalities that occur in regulatory proteins and genes lead to cartilage calcification and degradation.

Cartilage disease, like OA, is accompanied by synovitis. Synovitis is the inflammation of the lining of the joint capsule. Each joint has a capsule around it that contains the joint and the joint fluids. The synovial lining releases cytokines and matrix-degenerating enzymes into the joint and this leads to cartilage damage and the synovial cells continue to proliferate and produce even more damaging proteins. This, of course, results in progressive degeneration of the joint and joint tissues. The environment of increased levels of matrix metalloproteinases is responsible for the high level of proinflammatory cytokines that go on to damage the joint.

Today, many drug companies are looking for MMP-blocking agents to stop the cycle of inflammation. Another direction that drug companies are heading is toward blocking the smaller cytokines (IL-1, IL-6) that induce the MMPs to damage the cartilage.

Adipose tissue hormones and synovial products cause intense inflammation and are key to the development of OA. There is a correlation between the presence of inflammatory mediators and the development and progression of OA. It is well-known now that inflammation in the joint tissues is key for the start and progression of arthritis; the levels of inflammation also directly correlate to the levels of pain and dysfunction.

There are inflammatory markers that can be checked in serum to assess the activity level of the disease process. The overall balance of good and bad cartilage is disturbed in the pro-inflammatory environment of arthritis. There are higher levels of IL-1beta, IL-6, TNF-alpha that have been released by the damaged cartilage cells. These in turn induce more damage to cartilage cells. Worse, the inflammatory environment stops the chondrocytes from producing new matrix and cells as they should.

Joint trauma is often considered the cause of osteoarthritis and joint degeneration. After trauma, generally a surgeon will stabilize the joint. However, studies have shown that the re-stabilization of the joint does not reduce the risk of degeneration. This means that the problem is not the trauma, or even the change in shape or character of the joint.

Human studies have found that inflammatory mediators are very high just after an injury, but they also remain high later as compared to control groups. It has also been discovered that there is a protective role for the hemarthrosis (blood-joint) that forms after injury; this substance produces IL-10 and IL-4, both of which are protective of the joint and are there to counteract the effects of the increased levels of inflammatory proteins. More IL-10 is also found in joint fluids after exercise; it is known that exercise is also protective of joint tissues.

It is thought that in some people, the pro-inflammatory response that occurs just after injury is not controlled late. This is why some go on to form OA but not all do so. The ability to control and manage the inflammatory state of the joint has nothing to do with the trauma of course.

The strongest systemic influence on OA appears to be obesity. Obesity affects both weight-bearing and non-weight-bearing joints, therefore the problem can’t simply be load. Likewise, people of the same height but with more muscle than fat tend to have less arthritis than the counterparts.

The problem with obesity is that adipose tissue produces and promotes inflammation. Inflammatory substances found in the serum of the obese include certain free fatty acids, cytokines, adipokines and reactive oxygen species are very prevalent with obesity. For example, leptin and adiponectin have catabolic and inflammatory influence on cartilage. Likewise, weight loss is known to reduce circulating levels of IL-6 and TNF-alpha. This is true with or without any sort of joint trauma.

Weight loss protects cartilage. The beneficial effects of exercise seen on joints in overfed mice was found to be due to a reduction in inflammatory mediators, not the actual loss of poundage.

Inflammation happens without trauma most of the time. Beside the inflammation caused by the systemic condition of obesity, there are other mechanisms of inflammation and OA.

The body will produce what are known as ‘danger signals’ in the setting of damaged tissues, abnormal proteins or DNA, or infection. For example, the receptor for advanced glycation end products (RAGE) will pick up on the danger signals made by the advanced glycation end products (AGEs). AGEs are damaging proteins caused by oxidative stress, inflammation and hyperglycemia. Likewise, they are consumed in most Americans’ diets on a daily basis. The AGEs actively damage collagen and induce the inflammation associated with OA.

This happens just by living and is not due to any sort of wear-and-tear or traumatic incident. Rather, the danger signals are simply from the levels of chronic inflammation and reactive oxygen species that are prevalent in most modern humans right now.

Simply eating a more anti-inflammatory diet can have a large effect on the pain and symptoms of arthritis. A diet does nothing to change and so-called wear-and-tear, nor will a diet reverse any trauma or injury that may have occurred.

This leads one to wonder, how can what I eat modify the pain my joint feels? The answer is that the diet reduces the overall burden of the inflammatory proteins and the reactive oxygen species that are responsible for the pain of arthritis.

Foods found in the Mediterranean diet are high in omega-3 fatty acids, beta carotene, magnesium, fiber and olive oil (omega-9 fatty acids); all of these actively reduce the levels of inflammatory proteins in the body.

Just two weeks after switching to a plant-based diet, a group of people with painful arthritis had less pain (Arthritis. 2015). A research group followed 4000 patients for a different study and found that the ones that followed the Mediterranean diet were less likely to develop joint problems (Am S Nut. 2016). This means that arthritis must be caused by far more than simple wear-and-tear of life; it is clear that inflammation is the cause and most likely will be the cure.