Cytokines are some of the leading causes of joint inflammation. These proteins carry messages between cells & regulate immunity and inflammation. Two of the most important cytokines are tumour necrosis factor alpha ( TNF-a) and interleukin one beta (IL-1B). These are highly concentrated in the joints of people who have osteoarthritis.
Proteases, enzymes that cause the breakdown of proteins, also have been shown to create inflammation in the joint. Proteases are under the control of the cytokines. Some have anti-inflammatory qualities and some have pro-inflammatory (inflammation-creating) qualities. Obviously, in arthritis the pro inflammatory proteases are winning. Phagocytes (neutrophils) are attached to the inflamed joint in an attempt to clear this reaction and prevent damage to the cartilage and synovial living. But as explained in our earlier articles on auto-immune diseases, this inflammatory response is not always a good thing. Neutrophils can actually lead to more inflammation in the joint.
The ischemia-reperfusion phenomenon is a process that sounds difficult but is simple actually. As we use a weight bearing joint like knee or hip, the pressure created by our weight when we walk or especially when we run, blocks the blood flow to the cartilage. This is known as ischemia or lack of blood supply. When we take our weight off the joint, the pressure lessens and the blood is allowed to return to the cartilage (this is called reperfusion). This process, as well as the sources of inflammation causes excessive production of free radicals. In turn, the free radicals heavily tax the antioxidant defense system and cause oxidative stress.
When the antioxidant defense system is overwhelmed, oxidative stress within the joint cause damage to the cartilage and synovial lining of the joint. When the body cannot rebuild cartilage fast enough, the joint begins to deteriorate.