Rheumatoid Arthritis

Osteoarthritis is a degenerative joint disease that comes about because of the wear and tear of the cartilage in between joints.

For a long period of time, medics termed this disease as a non-inflammatory one. Pain is a common characteristic among all types of arthritis but the swelling and soreness is always directed to other forms of arthritis like rheumatoid arthritis.

With continued severity of osteoarthritis, the area around the joint becomes inflamed. This was attributed to a notion that cartilage would break down and irritate the synovium causing inflammation.

However, later discoveries have detected inflammation of the joint in the very early stages of OA through MRI images with the whole joint structure appearing intact. This brings the conclusion that inflammation in OA is evident.

Professors fro Cardiff and Leeds Universities deduced this through a study of varied tendons and ligaments around the joint.

Synovitis in OA

When the other types of arthritis notably rheumatoid arthritis and reactive arthritis were studied, they indicated a large proportion of the presence of leukocytes in the synovial fluid as compared to those in Osteoarthritis.

A similar study indicated the inflammation of synovial membrane also known as ‘post traumatic synovitis’ which is today a characteristic in many osteoarthritis patients.

This is however not a conclusion that the pathogenesis of osteoarthritis is tied to the synovium but rather synovitis is a disorder that propagates as a secondary outcome from cartilage damage induced by innate immune activation.

Of all joint diseases, osteoarthritis is the most common with 27 million patients in the United States. Another study from the Stanford University School of Medicine has indicated that osteoarthritis progression is enhanced by some low-grade type of inflammation processes.

The senior author of the study, Dr. William Robinson states in an objection of the view that it is not how people view it. Like the gradual wear and tear of tires in a car.

It is rather more defined by blow-outs like meniscus tear and other trauma causing damages to the joint.

The same study has shown that when a joint suffers osteoarthritis, it has the capacity to hold numerous migratory inflammation cells and some of the secretions from these cells.

The number of these inflammatory cells is quite lower compared to these present in rheumatoid arthritis joint which its characteristics brand it an autoimmune disease.

Those in osteoarthritis are numerous enough to keep us questioning the role inflammation plays in the progression of osteoarthritis.

The Compliment System

On the onset of damage to osteoarthritis joint triggers a progressions of molecular changes that in turn sets in to motion the compliment system.

It is this system that defends the body against bacterial, viral or any foreign material attack. The compliment system works by initiating a series of reactions referred to as complement cascade.

The complement cascade in osteoarthritis begins on its early stages. The building blocks of the complement system are blood proteins.

A viral or bacterial attack to the body triggers the action of these proteins. They act by engaging in a complex activity where some enhance while others inhibit the activity of the other.

The climax of these complex activities is the activation of MAC (Membrane Attack Complex). MAC is another cluster of proteins in the body’s defense system which acts on foreign bodies invading the body by inflicting holes in their membranes.

The viruses and bacteria end up dying and that is how the MAC helps to get rid of infections.

Role of MAC in Osteoarthritis

When joint fluid from an osteoarthritis patient was compared with that of a healthy person that of OA patient showed the presence of a high level of proteins as compared to that of a healthy person.

An OA joint tissue harbors a large amount of proteins that serve as enhancers to the complement cascade and there are also proteins acting as inhibitors of the process on the side.

On the same healthy versus OA patients, genes (components of protein) in the joint lining tissue were more active in OA patients.

A series of studies indicated that the MAC, which is a great weapon in the defense system of the body, was causing damage on joint tissue cells. It was not acting on the joint tissue cells like it does on bacteria and virus by punching holes.

This time it does it a bit differently by binding up the cells that produce cartilage in the joint tissue.

This in turn makes these cells to emit secretions inform of inflammatory chemical and enzymes which are active enough to eat up the cartilage in between the cells. This indicates how the complement system has the ability to maintain a continual inflammation and damage of the joint cartilage.

Can the Activation of the Complement System be treated?

The complement system through this study was found to be an inflicting real damage to the joint tissue. If the compliment system activation fails specifically on the OA infected joint, chances are that the progression of the disease will be minimal.

Research has ruled that a form of low-grade complement activation results to the progression of degenerative diseases like Alzheimer’s and OA may be another to add on the list as the authors of this study suggested.

There are drugs that act to inhibit the complement system. For people who suffer joint injuries may find a remedy to stop the onset of OA in future.

It may be too risky though to inhibit the complement system because it is the sole guard against infections. When the guard is killed then bacteria and viruses will find an open door to steal your whole health.

May be administering them for a short period of time to patients on their early developmental stages of OA can be of help.

As per mow, medics have not come up with one possible cure to OA. It is evident that inflammation plays a role in the development of the disease and hopefully the breakthrough in finding out this will lead to more advanced treatments.

REFERENCES:

  • Role of inflammation in the pathogenesis of osteoarthritis: latest findings and interpretations http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3638313/
  • Osteoarthritis results from inflammatory process, not just wear and tear, study suggests http://med.stanford.edu/news/all-news/2011/11/osteoarthritis-results-from-inflammatory-process-not-just-wear-and-tear-study-suggests.html