What Causes Rheumatoid Arthritis Damage?

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The sabre rattling of Rheumatoid Arthritis damage

Do you ever look down at the invisible stabbing pain and wonder what’s going on inside your joints? Do you wonder whether damage is occurring when you feel your joints sticking or twisting or popping? Or red or puffy?

What exactly causes Rheumatoid Arthritis damage? Over the years, some have supposed it is correlated with the Rheumatoid factor or the anti-CCP. Many rheumatology doctors were taught to rely strictly upon ESR / sed rate or CRP for measure of invisible disease activity. Most textbooks say that synovitis (swollen, thickened synovium) is responsible for bone erosions while others more specifically blame immune cells called cytokines which are produced there.

I don’t think anyone knows yet exactly how various types of damage happen or how to predict or prevent Rheumatoid Arthritis damage in spite of what some lovely hospital sites say. There is evidence of it occurring before there is much pain or indication of disease activity. There are even examples of high blood test markers and modest damage. There are trends, but little substantiation.

How many times have we heard a rheumatology doc say “disease activity is low” based on a blood test? That’s often the point when people look for answers online and write to me saying, “Now what do I do?” Are all of our joint symptoms just sabre rattling if a blood test says so?

Clues to Rheumatoid Arthritis damage?

You know the old saying about how you can tell some people are lying? Their lips are moving. Well, it’s true of RA, too. There’s one definite way to know that Rheumatoid Arthritis damage can occur: by having it. If you have RA, then it is probably damaging you. Think of RA as a liar whose lips are moving even when it whispers.

  • This month at EULAR, a study was presented which demonstrates that CRP is not as important as actual clinical measures (Ann Rheum Dis 2010; 69). In this study, clinical measure was swelling. Swelling, of course is subjective; my current rheumatology doctor can detect swelling that another one could not. Of course, that previous doctor examined me from the other side of the room. Obviously, this clinical method of detecting disease activity requires expertise some rheumatology docs don’t have.
  • It is believed that inflamed synovium (that thickening that a good rheum doc can feel) produces more immune cells that destroy bone and cartilage tissue. However, surrounding muscles, tendons, and ligaments can be suddenly weak and allow for unnatural loosening of a joint. I have not found a good explanation of what causes this weakness. (See NIH explanation of what happens in Rheumatoid Arthritis.)
  • Inflammation is not everything. There is proof that muscle loss continues even after inflammation markers improve (2009, Arthritis Research and Therapy). “Rheumatoid cachexia may be an important risk factor for cardiovascular disease and excess mortality in RA.”
  • A 2006 study found that certain “biomarkers of cartilage collagen and proteoglycan turnover” are related to RA damage. Other collagen biomarkers are not. “Specifically, C2C (the marker for collagen type II damage) could predict subsequent short-term as well as long-term radiographic damage in RA, and more specifically joint space width narrowing” (Arthritis Research and Therapy).
  • Last year, some researchers found that “MRI bone edema, representing osteitis, has been further implicated as a forerunner to bone erosion” (Arthritis Research and Therapy). So bone inflammation precedes erosion. Is that why my joints look bigger? Hope not.

There are definitely some pieces to this puzzle missing. I guess the more we know about how they fit together, the better our chances of stopping Rheumatoid Arthritis damage. We need to study the picture on the box lid some more: the RA patient.

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Kelly Young. All rights reserved.

This entry was posted on Wednesday, June 30th, 2010 at 7:09 am and is filed under RA Research, Resources, and Rheumatology. You can follow any responses to this entry through the RSS 2.0 feed. You can leave a response, or trackback from your own site.


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