Arthritis Joint Pain Plays a New Role in Osteoarthritis
By JR Rogers, CEO of Synflex
March 03, 2013
We have some new things to consider when talking about osteoarthritis. We now know that the arthritis joint pain that we experience with arthritis is actually part of the cause of this debilitating disease. That’s right. Pain is part of reason that you get arthritis in your joints.
It is pretty well established that arthritis is caused by “wear and tear” in cartilage of the joints where we have the problems. Or, at times it can be secondary to a joint injury. Either way, joint cartilage begins to deteriorate so its role as a protective cushion between your bones is lost. The result is pain and eventually, limited mobility. But to add this new finding about pain is big news.
As simply as you put it, pain is the realization that you have discomfort somewhere in your body. But, before you realize that, the pain signals have to travel along nerve cell pathways from your bad joint to pain processing centers in the dorsal horns of your spinal cord. That process is called nociception. So, you have this “crosstalk” between your injured joint and your spine that enables the arthritis to transmit this inflammation into your spinal cord and brain. From there, it passes through your central nervous system from one joint to another.
Do you see the implications here? In effect, pain is increasing and actually causing arthritis by itself. That runs contrary to what we believed about what caused arthritis. That is, the cartilage begins to deteriorate so its role as a protective cushion between your bones is lost. And, the result is deformity and increasing pain problems. However, this clinical study has now shown us that pain is playing a major role in the development of arthritis.
The author of this study, Stephanos Kyrkanides, D.D.S., PhD., stated the equation this way.“Until relatively recently, osteoarthritis was believed to be due solely to wear and tear, and an inevitable part of aging.” He went on to say that these studies reveal that specific biochemical changes contribute to the disease. He added that, “Our study provides the first solid proof that some of these changes are related to pain processing, and suggests the mechanisms behind that effect.”
When that pain signal is processing back to the site of the arthritis, it actually increases the disease. The researchers found that when they disrupted that pain signal using a gene therapy, not only did the pain ease but the joints improved as well. Although this study was conducted using mice, the same principals would apply to humans.
What this means is that the progression of the arthritis was slowed by controlling the pain signals that moved between the sites of the arthritis by intercepting that pain signal. In brief, it means that pain itself plays a major role in the development and progression of arthritis. So by treating the arthritis joint pain you are affecting the disease itself.
Studies conducted prior to this one have found that nerve pathways become more sensitive as pain travels through them frequently. And further, that since the cells that surround sensory nerve cell pathways expand the affected cells to surrounding cells. So, they too are affected by this ‘crosstalk’ of pain signals. This causes the expansion of the field of inflammation. Under these findings, increased inflammation in the central nervous system is then able to send signals back down the nerve pathways to joints. This in turn would cause the release of inflammation there.
“Our study results confirm that joints can export inflammation along the sensory nerve pathways to the spinal cord, and that (this) in and of itself is sufficient to create osteoarthritis in peripheral joints, “Kyrkanides said. “We believe this to be a vitally important process contributing to orthopedic and neuorological diseases in which inflammation is a factor.”
In the past, clinical studies demonstrated that those nerve pathways where pain travels constantly became more sensitive to pain with use. Pain has always had a relationship to inflammation. And, that the same chemicals that cause inflammation also may increase the sensation of pain.
Dr. Kyrkanides, and his colleagues found that this communication of pain was exacerbating the pain issue. “This cross talk is oil to the fire of arthritis,” Kyrkanides tells WebMD. “Trying to stop joint inflammation with the traditional drugs we have is inadequate—because it tries to address the joint but fails to address this newly-discovered mechanism where it is progressing along the nerve from the spine.”
In this study, the researchers used a gene therapy to block this chemical messenger and the mice used in this study stopped demonstrating pain. And, according to the study their joints improved.
That would mean that traditional methods of treating osteoarthritis by limiting inflammation is less effective. That would be because the treatments fail to address this “communication of pain” that is occurring in your body.
In brief, Dr. Kyrkanides and his research team concluded that pain can no longer be considered simply a symptom of arthritis. Rather, their findings are clear that pain causes arthritis.
As it now stands, there is a gene therapy available for those suffering from Rheumatoid Arthritis. Certainly, medical science will soon develop a similar therapy for those suffering from Osteoarthritis.
*The principal study conducted by Dr. Kyrkanides was published by the University of Rochester School of Medicine and Dentistry and funded in part by grants from the National Institutes of Health. Dr. Dyrkanides was joined in this work by M. Kerry O’Banion, M.D., PhD., Ross Tallents, D.D.S., J. Edward Puzas, Ph.D. and Sabine M. Brouxhorn, M.D. Paolo Fiorentino was a student contributor and Jennie Miller was Involved as Dr. Kyrkanide’s technical assistant. Maria Piancino led a collaborative effort at the University of Torino, Italy.