Pain may not be a symptom of arthritis; it may actually be the cause. If we were asked to give a definition of the word “pain,” we would more than likely say that it is the response, or reaction, to something physically, emotionally, or mentally unsettling. For instance, if we were to stub our toe on the corner of the sofa, we would say that the pain was the result of our toe coming into contact with an inanimate object. We would not say that the pain itself caused our toe to make contact with the sofa. According to a new study, when it comes to arthritis, our traditional approach to pain is not true. The study discloses this information based on the most common form of arthritis which is osteoarthritis.
Osteoarthritis presently affects more than 21 million people in the U.S. alone. Osteoarthritis has a stigma of being a disease for the old, probably because it deals with the wear and tear of the joints. The cartilage around the joint begins to deteriorate, resulting in pain and discomfort. The knees, hips, and fingers are among the most commonly affected joints on the body. Most individuals do not even realize that they have the disease until it has rapidly progressed. Stiffness and swelling of the joints are often noticed, followed by pain. The pain may ultimately be contributing to, and controlling, your condition.
A new study at the University of Rochester in New York, lead by Dr. Stephanos Kyrkanides, has given new insights into the cause of arthritis. Dr. Stephanos has a Ph.d in Orthodontics and Dentofacial Orthopedics. You may wonder how that relates to arthritis. He has studied one of the most common sites of arthritis, the jaw joint. He also has a Ph.d in Neurobiology and Anatomy that has launched his interest in pain research. The research indicates that pain is not a symptom of arthritis. Pain actually causes the condition to persist and progress. He found that pain sensors travel along the spine from the arthritic joints, along the nerve pathways, and back again to the joints. This is called “crosstalk,” where there is a potential to develop the disease at both ends. It is believed that this road of signaling can lead to the brain as well, thereby open to all of the central nervous system.
Researchers on this project studied engineered mice, and their reaction to an increase of a pro-inflammatory chemical called Interlekin 1-beta (1L-1B). An increase in this chemical, which produces pain and inflammation, allowed an increase of pain receptors to travel through the spinal cord. The pain that was increased sent out an alarm, resulting in a surge of 1L-1B chemicals. The researchers then utilized a gene therapy on the mice that blocked the signals. The message would not transmit and the chemicals were blocked. The pain was unable to go past its primary origin. The brain did not have to process the pain reactions, and the mice noticeably were relieved of the symptoms.
The study shows that if we can block the transmission of pain, then we may have (at the least) a treatment for osteoarthritis. This therapy may work with medications that are already readily available, those that can interfere with the inflammatory receptors. Kyrkanides states, “We believe this to be a vitally important process contributing to orthopedic and neurological diseases in which inflammation is a factor.” He believes that other conditions, such as Alzheimer’s disease, that are connected to the “crosstalk” theory, may be advanced scientifically by this new finding.