There are no perfect arthritis drugs, but ongoing studies that delve deeper and deeper into the source of chronic pain provide hope that someday there might be.

Since pain is directly related to your nervous system, understanding how that system works can help you understand how medical researchers approach pain, and develop treatments to control it. One brain chemical known as "Substance P" is providing insight into pain—and how to treat it.

What Is Substance P?
Neurotransmitters are brain chemicals that carry signals between nerve cells, and connect your nervous system to your organs and muscles. A neurotransmitter known only as "Substance P" (SP) appears to hold the key to unlocking the mysteries of severe arthritis pain. When an injury occurs in a joint, SP is released into the synovial fluid that lubricates the joint. This release alerts sensory receptors, or nerve endings, in the joints to signal pain.

How Substance P Works
Research into Substance P began several decades ago, when a study in Science found that the fluids surrounding the joints of laboratory rats with severe arthritis contained higher levels of SP than joints with less damage. Shortly thereafter, researchers discovered that releasing SP into joint tissue causes swelling and inflammation. A few years later, Italian investigators discovered that people with arthritis have significantly higher levels of SP in the blood than people without arthritis. These early studies helped scientists understand the role of the nervous system in the development of rheumatoid arthritis.

SP in Arthritis Treatments Today
Understanding the role of SP in the body has helped researchers develop better arthritis treatments and may help them produce more in the future. For now, researchers know, for instance, that capsaicin cream, when applied to the skin around a joint, ultimately depletes that area of SP and temporarily alleviates pain. The reason it works is that capsaicin, which is made from cayenne peppers, causes burning pain and tricks the nervous system into responding to an injury that hasn't actually occurred. Nerve cells promptly release SP into the area that burns. With repeated application of the cream, the body builds up a sort of tolerance, and the body stops releasing SP. When the joint area becomes depleted of SP, you no longer feel pain.

SP and Rheumatoid Arthritis
A 2011 study Modern Rheumatology found that injection of the autoimmune drug etanercept significantly reduced levels of SP and reduced disease activity in 11 patients with rheumatoid arthritis. While etanercept is currently used to treat rheumatoid and other types of inflammatory arthritis, potentially harmful side effects require doctors to carefully monitor its use. Blocking Substance P may be the key to relieving pain and slowing down the progression of disease, but scientists have yet to come up with a truly effective medication that can accomplish this without the risk of side effects.

 

Sources:

Anichini M, et al. "Substance P in the Serum of Patients with Rheumatoid Arthritis." Revue du rheumatisme (English ed.) 1997; 64(1): 18-21. Web 23. May 2012. http://www.ncbi.nlm.nih.gov/pubmed/9051855

Levine JD, et al; "Intraneuronal Substance P Contributes to the Severity of Experimental Arthritis." Science 2 Nov. 1984; 226(4674):547-549. Web. 23 May 2012. http://www.sciencemag.org/content/226/4674/547

Lots M, et al. "Substance P Activation of Rheumatoid Synoviocytes: Neural Pathway in Pathogenesis of Arthritis." Science 1987; 235 (4791) 20:893-895 Web. 23 May 2012.

Marshall KW, et al; "Substance P and Arthritis: Analysis of Plasma and Synovial Fluid Levels." Arthritis and Rheumatism 1990; 33(1):87-90. Web. 23 May 2012

http://www.ncbi.nlm.nih.gov/pubmed/1689161

New York University Langone Medical Center: Cayenne. August 2011. Web. 23 May 2012. http://www.med.nyu.edu/content?ChunkIID=21645

Origuchi T, et al. "Reduction in Serum Levels of Substance p in Patients with Rheumatoid Arthritis by Etanercept, a Tumor Necrosis Factor Inhibitor. 2011; 21(3):244-50. Web. 23 May 2012. http://www.ncbi.nlm.nih.gov/pubmed/21188454