As we get older, way too many of us begin to notice the snap, crackle, and pop of some of our most-used joints as we try to go about our day bending and twisting as we did in our youth. We might go throughout our day in extreme discomfort asking ourselves, “Whatever happened to my rubber band-like tendons?” The reality is that wear and tear, disease, and genetics have a lot to do with the pain involved in each step and bend throughout our day and it doesn’t seem to get any better as time goes by. So, as cartilage decays or gets inflamed, the question asked now is, “what kind of drug, supplement, or procedure is available to stop the pain?” Let’s attempt to answer these questions as we explore treatments for different types of arthritis.
What is Osteo Arthritis?
The word “arthritis” literally means arthron (joint) and -itis (inflammation) and is defined as painful inflammation and stiffness of the joints. Osteo arthritis is the most common form of arthritis and usually affects large and small “arthrons” of our bodies (knees, wrists, ankles, etc). The most common reason individuals acquire osteoarthritis is due to progressive wear and tear of a given joint, although a major trauma to the area can also cause an osteoarthritic state. Osteoarthritis starts in the connective tissue region of the joint and eventually begins to bridge the two opposing bones to graft or fuse into each other. This phenomenon causes for a very uncomfortable and often painful condition. Some of the most common causes of this type of arthritis are obesity, immobility, and prior joint trauma1, just to name a few.
What is Rheumatoid Arthritis?
Rheumatoid arthritis (or RA) is denoted as an autoimmune disorder in which the immune cells of our bodies attack our own tissues, in this case our connective tissues or joints. The result of this attack is inflamed joints followed by stiffness and pain. Although this disease can and will act upon other parts of the body involving larger joints, the typical areas of attack are the wrists and hands. These symptoms can develop either quickly or gradually over longer periods of time. The result of rheumatoid arthritis doesn’t only involve typical arthron, but can lead to inflammation of the lungs and heart as well as decreased erythrocyte count2-4. To date, approximately 1.3 million people in the United States suffer from RA5.
What are the Key Players?
To understand the pathophysiology involved in osteo and rheumatoid arthritis, it is important to know what molecules are involved. For example, during the initiation of osteoarthritis, the collagen meshwork within the joint becomes more and more disorganized and there is a net decrease in proteoglycan content within cartilage. Without the nice cushion-like barrier of the proteoglycan strands, the collagen fibers within the cartilage become susceptible to degradation. This, in turn, causes inflammation within the synovial space in the joint area because cells lining the joint attempt to remove the degraded pieces of cartilage and use inflammatory cytokines to do so.
In RA, it is a little more complex. It all begins with a trigger in a particular joint (or other tissue) where a complex cellular “activation” series of events takes place, followed by a swelling of the synovial membrane which attracts immune cells. The entire process takes place in three basic phases: the non-specific inflammation phase, the amplification within the synovium phase, and chronic inflammatory phase. In the non-specific phase, genetic and/or environmental factors (smoking, diet, etc.) can often set off this spark. The amplification phase is usually due to B lymphocytes mass producing little chemicals known as immunoglobulins (IgG and IgM in particular), which really get macrophages excited and intensifies the inflammation response. Finally, in the chronic inflammation phase, the synovial lining begins to form granulated tissue as a defense mechanism, and more immune cells flock to this neoplastic-like tissue, chewing it up as they arrive using hydrolytic enzymes, which in turn creates more inflammation. The key players in all of this are CD4 and CD8 T-cells, macrophages and dendritic cells, B cells, monocytes, and osteoclasts, and of course our favorite immune molecules TNF-a, and interleukins 1,6,15, and 17. A whole army of immune cells and their respective cytokines are now found coming to attack and destroy a targeted tissue.
How Do You Treat Arthritis?
Although there is no known cure for osteo or rheumatoid arthritis, there are many treatments. Joint replacement surgery, medication, diet and exercise, nutritional supplements, etc. are all viable options. Physical therapy in some cases has been shown to decrease pain and delay the need for surgery6. Prescription medications such as Methotrexate, Anakinra, and anti-TNF drugs have been shown to assist in reducing inflammation by cutting it off at the source7. Conversely, non-prescription (ie, OTC) medications such as acetaminophen and ibuprofen are very successful in reducing pain and inflammation by acting as antinociceptive and non-steroidal anti-inflammatory drugs8. Holistic medicine has also risen to the challenge with new discoveries of fascinating molecules found in plants and even animals. For example, Hyaluronic acid is used as a treatment for osteoarthritis, creating an analgesic effect as well as rebuilding and cushioning knee cartilage9. Methylsulfonylmethane (MSM) is an organic, sulfur-containing compound found in certain foods and is known to have some pretty amazing anti-inflammatory properties10. And then, of course, the ever so popular amino sugar, glucosamine. It is one of the most abundant monosaccharides in our bodies and actually does wonders for repairing and reducing the inflammation of some of our most-used joints11,12. So, whether one chooses holistic medicine, prescription drugs or physical therapy, arthritis can be treated.
The inevitable is that over time, whether genetically or environmentally influenced, connective tissue degradation does in fact occur. Some faster, some slower than others. Although there is no magic pill or therapeutic exercise that will give us back our teenage joints, science and technology have caught up with the times to offer us helpful suggestions on how to keep our most-used joints healthy and happy.
Author: Chad Brey, a California State University, Northridge alumnus, has since worked as a chemist for various analytical and research facilities such as Amgen, Baxter, and Nusil Technology. Since 1997 he has worked in the dietary supplement industry for companies such as Earthwise Nutrition (formerly known as Great Earth Vitamins) and has earned a number of certificates as an IACET-certified dietary supplement specialist. Chad has written dozens of technical articles on the specifics of how certain dietary supplements work. Chad has formulated and developed small and large molecules in research and development laboratories since 2003 and continues to consult others in R&D today.
1. Yuqing Zhang, D.Sc and Joanne M. Jordan, MD, MPH. Epidemiology of Osteoarthritis. Clin Geriatr Med. 2010 Aug; 26(3): 355–369.
2. Staroń A, Mąkosa G, Koter-Michalak M. Oxidative stress in erythrocytes from patients with rheumatoid arthritis. Rheumatol Int. 2012 Feb;32(2):331-4.
3. Zulma X. Yunt, MD and Joshua J. Solomon, MD. Lung Disease in Rheumatoid Arthritis. Rheum Dis Clin North Am. 2015 May; 41(2): 225–236.
4. Cynthia S Crowson, MS, Katherine P Liao, MD MPH, John M Davis, III, MD, Daniel H Solomon, MD MPH, Eric L Matteson, MD MPH, Keith L Knutson, PhD, Mark A Hlatky, MD, and Sherine E Gabriel, MD MSc. Rheumatoid Arthritis and Cardiovascular Disease. Am Heart J. 2013 Oct; 166(4): 622–628.e1.
5. Clough JD. The Cleveland Clinic Guide to Arthritis. New York, NY: Kaplan Publishing; 2009.
6. Fransen M, Crosbie J, Edmonds J. Physical therapy is effective for patients with osteoarthritis of the knee: a randomized controlled clinical trial (2001). J. Rheumatol. 28 (1): 156–64.
7. J. Michelle Kahlenberg, M.D., Ph.D.a and David A. Fox, M.D.b. Advances in the Medical Treatment of Rheumatoid Arthritis. Hand Clin. 2011 Feb; 27(1): 11–20.
8. Mart van Laar, Joseph V Pergolizzi, Jr, Hans-Ulrich Mellinghoff, Ignacio Morón Merchante, Srinivas Nalamachu, Joanne O'Brien, Serge Perrot, Robert B Raffa. Pain Treatment in Arthritis-Related Pain: Beyond NSAIDs. Open Rheumatol J. 2012; 6: 320– 330.
9. Puhl W; Scharf P (July 1997). Intraarticular hyaluronan treatment for osteoarthritis. Ann Rheum Dis 56 (7): 637–40.
10. Murav'ev IuV, Venikova MS, Pleskovskaia GN, et al. Effect of dimethyl sulfoxide and dimethyl sulfone on a destructive process in the joints of mice with spontaneous arthritis. Patol Fiziol Eksp Ter 1991; (2):37–9.
11. Largo R, et al. Glucosamine inhibits IL-1beta-induced NFkappaB activation in human osteoarthritic chondrocytes. Osteoarthritis Cartilage. 2003 Apr;11(4):290-8.
12. Bassleer C., et al. Stimulation of proteoglycan production by glucosamine sulfate in chondrocytes isolated from human osteoarthritic articular cartilage in vitro. Osteoarthritis Cartilage. 1998 Nov;6(6):427-34.
(Originally published on Health & Nature News with permission)