Arthritis is the inflammation of a joint accompanied by pain and swelling. An estimated 97 million Americans suffer from severe arthritis Relieving swelling and inflammation is one of the oldest recorded uses of cannabis. Modern science is currently exploring a newly discovered network of cannabinoid receptor sites located throughout the body. The new understandings of cannabinoid research clearly support historical references on treating inflammation with marijuana.
While synthetic THC has been found beneficial as an analgesic, clinical studies indicate that several other cannabinoids have more effective anti-inflammatory properties. Non-psychoactive cannabis compounds such as CBD and CBG have greater anti-inflammatory properties than the legal THC pill. One prominent researcher reported that CBC a non-psychoactive cannabinoid found abundant in certain strains of African cannabis, and some non-cannabinoid constituents of cannabis, olivitol, and cannoflavin, all have marked anti-inflammatory properties. 
In 1997, Kenneth Hargreaves of the University of Texas reported on research he conducted while at the University of Minnesota. In his words, “These results suggest that local administration of the cannabinoid to the site of injury may be able to both prevent pain from occurring and reduce pain which has already occurred without producing side-effects.” The Institute of Medicine report of 1999 recommends further study of these cannabinoids: “Because different cannabinoids appear to have different effects, cannabinoid research should include, but not be restricted to, effects attributable to THC alone” In 2008, the IOM recommendations were confirmed by a biologist at the Institute of Pharaceutical Sciences in Zurich, Switzerland. “We were stunned to find a totally different compound within the same plant with anti-inflammatory properties,” said Jurg Gertsch. His Swiss team extracted a previously little-studied component of natural cannabis, beta-caryophyllene, and demonstrated how it acts on CB2 receptors found throughout the human body to reduce inflammation without affecting the brain or causing psychoactive effects.
In August 2000 researchers from the Kennedy Institute for Rheumatology reported that cannabidiol (CBD) suppressed progression of arthritis in animals. CBD "effectively blocked progression of arthritis". The experimental cannabinoid derivative, HU-320 has also been shown to protect joints from arthritis in animals. Japanese researchers summarized the available literature in 2005, "Cannabinoid therapy of Rheumatoid Arthritis could provide symptomatic relief of joint pain and swelling as well as suppressing joint destruction and disease progression".
Despite these promising recommendations, political and economic considerations rule the pharmaceutical marketplace. At the present time, marijuana remains the only available source of these naturally occurring anti-inflammatory compounds.
Related sections: Analgesia, Replacement of Medications.
 “Pot chemical can relieve serious pain.” Los Angeles Times, August 27, 1998
 Formukong, Evans, and Evans, “Analgesic and anti-inflammatory activity of constituents of cannabis sativa L.” Inflammation, Vol. 12, No. 4, p. 361-371, 1988
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 Symposium Syllabus: Functional Role of Cannabinoid Receptors. August, 26, 1998
 Institute of Medicine, Marijuana and Medicine: Assessing the Science Base. Washington DC: National Academy Press, 1999
 “Curative Leaf – Compound in marijuana reduces inflammation without the psychological effects” Amy Maxmen, Science News, June 23rd, 2008 www.sciencenews.com
 "The non-psychoactive cannabis constituants cannabidiol is an anti-arthritic therapeutic in murine", Mailfait, et al. Journal of the National Academy of Sciences 97: 9561-9566, 2000
 "A novel synthetic, non-psychoactive cannabinoid acid (HU-320) with anti-infammaitory properties in murine collagen-induced arthritis", Sumeriwalla et al. Arthritis and Reumatism 50: 985-998, 2004
 "Cannabinoids and the immune system: Potential for treatment of inflammatory diseases", Jounral of Neuroimmunology 166: 3-18, 2005