Nearly one third of the world's adult population suffers withthe pain of arthritis. While NSAIDs and COX-2 inhibitors offer thepromise of relief, these drugs also bring the risk of adverse effects,from stomach ulcers to heart attack. Recent studies have suggested thepotential of tapping into the body's supply of painkilling peptides asa safe, natural approach to arthritis pain management.
Extraneous substances such as morphine can be disadvantageous inarthritis pain therapy due to a large number of adverse side-effectsassociated with these compounds. In addition, the lack of selectivityof morphine means that precise targeting of u-opioid receptors tocontrol chronic pain has proven to be problematic. What's more, severalclinical and experimental studies of m-opioid therapy have shownambiguous results.
The recent discovery of a natural morphine-likecompound in joints called endomorphin 1 could circumvent thesetherapeutic drawbacks due to its greater selectivity for the u-opioidreceptor. Endomorphin 1 has the potential, therefore, to be a majorpainkilling agent in the body with less chance of risk.
Researchers at the University of Calgary set out to determine theeffectiveness of endomorphin 1, with a painkilling capacity equal to orgreater than morphine – on knee joint pain. Their subjects were malerats with induced arthritis, both acute and chronic. Their findings,featured in the October 2005 issue of Arthritis & Rheumatism(http://www.interscience.wiley.com/journal/arthritis), shed light onwhy u-opioid therapy may not work to control long-term arthritis pain.
Previousresearch into u-opioid therapy for arthritis has primarily focused onchanges occurring in the hours immediately following tissueinflammation. This study is the first to examine the impact on chronicinflammation. The rat models were randomly assigned to the differenttreatment groups: acute (48-hour) inflammation, chronic (1-week and3-week) inflammation, and normal controls. Under anesthesia,endomorphin 1 was injected into the arthritic knee joints of allaffected rats. Therapeutic effectiveness was assessed by measures ofjoint edema formation and sensory nerve activity associated with pain.
Inrats with acute arthritis, endomorphin 1 worked to significantly reducethe hypersensitivity of joint nerves by as much as 75 percent. In therats with chronic arthritis, however, endomorphin 1 had no observableeffect on the telltale triggers of pain. On the strength of thesefindings, researchers concluded that chronic inflammation negates thepain-relieving benefits of the body's u-opioid receptors.
"Theseobservations highlight a possible inadequacy of the endogenous opioidsystem to alleviate chronic arthritis pain," notes study author Dr.Jason McDougall. By offering clear insights into the disappointment ofu-opioid therapy, this study suggests the need for rethinking the bestuse of endomorphin 1 and redirecting pain management research towardmore promising alternatives for long-term arthritis sufferers.
Article:"Chronic Arthritis Down-Regulates Peripheral u-Opioid ReceptorExpression With Concomitant Loss of Endomorphin 1 Antinociception,"Zongming Li, David Proud, Chunfen Zhang, Shahina Wiehler, and Jason J.McDougall, Arthritis & Rheumatism, October 2005; 52:10; pp.3210-3219.
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