Osteoarthritis (OA) is the most common degenerative joint disease, which leads to pain during joint loading and to chronic physical disability. The management of OA is often frustrating for both patients and physicians as adequate pain relief is difficult to achieve and no treatment modality seems to reverse the disease progression. Clearly, OA is a large, unmet medical need, there is a strong need to develop new treatments for OA. Considerable evidence has uncovered new mechanisms underlying the generation and transduction of pain, many of which represent new targets for pharmacological intervention. The endogenous agonist of cannabinoid receptor 1 (CB1), anandamide (AEA), also stimulates transient receptor potential vanilloid channel-1 (TRPV1) channels, which instead plays a key role in the induction of inflammation and the development of pain associated with OA. AEA degradation by fatty acid amides hydrolase (FAAH) limits its activity. Inhibiting FAAH, and TRPV1 with the same molecule might produce more efficacious anti-hyperalgesic actions than the targeting of FAAH or TRPV1 alone. An update of the relationship CB1 and TRPV1 channels and their possible implications for OA pain will also be provided. Bases for the possible future development of new therapeutic approaches that might be used for the treatment of pain will be suggested.
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