# Tapping into the Endocannabinoid System to Ameliorate Acute Inflammatory Flares and Associated Pain in Mouse Knee Joints > **Author:** Benjamin Caplan, MD (ABFM Board Certified, MA Lic. #240562, NPI: 1962722637) > **Publisher:** CED Clinic (https://cedclinic.com) > **Canonical URL:** https://cedclinic.com/faah-inhibition-arthritis-pain-endocannabinoid-relief/ > **Published:** 2022-08-30T19:41:33-04:00 | **Last Modified / Clinically Audited:** 2026-09-28T11:16:27-04:00 > **Clinical Summary:** Explore FAAH inhibition arthritis pain as a promising approach to reduce joint inflammation and discomfort via the endocannabinoid system. --- The cannabinoid system of the human body is composed of lipid molecules called endocannabinoids, [cannabinoid receptors](https://cedclinic.com/citral-cannabinoid-receptor-2-activation-pain-relief/) they bind to – namely CB1 and CB2, and enzymes – molecular machineries that synthesize and degrade the endocannabinoids. Endocannabinoids have been found to play important roles in many biological processes; for instance, the endocannabinoid anandamide, which can activate CB1 and CB2, has both anti-inflammatory and pain-relieving powers. Patients with arthritis often experience frequent but intermittent flares in which the joints become acutely inflamed or painful. The cannabinoid system is a promising target for treating arthritis because of the localization of CB1 and [CB2 receptors](https://cedclinic.com/cannabinoid-receptor-type-2-schizophrenia/) to the joints. For example, in a rat model of arthritis, activation of joint [CB1 receptors](https://cedclinic.com/cb1-receptor-modulation-mira-55-no-cns-side-effects/) was found to significantly decrease activity of pain receptors and administration of synthetic cannabinoids was found to regulate blood flow and inflammation. This potential to ameliorate joint pain and inflammation of the cannabinoid system, however, is limited since endocannabinoids are broken down rapidly. A major enzyme responsible for breaking down anandamide is fatty acid amide hydrolase (FAAH). Inhibition of FAAH, therefore, has emerged as a promising avenue of modulating pain and inflammation in arthritis patients. Experiments on murine models of this condition, in fact, supported this possibility. Specifically, administration of a potent and specific FAAH inhibitor decreased leukocytes rolling and adherent – a measure of inflammation, as well as inflammation-induced excess blood flow at the joint. It also reduced joint pain, as quantified through hindlimb weight bearing test and von Frey hair algesiometry. Additional experiments in mice further proved that the anti-inflammatory effect of FAAH inhibition was facilitated by both CB1 and [CB2 receptors](https://cedclinic.com/cannabinoid-receptor-type-2-schizophrenia/), while the pain-relieving effect by the CB1 receptor only. [More access here](https://cedclinic.com/) [https://cedclinic.com/contact/](https://cedclinic.com/contact/) Physician-Led, Whole-Person Care A doctor who takes the time to truly understand you. Personal care that starts with listening and is guided by experience and ingenuity. 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[Learn More](https://cedclinic.com/citral-cannabinoid-receptor-2-activation-pain-relief/) [Neurological and Neurodegenerative Conditions, Physical Activities, and the Endocannabinoid System – How Might All These Be Linked?](https://cedclinic.com/endocannabinoid-system-neurological-disorders-link/) An insightful article discussing the connections between the [endocannabinoid system](https://cedclinic.com/endocannabinoid-system-fear-extinction/), [neurological health](https://cedclinic.com/benzodiazepine-discontinuation-rates-medical-cannabis/), and physical activity. [Discover Insights](https://cedclinic.com/endocannabinoid-system-neurological-disorders-link/) Have thoughts on this? 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