Cannabidiol Prevents Pain and Nerve Damage in a Rat Model of Osteoarthritis

by | Apr 29, 2021 | 2017, Alternative Therapies, Arthritis, CBD, Joint Health

Written by Angeline A. De Leon, Staff Writer. CBD significantly blocked transient osteoarthritis pain, while prophylactic CBD treatment significantly prevented the later development of pain and nerve damage in the OA joints of a rat model.

Although osteoarthritis (OA) has been traditionally classified as noninflammatory arthritis, research now shows that synovitis (inflammation of the joint lining) is present in a significant portion of patients with primary OA and may even be involved in the pathogenesis of the chronic disease 1. Low-level inflammation is now believed to play a role in the neuropathic pain experienced by OA patients 2. Drugs which target the endocannabinoid system (ECS), involved in regulation of inflammatory processes and pain, 3 have been shown to be helpful in modulating joint pain 4 and may have therapeutic potential for inflammatory joint disease. Through its interaction with the ECS, cannabidiol (CBD), a phytocannabinoid derived from the cannabis plant, shows the ability to influence the protein receptor pathways which play a role in the development of OA 5. Preliminary research, for example, indicates that CBD can attenuate collagen-induced arthritis by decreasing inflammatory cytokine production 6, essentially acting as an anti-arthritic therapeutic. Given the promising clinical effects of CBD in musculoskeletal disease models, a research study 7 published in Pain (2017) aimed to determine whether local administration of CBD in a rat model of OA would reduce OA synovitis, OA pain, and OA joint neuropathy.

A group of male Wistar rats (150-175 g) were administered an intra-articular injection of sodium monoiodoacetate (MIA, 3 mg) in the right knee joint, inducing OA. After the onset of OA (14 days post-MIA), a baseline measurement of joint afferent mechanosensitivity (response of joint to mechanical stimulation) was obtained using electrophysiological recordings. CBD (100-300 µg in 100 µL) or vehicle solution (100 µL) was administered and afferent firing measured for an additional 15 minutes (washout period of 50 minutes between administration of CBD doses and vehicle). On Day 14, pain behavior was also evaluated using the Von Frey hair test (measuring tactile sensitivity of skin) and hind limb incapacitance (measurement of hind limb weight bearing) at 30 to 240 minutes following administration of CBD (100-300 µg/50 µL) or vehicle (50 µL). One day following MIA (peak of inflammation in OA model), acute joint inflammation, knee joint blood flow, and leukocyte-endothelial interactions (involved in inflammation response) within the knee joint were measured at 5 to 180 minutes following topical application of CBD (300 µg/50 µL) or vehicle over the exposed knee joint.

On Days 14-19 following MIA induction, administration of CBD was found to reduce movement-evoked firing of knee afferent fibers in a dose-dependent manner (p < 0.0001), with the 300 µg dose decreasing firing by 22.8% +/- 1.2% overall (p < 0.0001). Although low doses of CBD showed no effect on pain behavior, the 300 µg dose significantly increased hind paw withdrawal threshold and hind limb weight bearing (p < 0.0001), relative to vehicle. On Day 1 post-MIA, topical administration of CBD, compared to vehicle, also significantly reduced leukocyte trafficking (p < 0.0001) and moderately lowered knee joint blood flow (p < 0.05) over the 3-hour time course, indicative of diminished transient joint inflammation. Finally, prophylactic treatment with 300 µg CBD (on Days 0-3 of MIA) was shown to significantly reduce development of tactile allodynia (touch-induced pain) over the next 14 days (p < 0.0001).

Overall, data from the study indicate that local administration of CBD can attenuate pain and peripheral sensation in an animal model of OA. Not only did cannabidiol reduce leukocyte trafficking and block acute inflammation, pre-treatment with CBD also appeared to effectively suppress severity of disease pain at later stages of OA development. Thus, researchers corroborate preliminary research proposing the beneficial role of CBD as an anti-inflammatory, anti-nociceptive agent in OA, providing novel evidence for the analgesic effects of CBD when administered locally around the joint. With a relatively low incidence rate of adverse side effects (10) as well, CBD presents as a promising therapeutic option for the treatment of OA. Findings remain to be replicated in human models of OA, and the efficacy of CBD deserves further testing at different stages of disease severity.

Source: Philpott HT, O’Brien M, McDougall JJ. Attenuation of early phase inflammation by cannabidiol prevents pain and nerve damage in rat osteoarthritis. Pain. 2017; 158: 2442-2451. DOI: 10.1097/j.pain.0000000000001052.

Copyright © 2017 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of the International Association for the Study of Pain. This is an open-access article distributed under the terms of the Creative Commons Attribution-Non Commercial- No Derivatives License 4. (CCBY-NC-ND), where it is permissible to download and share the work provided it is properly cited. http://dx.doi.org/10.1097/j.pain.0000000000001052

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Posted March 4, 2019.

Angeline A. De Leon, MA, graduated from the University of Illinois at Urbana-Champaign in 2010, completing a bachelor’s degree in psychology, with a concentration in neuroscience. She received her master’s degree from The Ohio State University in 2013, where she studied clinical neuroscience within an integrative health program. Her specialized area of research involves the complementary use of neuroimaging and neuropsychology-based methodologies to examine how lifestyle factors, such as physical activity and meditation, can influence brain plasticity and enhance overall connectivity.

References:

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