24 Sep Could CBD Oil Be Used For Bone Disorders ?
The most prominent form of synovial joint disease, osteoarthritis (OA), is characterized by joint degeneration, pain, and in some patients, articular neuropathy. Chronic pain associated with OA is a major concern for which there are few viable treatments. The first line therapy used to treat OA pain is non-steroidal anti-inflammatory drugs (NSAIDs); however, withlong-term use their efficacy declines and they can lead to major adverse gastrointestinal and cardiovascular events. Historically, OA has been classified as a non-inflammatory arthritis; however, there is now overwhelming evidence that synovitis can occur in response to pro inflammatory mediators being released into the joint. It is believed that this low-level inflammation contributes to degenerative changes that affect the entire joint leading to the development of peripheral sensitization and nociceptive pain . In addition to structural defects, there is growing evidence to suggest that approximately 30% of OA patients suffer from neuropathic pain. Thus, a therapeutic which can block inflammation, neuropathy, and pain is sorely needed The endocannabinoid system (ECS) plays an important physiological role in the regulation of tissue inflammation and pain. A functional ECS has been demonstrated in the joints of animals and humans, which acts tonically to maintain joint homeostasis.
Immunohistological and pharmacological evidence confirm that cannabinoid 1 (CB1) and cannabinoid 2 (CB2) receptors are expressed on the neurones and microvasculature that supply rat knee joints. Additionally, CB2 receptors are co-localized with pronociceptive transient receptor potential vanilloid-1 (TRPV1) channels where, through common intra-cellular
pathways, they act together to modulate joint pain. This suggests that drugs which target the ECS have the potential to regulate painful arthritis and inflammatory joint disease. Cannabidiol (CBD) is the main non-euphoria producing component of the cannabis plant.
Pharmacologically, CBD has a complex signalling mechanism whereby it can both activate and silence classical cannabinoid receptors as well as modulate non-canonical cannabinoid receptor pathways. In in vitro studies, CBD has been shown to be an inverse agonist at CB2 receptors, and a full antagonist at CB1 receptors and G protein-coupled receptor-55
(GPR55). In vitro, CBD was found to be an agonist at TRPV1 and transient receptor potential ankyrin 1 (TRPA1), which play a central role in the development of OA. In musculoskeletal disease models, systemic administration of CBD suppressed the progression of collagen-induced arthritis by reducing inflammatory cytokine production. While these preliminary findings indicate a possible role for CBD in relieving joint inflammation, the local effect of articularly applied CBD on OA and joint pain has not been investigated.
The initial aim of the present study was to assess the effect of locally administered CBD on joint pain in animals with end-stage OA. Since acute inflammation can contribute to the long-term development of OA joint pain, the ability of CBD to reduce acute OA synovitis and prevent the subsequent progression of chronic persistent OA pain was also investigated. Finally, the effect of prophylactic CBD treatment on OA joint neuropathy was assessed by the authors.
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