Arthritis is the number one cause of disability in the United States. 'Potent anti- arthritic effect': Science shows CBD could slow progression of arthritis and CBD seemed to slow the progression of damage to the joints. Recent medical research indicates that CBD could be a promising treatment for Arthritis. Other studies also show swelling, inflammation, and pain relief can come CBD Has “Potent” Anti-Inflammatory Effect; How CBD Treats Arthritis . help those who have early stage arthritis slow down its progression. These potentially anti-inflammatory properties of CBD, together with the lack of . of CBD Has an Equally Potent Therapeutic Effect on Established Arthritis. shown to effectively suppress progression of disease over a study period of 4 weeks (Fig. .. Nevertheless, we could not find suppression of TNF release by arthritic.
Shows Arthritis Of Could Cbd Science Progression ‘Potent Anti-arthritic Slow Effect’:
Arthritis is a condition characterized by joint pain. There are different types of arthritis, according to the Arthritis Foundation, but common symptoms among all the types include swelling, pain, stiffness and decreased range of motion.
The most common type of arthritis is osteoarthritis, or degenerative joint disease, which is the wearing down of the protective cartilage on the ends of bones. Other more common types of arthritis include juvenile arthritis, which develops in children; psoriatic arthritis, which affects people with psoriasis; infectious arthritis, which is an infection that spreads to a joint; and gout, which is caused by the buildup of uric acid. The pain, swelling and stiffness associated with arthritis can fluctuate in severity and varies between individual.
Severe arthritis can cause such intense chronic pain that the ability to maintain daily activities is affected. Arthritis treatment focuses on relieving pain and swelling with medications, physical therapy, and in some cases, surgery. Preclinical trials suggest that cannabis can help limit the damage of different types of arthritis.
In an animal trial, cannabidiol CBD , a major cannabinoid found in cannabis, effectively blocked the progression of arthritis.
Researchers found that CBD protected joints against severe damage and concluded that CBD offers a potent anti-arthritic effect 6. Other studies have found that cannabinoids offer strong anti-inflammatory and immunosuppressive properties and reduce joint damage in mice with osteoarthritis 8,9.
Most recently, cannabinoid treatments were found effective for reducing osteoarthritis-related cartilage breakdown 4. Research has also shown that cannabis can help manage the pain and inflammation associated with arthritis.
CBD, and another major cannabinoid found in cannabis — tetrahydrocannabinol THC — activate the two main cannabinoid receptors CB 1 and CB 2 of the endocannabinoid system within the body. These receptors regulate neurotransmitter release and central nervous system immune cells to reduce pain Activating the CB 1 receptor has been specifically found to reduce pain sensitivity in the osteoarthritic knee joints of rats 7.
One study found that cannabis-based medicine significantly improved pain during joint movement, pain while at rest, and quality of sleep in patients with rheumatoid arthritis 3. Currently, Arkansas , California , Illinois osteoarthritis, rheumatoid arthritis , and New Mexico have approved medical cannabis for the treatment of arthritis. However, in Washington D. In addition, various other states will consider allowing medical cannabis to be used for the treatment of arthritis with the recommendation from a physician.
Activating CB 2 receptors reduces osteoarthritic knee pain. CBD found to have anti-inflammatory and immunosuppressive effects, and therefore shown to be a potent anti-arthritic. The nonpsychoactive cannabis constituent cannabidiol is an oral anti-arthritic therapeutic in murine collagen-induced arthritis.
Your email address will not be published. Federal Tax ID Finally, using an LKB Huxley ultramicrotome with a diamond knife, the samples were sectioned into nm thick slices. The microscope was set at a voltage of One nerve cross-section image was visually partitioned into 9 quadrants and 3 images were captured from quadrants 1, 5, and 9.
All fibres were assessed using the G-ratio plugin in ImageJ processing software. The G-ratio was calculated using the equation where, a is the internal axonal area and A is the total axonal area of the fibre. The higher the G-ratio the higher the degree of demyelination. Cannabidiol 2-[ 1 R ,6 R methyl 1-methylethenyl cyclohexenyl]pentyl-1,3-benzenediol was obtained from Tocris Bioscience Bio-Techne, Abingdon, United Kingdom. AM CB 1 receptor antagonist; 1- 2,4-dichlorophenyl 4-iodophenyl methyl-Nmorpholinyl-1H-pyrazolecarboxamide and AM CB 2 receptor antagonist; 6-iodomethyl 2-morpholinylethyl indolyl]- 4-methoxyphenyl methanone were obtained from Cayman Chemicals Ann Arbor, MI.
Data were tested for Gaussian distribution by the Kolmogorov—Smirnov test. A P value less than 0. A total of 17 afferent fibres were recorded in this study. On days 14 to 19 post-MIA induction, close i. Example of a single-unit recording whereby CBD attenuated firing evoked by noxious rotation A. The dose-dependent effect of CBD treatment on afferent firing rate was averaged over the 15 minutes after administration C.
Effect of contralaterally administered CBD on ipsilateral pain behaviour. Contribution of cannabinoid and noncannabinoid receptors to the analgesic effects of CBD. One day after i. Contribution of cannabinoid and noncannabinoid receptors to the anti-inflammatory effects of CBD. Pain and disease progression are poorly managed in many patients with OA because of the multifactorial nature of the disease. Intra-articular injection of MIA produces monoarthritis with several features that resemble human OA, including joint pain, intermittent inflammation, and joint nerve damage.
This study aimed to address, for the first time, whether the inflammatory and neuropathic pain associated with MIA could be blocked by local administration of the noneuphoria producing phytocannabinoid CBD. It has previously been shown that the pain associated with the MIA model of OA is mediated in part by the sensitisation of joint afferent fibres. These electrophysiology data confirm that CBD has a peripheral site of action in knee joints.
These observations, along with our electrophysiology data, assert that CBD acts locally in the joint to reduce joint mechanical pain as revealed by improved weight bearing as well as a reduction in centrally mediated secondary allodynia as determined by hind paw withdrawal threshold.
Contralateral injection of CBD had no discernible effect on ipsilateral secondary allodynia confirming that the analgesic effect of intra-articular CBD was localised to the site of administration for this pain test.
This may be because electrophysiology is a highly sensitive technique that detects subtle response to test agents in the periphery, whereas pain behaviours are more complex and encompass the entire pain pathway. The rationale for using two pain behavioural tests in this study was to interrogate different aspects of the pain pathway. Dynamic incapacitance is a measure of spontaneous pain that is associated with joint degeneration or inflammation arising from peripheral sensitisation.
Thus, it seems that local injection of CBD is effective at reducing direct nociceptive and inflammatory pain in the joint as well as ameliorating neuropathic features of OA pain.
Both CB 1 and CB 2 receptor antagonists failed to block the CBD-mediated improvements in hind paw withdrawal threshold and weight bearing. Although CBD has been shown to act as an inverse agonist at CB 2 receptors and a full antagonist at CB 1 receptors, 40 it has also been shown to act through GPR55, serotonin receptors eg, 5-HT 1A , and various transient receptor potential ion channels.
Transient receptor potential vanilloid-1 is known to be involved in MIA-induced peripheral sensitisation, 17 therefore, antagonist experiments were performed to test the involvement of this ion channel in CBD-mediated analgesia. This mechanism of action has been previously reported in in vitro studies using human embryonic kidney HEK cells and using cell membranes from mouse and rat brains.
Cannabidiol has been shown to inhibit fatty acid amide hydrolase FAAH and the uptake of anandamide. Intra-articular injection of MIA produced an acute inflammatory response on day 1 after injection. This acute phase of inflammation was evinced by an increase in leukocyte trafficking and a moderate increase in joint blood flow. Local application of CBD significantly reduced these acute, inflammatory changes corroborating what has previously been reported in other inflammatory models.
Opening of TRPV1 ion channels causes the peripheral release of inflammatory neuropeptides which promote neurogenic inflammation and enhanced leukocyte trafficking in joints. A central hypothesis of this study was that early inhibition of OA-related inflammation with CBD would reduce the development of persistent joint pain.
Prophylactic treatment of OA joints with CBD on days 1 to 3 after MIA induction prevented secondary allodynia at day 14, but had no effect on hind limb weight bearing. Inflammation associated with MIA diminishes by day 7, 4 therefore the pain associated with end-stage OA in this model is largely due to joint degeneration and peripheral neuropathy.
Thus, by abolishing early inflammation with prophylactic treatment, CBD attenuates central sensitisation and neuropathic pain development in OA. The G-ratio data would benefit from future studies examining the expression of a biomarker for peripheral nerve damage to further support this finding.
Several cannabis compounds, including CBD, have been shown to be neuroprotective in other musculoskeletal disorders. In a preclinical model of multiple sclerosis, CBD was shown to improve clinical recovery and rotarod scores in animals, correlating with and indicative of a neuroprotective effect. Cannabidiol is a noneuphoria producing compound and has a more desirable side effect profile compared with other cannabinoid compounds and commonly prescribed analgesics. Animal studies where CBD was administered systemically showed that the animals had no signs of adverse side effects.
Successful relief of OA symptoms by peripherally administered CBD suggests a therapeutic option that has a low chance of adverse effects which is more desirable for patients. This study showed for the first time that local CBD administration inhibited pain and peripheral sensitisation in established OA.
By attenuating this initial inflammatory response with CBD, end-stage OA pain and peripheral neuropathy were abrogated. Thus, CBD may be a safe therapeutic to treat OA pain locally as well as block the acute inflammatory flares that drive disease progression and joint neuropathy.
All experimental protocols were approved by the Dalhousie University Committee on Laboratory Animals, which acts in accordance with the standards put forth by the Canadian Council for Animal Care. Availability of data and materials: Philpott conducted the pain behaviour experiments, the inflammation measurements IVM and LASCA , performed the G-ratio measurements, analysed data, and helped draft the manuscript.
O'Brien conducted all electrophysiology experiments, analysed the data, and helped draft the manuscript. McDougall conceived the study, participated in its design and coordination, helped analyse data, and helped draft the manuscript.
All authors read and approved the final manuscript. Sponsorships or competing interests that may be relevant to content are disclosed at the end of this article. National Center for Biotechnology Information , U. Published online Sep 1. Author information Article notes Copyright and License information Disclaimer.
Published by Wolters Kluwer Health, Inc. The work cannot be changed in any way or used commercially without permission from the journal. This article has been cited by other articles in PMC. Abstract Osteoarthritis OA is a multifactorial joint disease, which includes joint degeneration, intermittent inflammation, and peripheral neuropathy. Cannabinoids, Osteoarthritis, Pain, Neuropathy, Inflammation.
Introduction The most prominent form of synovial joint disease, osteoarthritis OA , is characterised by joint degeneration, pain, and in some patients, articular neuropathy.
Experimental timeline On day 14 post-MIA induction, 3 sets of noxious rotations, each lasting 5 seconds, were applied 5 minutes apart as a baseline measurement of afferent activity. Behavioural pain measurements 2. Von Frey hair mechanosensitivity Von Frey hair mechanosensitivity was used as a measure of secondary allodynia. Intravital microscopy Both hind limbs were immobilised and the capsule of the ipsilateral knee was exposed by surgically removing a small ellipse of the overlying skin and superficial fascia.
Experimental timeline Inflammation measures were conducted on day 1 post-MIA induction, which corresponds to the peak of inflammation in this OA model. G-ratio analysis of the saphenous nerve A segment of the saphenous nerve was isolated proximal to the ipsilateral knee joint and placed in 2.
Drugs and reagents Cannabidiol 2-[ 1 R ,6 R methyl 1-methylethenyl cyclohexenyl]pentyl-1,3-benzenediol was obtained from Tocris Bioscience Bio-Techne, Abingdon, United Kingdom. Effect of acute administration of cannabidiol on joint afferent mechanosensitivity A total of 17 afferent fibres were recorded in this study. Table 1 Characterisation of the recorded fibres in the electrophysiology experiments. Open in a separate window. Effect of acute administration of cannabidiol on sodium monoiodoacetate—induced inflammation One day after i.
Discussion Pain and disease progression are poorly managed in many patients with OA because of the multifactorial nature of the disease. Conclusions This study showed for the first time that local CBD administration inhibited pain and peripheral sensitisation in established OA.
Conflict of interest statement The authors have no conflicts of interest to declare. This work was supported by an operating grant provided by The Arthritis Society. Acknowledgements The technical assistance of Allison Reid is gratefully acknowledged. Footnotes Sponsorships or competing interests that may be relevant to content are disclosed at the end of this article.
Use of the painDETECT tool in rheumatoid arthritis suggests neuropathic and sensitization components in pain reporting. J Pain Res ; 7: Leukocyte trafficking and pain behavioral responses to a hydrogen sulfide donor in acute monoarthritis.
Molecular targets for cannabidiol and its synthetic analogues: Br J Pharmacol ; Weight bearing as a measure of disease progression and efficacy of anti-inflammatory compounds in a model of monosodium iodoacetate-induced osteoarthritis. Osteoarthr Cartil ; Quantitative assessment of tactile allodynia in the rat paw. J Neurosci Methods ; Antihyperalgesic effect of a cannabis sativa extract in a rat model of neuropathic pain: Phytother Res ; Vanniloid TRPV1 receptor mediates the antihyperalgesic effect of the nonpsychoactive cannabinoid, cannabidiol, in a rat model of acute inflammation.
Oral anti-inflammatory activity of cannabidiol, a non-psychoactive constituent of cannabis, in acute carrageenan-induced inflammation in the rat paw. Naunyn Schmiedebergs Arch Pharmacol ; Effects of cannabinoids and cannabinoid-enriched Cannabis extracts on TRP channels and endocannabinoid metabolic enzymes.
Neuropeptides in the synovium of patients with rheumatoid arthritis and osteoarthritis. J Rheumatol ; Assessment of synovitis with contrast-enhanced MRI using a whole-joint semiquantitative scoring system in people with, or at high risk of, knee osteoarthritis: Ann Rheum Dis ; Transdermal cannabidiol reduces inflammation and pain-related behaviours in a rat model of arthritis.
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The first-line therapy used to treat OA pain is nonsteroidal anti-inflammatory Thus, a therapeutic which can block inflammation, neuropathy, and pain is of CBD suppressed the progression of collagen-induced arthritis by reducing Finally, the effect of prophylactic CBD treatment on OA joint neuropathy was assessed. 3 days ago So what can cannabis for arthritis really do for those afflicted by a disease Simply put, arthritis is caused by the inflammation and, well, marijuana has been shown to help. Of the many cannabinoids present in cannabis, THC and CBD are CB1 and CB2 which control anti-inflammatory effects in the body. Research shows that certain compounds can be beneficial for health, without CBD oil contains one of those powerful components. form was a more effective anti-inflammatory than pure CBD, at least in mice (2). It has even shown anti- tumor effects and could be effective in inhibiting the progression of.