The Disease

OA is a degenerative joint disease, characterized by damage to the cartilages in joints, inflammation of the joints, thickening of the bone around the joint, and bone spurs.  These changes result in chronic pain, joint instability, stiffness, and joint space narrowing.  The cartilage between the bones absorbs and dissipates the load of our weight in our lower extremities or the shear force in our joints of our upper extremities when they are abused by repetitive grasping and pushing.  The cartilage in the joints gradually thins and ultimately results in bone sliding against bone.  OA is the most common form of arthritis, a leading cause of impaired mobility among the elderly and the most common cause for total hip and knee replacements.  Aging, joint trauma, obesity, and genetic predisposition are some of the risk factors for developing OA.

Research

With repetitive shear and loading forces to the cartilage, the normally quiet chondrocytes become “active” and start multiplying and producing more matrix.1  This increase in activity is associated with an increase need for energy which is supplied by the mitochondria inside the cell as they use food and oxygen to produce the energy needed.  With age, the mitochondria in the chondrocytes begin to dysfunction causing them to not utilize oxygen fully which results in the accumulation of Reactive Oxygen Species (ROS) inside the cell, called oxidative stress.2,3  This oxidative stress causes the cell to start producing MMPs (see above) which destroy the collage matrix.4  In addition, the chondrocytes start releasing inflammatory mediators which cause inflammation in and around the joint which, in turn, aggravates the chondrocytes more, resulting in a vicious cycle of progressive destruction of the joint.1  When the homeostasis of production and destruction of collagen is upset and destruction exceeds production, this marks the progression from reversible to  irreversible cartilage degradation and, ultimately, total destruction.3,4,5,6  Just when the process becomes irreversible is yet to be determined.  However, when compounds that reverse oxidative stress are added to damaged chondrocytes, the levels of MMPs decrease dramatically.4

Because CBD has well known anti-inflammatory activity, reduces oxidative stress, and has potential pain-relieving capabilities, it is well positioned to be possibly very effective in the treatment of OA.  In a veterinary clinic, dogs with OA treated with oral CBD at a dose of 2mg/kg twice daily showed a significant decrease in pain and a significant increase in activity.7  The only change in blood chemistry was a slight increase in the amount of alkaline phosphatase, which may have been due to remodeling of the bone in the affected joint secondary to improvement of the joint.  Other studies have shown that transdermal CBD (CBD lotion placed on the joint) significantly reduced swelling, spontaneous pain, immune cell infiltration, joint redness, and synovial thickening.8,9  In the one study, animals in endstage OA (thought to have irreversible damage) had significant improvement in their ability to support weight bearing that was dose dependent.9 

Bottom Line

Research has shown that CBD has the capabilities to alleviate the pain, inflammation, and swelling in OA.  In addition, it has the potential to reverse the cycle of cartilage destruction and joint degradation.  Multiple anecdotal reports are available on the internet, some with pictures, that suggest that CBD may be extremely helpful in the treatment of OA.  However, further studies are needed to determine the potential CBD may have.  At this time, the FDA has not approved CBD for the treatment of OA.

 

References:
  1. Houard X, etal. Homeostatic mechanisms in articular cartilage and role of inflammation in osteroarthritis.  Curr Rheumatol Rep 2013;15(11):375
  2. Bolduc JA, etal. Reactive Oxygen Species, Aging and Articular Cartilage Homeostasis. Free Radic Biol Med. 2018; Aug 31. pii: S0891-5849(18)31500-4.
  3. Portal-Nunez S, etal. Oxidative stress, autophagy, epigenetic changes and regulation by miRNAs as potential therapeutic targets in osteoarthritis.  Biochem Pharmacol. 2016;108:1-10.
  4. Reed KN, etal. The role of mitochondrial reactive oxygen species in cartilage matrix destruction.  Mol Cell Biochem. 2014;397(1-2): 195-201.
  5. Collins, Y, etal. Mitochondrial redox signaling at a glance. J Cell Sci 2012;125:801-6.
  6. Minocherhomju S, etal. Mitochondrial regulation of epigenetics and its role in human diseases.  Epigenetics 2012;7(4):326-34.
  7. Gambel L, etal. Pharmacokinetics, safety, and clinical efficacy of cannabidiol treatment in osteoarthritic dogs.  Frontiers Vet Sci 2018;5:165.
  8. Hammell C, etal. Transdermal cannabidiol reduces inflammation and pain-related behaviours in a rat model of arthritis.  Eur J Pain 2016;20(6):936-48.
  9. Philpott H, etal. Attenuation of early phase inflammation by cannabidiol prevents pain and nerve damage in rat osteoarthritis.  Pain 2017;158:2442-2451.

 

 

 

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