Conclusion Among patients with knee or hip OA using analgesics, more than half either discontinued analgesic use or shifted to lower risk analgesics following an 8-week structured exercise therapy and patient education programme (GLA:D). These data encourage randomised controlled trial evaluation of whether supervised exercise therapy, combined with patient education, can reduce analgesic use, including opioids, among patients with knee and hip OA pain.
The Stanford researchers figured out how to regrow articular cartilage by first causing slight injury to the joint tissue, then using chemical signals to steer the growth of skeletal stem cells as the injuries heal. The work was published Aug. 17 in the journal Nature Medicine.
“Cartilage has practically zero regenerative potential in adulthood, so once it’s injured or gone, what we can do for patients has been very limited,” said assistant professor of surgery Charles K.F. Chan, PhD. “It’s extremely gratifying to find a way to help the body regrow this important tissue.”
STANFORD MEDICINE (Aug 17, 2020): Researchers at the Stanford University School of Medicine have discovered a way to regenerate, in mice and human tissue, the cushion of cartilage found in joints.
Loss of this slippery and shock-absorbing tissue layer, called articular cartilage, is responsible for many cases of joint pain and arthritis, which afflicts more than 55 million Americans. Nearly 1 in 4 adult Americans suffer from arthritis, and far more are burdened by joint pain and inflammation generally.
Stanford has come up with a Promising new approach to the surgical treatment of osteoarthritis. Unfortunately for the suffering public, this approach is still in the rodent experimental stage.
The pain of osteoarthritis is caused by the LOSS of the CARTILAGE which insulates the bone of the joints. The wonderful cartilage coating prevents the pain which would result from the rubbing of bone on bone. The best solution in osteoarthritis would be to replace the cartilage, and I have no doubt that this will be possible some day.
STEM CELLS is the theoretical method most commonly imagined when it comes to replacing lost tissue.. Brain cells, cardiac muscle cells, and pancreatic islet cells are some of the research areas. The development of stem cells from the cells of the Patient herself (iSCs) obviates the need for immunosuppression, which plagues allographs ( stem cells or organs from other humans).
Recently, in situ transformation of neighboring cells has been described, which sidesteps the need to introduce any cells. For instance the transformation of astrocytes (a type of brain cell) into neuronal stem cells of the dopamine lineage would be a great boon to Parkinson’s disease.
The Stanford method somewhat resembles this last-mentioned technique. An injury is created where the cartilage is desired. Like any injury, bleeding, clotting, and cell infiltration follows, destined to form a scar. However, the researchers added BMP-2, which in this milieu causes the pro-fibroblasts to head toward the bone (osteoblast) lineage. Since cartilage forms first in a tissue destined to be bone, they then added a VEGF antagonist, which interrupts the transformation in the desired cartilage stage. Both BMP-2 and anti-VEGF have already been approved for use, facilitating the development of this attractive therapy.
The researchers have even identified an excellent potential Patient Population: Osteoarthritis patients scheduled for surgical removal of the first metacarpal articulation with the wrist. They could do their procedure on this area, and if there is no benefit, They could just go ahead with the original plan of removal. The thumb happens to be one of my most painful arthritic areas.
I will most interestedly follow their research.
Osteoarthritis (OA) was considered a Degenerative disease when I went to Med School in the late 50s. I am more interested in OA since I have developed it myself.
There is a 40-60% hereditary component. My father’s mother had arthritis badly in her hands, as did my mother’s mother, and so on. A lot of genome-correlation work has shown many different genes involved,
But without a single big contributor, OA appears to be “multifactorial”, similar to a lot of common diseases like Diabetes l. Trauma can be a factor. Old sports injuries, like an ACL tear, that you thought a thing of the past, may come back to haunt you in later years.
INFLAMMATION, the most popular explanatory cause of the decade, may be operating in OA. For instance, you can imagine that OBESITY would contribute to hip and knee OA simply through the traumatic force of gravity. But obesity is also a disease of Inflammation, and increases IL-6 and other cytokines as well.
My own OA involves the classic distal 2 interphalangeal joints (go to the wikipedia manekin for a color-representation of OA classic locations). The base of my thumb, neck and back are also a problem.
Strangely, but wonderfully, my “wheels”, the Hips and Knees, are spared. I have exercised a lot in my life. Clearly, you can’t “wear out” your joints with ordinary exercise.
Our joints have evolved to allow us to move. Since bone has a lot of pain fibres, it would be painful to move the joints, directly bone-on-bone. So we have cartilage on the ends of the bones and discs between the vertebrae. The cartilage is slick to reduce friction.
Cartilage has no blood to supply it with nutrients. Instead, it relies on the joint (synovial) fluid. The cartilage is like a sponge. Walking alternately compresses and relaxes the spongy cartilage, increasing the synovial fluid circulation, thus improving the nutrition of the cartilage. If the Cartilage disappears, there is pain.
I am not a fan of pain medication. My belief was strengthened by the side effects of the study of a medication designed to genetically block pain transmission by injection into the painful joints. The side effect was virtual dissolution of the joints in a fraction of those treated. I felt more comfortable with my pain after reading the article.
Although Acetaminophen helps a little, NSAIDs usually work better, perhaps because of their anti-inflammatory action.
If, like me, you have stomach issues, there are the COX-2 inhibitors like Celebrex. The one dose I recently took was almost magical in its effects. Maybe if you don’t use pain Meds much, they work better.
I do take Glucosamine-Chondroitin, thinking that providing building blocks for cartilage couldn’t hurt. Along this line I also EAT CARTILAGE whenever I eat Chicken or ribs, being careful not to damage my teeth in the act of of exercising my jaws.
I also take Curcumin, hoping to relieve some pain, in spite of the fact that it is poorly absorbed (some brave souls take it by injection). I don’t know if any of this helps, How can you know in such a variable disorder, in the absence of controlled studies.
And pain has no OBJECTIVE markers, and is notoriously hard to study. We literally know more about the surface of mars than we know about Pain.
SLEEP, DIET, and EXERCISE, by minimizing OA factors kike OBESITY and INFLAMMATION are the best bet for preventing and treating OA at present.
UCSF orthopedic surgeon Dr. Paul Toogood discusses the types and origins or Arthritis.