Joint Instability and developing degenerative joint disease and progressive osteoarthritis

Ross Hauser MD

When a joint is unstable, the body has three mechanisms to temporarily stabilize the joint to help get the injury to heal. These three are joint swelling, muscle guarding, and bony overgrowth. Bony overgrowth is more of a ‘last ditch effort’ to more permanently limit bone motion so that adjacent nerves are not injured and stability can occur.

When a ligament is injured, a cascade is activated to temporarily help limit joint motion through muscle spasms and joint swelling. This is supposed to allow for soft tissue healing. The injured ligament (s) responsible for stability (and thus causing the instability) contain nerve endings. These nerve endings are essentially non-stretchable.

3 things the body does to stabilize joints

So when this ligament(s) stretches excessively, so do the nerve endings within it, which sets off the ligamento-muscular reflex. (This is why muscles feel chronically tense, tight and tender. As the ligament laxity cannot limit joint motion, the joint capsule then stretches including its inner layer the synovium. One of the synovium’s job is to secrete extra joint fluid when it senses the joint is under attack by too much force. The joint swelling in osteoarthritis has three main functions: 1) temporary stabilization of the joint; 2) equalization of joint forces; and 3) further sensitize the joint to motion. The temporary stabilization of the joint protects the joint from further immediate damage and in essence reduces force on the injured ligament giving it a chance to heal. The extra joint fluid also causes a more even distribution of joint forces as in walking. The extra fluid also makes the joint more sensitive to any forces or movements that could injure it. Yes, it makes the joint more painful but it is trying to get the brain’s attention so the person will make a good decision as to what to do. Do you think in this scenario it is a good decision to take anti-inflammatory or narcotic medications or get any pain-reducing shot and then go out and walk and exercise excessively on the injury? So blocking the pain and even the muscle spasms is not a good idea because the muscle spasms and joint swelling are the joints and ligaments protective mechanism when they are injured. If you take the protection away and can’t feel pain because of the medications and continue to put damaging forces and motions on the joint, the tissue cells will die. This is why tendinosis, ligamentosis and articular cartilage degeneration are so prevalent in osteoarthritis. (In layman’s terms, these terms stand for tendon, ligament and cartilage cell death.) When there are fewer cells to make the tendons, ligaments and cartilage, then of course the tendons, ligaments and cartilage cannot be made quickly enough to keep up with the damage. The inflammatory cascade through which these tissues are made will continue in an effort to try and heal tissue, but in the presence of continued joint instability, tissue inflammation and degeneration will exceed regeneration. This is why both inflammation and degeneration can occur with osteoarthritis when joint instability is the underlying cause.

Degenerative joint disease (DJD) is a painful condition that results in the deterioration of the cartilage tissues that support the weight-bearing joints in the body. Once the cartilage is thinned or lost, the constant grinding of bones against each other causes pain and stiffness around the joint. Abnormal and excess bone formations (bone spurs) grow from the damaged bones, causing further pain and stiffness. These are the classic signs of joint instability. But is osteoarthritis ONLY about “no cartilage?”

Degenerative joint disease should be considered a “whole” joint disease and not simply the loss of cartilage

In an editorial in the British Medical Journal entitled: “Yet more evidence that osteoarthritis is not a cartilage disease,” lead author Ken Brandt of Indiana University School of Medicine and his team suggested:

(The origin) and progression of osteoarthritis should not be thought of as being invariably attributable to a single tissue, such as articular cartilage, but as possibly due to disease in any of the tissues of the affected joint, including the subchondral bone, synovium, capsule, periarticular muscles, sensory nerve endings and meniscus (if present). Supporting ligaments should be added to the list.

Although reviews of osteoarthritis often contain a statement to the effect that it is not merely a disease of cartilage, the large amounts of time, money and brainpower that have been invested in attempts to develop “chondroprotective” drugs and efforts to find the best ways to image minuscule (and clinically meaningless) changes in articular cartilage and to identify biomarkers of cartilage damage in osteoarthritis are evidence that we really do not believe what we write.1

The above editorial appeared in 2006. Even before that time we here at Caring Medical have published medical research and cited numerous studies that suggests that to treat joint osteoarthritis you must treat the whole joint. Additionally, as stated in the editorial, we have written that MRIs are clinically meaningless and the search for a magic drug is equally futile.

More than a decade after the above editorial, medicine is still looking for drugs and surgeries, treatments that have been shown to be ineffective for many, to offer patients justified by controversial MRI findings.

Bone spur injuring patellar tendon.

The importance of treating ligament injury in chronic joint instability cannot be overstated

It is important to note that, although associated with old age,osteoarthritis and degenerative joint disease are not simply a result of the aging process, nor are they a result of general wear and tear on joints.

Osteoarthritis and degenerative joint disease almost always begin as a ligament weakness resulting from injury.

Ligament laxity (a stretched, loose ligament) is an often overlooked but extremely important cause of chronic body pain in the degenerative condition.

The importance of treating ligament injury in joint instability cannot be overstated. Left untreated, or mistreated in many cases, ligament damage leads to further degeneration of the joint. Research has shown that laxity in the bone/ligament insertion (i.e., ligament laxity) leads to subchondral bone changes (bone destruction) that leads to cartilage changes which in turn leads to osteoarthritis.2

  • In other words: If the ligaments become weak and untreated, it will lead to breakdown of cartilage, bone on bone, and a recommendation to joint replacement.

The above described process is not well understood in medicine. In one of the more recent papers on the true origins of knee osteoarthritis researchers made these observations:3

  • According to these researchers, thanks to new MRI techniques and arthroscopic surgery we have a better understanding of how knee osteoarthritis begins. For my opinion on these statements I invite the reader to review these articles on our website: Is My MRI Accurate? and Arthroscopic Knee Surgery for Osteoarthritis. In these articles you will find my comments on personal observations of misguided treatments based on MRI and unnecessary knee surgeries that accelerated the joint degeneration.
  • In their defense, the researchers of the above cited paper had this to say: “The significance of MRI findings such as cartilage defects, bone marrow lesions, synovial inflammation/effusions and meniscal tears in patients without radiographic signs of osteoarthritis is not fully understood. Nevertheless, early joint tissue changes are associated with symptoms and, in some cases, with progression of disease.”ibid

Twenty years ago, an article published in Gerontology disagreed with the notion that wear and tear is the origin of osteoarthritis and conducted a literary review to prove that osteoarthritis starts with ligament damage. Reviewing numerous research articles, the authors conclude that subchondral bone (the bone just beneath cartilage) changes precede any cartilage change associated with osteoarthritis.

These bone changes are due to a loss of tension on bone at the ligament/bone insertion. In other words, ligament laxity causes bone changes that in turn cause cartilage change and damage. This idea appears again and again in the literature and this article – ligament laxity causes joint instability and degenerative joint disease.

When discussing knee osteoarthritis, the authors point to the importance of joint stability in the development of osteoarthritis.

 “It should be remembered that the knee joint functions as an organ with every tissue contributing to its mechanical stability.  Ligaments, subchondral bone, meniscus and joint capsule all subserve the need for stability. . . the earliest change appears to be at the ligament-bone insertions site.  However, we propose that it is a change in the ligament that leads to an alteration in the tension on the bone at the bone-insertion site which precipitates bone remodeling (injury to subchondral bone) [emphasis added].”4

 Taking account of the progression of osteoarthritis, it becomes clear that the ligament integrity or lack of integrity is what needs to be treated to prevent further joint destruction and this applies to all joints:

“The health and integrity of the overlying articular cartilage depends on the mechanical properties of its bony bed.  Ligament injury precedes the subchondral bone changes and these changes occur before articular cartilage degeneration. ‘The proposed reversal of the current concepts of the aetiology of osteoarthritis from cartilage to bone and ligament suggests that research and therapeutic strategies could be effectively redirected.”4

That was twenty years ago and still pain management medicine continues to search for drugs, devices and surgical procedures to eliminate the chronic pain associated with osteoarthritis and degenerative joint disease and then fesses up that this is still not a fully understood science.

Ligament regeneration and repair – Progression of degenerative joint disease addressed by comprehensive Prolotherapy

As mentioned above in the more recent paper: The standard osteoarthritis treatment involve symptom management such as nonsteroidal anti-inflammatory medications, cortisone shots and even surgery to provide pain relief. Cortisone and other steroid shots have adverse affects on bone, cartilage and soft tissue healing, this has been well documented.

Since osteoarthritis begins with ligament damage it would make sense to treat the ligaments early.

Understanding ligament damage:

  1. A ligament is damaged through overuse or trauma, such as a sports injury or an accident.
  2. Because of the ligament’s poor blood supply, it does not heal (unlike muscles, which have a good blood supply and heal quite easily).
  3. Over time, the injured ligament weakens, like a stretched rubber band that has lost its elasticity.
  4. Since ligaments function as joint stabilizers, the injured ligament is no longer capable of doing its job.
  5. As a result, the muscles must compensate. They begin to ache and spasm and, eventually, the joint or vertebra in the area begins to compensate as well.
  6. Overgrowth of bone occurs to help stabilize the injured ligament, which leads to arthritis, and a whole new level of pain and disability.

Stem Cells and Prolotherapy for degenerative joint disease and Instability

This downward spiral of pain can be halted and reversed only by stimulating healing at the source—the ligament. The only proven procedure that stimulates this kind of healing is Prolotherapy.

Recently we published our findings on Stem Cell Therapy, as part of a comprehensive Prolotherapy program for advanced arthritis. In this paper we were able to describe our experience with a simple, cost-effective regenerative treatment using direct injection of unfractionated whole bone marrow (stem cells from a patient’s own bone marrow), into osteoarthritic joints in combination with simple dextrose Prolotherapy. Seven patients with hip, knee or ankle osteoarthritis received two to seven treatments over a period of two to twelve months. All patients reported improvements with respect to pain, as well as gains in functionality and quality of life. Three patients, including two whose progress under other therapy had plateaued or reversed, achieved complete or near-complete symptomatic relief, and two additional patients achieved resumption of vigorous exercise. Learn more about stem cell therapy for osteoarthritis and Prolotherapy at pages on our website.

In my opinion and documented by scores of medical papers, Prolotherapy is the safest and most effective treatment for repairing tendon, ligament and cartilage damage is Prolotherapy. Prolotherapy stimulates the body to repair painful areas. It does so by inducing a mild inflammatory reaction in the weakened ligaments and cartilage. The inflammation causes the blood supply to dramatically increase in the ligament, alerting the body that healing needs to take place. In the simplest terms, Prolotherapy stimulates healing.

Furthermore, Prolotherapy offers the most curative results in treating osteoarthritis and degenerative joint disease bone repair. It effectively eliminates pain because it attacks the source: the fibro-osseous junction, an area rich in sensory nerves. What’s more, the tissue strengthening and pain relief stimulated by Prolotherapy is permanent.

1 Brandt KD, Radin P, Dieppe P, Putte L. Yet more evidence that osteoarthritis is not a cartilage disease. Ann Rheum Dis. 2006;65(10):1261-1264. [British Medical Journal]

2 Bailey AJ, Mansell JP. Do subchondral bone changes exacerbate or preceded articular cartilage destruction in osteoarthritis of the elderly? Gerontology 1997;43:296-304.

3. Favero M, Ramonda R, Goldring MB, Goldring SR, Punzi L. Early knee osteoarthritis. RMD Open. 2015 Aug 15;1(Suppl 1):e000062. doi: 10.1136/rmdopen-2015-000062. eCollection 2015.

4. Bailey AJ, Mansell JP. Do subchondral bone changes exacerbate or precede articular cartilage destruction in osteoarthritis of the elderly? Gerontology 1997; 43:296-304.


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