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An alternative medicine approach to treatment and management. Part I

flower-boswellia-serrataOsteoarthritis (OA) is one of the most common and debilitating conditions in our modern American society. Let’s explore what we know and how to fix OA. First a review of current literature.

Understanding Osteoarthritis (OA)

When we understand the basis for a condition such as OA we can be more effective clinically in treatment. OA is commonly thought of as being a result of mechanical stress upon the joint and that the repair mechanisms about the joint are faulty. We are commonly focused on just the cartilage in degeneration but we have to think of the synovial joint as being an organ and this involves all of the structures. So we have to also focus on the meniscus, the synovial membrane and all of the ligamentous and muscular tendinous structures about that organ. In terms of OA there are changes that take place particularly in subchondral bone where we see joint space narrowing and osteophyte formations along the edges. If we think of synovial joints as an organ then all of these structures, the articular cartilage and  the underlying subchondral bone have to be kept in a state of metabolic health and a state of balance. From a biochemical point of view, what goes wrong in OA is that the balance that is maintained within the joint gets lost. The catabolic events, the things that form the wear and tear at that biomechanical level outstrips the ability of the anabolic capacity in the joint to do the necessary rebuilding. In OA the scale tips in favor of those catabolic events.

The real question that I want to explore though is, “why is that.”

Mechanical stress plays a role but lets look at more of what is going on after the stress sets the degenerative process in motion. The common joints that are affected are the knees, hips, hands and spine but any synovial joint can be affected. Age is definitely one of the major risk factors as we see significant increases as we age. If we look at the age group from 18 to 24  there is approximately 8% afflicted and from 45 to 60 it jumps up to 30% and above 60 is 50% of the population. It is difficult to get population numbers but it is estimated that 15% of Americans suffer from OA, which is about 40 to 50 million people. OA is a huge problem and is definitely the leading cause of disability amongst the elderly. We are seeing a significant increase in the incidence and a definite exponential growth of OA  in the aging population.

Understanding Risk Factors

One of the ways we get to how to manage and treat a disease process is to understand the risk factors. The risk factors in any complex disease process are often a work in progress and there are nuances that get added as we go through time and as research develops new understandings.  Risk factors become our clinical guide and extends our clinical understanding in meaningful ways and allows us to be more effective in a broader range of people. Aside from age, obesity is another risk factor. As we increase our weight there is an increase in the mechanical stress upon the joint, but when you look into obesity in more detail obese patients have more hand based OA.

Why is that?

There is obviously no extra mechanical stress from obesity associated with the hands. This is where OA gets very interesting because it takes us into a whole range of metabolic disorders. Insulin resistance, Type II diabetes, elevated leptin for examples, are all risk factors that are quite well acknowledged that play an important role in the life long development of OA. You could argue that patients with OA are on that metabolic tract and could end up with diabetes, cardio-vascular disease and cognitive disorders as they age. Joint injuries and joint misalignments are also factors as are genetics and an inactive lifestyle.

Let’s first look at the cartilage and “Cross Talk”

OA results from a complex interaction of mechanical, biochemical, molecular and enzymatic feedback loops or chemical cross talk, which sets the scene for joint destruction. Within the articular cartilage very early on, there is an increase in water and a decrease in the proteoglycans or the aggrecans. The aggrecans are the large molecules that contain chondroitin sulfate and keratan sulfate. These are important for the weight bearing properties of the joint. In the early stages as these molecules decrease, and Type 2 collagen is involved in this as well, the cartilage can’t withstand the regular pressure and impact of the normal joint. The predominant enzymes responsible for the breakdown in OA are things called matrix metalloproteinases. MMPs for short. Aggrecanases are also important. When there is an inflammatory process within the joint one of the end stages in this chain of events is the release of these enzymes which breaks down the cartilage. Later on in OA the cartilage can become mineralized which is a unique feature of the advanced process. As the chemical environment in the articular cartilage changes some unique things begin to happen.

Embryology of Chondrocytes

If we look at the embryology of chondrocytes they are really cells that have been arrested in their development and they have not become bone. When a bone is being produced the chondrocytes that will form the articular cartilage are put into an arrested state of development so that they retain their chondrocyte characteristics to form the cartilage. In OA when we have these metabolic disturbances it has the ability to unlock that embryological metabolic break and those chondrocytes start to differentiate into bone and that is one of the reasons that they become mineralized. If we were to look at a cross section of a piece of cartilage you would have cartilage across the top and underneath the cartilage there is a layer of calcified cartilage and underneath that you would see the subchondral bone. In OA one of the hallmarks is that the subchondral bone plate thickens, the calcified cartilage plate gets larger and the articular cartilage starts to shrink. The subchondral bone becomes a key feature in the development of OA. The subchondral bone plate is in direct contact with the articular cartilage as it is in contact with the mineralized layer. There is good evidence to show that the nutrients that are being delivered by the underlying vascular supply in the subchondral bone supply about 50% of the nutrients that the lower layers of the cartilage needs. Glucose, oxygen and water and all of the necessary nutrients come through the subchondral bone. There is now very strong evidence to show that in humans subchondral bone alterations may in fact precede cartilage degeneration. Keeping an eye on the vascular supply in the subchondral bone becomes a key  in supporting the bone health and joint healing ability. One of the factors that emerges particularly with knee OA are things called bone marrow lesions or bone cysts. These lesions play an important role in the pathogenesis of knee OA. They are very strongly associated with radiological progression and bone marrow lesion enlargement predicts an increased cartilage loss. If you can repair those bone marrow lesions it actually predicts a reversal of the OA. Clinically we need to place a lot of our attention on what is happening with the subchondral bone.

Synovium is Significant

The synovium is also involved and it is quite significant in the early development of OA. One of the issues has to do with what is happening at the surface of the articular cartilage. If you have fragments of cartilage that have become detached from a damaged cartilage surface or if you have bits of meniscus that are being rubbed of f (when a meniscus gets worn it is kind of like the rough end of a piece of carpet where all of the threads start to come out) you have fragments of tissue from the cartilage and pieces of meniscus that are detached and floating around in the synovial fluid. These tissue fragments ultimately become attached to the synovial membrane and are seen by the immune system as foreign bodies. Those bits of dead and dying tissue, which are necrotic, are releasing compounds that will develop an immune response. When those compounds arrive at the synovial membrane they get received as foreign bodies and that developes an inflammatory response which results in the early signs of synovitis. This type of synovitis then recruits all sorts of immune cells into the area such as activated T and B cell lymphocytes. Those inflammatory mediators then leak into the synovial fluid which migrates through the synovial fluid. The areas of the articular cartilage that are most directly related physically to the area of inflammation  then start to experience the inflammatory effects of those inflammatory mediators that have leaked through the synovial fluid.

Be Sure to check out Part 2

One of the keys in helping the patient with OA is by reducing their inflammation which causes pain and debilitation. In Part 2 we will discuss the herbals and dietary approaches that we utilize to help OA. You may have already guessed that Chiropractic, Boswellia Serrata and the Young Living Essential Oil of Frankincense will be a large part of the topic. Until we meet again. Dr. John Weisberg

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