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The Carousel of Joint Degeneration: Osteoarthritis Part 1



Terms:


hypertrophy: growth of tissue

atrophy: diminishment of tissue

pathology: etiology (cause and origin) as well as nature of a disease process

aneural: without nerve supply

avascular: without blood supply



The process of osteoarthritis is multi-factorial and cyclical in nature. This is both a bummer and extremely good news.

It’s why we haven’t found a pill or injection that works to control the cycle of degeneration, and why we likely never will. Working with osteoarthritis requires a multi- faceted approach- movement, diet and nutrition, lifestyle and educational changes. Let’s flush out some of the education concepts so we can learn to work with our arthritic changes more autonomously.


Multifactorial Vs. Genetics

Please note that genetic markers play a part in the development of osteoarthritis (OA)- but the amount of involvement seems minimal and is not well understood. (The exception here is the people born with hip dysplasia). We have many more lifestyle choices that affect the development of OA.


When I hear people say, “my mom had a bunion, my grandma had a bunion and I have a bunion” I am struck by the lack of connection with the true multifactorial nature of the disease. Similar to cardiovascualr disease, OA can have genetic predispositions, and also similar to cardiovascular disease, you can really influence the disease process through your own behaviors and beliefs.

Recall that how we move (how we stand, how we walk) is socialized- we learn to move and speak like our parents and siblings and family because they are our social network. It is time to move away from blaming bunions on genetics, to understanding how to control the biomechanics of your own body.


When thinking about arthritis, it is important to keep in mind the different types of arthritis, and their different causes:


- Gout: caused systemically by excess uric acid within the body, along with genetic propensity

- Autoimmune Mediated Arthritis: Rheumatoid arthritis, lupus, psoriatic arthritis, juvenile idiopathic arthritis. These conditions are caused by an autoimmune issue of not totally understood origin

- Osteoarthritis (OA): due to mechanical stressors on the joint that change the structure of a joint over time (wearing thin cartilage, stiffening joint capsule and causing hypertrophy of bone).


Be clear, what most of us have and what I’ll be exploring is related to osteoarthritis specifically.


Please think of mechanical stressors are physical forces- think back to your days in physics- forces acting on your joints such as compression created by gravity or caused by muscular contraction, forces created by the ground as it interacts with your feet and rotational and shearing forces created by our movement.

Osteoarthritis is like a Carousel:

Every pathology (disease process) we see has a certain nature or flavor to it. A bone fracture is like falling off a cliff- you are fine one moment, and the next you are in a cast, immobilized. You have a slow climb back to recovery, and then at a certain point, you are mostly “normal” again.


It is easy when you are not familiar with pathology to think of disease like a light switch- either you have it or you don’t.

Osteoarthritis is like a carousel. It is cyclical in nature. In this way, it is more like cardiovascular disease or Type II diabetes. You may have flares when your sugar or blood pressure is out of control, but you can bring it back under your control through behaviors and actions you take.

Though you may not be 100% in control of getting on the cycle of arthritis in the first place (because of past injuries or movement predispositions) you can control the speed with which the cycle goes, and how long you stay in it.


Within the lifetime of say, a knee joint, someone with OA may experience 100s or even 1000s of arthritic degenerative cycles before the joint surface becomes so degraded that a surgeon recommends a joint replacement.


Movement Extremes (Behavior and Belief) Seem to Exacerbate OA:

In the clinic, I see two types of folks who develop osteoarthritis most often:


1) People who have moved a lot in their life and have not spent time improving their biomechanics (understanding the forces they are subjecting their bodies to as they move)

2) People who have done very little movement in their lifetime- or who only move in a certain way, in a specific direction.


Folks who have learned to inhabit the middle ground tend not to have so many issues with osteoarthritis as they move into their 80s and 90s.


I’ll come back to this middle road of movement concept in later writing, but for now, let’s focus on to the pathology of osteoarthritis, specifically, the nature of the disease process.



The Cycle of Osteoarthritis (please see the pic below):


1) Excessive forces/ poor nutrient exchange across the cartilage surface


Recall from our last post that cartilage is avascular (without direct blood supply, it also does not have a lymphatic supply) and it relies on simple diffusion to “breathe”.

In order to maintain health, cartilage requires imbibition to allow diffusion of synovial fluid rich with nutrients into its cells, and compression to squeeze old synovial fluid with waste products out. This compression and imbibition is created by controlled motion across the joint surfaces.


When adults stand excessively (or sit, or lie down etc. for extended periods without moving), cartilage cannot breath. If we are standing, there are certain places where cartilage cannot bring in new fluid, despite needing it, because of the weight loading down the joints. But the strangest thing is that we don’t feel this starvation. There are no sensory neurons to communicate to our brain that a danger level has been reached. Unlike holding our breath, there are no cues from our cartilage that we need to move and so cartilage starves quietly.


Excess forces come into play when adults gain weight excessively (creating too much compression and fatiguing cartilage), move excessively creating forces they cannot control. I see this every day in the clinic when I ask clients to do a squat and their knees knock together, or they shrug shoulders to ears in an overhead reach of their shoulder.


Think about shearing forces like trying to stand on one leg on ice. Shearing is the side to side slip in the joint- no joint likes these.

In our Practical Strength class, movers learn to watch for and monitor good hip, knee and ankle mechanics during functional movement. They also learn to strength train all while maintaining a stable spine.

This type of training helps to control excessive forces across the weight bearing joints.


If you have OA and you do the above mentioned activities, get them checked by a Physical Therapist to make sure your mechanics are good- really they should be great.


In the presence of excessive forces and poor nutrient exchange, without intervention we start to experience cell death, the second stop in our cycle.


2) Cartilage Cell death


Like all cells, cartilage cell death creates a cascade of repercussions.

There is an increase in inflammatory signaling and new cells migrate into the area to help clean up the dead cell debris. You can think of this team as a cal-trans cleanup crew. The cells bring with them inflammation and increased white blood cells.


As cartilage cells die, unlike muscle or peripheral nerve, they cannot repair themselves and make a comeback. This is how we have atrophy of our articular cartilage- we cannot replace chondrocytes.

To find a tissue that is regenerative, look for one with a high blood and nerve supply (such as bone). Poor avascular, aneural cartilage doesn’t stand a chance.

There are byproducts that occur as a result of this increased inflammation.


3) Stiffening of the Joint Capsule


Recall the incredible joint capsule from our last blog- the deep ligaments surrounding the end of the bones and providing stability, support and the beautiful synovial fluid?


Inflammation has an impact on the chemistry of both the synovial fluid, and the joint capsule itself.

Inflammation, left uncontrolled over time, contributes to an increase of stiffness, loss of pliability within the joint capsule. The joint capsule is the deepest structure that limits and controls movement.


When the ligaments get too stretched (such as with hypermobility or overstretching) we lose integrity and proprioception.

In OA, the ligaments surrounding the joint get hypomobile- they develop stiffness and adhesions and move less than normal.


This is a HUGE point for productive intervention, but unlike Actions #1 and 2, we cannot do this work on our own.


Please also note, this is a place many of us are in following an acute injury. This is also why acute or traumatic injuries are connected with future OA. After my ankle break, I will need help getting my joint capsule motion back to “normal” qfter long standing inflammation and immobility..


4) Reduction in Surface Area- further changes in increased compression/ excessive forces


Without restoration of normal joint capsule motion, your joint will experience unmitigated stiffness. You will no longer have the same mobility you once had (or that you have on the other limb), and you will not be able to restore it on your own. This reduced capsule mobility, causes a smaller surface of the joint to experience adequate compression and imbibition. You begin to have even more compression and tension.

Recall, smaller surface areas cause more compressive forces when other factors are kept constant. If you reduce the mobility at your knee, and maintain your body weight, you are going to fatigue your cartilage and wear it out that much faster.


This decrease in surface area, causes an increase in compression which in turn causes bone underneath the cartilage to hypertrophy. When this process occurs, pain usually kicks up a notch as bone is highly innervated both with blood and nerve. This is when you may be diagnosed with stenosis or bone spurring.


This increase in compression and excessive forces without adequate nutrition exchange, takes us back to the beginning of this yucky cycle.


As a result, many folks get stuck get stuck going round and round, like a bad carnival ride they can’t get off.


The good news, is that you have many points in the cycle where you can get off this ride. The interesting observation I have had through the years, is that very few people take advantage of working all of these points.

And even if you have had permanent cell death of your cartilage (which you cannot regrow), you can still:

1) control inflammation using P.R.I.C.E.

2) open your joint capsule back up (with the hands of a skillful provider) thereby expanding the joint surface loading area

3) understand how to reduce loading and compression at your joint through education and ergonomics and functional training

4) Ultimately, restore strength and good biomechanics thereby preserving your function


We’ll explore these OA Actions, or the exit points on the carousel ride of degeneration that you can use to slow and even exit this degenerative cycle, in our post next week. Slowing the cycle and taking breaks from it extends the longevity of your joints.


I hope the information on the cyclic nature of OA has been helpful and also inspired you to being open to investigating the actions you can take to help reduce the speed and duration of your OA cycling.


Until then, happy moving!

Trina








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