Recent developments in science are telling us we need to re-think osteoarthritis.
Regularly, I see imaging of joints that look textbook normal, but the owner of those joints has terrible pain and debility. Likewise, I see spectacularly awful images of joints where the person has no (or minimal) pain or dysfunction in the joint at all. In the former case, the symptoms the person is suffering would imply they have osteoarthritis (OA) and in the latter example, the imaging screams OA, but something doesn’t add up here.
Research now shows that changes on imaging (x-ray, CT scans and MRI) DO NOT tell us much about current pain status, the future amount of pain a person will feel (so not a crystal ball), nor are they indicative of how much activity that person can do at the time of imaging (1,2) [you can read more about this here]. In fact, the bony changes we see on joint imaging are often a reflection of the vintage of the subject ~ they’re just wrinkles on the inside. Some people with wrinkles inside and out are active, vital and pain free. Others are not. It turns out that the wrinkles are not the thing that matters.
Bette Calman is 83 in these photosIt's also worth noting that the idea of OA developing in joints that are overused, or that wear and tear causes OA, is a furfy too. Here’s the evidence:
The research on cartilage is quite clear ~ cartilage does not wear out from excess usage and to be at its best it requires load bearing exercise. So the old way of thinking about cartilage wear/damage causing OA and needing to protect joints showing cartilage wear on x-ray by not using them as much with the goal of slowing OA progression ~ complete waffle!!
There is also a theory out there that people who are overweight or obese are more likely to develop OA. There is some truth to this, but not in the way you might think.
It turns out that:
…and
It has been postulated that it is the body wide pro inflammatory state [read more here], which is associated with increased body fat (and thus increased weight), that is the significant factor when it comes to the development of OA. Another interesting observation on increased pro inflammatory state is that its prevalence is known to increase with age, as does OA.
Remember at the start of this blog where I mentioned how medical imaging of joints reflects neither the relative ability of the joint being imaged nor the level of pain a person is experiencing in that joint? Let’s talk about the pain of OA.
As we’ve discussed in other blogs, pain is a tool the brain uses to keep us safe [read more here] ~ it’s the stick in the carrot/stick-donkey metaphor (!). Our nervous system has inbuilt natural brakes and accelerators that allow this pain perception system to adapt to a body’s situation in real time. Very clever.
In OA the nervous system’s natural brakes and accelerators have been altered in response to the individual’s life experiences to promote the experience of pain (8, 9):
The upshot of this is that the brain and nervous system become overprotective. This means that people who have OA experience pain when using the affected joint well before there is any possibility of any further tissue damage. The pain is kicking in to protect the joint before there is any need to do so. As a result, the person is excessively limited in their perception of what the joint can safely do. They then do/move even less (much less than the joint is capable of) and, without exercise and weight bearing load of the joint, the joint deteriorates through lack of use. Another word for this is deconditioning. Ironically, the person thinks they are being sensible and reasonable protecting the joint by not using it and reducing the pain they are living with, but the lack of use is actually speeding the way to deterioration, dysfunction, and more pain.
Now for the good news: these systemic evolutions towards dysfunction and OA are the result of bioplasticity ~ the body’s adaptions to the world around it for that individual, in that particular environment, in that society. Bioplasticity is a two way street with optimal function up one end of the spectrum and dysfunction at the other (in the context of this discussion, a healthy joint is at one end of the spectrum and a joint debilitated by OA is at the other), and your every day choices determine which direction you are travelling on this spectrum. Bioplasticity is a feature of life right up and until we leap off the mortal coil as evidenced by people who build muscle, strength, and thicker cartilage when they do weight bearing exercise; or improve reaction times when we practice an activity. The same holds true for our pain and immune systems. If they have deteriorated, we can build them up again.
The science shows us that to manage a joint that is impacted by OA we need to:
At the Adelaide Chiropractic Centre we are helping people with OA pain every day. OA pain is complex, it’s not just about the joint. We are working with people to promote them being strong, fit, and able; to expand on what their brain sees as the limit of possibility for their frame; to shift their bioplasticity towards increased function and away from a slow downward spiral to dysfunction.
Be an active participant in preventing OA dictating what you can and cannot do. Please share this new science-based knowledge about OA with anyone you love who is living with OA. Healing begins with knowledge and understanding. If you have any questions, feel free to call the Adelaide Chiropractic Centre on 8221 6262 and make a time to have a chat with our chiropractors.