Osteoarthritis is the most common arthritic complaint among older adults with pain, loss of function, disability and reduction in quality of life being the result. Pain is reported to be the most common complaint for people to undergo a total knee replacement (TKR), with the understanding being that the damage in my joint is causing the pain, so take away the damage and no more pain! This common understanding is still accepted despite the growing body of evidence around the mismatch between structural changes on imaging and patient reported symptoms (Bedson & Croft, 2008; Finan et al., 2013; Lundblad et al., 2012).
There appears to be a mix of evidence regarding subjective and clinical improvement in knee OA following TKR. According to a number of studies it seems individuals that had less severe OA and had TKR were more dissatisfied post-operatively (Jacobs, Christensen, & Karthikeyan, 2015; Nyvang, Hedstrom, & Gleissman, 2016; Pouli, Das Nair, Lincoln, & Walsh, 2014; Vina, Hannon, & Kwoh, 2016).
The main reason most people choose to undergo TKR is because of pain (Nyvang et al., 2016), but it seems that there is a bit of a mixed bag of outcomes with some patients reporting no improvement in disability and worse pain following surgery and others saying the opposite. So I wanted to share some insights from the evidence, pain science and the relationship with knee osteoarthritis.
It is important to understand that there are other factors involved such as genetics, age, obesity, sex and ethnicity and also previous trauma, such as ACL injuries and where they might be a risk factor towards developing knee OA they may not individually be a cause of pain (Grindem, Eitzen, Engebretsen, Snyder-Mackler, & Risberg, 2014; Grotle, Hagen, Natvig, Dahl, & Kvien, 2008; Silverwood et al., 2015; Timmins, Leech, Batt, Edwards, & Bchir, 2016).
Osteoarthritis is understood to be a degenerative (I hate that word!) process of a joint surface. It is commonly understood that the cartilage in the joint is the culprit for pain and swelling as it can cause what is known as a synovitis –inflammation of the synovial capsule. The cartilage itself is aneural (does not have a nerve supply) yet the underlying bone has a large nerve supply. It is understood that nerves grow from the exposed underlying bone into the cartilage and so a tissue that does not normally have a nerve supply can become a source of pain.
Here’s the rub. Pain by definition is ‘an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage’ (IASP, 2012). Yet one of the issues as previously mentioned, is we know from many imaging studies that there are people walking around without pain who have osteoarthritis. So perhaps another definition might be ‘Pain is whatever the experiencing person says it is, existing whenever the experiencing person says it does’ (McCaffery & Beebe, 1989).
So, what’s going on here? Well I want to use a metaphor by my colleague Greg Lehman @greglehman. He describes the understanding of degeneration and pain as kindling and a spark that starts the fire (the fire would be pain). The kindling represents the degenerative change in the joint (this is not pain at this stage) and the spark is a sensitizing agent. This agent could be a physical stimulus or perhaps it could be a stressor like work overload or pressure from your boss. It could be an emotional stressor such as fear or anxiety or it could be a social stressor such as a family member having the same symptoms. The sensitizing agent can be what starts the fire.
Let’s say you decide to undergo TKR surgery, which means you remove the kindling (the osteoarthritis). Some people continue to report pain which is now a new pain which appears to be a result of the major surgery. The issue here is that although you have put the fire out metaphorically speaking, the embers are still glowing and another sensitizing agent comes along and sparks off a new fire or the wrong sensitizing agent was addressed or because pain is multidimensional there was potentially more than one. Now I admit pain is a really REALLY shitty thing but it is just not as simple as ying and yang or on and off. Furthermore, it has been known for sometime that our expectations and how we feel about something can have a strong influence on our pain experience (Atlas & Wager, 2012; Pulvers & Hood, 2013). So, if you are deciding to undergo TKR surgery it’s definitely worth exploring all the options and discussing it with a qualified health professional preferably one that is specialized in pain science.
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Let’s look at bracing. There are lots of knee braces out there that are designed to offer you stability and support. The most common reason for bracing when it comes to OA is to modify the mechanical stress on the symptomatic (or painful) joint (Rannou, Poiraudeau, & Beaudreuil, 2010). It is understood that bracing does offer symptomatic relief but I want to cast your eyes back to the beginning of this blog. If we accept that pain is associated with tissue damage then why does a brace provide relief to a damaged knee? Has the brace miraculously cure the damaged joint?
Some may argue that bracing helps to provide support with movement, but by reducing movement through bracing immobilises the joint and this can cause further problems in terms of bone strength and soft tissue strength. Just place your arm in a cast for 6 weeks and see the outcome. Furthermore, people report problems with braces including irritation, to restrictive, cumbersome, lack of prolonged symptomatic relief and swelling (Squyer, Stamper, Hamilton, Sabin, & Leopold, 2013). A final message here is that humans are biological beings constantly adapting, movement actually maintains the health of the joint. The fluid in your knee brings nutrients into the joint and movement and compression helps to force the nutrients into the cartilage cells. So where bracing might provide symptomatic relief it may actually be contributing to further problems with an OA knee due to the reduction in movement.
A wee mention to something called nociception. It is the process of the nervous system responding to potentially harmful stimuli. I’m sure most would agree that damaged tissue is harmful, right? So, if the harmful stimuli is damaged tissue and that is causing our pain (so we believe) why is it that an osteoarthritic knee can feel better when we put a brace on it? This doesn’t make sense. Pain is weird and we know that nociception (harmful stimuli) is neither necessary nor sufficient for us to feel pain. In fact, I’d bet that nociception is probably happening all the time, just like smell, hearing, touch or sound stimuli. It depends on whether it’s important to take attention of it. I suspect you don’t feel the clothes you are wearing most of the time yet they are still touching your skin.
So on to exercise (or activity). We all know that exercise is good for us, right? Right!?. Yet exercising with knee osteoarthritis is not everyone’s cup of tea. Why? Because it hurts! It is often the case that we do too much too soon and because you already have a sensitized nervous system (remember the embers and sensitizing agent) it is very very easy to push ourselves over our capacity.
Contrary to popular belief there are many misconceptions about exercise. For example, running is believed to be bad for our knees because of the pounding to the joints. See here for more on running and knee joints. The problem is that the evidence behind these theories doesn’t really hold up. Our bodies are not mechanical machines they are biologically adapting all the time. Even knees that have osteoarthritis benefit from exercise (Fingleton, Smart, & Doody, 2016). Strength training has been shown to increase cartilage density in the knee (Grzelak et al., 2014) albeit in elite weight lifters yet a recent systematic review found no further OA progression in elderly people when they followed a regular exercise program (Quicke, Foster, Thomas, & Holden, 2015).
The problem is that we often don’t know what our tolerances are and as previously mentioned there is a bit more too it than just addressing the tissue. We are living, adapting, opinionated beings, just look at politicians!! If we all adopted the one policy, chaos would ensue, healthcare is no different. There is hope on the horizon we are understanding pain more and more and identifying other mechanisms. For example, it seems that there is a problem with the endogenous opioid pathway (happy hormones/bodies own painkillers) in some people who live with knee OA (Fingleton et al., 2016), this is common in other long term conditions such as fibromyalgia, chronic low back pain and chronic fatigue syndrome. All of these conditions point to changes in the nervous system.
So, if you or you know someone who has been living with knee OA for a long time it is worth speaking to a clinician that has a sound understanding of pain science. Clinicians range from physiotherapists, Occupational therapists, chiropractors, nurses, doctors even massage therapists. Just check with your health professional, don’t be afraid to ask.
That wraps up another blog for the naked physio. Please do get in touch, always happy to engage in healthy debate or discuss concerns with people.
Thanks again for having a read.
TNP
References
Atlas, L. Y., & Wager, T. D. (2012). How expectations shape pain. Neuroscience Letters, 520(2), 140–148. https://doi.org/10.1016/j.neulet.2012.03.039
Bedson, J., & Croft, P. R. (2008). The discordance between clinical and radiographic knee osteoarthritis: a systematic search and summary of the literature. BMC Musculoskeletal Disorders, 9, 116. https://doi.org/10.1186/1471-2474-9-116
Finan, P. H., Buenaver, L. F., Bounds, S. C., Hussain, S., Park, R. J., Haque, U. J., … Smith, M. T. (2013). Discordance between pain and radiographic severity in knee osteoarthritis: Findings from quantitative sensory testing of central sensitization. Arthritis and Rheumatism, 65(2), 363–372. https://doi.org/10.1002/art.34646
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