Wear and Tear
How we conceptualize our body, our joints and tissues, affects how we react to situations that involve those tissues. Our joints and tissues represent, in the minds of most laypersons, a static entity. That is, “they are what they are”. They can often be viewed as the sum of all stresses, where stresses are responsible for “wearing out” the tissues. This analysis can be misleading. How we conceptualize our tissues dictates, or at least influences, how we behave. In essence, we act out in the real world what we believe to be true about our bodies.
The “wear and tear” model of joint structure, while intuitive and rational in terms of what we know about the world (we all are well aware discontinuity of all things that exist, aside change), has some misconceptions when applied to the living adaptable system that is our body. The main misconception involves the belief that tissue wear itself is irriversable tissue degeneration. In a world where tissue wear = degeneration = pain, the body can be viewed much like a car, in that based on amount of use (ie at 200k miles) it requires a replacement.
I can't remember the reference, but I once read of a tribe whom held the belief that a human has a finite number of heart beats before death. The tribe would act in accordance to this belief, and move very slowly, avoiding any increase in heart rate. They became fragile, soft and sloth like sedentary citizens, and their king existed in a near immobile state, spoon fed and manually transported. Yes, their hearts beat slowly. But at what cost was this belief? Was what they were acting out advancing the intentions of their belief, or to their detriment?
There is mounting evidence and exposure on the tenuous link between tissue and damage, and the more we can re-conceptualize our bodies as adaptive, the less likely we are to fall in line with the aforementioned tribe, mistaking cure for disease.
Bringing this to light can be of therapeutic value in many ways. If we can change what someone believes about their condition, then we can change what they act out, which has incremental returns. The job doesn’t end with just stating information about the body being adaptable. In order for a person to make an informed decision to change how they react to their pain, they need to find this new conceptualization of an adaptable system interesting. If it isn’t interesting, then there is likely no cognitive shift in understanding, and behavior would be unlikely to change.
The idiom “Wear and Tear” (a phrase also labeled by Butler/Moseley to be a particularly “sticky” neuro-tag in is roll-off-the-tongue ease) is usually somewhere in the mind of a patient. In reality, there is tear. There is breakdown. It is completely unavoidable. What can be missed though in the patient-physio interaction is the education that tissue “learns”, changes and responds. This is part and parcel of what Butler and Moseley are bringing to the rehab table. There are too many real interactions between the immune system, thoughts and beliefs, stress and sleep, behavior etc… to view pain in a purely isolated biological tissue mechanistic sense. That is, it isn’t exactly the painful joint (or the muscle or body part) but how that body part is acting in its environment. The “how it is acting” has implications both at the tissue state, and at the individual tissue owner’s state.
I am reminded of a recent PT visit of a woman in her 80’s that had severe scoliosis and it was affecting her gait. She wasn’t coming in because of pain, as she didn’t have any. She was just concerned about the way her walk looked, and her balance. Here is a great example of wear and tear, structural changes and tissue “dysfunction” over the course of an entire life without manifesting any mentionable pain level. But when we are under the influence of pain, it is much more difficult to zoom out and look at the big picture: there exists a present reminder of pain that can consistently confirm our beliefs that something is wrong, that we are at 200k on that tissue. It is difficult to imagine the educational messages of adaptation outweighing innate messages of pain (yes pain is output, but its output circles back around to a cognitive psychological input). But part of that depends on how relieved the patient is to find out the truth about their condition (this goes back to the interest). If for months you suspected a sneaking terminal cancer, awaking in the middle of the night dreading it and imagining and feeling symptoms that confirmed this daily, and finally getting to a specialist only to find that your symptoms were, all from say a gluten allergy, imagine your relief. Its not terminal cancer! Its just an allergy! A weight is lifted…this can change.
Can we shift our views, in a similar sense, when we think about low back pain, neck pain or knee pain? Are our pains conformation of a static and irreversibly damaged tissue? Or could they be a feared cancer without any relevant diagnosis? What would lift the weight of our concerns? Part of this is education. The other part is learned through experience, when the person starts to behave differently and treat the tissue based on what they may have learned through the education. We act out what we believe (we hobble on a joint we believe to be fragile, we move carefully and slow when expecting pain, we change what we do if we are afraid that activity will cause damage, we tense up with pain, and we avoid positions and loads that our tissues have disliked in the past). These behaviors can have their place, but their protection can often quickly become unwarranted.
Back to wear and tear, lets take a metaphor. Imagine a small cabin in the forest of Alaska. In that cabin lives a particularly industrious jack-of-all trades woodsman. His goal is survival, and to survive he keeps his cabin fortified. He learns how to properly fortify his cabin based on what he experiences over the years; wet falls, heavy winters, bears in the summer clawing their way in…you might liken that cabin to your body, where its under constant surveillance of your nervouse system and brain. The tissues are constantly being monitored, and changing in small ways based on what they experience. In a simple mechanical sense, these could be stress, strain, and all things detected by “mechanoreceptors”. In an immunological sense, these could be chemical changes, cellular response, and all things “chemoreceptor”. The cabin does eventually break down over 100 years. Tissue will always eventually degenerate. But, it also gets fixed up along the way, making areas of weakness more robust, and adding support where it is most needed. In a living system, there is adaptation.
Disk degeneration, or “DDD” is a common term brought up by patients with back pain. One argument against some of the medical overemphasis on disc loading strategy is disk research is conducted in-vitro to “non-living” tissue, and doesn’t respond the same to actual living tissue. But even then, disc degeneration doesn’t necessarily have anything to do with pain (back to the woman with severe scoliosis, and all sorts of disc degeneration). There are many angles we can help address where the body is working for the bothersome tissue, not against it. This may come in the form of load management, sleep education, graded exposure to reduce sensitivity, getting stronger globally to support the painful area, increasing cardio for improved blood flow (this could be an arm bike for a person with knee pain, or a leg bike for a person with neck pain… just something to globally improve vascularity).
Not only is the term “wear and tear” misleading (as it should be more something like “wear/load, and create adaptations to best/better tolerate future wear/load”), it also isn’t strongly correlated with pain, which is almost always the primary complaint. Take knee OA for example. Researchers are now referring to this condition as “symptomatic knee OA” (and more and more conditions are allowing this discriminating preamble) because radiographic knee OA does not equate pain.
The consensus is clear that as age and OA findings have a linear relationship, which does not come as a surprise. But remember, OA does not equal pain. The Framingham Osteoarthritis Study found that 10% of people aged 63 years and over had symptomatic knee OA (pain) in the presence of radiographic changes (1). In people with severe OA, it seems about half report pain (2). Although some studies find the link of reported pain and OA severity less clear, some large scale studies (4000 subjects) finds a clear relations between the roughly 40% of persons with radiographic OA and pain (3). Even in these studies, 60% of the persons with radiographic OA did not have pain. Further, can the 40% improve? If so, their “radiographic” OA isn’t changing….
Back to the education component. A study I like to reference is a recent “JOSPT perspective for patients.” (4) The important part to get across is, the more you load the tissue doesn’t necessarily mean the worse off the tissue is. Again, the structural life of tissue is not a ticking clock that only that only counts down to zero. People that don’t jump around, load and move (sedentary individuals) have a higher chance of radiographic knee OA than recreational runners. And people that are obsessive about running (over 57 miles/week runners) only have slight more signs of usage than sedentary people! The take home point is that, to a large level, tissue adapts and becomes more robust, depending what it is introduced to and how it is introduced (ie graded VS overworked). I also like to bring up the fact that people can train themselves to run 26 miles, without their body reacting to that load with severe pain and inflammation. If a runner runs 15 miles in the first month, they may be hobbling in pain for a few weeks. If they train, running 3, 2, 5, 4, 8, 3, 3, 8, 4, 10 miles and so on, they can undergo the same “wear and tear” load, with a totally different response. The response is different not because the person is just stronger or more fit (even though that may be part) but because the body gets familiar with the jolts and pounding of running, and has time to adjust to this and not be alarmed by it. If it (the brain) isn’t alarmed, then the alarm signals (pain) are not present. I also like to reference the Moseley / Butler diagram of “twin peaks” (5). This illustrates that the alarm is going to be set at a lower threshold after injury (even though the actual tissue tolerance can be still robust, especially after proper healing time).
I like tangible examples that don’t get too deep in the physiology of pain. We don't want to move into a completely mechanistic explanation of neurophysiology to replace a mechanistic explanation of structure. There are a lot of simple examples out there that can be used to open up a conversation about the pain in question and how it relates to structure. There is growing evidence that many things influence pain, and how we understand the issue may dictate how we then interact with the world. Not only do we need to change beliefs through our rhetorical explanations, we need to disconfirm beliefs (a term used by Peter O’sullivan in his CFT workshop) in a physical, real body activity and movement sense.
There will always be cases where structure wins, where structure truly needs to be replaced, or “fixed”. Unfortunately, for the same reason we mention tissue damage doesn’t equate pain, fixing the structure doesn’t promise pain relief, and we can look to lumbar fusion outcomes to see it isn’t a cure-all to decompress and immobilize areas reported painful. Some areas respond better to "fixing" than others. We can often mistake symptoms for a disease, and be confused on the relevancy of a patient with one, or both of those variables. Either way, if we are going for conservative treatment, we need to go about it right, with the right outlook and information. This conceptualization should act as a critical foundational understanding to which the rest of the rehab experience can fall under. Following a narrative of adaptation, strength, desensitization and graded exposure, patients will have a better understanding of what physical therapy means, and their individual role in rehab from the specific irritable tissue to the global influencing factors in their lives.
-Tal Blair, DPT
1) D. T. Felson, A. Naimark, and J. Anderson, “The prevalence of knee osteoarthritis in the elderly. The Framingham Osteoarthritis Study,” Arthritis and Rheumatism, vol. 30, no. 8, pp. 914–918, 1987.
2) Hannan MT et al. Analysis of the discordance between radiographic changes and knee pain in osteoarthritis of the knee. J Rheumatol. 2000 Jun;27(6):1513-7.
3) Laxafoss E et al. Case definitions of knee osteoarthritis in 4,151 unselected subjects: relevance for epidemiological studies: the Copenhagen Osteoarthritis Study. Skeletal Radiol. 2010 Sep;39(9):859-66. doi: 10.1007/s00256-009-0856-x. Epub 2010 Jan 30.
4) Teyhen et al. Journal of Orthopaedic & Sports Physical Therapy, Volume 47, Number 6, June 2017, 391
5) Moseley L, Butler D. Explain Pain Supercharged. The Clinician’s Manual. Moseley & Butler. Noigroup Publications, Pg. 4.