The 'Wear and Tear' Myth

There have be recent advances in osteoarthritis (OA) and cartilage research that have changed what we know to be true about OA. In light of new evidence, clinicians should alter their interactions and protocols with regard to patients affected by OA. It has been widely believed for many year that people suffering with arthritis will need a joint replacement eventually and that that is the only option. It is also widely believed that cartilage will not regrow or become healthy again.

Patients are often told that reducing weight is the most effective way to decrease OA associated joint pain because it decreases the impact on the joint and the stress on the cartilage. However, recent research has shown that it is not so much the weight, but the percentage of body fat (1). A higher percentage of body fat has been shown to increase cartilage loss over time, while a higher percentage of lean muscle mass is associated with maintaining cartilage over time. Obesity has been shown to predict the progression of hand OA, which is not a weight bearing joint, so how does increased weight contribute to that? Further research found that obesity contributes to inflammatory responses in the joint which affects the cartilage and its ability to repair and thus can add to the progression of OA.

A commonly held belief is that once there is no cartilage left on a joint surface it will only get worse with more activity. Activities like bike riding, which don’t involve impact or loading of the joint, are preferred because they don’t wear the cartilage down more. As it turns out, cartilage loves loading. It has been found that astronauts after having spent substantial time in space have thinner cartilage upon returning to earth which is less healthy. In contrast, marathon runners have been shown to have thicker, more healthy cartilage than “normal” individuals (2). Cartilage doesn’t get its nutrients like other tissues of the body because cartilage doesn’t have a blood supply. Cartilage gets it nutrients through compression and load, by physically pushing the nutrients into the cartilage tissue. Furthermore, compression and load stimulates chondrocytes (the cells of cartilage) to make collagen and aggregan (parts of your cartilage) and loading also creates daughter cells that help repair cartilage. Instead of the “wear and tear” that we always think of, cartilage can “wear and repair”

Lastly, another part of this myth is the psychologic message that “wear and tear” sends. It casts the shadow that joint replacement is inevitable and there are no alternatives. It assumes that he joint will continue to wear out so you’d better get used to it. These ideas are, however, not evidence based. The body, even the cartilage, is “bioplastic”. That means that the body has the ability to change and adapt, even the bones and cartilage. Exercise and activity has been shown to improve cartilage health in people with OA and to decrease the system wide inflammation associated with OA (5, 6).

This isn’t to say that all joint replacements are unnecessary and ill-advised. Certainly many people need this procedure and have favorable outcomes. There are 10-34% who do have unfavorable long term outcomes, such as moderate to severe pain, two to five years after a total knee replacement (7).

1. van der Kraan PM. Osteoarthritis year 2012 in review: biology. Osteoarthritis Cartilage. 2012 Dec;20(12):1447-50. doi: 10.1016/j.joca.2012.07.010. Epub 2012 Aug 13. PMID: 22897882.

2. Smith, David & Gardiner, Bruce & Zhang, Lihai & Grodzinsky, Alan. (2019). Articular Cartilage Dynamics. 10.1007/978-981-13-1474-2.

3. Berthelot JM, Sellam J, Maugars Y, Berenbaum F. Cartilage-gut-microbiome axis: a new paradigm for novel therapeutic opportunities in osteoarthritis. RMD Open. 2019;5(2):e001037. Published 2019 Sep 20. doi:10.1136/rmdopen-2019-001037

4. Gwilym SE, Keltner JR, Warnaby CE, Carr AJ, Chizh B, Chessell I, Tracey I. Psychophysical and functional imaging evidence supporting the presence of central sensitization in a cohort of osteoarthritis patients. Arthritis Rheum. 2009 Sep 15;61(9):1226-34. doi: 10.1002/art.24837. PMID: 19714588.

5. Naugle KM, Ohlman T, Naugle KE, Riley ZA, Keith NR. Physical activity behavior predicts endogenous pain modulation in older adults. Pain. 2017 Mar;158(3):383-390. doi: 10.1097/j.pain.0000000000000769. PMID: 28187102.

6. Wallis JA, Taylor NF. Pre-operative interventions (non-surgical and non-pharmacological) for patients with hip or knee osteoarthritis awaiting joint replacement surgery--a systematic review and meta-analysis. Osteoarthritis Cartilage. 2011 Dec;19(12):1381-95. doi: 10.1016/j.joca.2011.09.001. Epub 2011 Sep 10. PMID: 21959097.

7. Beswick AD, Wylde V, Gooberman-Hill R, Blom A, Dieppe P. What proportion of patients report long-term pain after total hip or knee replacement for osteoarthritis? A systematic review of prospective studies in unselected patients. BMJ Open. 2012 Feb 22;2(1):e000435. doi: 10.1136/bmjopen-2011-000435. PMID: 22357571; PMCID: PMC3289991.

Muscle Tension and Motor Control

When treating patients I commonly find tight and painful muscles directly or indirectly associated with the major complaint the patient is being treated for. I hear “Why is that muscle tight? It’s not even near my pain.” or “I didn’t even know that muscle was so tight!”

Tightness is often a way that the body uses parking brakes in the absence of real, authentic braking systems. The braking system that the body has is called motor control and it is finely tuned to input, processing and appropriate output. When a fault is present somewhere in that system—somewhere in movement, somewhere in that coordination, timing and symmetry—a dysfunction is observable.

The body is set up to do what you ask of it, and in a situation where the strength or coordination are not present, it simply creates a parking brake system—one that tends to stay engaged, slow you down and keep you out of trouble. This parking brake is a fail-safe in the presence of fatigue, injury, protection of other structures and avoidance of pain. You may have some limited improvement in control, but you also waste energy and lose efficiency. The weakness issue remains evident. It is often deconditioning; it’s body-wide and not isolated and it’s easily fixed by getting up and moving today  . . . and then moving a little more tomorrow. However, isolated weakness is rarely just weakness.

Isolated inhibition of a single muscle or group of muscles is best diagnosed in rehabilitation as a neurological problem or impairment resulting from injury, disease or dysfunction. The subtle and background inhibition I’m speaking of is the inability for a muscle to take a command to an appropriate level of tone to execute a posture or a pattern. Our real problem here is when we simply discuss tightness or weakness of a muscle, we can go down the rabbit hole thinking it’s a muscle problem. Very often, it’s a coordination problem.

If there is tissue tightening, everything from deep fascia to superficial scarring or scar tissue from a previous injury, the muscles will be told to tighten prematurely or even maintain a significant amount of resting tone simply to protect the kink in the system. This tightness can also be preserved not from a signal from other tissues but it can be left over from a previous injury that has already been resolved. The muscles never got the memo.

Sometimes patients are confused when I prescribe exercise for a chronically tight muscle. “Isn’t the muscle too strong already?”. The simple answer is “no”. Because of a lack of strength, poor coordination, or engrained guarding from a previous injury, the brain thinks it’s only option is to contract that muscle as hard as possible to provide the only control it can. By improving the connection of the brain to the muscle (coordination), improving strength, or retraining movement patterns the brain can finally create a new habit or movement (incorporating strength and coordination) which allows those muscle to relax to a “normal” level.