Don’t count inflammation out of tendinopathy quite yet

Photo by Pete, Public Domain Mark 1.0

For a long time now, it’s been the counterintuitive conventional wisdom among better-informed healthcare professionals that tendinitis does not actually involve inflammation, that it’s more about degeneration of the tendon, and that the “itis” suffix should be replaced: it’s tendon disease (tendinopathy), not tendon inflammation.

That idea was always based mainly on the absence of relatively obvious signs, the classic clinical and pathological signs of a vigorous immune response. Basically, it doesn’t look like it’s inflamed.

But it certainly feels inflamed.

There’s probably more to inflammation than redness and white blood cells swarming the tissue like police trying to control a riot. Inflammation is not one thing: it’s a dizzingly complex spectrum of cells, molecules, and processes, many of which are absent or different or just subtler in RSIs than they are in infection or acute injury. In fact, “classic” inflammation is probably a relatively minor tip of a much larger physiological iceberg.+Medzhitov R. Origin and physiological roles of inflammation. Nature. 2008 Jul;454(7203):428–35. PubMed 18650913 ❐ Medzhitov explains that “although infection-induced inflammation is vital, it might be a special case.” Indeed, classic inflammation seems to be an oddball, and has relatively little in common with lots of other “inflammation” — the immune response to infection is dramatic and conspicuous, but perhaps exceptional and distinctive within the broader context of the biology of healing and adaptation … which is so diverse that it really doesn’t fit comfortably under one umbrella term like “inflammation.” Consider that some inflammation is an actual malfunction, a straight-up case of mistaken identity — I’m referring to autoimmune disease, but also a more common “normal” mistake that affects everyone.+Ruslan Medzhitov (emphasis mine): “ … whereas the physiological rationale [clear biological purpose] of infection-induced inflammation is clear, many other types of inflammatory response are only known in pathological settings, and there is no clear understanding of their physiological counterparts. It is not even clear whether there is any physiological counterpart for some inflammatory conditions … The standard view of inflammation as a reaction to infection or injury might need to be expanded to account for the inflammatory processes induced by other types of adverse conditions.” In other words, sometimes inflammation seems to happen for no reason whatsoever.

maybe it’s not an absence of inflammation, but a definition of inflammation that’s too narrow. Maybe it should include a bunch of other healing and adaptation biochemistry. An infected cut hosts a soup of cells and chemicals, and biologists know quite a lot about the recipe for that soup. They know almost nothing at all about what’s going on in RSIs.+Medzhitov yet again: “The mechanisms of infection-induced inflammation are understood far better than are those of other inflammatory processes. It is unclear how applicable knowledge of infection-induced inflammation is to other types of inflammation.” Also: “Unlike the signals that report infection and injury, the signals that report tissue stress and malfunction, and the molecular sensors that detect these signals, are largely unknown.”

But that is starting to change; experts have started to talk more about this. In a 2009 paper, tendinitis experts Cook and Purdam acknowledge that their basically non-inflammatory model of tendinitis nevertheless “can even encompass … some form of inflammation underpinning the cell and matrix response.”+Cook JL, Purdam CR. Is tendon pathology a continuum? A pathology model to explain the clinical presentation of load-induced tendinopathy. Br J Sports Med. 2009 Jun;43(6):409–16. PubMed 18812414 ❐ This paper is required reading for pros, by the way. More recently, in 2017, researcher Stephanie Dakin wrote: “the absence of clinically evident inflammation does not preclude an integral role for inflammatory mediators during the pathogenesis and healing of tendon injuries at a cellular level.”+Dakin SG, Newton J, Martinez FO, et al. Chronic inflammation is a feature of Achilles tendinopathy and rupture. Br J Sports Med. 2017 Nov. PubMed 29118051 ❐

Translation: just because you can’t see it, doesn’t mean it’s not there, or wasn’t there earlier. Maybe you just have to look better.

Which Dakin and her colleagues did. They simply looked for more subtle signs of inflammation … and found them, seemingly without much ambiguity. Their paper in British Journal of Sports Medicine showed that painful and ruptured Achilles “show evidence of chronic (non-resolving) inflammation.”

That paper now stands as the best available evidence so far that rumours of inflammation’s demise in tendinopathy are greatly exaggerated. But there are no other important sources I’m aware of — Dakin et al. cite only their own evidence on this.

As it so often is, the truth is in the middle

Looking at Dakin et al.’s results, it’s tempting to just concede that inflammation has made a comeback — it was never absent after all, it was just more subtle than the experts thought. Silly experts! It wouldn’t be the first time that kind of oversight has happened in medical science, not by a long shot.

But calling it “inflammation” may be largely meaningless if it doesn’t resemble classic inflammation or respond to anti-inflammatory treatments. Most anti-inflammatory treatments are aimed straight at classic, acute inflammation. Who cares if a tendon is “technically” inflamed if taking a drug designed to blunt a classic immune response is largely pointless?

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