How to tendinopathy: 1
About tendon injury
Tendinosis is tendinitis that can’t be proven to be associated with inflammation, but tendinitis is. Or maybe tendinosis might be failed repair of a previously inflamed tendon, so might be tendinitis then not tendinitis. Also, tendinosis is chronic and is not painful except when it is painful, and then maybe it’s tendinitis again. Unless its tenosynovitis, which definitely is inflammatory. Or maybe that was paratenonitis.
Confused yet?
If you are, you are part of long list of health care providers and researchers who have struggled with tendon pathology, the terminology used to describe it, and what to do about it when it is detected.
For some time authorities have been calling for a revision in the terminology used to describe tendon disruption and to more clearly explain the apparent discrepancies in understanding of how pain and structural change interact. For example, in 19981, research was published calling for just this, and suggesting that in fact the clinical entity that is expressed by pain, performance interruption and swelling should perhaps better be called tendinopathy.
Enter Jill Cook and colleagues, who, across two important publications, have proposed and revised a continuum model of tendon pathology, and refuted much of the current thinking regarding the pathophysiology of tendinopathy2,3 Their continuum model describes three phases of tendinopathy, with the reactive and degenerative phases straddling an intermediate tendon dysrepair phase2. They point out that the tendon is a dynamic structure, primarily acting to store and release energy, that responds and adapts to loading, and that structural change and nociception after a period of abusive loading2, analogous to injury, can occur at any point in the continuum3. They further suggest that models of tendon pathology which characterise pain by mechanisms of collagen disruption/tearing or inflammation are unlikely to be accurate3.
It is well worthwhile reading the two papers here and here.
It is also worth noting that the stages of the continuum model can be visualised with ultrasound imaging (see Figures A-D). Such imaging, incorporated into a clinical picture of tendinopathy characterised by a patient’s presentation and the specific interaction of pain, tissue change and function (more next time), is likely to help direct management of tendon pathology.
Figure A: the supraspinatus tendon that while thickened (7 mm thick) and mildly reduced echogenic, retains its normal collagen organisation.
Figure B: the common extensor origin at the lateral epicondyle of the elbow. The tendon has an increase in ground substance, the black bits are more prominent with a microcystic appearance.
Figure C: the Achilles tendon with collagen disorganisation speckled appearance, ‘white bits’ are disrupted.
Figure D: the Achilles tendon with extensive loss of collagen fibrillar echopattern, ‘white bits’, markedly disrupted, moderate to marked increase in ground substance ‘black bits’, and marked thickening (left of image). Intrasubstance tears will be present.
References:
Maffulli N, Khan KM, Puddu G. Overuse tendon conditions: time to change a confusing terminology. ArthroscJ Arthrosc Relat Surg Off Publ Arthrosc Assoc North Am Int Arthrosc Assoc. 1998;14(8):840–3.
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;43:409–16.
Cook JL, Rio E, Purdam CR, Docking SI. Revisiting the continuum model of tendon pathology: what is its merit in clinical practice and research? Br J Sports Med [Internet]. 2016;bjsports-2015-095422-. Available from: http://bjsm.bmj.com/content/early/2016/04/28/bjsports-2015-095422.short?rss=1