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Chronic inflammation is a feature of Achilles tendinopathy and rupture

PainSci » bibliography » Dakin et al 2017
updated
Tags: etiology, tendinosis, inflammation, inflam-sys, counter-intuitive, pro, pain problems, overuse injury, injury

Eighteen pages on PainSci cite Dakin 2017: 1. Icing for Injuries, Tendinitis, and Inflammation2. The Complete Guide to Trigger Points & Myofascial Pain3. The Complete Guide to IT Band Syndrome4. The Complete Guide to Low Back Pain5. The Complete Guide to Patellofemoral Pain Syndrome6. Complete Guide to Plantar Fasciitis7. Tennis Elbow Guide8. The Complete Guide to Muscle Strains9. Heat for Pain and Rehab10. Voltaren Gel: Does It Work?11. Guide to Repetitive Strain Injuries12. Anti-inflammatories and tendons13. Don’t count inflammation out of tendinopathy quite yet14. Pictures of spinal inflammation: a correlation kerfuffle15. The Proteins of Pain: Part 3, Spice Therapy (Member Post)16. Two reasons further research is perpetually needed17. What happened editorially on PainScience.com in 201818. Exercise is anti-inflammatory medicine for injuries (Member Post)

PainSci notes on Dakin 2017:

This paper now stands as the best available evidence so far that rumours of inflammation’s demise in tendinopathy are exaggerated/oversimplified. There are no other important sources I’m aware of so far (as of early 2020), and Dakin et al. cite only their own evidence on this.

original abstract Abstracts here may not perfectly match originals, for a variety of technical and practical reasons. Some abstacts are truncated for my purposes here, if they are particularly long-winded and unhelpful. I occasionally add clarifying notes. And I make some minor corrections.

BACKGROUND: Recent investigation of human tissue and cells from positional tendons such as the rotator cuff has clarified the importance of inflammation in the development and progression of tendon disease. These mechanisms remain poorly understood in disease of energy-storing tendons such as the Achilles. Using tissue biopsies from patients, we investigated if inflammation is a feature of Achilles tendinopathy and rupture.

METHODS: We studied Achilles tendon biopsies from symptomatic patients with either mid-portion tendinopathy or rupture for evidence of abnormal inflammatory signatures. Tendon-derived stromal cells from healthy hamstring and diseased Achilles were cultured to determine the effects of cytokine treatment on expression of inflammatory markers.

RESULTS: Tendinopathic and ruptured Achilles highly expressed CD14+ andCD68+ cellsand showed a complex inflammation signature, involving NF-κB, interferon and STAT-6 activation pathways. Interferon markers IRF1 and IRF5 were highly expressed in tendinopathic samples. Achilles ruptures showed increased PTGS2 and interleukin-8 expression. Tendinopathic and ruptured Achilles tissues expressed stromal fibroblast activation markers podoplanin and CD106. Tendon cells isolated from diseased Achilles showed increased expression of pro-inflammatory and stromal fibroblast activation markers after cytokine stimulation compared with healthy hamstring tendon cells.

CONCLUSIONS: Tissue and cells derived from tendinopathic and ruptured Achilles tendons show evidence of chronic (non-resolving) inflammation. The energy-storing Achilles shares common cellular and molecular inflammatory mechanisms with functionally distinct rotator cuff positional tendons. Differences seen in the profile of ruptured Achilles are likely to be attributable to a superimposed phase of acute inflammation and neo-vascularisation. Strategies that target chronic inflammation are of potential therapeutic benefit for patients with Achilles tendon disease.

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Specifically regarding Dakin 2017:

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