Achilles’ Tendon Rupture Caused by Microbial Influences: a Feasible Aetiology?
Refereed conference paper presented and published in conference proceedings

Full Text

Other information
AbstractAchilles’ tendon ruptures are typically associated with chronic Tendinopathic structural alterations. Given the insidious nature of Tendinopathy, failed tendon healing may result from exposure to direct or indirect risk factors with long incubation periods such as microbes. There are a number of examples of microbe-induced matrix degeneration, for example, chronic myocarditis may, in some cases, be linked to viruses and bacteria, which lead to activation of nucleotide-binding oligomerisation domain (NOD) containing proteins and results in cell apoptosis and matrix disturbance similar to that in Tendinopathy in peripheral tendons. At least three reported cases of Tendinopathy were found to be linked to bacteria, two cases to Borrelia burgdorferi (Lyme disease) and one case to Mycobacterium tuberculosis. We propose a theory that microbial influences may play a role in the development of chronic Tendinopathic changes, occasionally leading to complete tendon rupture.

We detected the presence of microbial footprints in 8 out of 24 operated Achilles’ tendon rupture samples, being positive for 16S rRNA (33.3%), while healthy hamstring tendon samples (n=24) were all negative. Serological findings also suggest higher microbial exposure in a similar sized group of patients with Achilles’ tendon rupture, than that in a control group of healthy subjects. As expression of NOD1 is prevalent in many Tendinopathy samples but not in healthy tendon samples, it is possible that these findings combined reflect an activation of NOD pathways in tendon cells which could contribute to pathological structural changes associated with failed tendon healing. In an experimental model, we treated cultured healthy tendon-derived stem cells with diaminopimelic acid (DAP; an agonist of NOD1) and demonstrated a significant up-regulation in NOD1 and interleukin-1 beta (IL-1β). As cyclic stretching (mimicking overuse) on tendon cells also leads to increased IL-1β expression and altered cellular activities related to failed tendon healing, the current evidences suggest that microbes may play a role in the pathogenesis of Tendinopathy.

Although a direct causal relationship between microbes, Tendinopathy and tendon rupture is not established, the implications of further supportive evidence may lead to novel, evidence-based treatment for Tendinopathy, which may potentially prevent some complete tendon ruptures, in the long-run.
All Author(s) ListROLF Christer, HOPKINS Chelsea
Name of Conference5th CUHK International Symposium on Stem Cell Biology and Regenerative Medicine
Start Date of Conference12/11/2015
End Date of Conference12/11/2015
Place of ConferenceHong Kong
Country/Region of ConferenceHong Kong
Place of PublicationChina, Hong Kong
LanguagesEnglish-United Kingdom

Last updated on 2021-07-05 at 11:06