British Journal of Sports Medicine 2009;43:265-268
Original articles
Reviving the "biochemical" hypothesis for tendinopathy: new findings suggest the involvement of locally produced signal substances
Dr P Danielson, Department of Integrative Medical Biology, Anatomy, Umeå University, SE-901 87 Umeå, Sweden; patrik.danielson@anatomy.umu.se
Accepted 9 October 2008
| The first 150 words of the full text of this article appear below. |
"A hypothesis is... the obligatory starting point of all experimental reasoning. Without it no investigation would be possible and one would learn nothing...". These are the words of the 19th-century French scientist Claude Bernard, widely considered as the father of modern experimental physiology.
Many hypotheses have been put forward over the years in attempts to explain the still incompletely clarified aetiology and pathogenesis of chronic tendon pain (tendinopathy). At the turn of the millennium, Khan et al made new intriguing suggestions,1 partly contradicting previously presented theories on the cause of tendinopathy. They speculated that biochemical mediators in the tendon tissue might influence or irritate nociceptors in or around the tendon. Half a decade later, novel findings of non-neuronal production of signal substances in human tendon cells (tenocytes) in tendinopathy seem to give new support to such a "biochemical" hypothesis.
Old "tendinitis" theories, assuming an inflammatory process as the
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