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“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 cause for chronic tendon pain, have already been discarded, as microdialysis studies showed no increase in prostaglandin E2 levels in chronically painful tendons compared with asymptomatic ones,2 3 and because no inflammatory cells are detected in histological examination of tendon tissue from patients with tendinopathy.4 The histological findings instead clearly point in another direction, implying that the condition is better characterised as a degenerative-like process, sometimes defined as “tendinosis”.4 A traditional theory regarding the cause of the pain is that pain derives from the separation of collagen fibres in severe cases of tendinopathy, but this suggestion has been heavily contradicted with convincing arguments by Khan et al,1 one such strong argument being that collagen excision from patellar tendons in autograft harvesting causes minimal pain to the donor site. Nevertheless, the physical strain to which the tendon is exposed is generally thought to be one of …
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