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We read with interest the paper by Nwosu et al1 recently published in Annals of the Rheumatic Diseases. They clearly provided evidence that blocking tropomyosin receptor kinase A (TrkA), the p140 high-affinity receptor of nerve growth factor (NGF), by a selective TrkA inhibitor AR786 relieves pain in two different rat models of osteoarthritis (OA). A reduction of synovitis was also shown by histopathology, suggesting that NGF inhibition exerted its effect at peripheral level on extraneural tissues. Authors concluded that inhibition of NGF activity might be an effective strategy as treatment of OA pain. Indeed, NGF may have pleiotropic effects, and we would like to speculate on the possible role played by NGF and its counter-receptor …
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