Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
9354060 | Journal of Orthopaedic Research | 2005 | 8 Pages |
Abstract
The observed SP and CGRP upregulation in the paratenon and bony insertion suggests a pathophysiological role in paratenonitis and enthesitis often seen in patients with rheumatoid arthritis. Presumably Achillodynia originates in the tendon envelope rather than the tendon proper. The observations could be used to define new pharmacological targets for mitigating symptoms from tendons in rheumatoid arthritis and possibly also in other disorders. Whether a neuronal pathogenic mechanism underlies tendon overuse disorders in non-arthritic tendinopathies and the development of degeneration, i.e. tendinosis, remains to be studied.
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Authors
Daniel K.-I. Bring, Marie-Louise Heidgren, Andris Kreicbergs, Paul W. Ackermann,