We know surprisingly little about the precise pharmacological effects of corticosteroids when they are injected directly into joints and soft tissues3 4 , 2 0 6.
Local steroid injections are thought to work by:
• Suppressing inflammation in inflammatory systemic diseases such as rheumatoid or psoriatic arthritis, gout, etc2 8 , 3 1 , 3 4 - 3 6 , 1 9 4 , 2 1 8
• Suppressing inflammatory flares in degenerative joint disease3 1 , 3 2 , 3 7 - 4 0 . The classic distinction between osteoarthrosis and osteoarthritis is not helpful, and there are no reliable clinical features to tell us how much 'osis' (wear and tear) and how much 'itis' (inflammation) is contributing to a particular
symptomatic joint4". Often, the only way to find out is to treat it
• Breaking up the inflammatory damage-repair-damage cycle, which is postulated to set up a continuous low-grade inflammatory response, inhibiting tissue repair and sound scar formation, while forming adverse adhesions4 1 , 4 2 . There is little direct evidence to support this, however
• Possibly a direct chondroprotective effect on cartilage metabolism or other effects not related to anti-inflammatory activity of the steroids, e.g. promotion
of articular surfactant production3 2 , 4 3 , 4 4 , 2 0 6 , 2 1 6 , 2 2 4 - 2 2 6 , 2 41
Inflammation is a complex cascade of molecular and cellular events that is often poorly understood by the clinicians who treat it3 1 6 , 3 1 7 . The precise
role of inflammation in 'tendinitis' is the subject of considerable debate, and many authors prefer the terms 'tendinosis' or 'tendinopathy' to describe the pathological changes4 5 - 4 8 . The pain might not be due to inflammation (tendinitis) or structural disruption of the tendon fibres (tendinosis), but to the stimulation of nociceptors by chemicals released from the damaged tendon4 9 . Corticosteroids (and possibly local anaesthetics) might affect
the release of noxious chemicals and/or the long-term behaviour of local nociceptors.
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