Peri-tendinous injection of local anaesthetic,
both alone and in combination with corticosteroids, is commonly performed
in the treatment of tendinopathies. Previous studies have shown
that local anaesthetics and corticosteroids are chondrotoxic, but
their effect on tenocytes remains unknown. We compared the effects
of lidocaine and ropivacaine, alone or combined with dexamethasone,
on the viability of cultured bovine tenocytes. Tenocytes were exposed
to ten different conditions: 1) normal saline; 2) 1% lidocaine;
3) 2% lidocaine; 4) 0.2% ropivacaine; 5) 0.5% ropivacaine; 6) dexamethasone
(dex); 7) 1% lidocaine+dex; 8) 2% lidocaine+dex; 9) 0.2% ropivacaine+dex;
and 10) 0.5% ropivacaine+dex, for 30 minutes. After a 24-hour recovery
period, the viability of the tenocytes was quantified using the
CellTiter-Glo viability assay and fluorescence-activated cell sorting
(FACS) for live/dead cell counts. A 30-minute exposure to lidocaine
alone was significantly toxic to the tenocytes in a dose-dependent
manner, but a 30-minute exposure to ropivacaine or dexamethasone
alone was not significantly toxic. Dexamethasone potentiated ropivacaine tenocyte toxicity at higher
doses of ropivacaine, but did not potentiate lidocaine tenocyte
toxicity. As seen in other cell types, lidocaine has a dose-dependent
toxicity to tenocytes but ropivacaine is not significantly toxic.
Although dexamethasone alone is not toxic, its combination with
0.5% ropivacaine significantly increased its toxicity to tenocytes.
These findings might be relevant to clinical practice and warrant
further investigation.
Osteoarthritis (OA) is an important cause of
pain, disability and economic loss in humans, and is similarly important in
the horse. Recent knowledge on post-traumatic OA has suggested opportunities
for early intervention, but it is difficult to identify the appropriate
time of these interventions. The horse provides two useful mechanisms
to answer these questions: 1) extensive experience with clinical
OA in horses; and 2) use of a consistently predictable model of
OA that can help study early pathobiological events, define targets
for therapeutic intervention and then test these putative therapies.
This paper summarises the syndromes of clinical OA in horses including
pathogenesis, diagnosis and treatment, and details controlled studies
of various treatment options using an equine model of clinical OA.