more likely to have trophic and anti-inflammatory roles rather than a direct
structural effect. There are a number of different sources of MSCs, with bone
marrow and fat being the most commonly used.
When tested in the CSU equine OA model, injection of MSCs resulted either
in significant improvement in PGE2 level for bone marrow derived MSCs but
significant increase in TNFa level for fat derived MSCs. However, neither stem
cell preparation was able to improve lameness associated with OA. Therefore
the authors concluded the use of MSCs could not be recommended for
treatment of OA (Frisbie et al 2009).
One study has supported the treatment of soft tissue injuries in the
femorotibial joint with arthroscopy and concurrent MSC injections as more
favourable results were claimed in comparison with historical data of horses
treated with arthroscopic debridement alone (Ferris et al. 2009 and 2014). Our
experience with MSCs has been poor in any joint with obvious OA changes.
SYSTEMIC MEDICATIONS
Non steroidal anti-inflammatory drugs
Anti-inflammatory therapy is required to resolve or control the pain resulting in
lameness. Generally, the best plan is to do the minimum required to keep the
horse effectively in work, because more treatment will probably be required
eventually. Each horse is different and requires discovery of an effective
treatment schedule. A starting point includes systemic phenylbutazone (2.2
mg/kg, BID), which can be continued for an extended period of time in most
horses or given only when the horse is worked.
All NSAIDs inhibit cyclooxygenase (COX) activity to some degree, but more
recently two different isoenzymes called COX-l and COX-2 were reported with
potential importance in the horse. COX-2 is associated with inflammatory
events, especially those driven by macrophages and synovial cells, plays a
minor role in normal physiology, and is considered the “bad” or “inducible”
portion of the COX pathway. Drugs that preferentially inhibit COX-2 include
carprofen, firocoxib, metacam, ketroloac and etirocoxib, but the claims of
selective COX-2 inhibition and increased clinical benefit in the face of
improved safety relative to phenylbutazone remain unproven in the horse.
COX-2 inhibitors for horses are also a lot more expensive than
phenylbutazone.
A topical NSAID preparation, containing 1% diclofenac sodium cream could
be clinically beneficial while reducing systemic side effects and has promising
anti-inflammatory results.
Bis-phosphonates
Tiludronate and clodronate inhibit osteoclast activity and have been used in
horses with distal tarsal pain and navicular disease. In a limited double-blind
clinical trial of 8 horses with lameness confirmed to originate in the distal
tarsal joints given 1 or 2 single IV doses, 1 horse improved (Dyson 2004).
More recently, a larger study using 86 horses showed an average
improvement of 2 (out of 10) lameness grades in horses treated with an
infusion of tiludronate and a controlled exercise regime, which was
significantly better than the improvement seen in horses in the placebo group
15-‐18
February
2016
East
London
Convention
Centre,
East
London,
South
Africa
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