osteoarthritic lesions. For this reason, some authors have classified
corticosteroids as DMOADs through their inhibition of important mediators of
inflammation, interleukin-1 (IL-1), and tumor necrosis factor-α (TNF-α),
prostanoids, nitric oxide, matrix metalloproteinases (MMPs) and other related
proteinases. Pain relief in particular has been associated with their inhibition
of prostaglandin synthesis through blockage of the arachidonic acid cascade.
Moreover, some authors have attributed chondroprotective effects to
corticosteroids used at low concentrations, thanks to the inhibition of
interleukin-1 (IL-1) and tumor necrosis factor-a (TNFa). Frisbie et al. (1997)
demonstrated evidence of disease modification in an osteoarthritis model in
horses where cartilage from triamcinolone-treated (but not from
methylprednisolone- or betamethasone-treated joints) was found to have
superior mechanical properties in comparison with untreated control joints.
Other in vivo animal studies have demonstrated cartilage-sparing effects of
low-dose corticosteroids without marked effects on chondrocyte health.
Even so, descriptions of the deleterious effects of corticosteroids on cartilage
have been numerous in the past. There has been long-standing controversy
about the possibility of accelerated cartilage degeneration resulting in ‘steroid
arthropathy’. Deleterious efffects include loss of GAGs and decreased GAG
synthesis, inhibition of proteoglycan and hyaluronic acid synthesis,
chondrocyte necrosis, and hypocellularity. It has been suggested that these
detrimental effects on cartilage were due mainly to the high concentrations
and extended exposures used in earlier studies. Different clinical models have
shown less detrimental effects and even demonstrated some cartilage-sparing
effects especially with the use of low dose corticosteroids. Thus it was shown
that the levels required to influence cartilage matrix synthesis adversely
exceed those required to inhibit the synthesis of the inflammatory mediators of
degradation. It is clear that intra-articular corticosteroids can beneficial when
used judiciously. Adverse effects are still seen following indiscriminant use of
repeated injections of high doses of corticosteroids in vigorously exercised
horses, such as with so-called annual or bi-annual ‘maintenance’ injections
with corticosteroids practiced by some equine sports disciplines.
Post-injection flares are rarely associated with corticosteroids, but they may
be caused by the microcrystalline characteristics of corticosteroid
preparations. The incidence of infection related to corticosteroid injection is
low, and the onset of symptoms is usually delayed for up to 10 days due to
the powerful ability of corticosteroids to inhibit inflammation. It must be born in
mind that corticosteroids can falsely lower WBC count post CS injection.
Corticosteroid-induced laminitis is devastating but fortunately very rare. In one
study of 205 horses injected with triamcinolone at a dosage between 10 to 80
mg/treatment, only 1 of 205 horses was shown to have developed laminitis
related to the corticosteroid administration. It is generally felt that obese horse
or horses which may be predisposed to equine me tabolic syndrome are more
likely to develop this complication. Furthermore, the risk is probably greatest
in horses in which multiple joints are being treated.
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February
2016
East
London
Convention
Centre,
East
London,
South
Africa
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