Selection of treatments for joint disease in horses is complicated by the fact that there are so many options to choose from.
Consequently, the decision for use of a specific medication or group of medications is often dictated by subjective decision
making and word of mouth. With this in mind, the goals of using medication for management of joint disease are:
1. Relieve pain and inflammation in and around the joint
2. Restore the normal anabolic/catabolic balance within the joint
3. Improve strength and conditioning
4. Preemptively manage the disease process
Intraarticular corticosteroid use in horses is widespread and used in all breeds and disciplines. Information concerning the
use of corticosteroids for treating joint pain in horses has been in the literature for over 50 years. Since that time there
have been numerous objective studies, both clinical and experimental, that have evaluated the use of the medication. In vivo
studies have shown that betamethasone (BM) had no detrimental effects in an osteochondral fragment model of osteoarthritis.
However, it is only available at this time in compounded form, leading exposure of veterinarians to potential liability claims.
Methylprednisolone acetate (MPA) has been shown to cause a nonsignificant reduction in lameness in the same model, but also
to cause significant reduction in synovial fluid PGE2, and intimal hyperplasia and vascularity in the synovial membrane. However,
articular cartilage damage was worse in treated joints. Using these data, and data obtained from other studies, it has been
concluded that MPA causes articular cartilage damage in high-motion joints with repeated use. Triamcinolone acetanide (TA)
has also been studied using the OA model, and induced significant decrease in lameness, decrease in synovial fluid total protein,
increase in synovial fluid hyaluronan and glycosaminoglycan concentrations, and significant synovial membrane and articular
cartilage benefits both in treated and remote joints. This has lead to the conclusion that TA may actually be chondroprotective.
However, the biggest drawback to the use of TA is its perceived potential for causing laminitis, limiting its use for treatment
of multiple joints in a single horse.
Corticosteroid-induced laminitis is thought to result from the ability of glucocorticoids to induce insulin resistance in
cells. This has been shown experimentally in horses treated with systemic TA at a dose of 0.05 mg/kg, specifically resulting
in hyperglycemia, hyperinsulinemia and hypertriglyceridemia. The reduction in glucose use by the peripheral tissues has been
shown to induce separation between basal epidermal cells and their basement membrane, which is classic for hoof separation
in laminitis. However, a review of clinical cases in one hospital showed that for horses without a history of laminitis, 40
– 80 mg of TA per horse did not induce laminitis in 205 horses. Until publication of this paper, 18 mg per horse was the recommended
dose, which was based on review of clinical cases in which no incidence of laminitis resulted in 1500 doses of TA when given
at or below that dose. Regardless of these reports, however, there are still anecdotal reports of laminitis occurring shortly
after doses of TA are given, and widespread use of high doses. It is uncertain whether the McCluskey, et al paper has dictated
that the standard of care for TA dosing be raised.
Another contentious point often raised is the ability of MPA to induce ankylosis in low motion joints, specifically the distal
intertarsal and tarsometatarsal joints. Objective studies have repeatedly shown that MPA can induce significant articular
cartilage erosion in high motion joints. However, it is unknown whether the same can occur in low motion joints. There is
no clinical or experimental evidence to show that MPA induces ankylosis in low motion joints, and in fact, facilitated ankylosis
is often necessary due to failure of intra-articular medication to control joint pain.