Advances in musculoskeletal medications (Proceedings)
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:
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.