Glucocorticoids and laminitis in the horse

Although the administration of glucocorticoids to horses is widely believed to be associated with a risk of developing laminitis, attempts to experimentally induce laminitis with glucocorticoids have failed. In this chapter, we discuss potential pathophysiological mechanisms by which glucocorticoid treatment might predispose or exacerbate laminitis in the equine species. We will also introduce the concept that glucocorticoids may cause insidious structural changes in the hoof that resemble laminitis but that are not necessarily attended by pain and lameness. In this sense, conditions associated with glucocorticoid excess may lead to subclinical pathological changes at the pedal bone/hoof lamellar interface that resemble laminitis. We also review the role of 11(3-hydroxysteroid dehydrogenase in the regulation of cortisol in equine tissues and the extent to which changes in the cellular expression of this enzyme could promote cellular cortisol activity and lead to tissue changes associated with glucocorticoid excess.