Histopathogenesis of thickening of the hoof wall laminae in equine laminitis [Equus prezewalskii]

Histopathological observation was conducted mainly on the laminar layers of 17 affected and 13 unaffected hoofs from 10 laminitis-affected horses and also on the branches of digital nerves and the vascular nerves of digital arteries and veins from laminitis-affected and 20 control laminitis-unaffected horses. The laminar layer in the laminitis-affected hoofs thickened and was 22.2±8.3 mm thick (A), while 6.6±4.1 mm in the laminitis-unaffected (B) and 3.7±0.9 mm in 43 control hoofs (C); there were significant differences between A and B, A and C, and B and C, respectively. Principal changes in the laminitis-affected hoofs were: (a) in the epidermal laminae, irregular striking growths of the epithelium, hydropic degeneration of ebithelial cells, nonformation, defective formation or degeneration of onychogenic fibrils, and formation of keratohyalin granules; (b) in the dermal laminae and laminar corium, edema, capillary and venular dilatation, and edema of the nerve bundles. The peripheral nerves, including the vascular nerves, showed frequent edema and/or multifocal loss of nerve fibers in the nerve bundles. The morphological entity of the thickening of the laminar layer was regenerative growths of the epidermal laminae in the line of defective onychogenic process (squamous metaplasia). The changes in the laminar layer may have been effected by circulatory disturbances and such a disorder of vascular movement as is inferred from the organic disturbances in the peripheral nerves may have played an important role as the origin of the circulatory disturbances.