Studies on the pathology and treatment of equine navicular disease

Abstract

This present study arose following the hypothesis that vascular occlusion and progressive ischaemia were involved in the pathogenesis of navicular disease. The study was designed so that an evaluation of the radiographic and pathological changes in the navicular bones and surrounding structures could be carried out in horses in which a clinical diagnosis of navicular disease had been made and these compared with the results of similar examinations in control horses with no evidence of lameness. Using clinical criteria combined with an objective method of assessment based on radiographic findings, the effects of different treatments of navicular disease were examined with particular emphasis on oral warfarin therapy. Of the 265 horses examined clinically, 90 constituted a control population, 151 had a lameness which was diagnosed as navicular disease and the remaining 24 horses, although they displayed a fore foot lameness similar to navicular disease, it fulfilled less than half the required clinical criteria and they were thus designated "not yet diagnosed" NYD. No one clinical feature was diagnostic of navicular disease in itself but it was concluded that the clinical diagnosis should be based on the presence of a number of clinical signs, and the response to a number of diagnostic aids. It is considered from this study that the particular type of work performed by a horse does not in itself predispose the animal to navicular disease but that irregular work, and sudden or prolonged periods of rest in an otherwise hard worked horse are predisposing factors. From radiographic examinations of the navicular bones of the horses in this study, no particular radiographic feature was considered to be diagnostic of navicular disease. The significant radiographic changes in the navicular bone in navicular disease were, an increase in number and change in shape and distribution of the distal nutrient foramina, the presence of nutrient foramina in the proximal border and radiolucent areas in the body of the bone. Some of these radiographic changes were found in the navicular bones of the control horses. The distal nutrient foramina were identified and classified according to their morphology and position and 7 basic types were found. Distal nutrient foramina, shaped other than conical were considered as abnormal. Examination of serial radiographs at intervals showed that the distal nutrient foramina could increase in number and show changes in their shape which were part of a progressive series of changes. An objective method of assessing radiographs of the navicular bone was developed which consisted of a scoring system based on the number shape and anatomical position of the distal nutrient foramina. Significantly higher scores per navicular bone were found in the navicular disease group than in the control group, although there was a degree of overlap between the groups. It is considered that this navicular scoring system provides a useful method of evaluating radiographs of the navicular bone, but should not be used as the sole criterion in the diagnosis of navicular disease. Pathological examination, which included gross pathology, radiography, microangiography, fluorescent microscopy following the administration of intra-vital fluorochrome bone labels to a number of horses, and light microscopy, showed that pathological changes were present in all of the navicular bones and deep flexor tendons in the navicular disease cases, and also in a small number of control cases. These pathological changes were present to different degrees and could be fitted into a pattern of increasing severity. The main pathological changes found in the navicular bone were, degeneration of the fiborcartilage, disruption and loss of the subchondral bone plate of the fibrocartilage surface, an overall increase in the vascularisation, remodelling or the trabeculae in the medulla, and in the deep flexor tendon there was disruption of tendon fibres. A significant positive correlation was found between the degree of gross pathological change present in the navicular bones and deep flexor tendons and the navicular score. No evidence of occlusive vascular disease or of bone necrosis was found in any of the navicular bones examined in this study. These- results do not therefore support the hypothesis that occlusive vascular disease and progessive ischaemia are involved in the pathogenesis of navicular disease. However, the overall increase in vascularisation and active bone remodelling, in the absence of obvious vascular occlusion and bone necrosis suggests that hyperaemia rather than ischaemia may be involved in the pathogenesis of this condition. Although the cause of the hyperaemia has not been established, there is evidence that active and/or passive hyperaemia could be involved. The treatments used in this study were, rest, oral warfarin therapy, corrective shoeing, phenylbutazone, neurectomy and isoxsuprine hydrochloride. The results of the treatments were assessed clinically and radiographically using the navicular scoring system. No significant difference was found between the results of the different treatments at 3-4, and 6-8 months from the start of treatments, but significantly better results were found with warfarin therapy, 1 year from the start of treatments. It is considered from the results of this study that the positive effects of warfarin and isoxsuprine hydrochloride in the treatment of navicular disease may not be related to the anticoagulant or vasodilator effects but may be associated with their ability to reduce blood viscosity and thus improve blood flow