A study on the pathogenesis of equine sesamoiditis: the effects of experimental occlusion of the sesamoidean artery.

In this study the potential role of circulatory disturbances in the pathogenesis of sesamoiditis was investigated by studying the clinical and histological effects of experimental occlusion of the sesamoidean artery, which is the main nutrient artery of the proximal sesamoid bone (PSB). For this purpose, five adult Dutch Warmblood horses were used in which the sesamoidean artery was occluded with polyvinyl alcohol foam particles. Bone labelling was carried out with oxytetracycline and calcein. All animal were checked clinically three times a week and radiographically at days 14, 21, 28 and 35. At day 35 the animals were killed and the fetlock was dissected and macroscopically evaluated. The PSBs were isolated and radiographed and the soft tissues adjacent to the abaxial side of the PSBs were histologically examined [routine histology and for the neuropeptides substance P (SP) and calcitonin gene-related peptide (CGRP)]. The PSBs were divided into bony slices which were radiographed and evaluated histologically (routine, SP, CGRP, fluorescence). All horses showed a slight lameness that gradually diminished. Radiographically enlarged vascular channels were seen in only one horse. Histological data showed that on average 60% (range 37-89%) of the total area had been deprived of vascularization. In two horses an increase in the extent of the arterial network from the basal side of the PSB was seen. Only in the horse with the greatest extent of occlusion were bone necrosis and a reactively increased uptake of fluorochromes adjacent to the occluded arteries found. Bone density did not change. The distribution of neuropeptides in the surrounding soft tissues was not affected by the occlusion. From this study, it can be concluded that a large part of the arterial supply to the PSB can be interrupted without provoking histological and/or radiographic changes that are consistent with clinical sesamoiditis. Therefore, it seems very improbable that circulatory disturbances are a primary aetiopathogenic factor in the disease.