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Epiphyseal cartilage canal blood supply to the metatarsophalangeal joint of foals
Authors:K OLSTAD  B YTREHUS  S EKMAN  C S CARLSON  N I DOLVIK
Institution:1. The Norwegian School of Veterinary Science, Department of Companion Animal Clinical Sciences, Section for Equine Medicine and Surgery, Post Box 8146 Dep., N‐0033 Oslo, Norway;2. National Veterinary Institute, Section for Wildlife Diseases, Post Box 8156 Dep., N‐0033 Oslo, Norway;3. The Swedish University of Agricultural Sciences, Department of Biomedical Sciences and Veterinary Public Health, Division of Pathology, Pharmacology and Toxicology, Box 7028, SLU SE‐750 07, Uppsala, Sweden;4. The University of Minnesota, College of Veterinary Medicine, Department of Veterinary Population Medicine, 435H AnSci/VM, 1988 Fitch Avenue, St Paul, Minnesota 55108 USA.
Abstract:Reasons for performing study: It is presently unknown whether cartilage ischaemia plays any part in the pathogenesis of osteochondral fragmentation within the equine metatarsophalangeal joint, as no detailed studies on microcirculation in the area have been reported. Objective: To describe the developmental pattern of the blood supply to the epiphyseal growth cartilage in the metatarso‐phalangeal joint of foals. Methods: Eight Standardbred foals were sacrificed between birth and age 7 weeks to undergo a barium perfusion procedure to demonstrate vessels within growth cartilage canals of one hindlimb. The metatarso‐phalangeal joint was cleared in methyl salicylate and perfused vessels studied in the intact bones. The bones were sawed into 5 mm thick slabs, decalcified and radiographed. Selected slabs were cleared in methyl salicylate for a second time and examined at low magnification. The dorsal half of the sagittal ridge of the distal third metatarsal bone and the plantar half of the proximal phalanx were examined histologically. Results: Regions of the epiphysis with thick cartilage contained a greater number of perfused vessels than regions with thin cartilage. The cartilage canal vessels were oriented either parallel or perpendicular to the underlying ossification front. Cartilage canal vessels were incorporated into the ossification front during growth and became reliant on a subchondral arterial source. Macroscopically visible lesions were not detected in the current group of foals. On histological examination, pathological changes consisting of an area of chondronecrosis surrounded by fibrovascular granulation tissue were found in sections from the lateral proximo‐plantar eminence of the proximal phalanx in the 7‐week‐old foal. Conclusion: The same anatomical feature (traversing the ossification front to enter cartilage canals) reported to render vessels vulnerable to failure in the tarsus was also present in the metatarso‐phalangeal joint of foals. Potential relevance: Osteochondrosis may occur by the same pathogenetic mechanism in the metatarso‐phalangeal joint as in the tarsus of foals.
Keywords:horse  foal  metatarso‐phalangeal joint  cartilage canals  osteochondrosis
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