[Development and progression of pyogenic spondylitis in a canine experimental model].

An experimental model was prepared to investigate the process of inflammation in pyogenic spondylitis. Forty-seven mongrel dogs were used, involving 24 mature and 23 immature dogs. Under intravenous pentobarbital anaesthesia, the lumbar vertebral bodies were approached posterolaterally and inoculated using a small piece of gauze soaked in a staphylococcus aureus suspension. Roentgenographic and histological examinations were regularly performed for 24 weeks after the inoculation. Histologically, acute inflammation started within 1 or 2 weeks, and subsided by 5 or 6 weeks in both the mature and immature dogs. In 55% of the dogs, the inflammation was confined within the vertebral body, in 10% it invaded into the intervertebral disc, and in 35% inflammation invaded into the anterior longitudinal ligament. In the immature dogs, thickening of the trabeculae and the anterior cortex was observed around the inflammatory focus more often than in the mature dogs. The epiphyseal line acted as a barrier against invasion by the inflammation in the immature dogs. However, direct invasion of the inflammatory process into the disc could have occurred through the vascular buds which were the terminal branches of the metaphyseal artery close to the disc in both the mature and immature dogs. In contrast to the results reported by Ohno who inoculated the lumbar discs of mongrel dogs with staphylococcus aureus, in the present study, the disc space remained intact and was replaced by fibrous tissue. Consequently, it was concluded that pyogenic spondylitis should be defined as a different clinical entity from discitis.