Kristin Olstad

Background The neuro‐central synchondrosis (NCS) is a physis responsible for the growth of the dorsal third of the vertebral body and neural arches. When the NCS of pigs is tethered to model scoliosis, stenosis also ensues. It is necessary to describe the NCS for future evaluation of its potential role in equine spinal cord compression and ataxia (wobbler syndrome). Objectives To describe the NCS, including when it and other physes closed in computed tomographic (CT) scans of the cervical spine of foals, due to its potential role in vertebral stenosis. Study design Post‐mortem cohort study. Methods The cervical spine of 35 cases, comprising both sexes and miscellaneous breeds from 153 gestational days to 438 days old, was examined with CT and physes scored from 6: fully open to 0: fully closed . The dorsal physis, physis of the dens and mid‐NCS were scored separately, whereas the cranial and caudal NCS portions were scored together with the respective cranial and caudal vertebral body physes. Results The NCS was a pair of thin physes located in a predominantly dorsal plane between the vertebral body and neural arches. The mid‐NCS was closed in C1 from 115 days of age, and in C2–C7 from 38 days of age. The dorsal physis closed later than the NCS in C1, and earlier than the NCS in C2–C7. The dens physis was closed from 227 days of age. The cranial and caudal physes were closing, but not closed from different ages in the different vertebrae of the oldest cases. Main limitations Hospital population. Conclusions The NCS was a thin physis that contributed mainly to height‐wise growth, but also width‐ and length‐wise growth of the vertebral body and neural arches. The mid‐NCS was closed in all cervical vertebrae from 115 days of age. The NCS warrants further investigation in the pathogenesis of vertebral stenosis.

Recently, the central and third tarsal bones of 23 equine fetuses and foals were examined using micro-computed tomography. Radiological changes, including incomplete ossification and focal ossification defects interpreted as osteochondrosis, were detected in 16 of 23 cases. The geometry of the osteochondrosis defects suggested they were the result of vascular failure, but this requires histological confirmation. The study aim was to examine central and third tarsal bones from the 16 cases and to describe the tissues present, cartilage canals, and lesions, including suspected osteochondrosis lesions. Cases included 9 males and 7 females from 0 to 150 days of age, comprising 11 Icelandic horses, 2 standardbred horses, 2 warmblood riding horses, and 1 coldblooded trotting horse. Until 4 days of age, all aspects of the bones were covered by growth cartilage, but from 105 days, the dorsal and plantar aspects were covered by fibrous tissue undergoing intramembranous ossification. Cartilage canal vessels gradually decreased but were present in most cases up to 122 days and were absent in the next available case at 150 days. Radiological osteochondrosis defects were confirmed in histological sections from 3 cases and consisted of necrotic vessels surrounded by ischemic chondronecrosis (articular osteochondrosis) and areas of retained, morphologically viable hypertrophic chondrocytes (physeal osteochondrosis). The central and third tarsal bones formed by both endochondral and intramembranous ossification. The blood supply to the growth cartilage of the central and third tarsal bones regressed between 122 and 150 days of age. Radiological osteochondrosis defects represented vascular failure, with chondrocyte necrosis and retention, or a combination of articular and physeal osteochondrosis.