Fetal premature excess vertebral linear calcification: a case series

Author:

Bronshtein Moshe,Gover Ayala,Beloosesky Ron,Bachar Gal1ORCID,Khatib Nizar1

Affiliation:

1. Obstetrics and Gynecology, Rambam Health Care Campus, Haifa, Israel

Abstract

AbstractDuring embryogenesis, the vertebrae begin development during the 6th week of gestation via two lateral chondrification centers per segment. It was assumed that when disruptions occur in the process of somitogenesis during membranous vertebral body formation, chondrification and ossification will follow the anomalous membranous vertebral body scaffolding, resulting in an anomalous vertebral formation, such as a hemivertebra. Another hypothesis is that hemivertebra may result from anomalous distribution of intersegmental arteries of the vertebral column. There is no description in the medical literature of “excess linear calcifications” of part of the fetal vertebra, characterized by the presence of linear calcifications in the vertebrae of a developing fetus. In the first two trimesters of pregnancy, the fetal vertebrae usually show three calcified points in an axial section: the vertebral body and two transverse processes. Premature linear vertebral calcification was defined as an anterior or posterior echogenic connection between two of the points (Fig. 1). In this study, we describe seven cases of premature fetal linear vertebral calcification.

Publisher

Georg Thieme Verlag KG

Reference5 articles.

1. “Prenatal sonographic diagnosis of hemivertebra”;B Weisz;Journal of Ultrasound in Medicine,2004

2. “Genetics of non-isolated hemivertebra: A systematic review of fetal, neonatal, and infant cases;JE Powel;” Clinical Genetics,2022

3. “Microarchitectural and physical changes during fetal growth in human vertebral bone;S Nuzzo;” Journal of Bone and Mineral Research,2003

4. “Hemivertebra as a cause of scoliosis: A study of 104 patients;MJ McMaster;” Journal of Bone and Joint Surgery – Series B,1986

5. “Genetic aspects of early childhood scoliosis;JM Connor;” Am J Med Genet,1987

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