Human growth plate development in the fetal and neonatal period

Abstract

The development of the normal human upper tibial growth plate was studied at autopsy in 46 stillborns and 79 newborns of 20-41 weeks gestational age. During this time period, the histology of this plate evolves from a highly cellular structure with relatively poor columnar organization and matrix development to the well known structure seen later in postnatal life. The thickness of the growth plate, assessed in the area surrounding the longitudinal tibial axis, decreases continuously from 1.15 mm on the 20th week to 0.6 mm on the 38th week. This decrease results from losses of both matrix and cellular components, mostly of the latter. However, the relative fraction of area occupied by the matrix significantly increased (12%) and matrix area per cell increased 1.5 times over the last half of gestation, indicating a maturation process of the plate towards a more matrix-oriented structure with age. In this maturation process the number of cells per unit area does not change and the average size of the cells appears to decrease. Plate thickness does not decrease further in the final 3 weeks of pregnancy and increases in early neonatal life; this has no apparent influence on the tibial growth rate. In the period under study the relative anatomical participation of the upper tibial growth plate decreases from approximately 4% of the radiographic length of the tibia on the 20th week to less than 1% at term. Present data will provide fetal and neonatal growth plate standards needed to obtain a better understanding of this structure during both normal and abnormal conditions.

Lethal neonatal Hutchinson-Gilford progeria syndrome

“…The severe attenuation of the growth plate in the distal phalanges produced insufficient bone and, consequently, hypoplastic terminal phalanges. This finding could be related to a premature closure only in phalanx growth plate cartilages since the long bones were unaffected and normally developed [Rodríguez et al, 1992]. The present patient also showed premature regression of hair follicles and of the renal nephrogenic layer, other abnormalities that would be related to premature aging.…”

Quantitative analysis of trabecular morphogenesis in the human costochondral junction during the postnatal period in normal subjects

“…Quantitative studies of development at the growth plate have examined the cartilage matrix and chondrocytes (Buckwalter et al, 1986;Gruber and Rimoin, 1989;Gruber et al, 1990;Hunziker et al, 1987;Kember and Sissons, 1976;Kimmel and Webster, 1980;Mirralles-Flores and Delgado-Baeza, 1992;Rodriguez et al, 1992b), but failed to quantify the development of trabecular structure, which follows the orientation of cellular columns of the growth plate. In this study, the area within 3.78 mm of the resting zone starting point was sampled, representing the equivalent of ,17 days growth at the costochondral junction (based on a growth rate of 0.220 mm/day) (Emery and Kalpaktsoglou 1967).…”

Mechanism of longitudinal bone growth and its regulation by growth plate chondrocytes

“…In morphological appearance, the growth plate is unique and striking owing to its highly anisotropic and distinct cellular organization (Brighton, 1978;Hunziker et al, 1987;Rodriguez et al, 1992). The chondrocytes are arranged into vertical columns (see Fig.…”