The appearance and union of the various centers of ossification follow a fairly definite pattern and time schedule from birththrough adolescence. This process provides, through x-ray studies, a valuable criterion for estimating normal and abnormagrowth. The skeletal maturity of any person is known as the bone age.

Bone maturation is particularly influenced by theandrogenic and estrogenic hormones. In congenital adrenal hyperplasia, a deficiency of enzyme (21-hydroxylase in 80% ocases) causes an interruption in the pathway for production of Cortisol; the end result is hypersecretion of androgenicprecursors and clinical manifestations of virilism and protein anabolism.

In both males and females, muscles are welldeveloped and there is rapid growth in stature, with marked acceleration of osseous maturation. The result is early closureof epiphyses and failure to achieve full growth. Thyroid hormone appears to act as a primary stimulant to skeletalmaturation. Deficiency of thyroxine results in marked retardation of bone age.

Failure to thrive as a consequence ofprofound environmental deprivation is characterized by very low levels of circulating pituitary hormones and is associatedwith a delay in skeletal maturation. Removal of the child from the abnormal environment results in dramatic catch-up growtand a rapid return of hormone levels to normal.

Glucocorticoid excess, either endogenous or exogenous, is usuallyassociated with a decrease in the rate of growth and a delay in the onset of puberty, the exception being a case ofglucocorticoid excess resulting in significant virilization and rapid closure of growth plates. The effects of glucocorticoidexcess appear to be mediated at end-organ sites as part of the catabolic effects of these steroids..

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Bone age .-::80463::-.