Abstract
Glucocorticoids have a direct, inhibitory effect on the growth plate, as demonstrated by in vivo and organ culture studies. Glucocorticoids slow longitudinal bone growth by inhibiting chondrocyte proliferation, hypertrophy, and cartilage matrix synthesis. The molecular mediators of these effects are poorly understood. Glucocorticoids also delay growth plate senescence. The decreased rate of senescence appears to be a consequence of the growth inhibition and, in particular, may occur because glucocorticoids slow proliferation of stem-like cells in the resting zone and therefore conserve the limited proliferative capacity of these cells. This slowing of senescence appears to explain the phenomenon of catch-up growth following transient glucocorticoid exposure. After the exposure, the growth plate is less senescent, and therefore grows more rapidly than is normal for age. Glucocorticoids cause growth inhibition and subsequent catch-up growth not only in terms of longitudinal bone growth at the growth plate but also in terms of cross-sectional bone growth at the periosteum. Whether the underlying mechanisms are analogous to those at the growth plate is not known.