Abstract
Longitudinal bone growth is rapid in prenatal and early postnatal life, but then slows with age and eventually ceases. This growth deceleration is caused primarily by a decrease in chondrocyte proliferation, and is associated with other structural, functional, and molecular changes collectively termed growth plate senescence. Current evidence suggests that growth plate senescence occurs because the progenitor chondrocytes in the resting zone have a limited replicative capacity which is gradually exhausted with increasing cell division. In addition, recent experimental findings from laboratory and clinical studies suggest that growth plate senescence explains the phenomenon of catch-up growth. Growth-inhibiting conditions such as glucocorticoid excess and hypothyroidism delay the program of growth plate senescence. Consequently, growth plates are less senescent after these conditions resolve and therefore grow more rapidly than is normal for age, resulting in catch-up growth.