Epiphyseal Closure

Long bones lengthen at the epiphyseal growth plate, a cartilage disc where chondrocytes proliferate and are replaced by bone. Closure is the exhaustion and ossification of that disc, after which no linear growth is possible at that site. Growth hormone and IGF-1 set the rate of growth while the plate is open, but they do not decide when it shuts. That signal is oestrogen, acting through oestrogen receptor alpha on the plate itself, in both sexes.

The evidence comes from rare human mutations rather than animal work. Men with inactivating aromatase mutations, and a man described with a disruptive oestrogen receptor alpha mutation, continued growing into adulthood with radiographically open plates, tall stature and osteopenia despite normal or high testosterone. In the aromatase-deficient cases oestrogen closed the plates; in the receptor case it did nothing, which localises the effect to the receptor rather than to circulating hormone. Fusion usually completes in the middle-to-late teens, earlier in girls, and is staged on a hand and wrist radiograph read as bone age.

Closure is the hard boundary for any growth-promoting therapy. Growth hormone for short stature can only add height while the plates remain open, which is why bone age rather than chronological age governs starting and stopping. After closure the same excess produces the acromegalic pattern instead, with periosteal apposition thickening the skull, hands and feet.

The claim that recurs in adult peptide marketing is that growth hormone or a secretagogue can still add height. It cannot, and the observation offered as proof makes the point in reverse. Increasing shoe and ring size, a broadening jaw and coarsening features in an adult are the signature of appositional and soft-tissue growth on a closed skeleton, which is a sign of excess rather than renewed growth.