Oestrogen and growth plate fusion
Oestrogen determines when the epiphyseal growth plates (growing cartilage near the ends of the long bones, those of the arms and legs) fuse into solid bone, ending growth in height.
Remember
Oestrogen is the timer that decides when the growth plates fuse and growth ends, in both sexes. Growth hormone and insulin-like growth factor 1 (IGF-1, a hormone made mainly by the liver) drive growth without closing the plates.
Memory aid
Growth hormone and IGF-1 are the accelerator; oestrogen is the timer.
Picture growth hormone and IGF-1 as the accelerator that drives growth, and oestrogen as the timer that decides when it stops.
Growth in height happens at the epiphyseal growth plates, areas of growing cartilage near the ends of the long bones (the bones of the arms and legs). When a plate fuses, solid bone replaces the cartilage and the bone can no longer lengthen. Adult height is reached when the plates fuse.
Oestrogen, the main female sex hormone, determines when this happens: the more oestrogen exposure, the earlier the plates fuse. Laboratory studies suggest that oestrogen does not turn cartilage into bone directly. Instead, it speeds up the plate's programmed ageing (senescence), in which the cartilage cells gradually lose their ability to divide.
Females have higher oestrogen exposure, so their plates fuse sooner and their growth ends sooner. Males also make oestrogen, partly by aromatisation, the conversion of testosterone to oestrogen by the enzyme aromatase, and this oestrogen eventually closes their plates too. But they have lower oestrogen exposure early in puberty, so fusion is delayed and growth continues for longer. So men are, on average, taller than women mainly because fusion of their plates is delayed.
Growth hormone and IGF-1 drive growth rather than ending it: they are the accelerator, and oestrogen is the timer. Testosterone is not the main stop signal in its own right, because the oestrogen made from it by the enzyme aromatase contributes to fusion. In aromatase deficiency, a rare inherited condition in which the body cannot convert testosterone to oestrogen, affected men have high testosterone but keep growing into adulthood because their plates stay open.
Key facts
- What ends growth
- fusion of the epiphyseal growth plates, when solid bone replaces the cartilage and the long bones can no longer lengthen
- Oestrogen and timing
- the higher the oestrogen exposure, the earlier the plates fuse, and this applies in both sexes
- Why males end taller
- males are exposed to less oestrogen early in puberty, so their plates stay open longer and they keep growing for longer
- Spurt timing
- on average girls begin the growth spurt (the rapid rise in height of puberty) at about 9 years against about 11 years in boys
- Growth drivers
- growth hormone and IGF-1 support growth but do not close the plates
- Aromatase deficiency
- men who cannot convert testosterone to oestrogen have high testosterone yet keep growing, because their plates fail to close
Exam traps
- Testosterone is not what directly keeps the growth plates open, because oestrogen formed from it by aromatisation ultimately promotes fusion rather than preventing it.
- Growth hormone does not explain why males end up taller, because it works through IGF-1 to drive growth in both sexes and so affects how fast children grow rather than when growth stops.
- An earlier onset of the growth spurt in males is the reverse of the real pattern, because on average girls begin their spurt first, at about 9 years against about 11 years in boys.
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