Abstract

Longitudinal bone growth occurs in the growth plate through a process in which resting zone chondrocytes are recruited to start active proliferation and then undergo differentiation, followed by apoptosis and later mineralization. Bone growth is controlled by a multitude of genes encoding for hormones and growth factors acting systemically and/or locally in the growth plate. From studies of individuals with a mutated aromatase gene and a male patient with defective oestrogen receptor (ER) α, it has become clear that the action of oestrogen is indispensable for normal pubertal growth and growth plate fusion. As new aromatase inhibitors and specific modulators of ERs are developed, these could offer more specific ways to modulate longitudinal growth and growth plate fusion. It is difficult to extrapolate data obtained in experimental animals, as clear species differences exist, emphasizing the need for new models that will allow studies in human growth plate cartilage.

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