Lui Julian C, Baron Jeffrey
Endocr Dev. 2011;20:187-193. doi: 10.1159/000321244. Epub 2010 Dec 16.
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.
体内和器官培养研究表明,糖皮质激素对生长板有直接抑制作用。糖皮质激素通过抑制软骨细胞增殖、肥大和软骨基质合成来减缓纵向骨生长。这些作用的分子介质尚不清楚。糖皮质激素还会延迟生长板衰老。衰老速率降低似乎是生长抑制的结果,特别是可能因为糖皮质激素减缓了静止区类干细胞的增殖,从而保留了这些细胞有限的增殖能力。衰老减缓似乎可以解释短暂接触糖皮质激素后出现的追赶生长现象。接触后,生长板衰老程度较低,因此生长速度比同龄人正常生长速度更快。糖皮质激素不仅会导致生长板纵向骨生长受到抑制并随后出现追赶生长,还会导致骨膜处横向骨生长受到抑制并随后出现追赶生长。其潜在机制是否与生长板处的机制类似尚不清楚。