Ortoft Gitte, Andreassen Troels T, Oxlund Hans
Department of Connective Tissue Biology, Institute of Anatomy, University of Aarhus, DK-8000, Aarhus C, Denmark.
Bone. 2005 Jan;36(1):123-33. doi: 10.1016/j.bone.2004.07.015. Epub 2004 Dec 16.
We evaluated the effect of glucocorticoids (GC) and growth hormone (GH) on cortical and cancellous bone turnover in adult rats using random vertical sections giving valid measurements of bone surfaces and bone formation parameters. GH administration could reverse GC-induced osteopenia and low bone turnover of cortical bone. However, GH could not reverse the GC-induced low bone turnover of cancellous bone.
Seventy female Wistar rats, 7 months of age, were divided into five groups: (1) start control, (2) saline, (3) GC 9 mg/kg/day (Solu Medrol), (4) GH 5 mg/kg/day, and (5) GC 9 mg/kg/day + GH 5 mg/kg/day, and injected for 3 months. The vertebral body was examined using dynamic histomorphometry and biomechanical tests. Nonparametric methods were used.
Glucocorticoid administration induced a low bone turnover state of both the cortical and cancellous bone of the vertebral body, without altering the absolute amount of bone or the biomechanical competence of the vertebral body. GH administration induced a small increase in longitudinal bone growth and ventral modeling drift. This growth increased the total amount of cortical, endocortical, and cancellous bone in the vertebra. The biomechanical competence of a 3.5-mm-high cylinder of the central vertebral body was also increased due to an increase in the amount of cortical bone, whereas the total amount of cancellous bone in the cylinder was unaltered. The cancellous bone density (CBV) was, however, increased due to thicker trabeculae probably induced by an accelerated mineral appositional rate (MAR) induced by GH. GH also increased longitudinal and ventral modeling drifts in the GC-injected animals. GH increased the amount of cortical bone and also the amount of cancellous bone close to the epiphyseal growth plate, whereas the cancellous bone volume of the central vertebral cylinder was unaffected by GH administration in GC-injected animals. GH could also increase parameters of bone formation (bone mineralizing surface (MS) and MAR) on cortical bone surfaces in GC-injected animals, whereas parameters of bone formation [MS and bone formation rates (BFR)] on cancellous bone surfaces were even lower than those of animals injected with GC alone.
GH can reverse GC-induced low bone turnover on cortical but not on cancellous bone surfaces.
我们使用随机垂直切片评估了糖皮质激素（GC）和生长激素（GH）对成年大鼠皮质骨和松质骨骨转换的影响，该切片可有效测量骨表面和骨形成参数。给予GH可逆转GC诱导的骨质减少和皮质骨低骨转换。然而，GH不能逆转GC诱导的松质骨低骨转换。
将70只7月龄雌性Wistar大鼠分为五组：（1）起始对照组，（2）生理盐水组，（3）GC 9 mg/kg/天（甲泼尼龙），（4）GH 5 mg/kg/天，（5）GC 9 mg/kg/天+GH 5 mg/kg/天，并注射3个月。使用动态组织形态计量学和生物力学测试检查椎体。采用非参数方法。
给予糖皮质激素导致椎体皮质骨和松质骨均处于低骨转换状态，而不改变骨的绝对量或椎体的生物力学性能。给予GH导致纵向骨生长和腹侧塑形漂移略有增加。这种生长增加了椎体内皮质骨、骨内膜和松质骨的总量。由于皮质骨量增加，中央椎体3.5毫米高圆柱体的生物力学性能也有所提高，而圆柱体内松质骨的总量未改变。然而，由于GH可能诱导矿物质沉积速率（MAR）加快，导致小梁变厚，松质骨密度（CBV）增加。GH还增加了注射GC动物的纵向和腹侧塑形漂移。GH增加了皮质骨量以及靠近骨骺生长板的松质骨量，而在注射GC的动物中，中央椎体圆柱体的松质骨体积不受GH给药的影响。GH还可增加注射GC动物皮质骨表面的骨形成参数（骨矿化表面（MS）和MAR），而松质骨表面的骨形成参数[MS和骨形成率（BFR）]甚至低于仅注射GC的动物。
GH可逆转GC诱导的皮质骨低骨转换，但不能逆转松质骨表面的低骨转换。
