Glade M J, Krook L
Cornell Vet. 1982 Jan;72(1):76-91.
Changes in the developing femoral epiphysis, especially those concerning the osteocytes, were examined in pony foals systemically treated with daily intramuscular injections of either 0.5 or 5.0 mg of dexamethasone per 100 kg bodyweight for either 3, 8 or 11 months. Midsagittal sections of proximal femur from animals treated for 3 months contained significantly more bone tissue subchondrally and epiphyseally than did sections from untreated ponies. Large portions of the bone tissue appeared necrotic, although osteoblasts and patent capillaries were abundant. After 8 months the bone sections revealed marked osteoporosis. Abnormally dense bone was again observed after 11 months. There were significant increases in the severity of these changes in bone from the animals treated with the higher dosage. Calcium kinetics studies revealed an inhibition of calcium deposition (bone formation) in the treated animals after 2 and 7 months. However, calcium removal (bone resorption) was inhibited to a greater extent. Osteopetrosis (radiographic sclerosis) resulted from the initial resorption/formation imbalance, and was accompanied by osteonecrosis and osteocyte death. Continued treatment resulted in osteopenia, caused by the removal of necrotic bone debris and the inhibition of new bone formation. The primary event in the development of glucocorticoid-induced bone disease was shown to be suppression of osteolysis with the development of osteonecrosis.
对小马驹进行研究，这些小马驹每天按每100千克体重肌肉注射0.5毫克或5.0毫克地塞米松，持续3、8或11个月，然后检查其发育中的股骨骨骺的变化，特别是与骨细胞有关的变化。接受3个月治疗的动物的股骨近端矢状中切面，其软骨下和骨骺处的骨组织明显多于未治疗小马驹的切片。尽管有成骨细胞和开放的毛细血管，但大部分骨组织看起来已坏死。8个月后，骨切片显示出明显的骨质疏松。11个月后再次观察到骨密度异常增高。高剂量治疗的动物骨骼中这些变化的严重程度有显著增加。钙动力学研究显示，治疗2个月和7个月后，治疗组动物的钙沉积（骨形成）受到抑制。然而，钙的清除（骨吸收）受到的抑制程度更大。骨石化（影像学硬化）是由最初的吸收/形成失衡导致的，并伴有骨坏死和骨细胞死亡。持续治疗导致骨质减少，这是由于坏死骨碎片的清除和新骨形成的抑制所致。糖皮质激素诱导的骨病发展过程中的主要事件被证明是骨溶解受抑制并伴有骨坏死。
