发育期缺碘大鼠骨发育障碍的病理学观察

Pathological investigation of bone development retardation caused by iodine-deficiency

目的观察缺碘对大鼠甲状腺功能及骨发育的影响。方法复制两代碘缺乏大鼠动物模型,测定血清中TT3、TT4水平,拍摄X线片,并作股骨远端骨切片观察骨发育情况。结果20日龄缺碘大鼠的体质量明显低于对照组,甲状腺相对质量明显高于对照组;补碘组与正常组无明显差别。碘缺乏大鼠血清TT3水平与对照组相比无明显变化,但TT4水平显著降低。X线片中可见,碘缺乏大鼠的长骨较同日龄正常大鼠短且细,骨间隙增大,钙化不良。股骨远端骨骺病理切片显示,缺碘大鼠次级骨化中心形成迟缓且小,骨骺生长板中几个软骨细胞区域层次混乱,储备细胞数目减少,增殖区宽度较正常大鼠减少,生后补碘可以部分纠正上述改变。结论发育期碘缺乏会导致大鼠发育迟缓,骨骺软骨发育不良,钙化障碍。生后给碘缺乏大鼠补碘可以改善骨骼发育。

Objective To investigate bone development retardation caused by iodine-deficiency in rats. Methods The first and second generation of iodine-deficient rats was used as animal model, serum T3 and T4 level were measured, bone photographs were taken under X-Rays, pathological slices of rat femur were made. Results The body weights of iodine-deficient rats were significantly less than those of normal rats with a relatively heavier thyroid. In comparison of normal subjects, the radiophotograms showed that the bone length and thickness were lower and bone gap was larger. The histological results of femur showed iodine-deficiency animal models postponed the emergence of second ossification center that was, smaller than that in normal rats, the chondrocytes in epiphyseal plate were disarranged, the amount of reserve chondrocytes and the width of proliferation zone were decreased. These changes can be partially recovered in iodine-supplement rats. Conclusions These results suggests iodine-deficiency may cause both whole body and bone development retardation in rat, as well as impaired the calcified procedure. Iodine supplement to iodine-deficient rats after birth could improves their bone development.