Goodman W G
Kidney Int. 1987 Apr;31(4):923-9. doi: 10.1038/ki.1987.87.
Diminished parathyroid hormone (PTH) secretion may contribute to the accumulation of aluminum (Al) in bone and to impaired bone formation in Al-related bone disease. Therefore, intact (AL, N = 9) and thyroparathyroidectomized (TPTX-AL, N = 9) rats were given intraperitoneal injections of Al, 2 mg/day, for 42 days; intact control (C, N = 11) and TPTX control (TPTX-C, N = 9) animals received i.p. injections of vehicle only. Quantitative bone histology and measurements of mineralized bone formation (Rbf) using double tetracycline labeling were done for cortical and for trabecular bone; trabecular bone aluminum content (BA) was determined by histochemical methods. BA did not differ between AL and TPTX-AL, 33 +/- 13% versus 39 +/- 14%, and Rbf decreased similarly from control values in both Al-treated groups. In contrast, osteoid production was impaired to a greater extent in TPTX-AL than in AL. Thus, osteoid area and osteoid seam width were each lower in TPTX-AL than in TPTX-C; these values did not differ between AL and C. TPTX can aggravate Al induced reductions in osteoid synthesis, and low serum PTH levels may contribute to the pathogenesis of aplastic bone. However, reductions in Rbf during Al loading are not mediated by PTH.
甲状旁腺激素（PTH）分泌减少可能导致铝（Al）在骨中蓄积，并导致铝相关性骨病中骨形成受损。因此，对完整大鼠（AL组，n = 9）和甲状旁腺切除大鼠（TPTX-AL组，n = 9）腹腔注射铝，剂量为2mg/天，持续42天；完整对照组（C组，n = 11）和TPTX对照组（TPTX-C组，n = 9）动物仅腹腔注射赋形剂。对皮质骨和小梁骨进行了定量骨组织学分析，并使用双四环素标记法测量了矿化骨形成（Rbf）；通过组织化学方法测定小梁骨铝含量（BA）。AL组和TPTX-AL组的BA无差异，分别为33±13%和39±14%，且两个铝处理组的Rbf均较对照组值有相似程度的下降。相比之下，TPTX-AL组的类骨质生成受损程度比AL组更大。因此，TPTX-AL组的类骨质面积和类骨质缝宽度均低于TPTX-C组；AL组和C组之间这些值无差异。甲状旁腺切除可加重铝诱导的类骨质合成减少，低血清PTH水平可能在再生障碍性骨病的发病机制中起作用。然而，铝负荷期间Rbf的降低并非由PTH介导。
