Ellis H A, Peart K M
J Clin Pathol. 1973 Feb;26(2):83-101. doi: 10.1136/jcp.26.2.83.
The histopathology of bone is described in 60 patients with chronic renal failure due to a variety of renal diseases. Changes of azotaemic renal osteodystrophy included osteitis fibrosa, osteomalacia, and osteosclerosis. Quantitative histology using a point-counting technique revealed a significant increase in total bone, mineralized bone, and osteoid in comparison with a control group of 68 individuals. Osteitis fibrosa due to secondary hyperparathyroidism occurred in 93%, osteomalacia in 40%, and osteosclerosis in 30% of patients. Woven bone formation was a characteristic feature and was related to the severity of osteitis fibrosa. There were significant correlations between the weights of parathyroid glands and the number of osteoclasts, amounts of woven bone, and marrow fibrosis in the ilium. Hyperparathyroidism caused degradation of mineralized bone but the loss was balanced or exceeded by the aggradation of woven mineralized bone. Woven bone formation together with excess osteoid gave rise to osteosclerosis. The histological findings indicate that hyperparathyroidism and osteitis fibrosa usually occur early in chronic renal failure and that osteomalacia develops subsequently.
本文描述了60例因各种肾脏疾病导致慢性肾衰竭患者的骨骼组织病理学情况。氮质血症性肾性骨营养不良的变化包括纤维性骨炎、骨软化症和骨硬化症。采用点计数技术的定量组织学研究显示，与68名个体组成的对照组相比，患者的总骨量、矿化骨量和类骨质均显著增加。继发于甲状旁腺功能亢进的纤维性骨炎在93%的患者中出现，骨软化症在40%的患者中出现，骨硬化症在30%的患者中出现。编织骨形成是一个特征性表现，且与纤维性骨炎的严重程度相关。甲状旁腺重量与破骨细胞数量、编织骨量以及髂骨骨髓纤维化程度之间存在显著相关性。甲状旁腺功能亢进导致矿化骨降解，但编织矿化骨的增生可平衡或超过这种损失。编织骨形成以及类骨质过多导致了骨硬化症。组织学研究结果表明，甲状旁腺功能亢进和纤维性骨炎通常在慢性肾衰竭早期出现，随后发展为骨软化症。
