Naito S, Ito M, Sekine I, Ito M, Hirano T, Iwasaki K, Niwa M
Department of Pathology, Nagasaki University School of Medicine, Japan.
Bone. 1993 Sep-Oct;14(5):745-53. doi: 10.1016/8756-3282(93)90206-p.
Necrosis of the femoral head and osteopenia were examined histopathologically in stroke-prone spontaneously hypertensive rats (SHRSPs) aged 6 to 36 weeks and compared with that of spontaneously hypertensive rats (SHRs) and Wistar-Kyoto rats (WKYs). Avascular necrosis of the femoral head was frequently observed, mainly in the young SHRSPs and SHRs (about 8 to 15 weeks of age). SHRSPs had the highest incidence of femoral head necrosis among the three strains. This necrotic change in the femoral head was considered to be secondary ischemia induced by angiospasm or arteriosclerosis, similar to the disorders observed in the brain, kidney, and heart in SHRSPs. However, the complication occurred in spite of treatment with antihypertensive agents (ACE inhibitor: enalapril, spirapril) even though other ischemic disorders such as brain hemorrhage and renal infarction were prevented, indicating that the femoral head necrosis in SHRSPs was not due to hypertensive complications induced by angiospasm or arteriosclerosis. Bone mineral density (BMD) of the femoral bone was significantly lower in SHRSPs, and the femoral heads in this strain were the most easily deformed by loads applied during compression tests. Histopathologically, the infarctions were encountered on the lateral side of the epiphysis, but no thrombi were observed. The lateral side of the epiphysis is the anatomic site where the weight load is greatest and the site where the nutritive artery enters. Our results strongly suggest that the coexistence of vulnerable bone matrix and physical weight load to the nutritive artery plays a crucial role in the occurrence of femoral head necrosis in SHRSPs, whether based on generalized or localized osteopenia.
对6至36周龄的易卒中型自发性高血压大鼠（SHRSP）的股骨头坏死和骨质减少进行了组织病理学检查，并与自发性高血压大鼠（SHR）和Wistar-Kyoto大鼠（WKY）进行了比较。股骨头缺血性坏死经常被观察到，主要发生在年轻的SHRSP和SHR（约8至15周龄）。在这三个品系中，SHRSP的股骨头坏死发生率最高。这种股骨头坏死变化被认为是由血管痉挛或动脉硬化引起的继发性缺血，类似于在SHRSP的脑、肾和心脏中观察到的疾病。然而，尽管使用了抗高血压药物（ACE抑制剂：依那普利、螺普利）进行治疗，尽管预防了其他缺血性疾病，如脑出血和肾梗死，但并发症仍会发生，这表明SHRSP的股骨头坏死不是由血管痉挛或动脉硬化引起的高血压并发症所致。SHRSP的股骨骨矿物质密度（BMD）显著降低，并且在压缩试验过程中，该品系的股骨头最容易因施加的负荷而变形。组织病理学检查发现，梗死发生在骨骺的外侧，但未观察到血栓。骨骺的外侧是体重负荷最大的解剖部位，也是营养动脉进入的部位。我们的结果强烈表明，无论基于全身性或局部性骨质减少，脆弱的骨基质与营养动脉的物理体重负荷共存，在SHRSP股骨头坏死的发生中起着关键作用。
