Croucher P I, Garrahan N J, Compston J E
Department of Medicine, University of Cambridge Clinical School, UK.
Bone Miner. 1994 May;25(2):111-21. doi: 10.1016/s0169-6009(08)80253-x.
Osteoporosis is characterised by reduced bone mass and disruption of cancellous bone architecture; however, it is unknown whether these changes arise from a specific disease process or represent one extreme of physiological bone loss. We have quantitatively assessed cancellous structure in 35 patients with primary osteoporosis and 41 normal subjects. Cancellous microstructure was assessed by computerised strut analysis and by calculation of trabecular width, separation and number. Node to terminus ratio, node to node and node to loop strut length were significantly decreased in patients with osteoporosis when compared to normal subjects (P < 0.001), whereas terminus count and terminus to terminus strut length were significantly increased (P < 0.001). When two subgroups were matched for age these differences remained highly significant (P < 0.005). However, when two subgroups were matched for cancellous area, no significant differences were observed in any of the structural indices except terminus count (P < 0.05). Mean trabecular width and number were significantly lower and trabecular separation significantly higher in the patients with osteoporosis before and after age-matching but their differences disappeared after matching for cancellous area. Multiple regression analysis confirmed highly significant correlations between cancellous bone area and structural indices after adjustment for age, sex and disease status (P < 0.001). Our data demonstrate that for a given cancellous area, structural changes in primary osteoporosis are similar to those observed during age-related bone loss in normal subjects. These findings support the hypothesis that primary osteoporosis is the result of greater biological ageing rather than a specific disease process and are consistent with evidence from other sources that low bone mass is associated with increased mortality from diseases unrelated to osteoporosis.
骨质疏松症的特征是骨量减少和松质骨结构破坏；然而，尚不清楚这些变化是由特定的疾病过程引起的，还是代表生理骨质流失的一个极端情况。我们对35例原发性骨质疏松症患者和41名正常受试者的松质结构进行了定量评估。通过计算机化支柱分析以及计算小梁宽度、间距和数量来评估松质微结构。与正常受试者相比，骨质疏松症患者的节点到末端比率、节点到节点以及节点到环支柱长度显著降低（P < 0.001），而末端计数和末端到末端支柱长度显著增加（P < 0.001）。当两个亚组按年龄匹配时，这些差异仍然非常显著（P < 0.005）。然而，当两个亚组按松质面积匹配时，除了末端计数外（P < 0.05），在任何结构指标上均未观察到显著差异。年龄匹配前后，骨质疏松症患者的平均小梁宽度和数量显著较低，小梁间距显著较高，但在按松质面积匹配后，这些差异消失。多元回归分析证实，在调整年龄、性别和疾病状态后，松质骨面积与结构指标之间存在高度显著的相关性（P < 0.001）。我们的数据表明，对于给定的松质面积，原发性骨质疏松症的结构变化与正常受试者年龄相关骨质流失期间观察到的变化相似。这些发现支持了原发性骨质疏松症是生物衰老加剧的结果而非特定疾病过程的假说，并且与其他来源的证据一致，即低骨量与与骨质疏松症无关的疾病导致的死亡率增加有关。
