原发性骨质疏松的骨小梁丢失的结构机制:特定的疾病机制还是早期衰老?

P.I. Croucher , N.J. Garrahan , J.E. Compston
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引用次数: 35

摘要

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疾病过程引起的,还是代表生理性骨质流失的一种极端。我们定量评估了35例原发性骨质疏松症患者和41例正常人的松质结构。松质结构通过计算机化的结构分析和计算小梁宽度、间距和数量来评估。与正常受试者相比,骨质疏松症患者的淋巴结与终末比、淋巴结与淋巴结、淋巴结与环支杆长度均显著减少(P <0.001),而末端计数和端到端支撑长度显著增加(P <0.001)。当两个亚组的年龄相匹配时,这些差异仍然非常显著(P <0.005)。然而,当两个亚组对松质面积进行匹配时,除末端计数外,其他结构指标均无显著差异(P <0.05)。骨质疏松患者年龄匹配前后的平均小梁宽度和数量显著低于对照组,小梁分离率显著高于对照组,但匹配松质区后差异消失。多元回归分析证实,调整年龄、性别和疾病状态后,松质骨面积与结构指标高度相关(P <0.001)。我们的数据表明,对于给定的松质区域,原发性骨质疏松症的结构变化与正常受试者中与年龄相关的骨质流失相似。这些发现支持了一种假设,即原发性骨质疏松症是更大的生物老化而不是特定疾病过程的结果,并且与其他来源的证据一致,即低骨量与骨质疏松症无关疾病的死亡率增加有关。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Structural mechanisms of trabecular bone loss in primary osteoporosis: specific disease mechanism or early ageing?

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.

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