Matsushita M, Tsuboyama T, Kasai R, Okumura H, Yamamuro T, Higuchi K, Higuchi K, Kohno A, Yonezu T, Utani A
Am J Pathol. 1986 Nov;125(2):276-83.
Age-related changes of the femoral bone mass in several strains of the senescence-accelerated mouse (SAM) were investigated. Microdensitometrically, all strains exhibited essentially the same patterns of age changes, that is, bone mass corrected by the diameter of the shaft reached the peak value when the mice were 4 or 5 months of age and then fell linearly with age up to over 20 months of age. Two strains, SAM-R/3 and SAM-P/6, which originated from the same ancestry on pedigree, had a significantly lower peak bone mass than other strains (SAM-R/1, SAM-R/2, SAM-P/1, and SAM-P/2). On the other hand, the strains with a low peak bone mass had the same rate of decrease as other strains. Mineral and collagen contents per dry weight of bone showed little difference among the strains. Histologic studies of tibia, femur, and lumbar spine revealed that the osteopenia was not due to osteomalacia but, rather, to osteoporosis. The elderly mice in these two strains were prone to fracture, thus should be important models for study of senile osteoporosis seen clinically.
研究了几种衰老加速小鼠(SAM)品系股骨骨量的年龄相关性变化。通过显微密度测定法,所有品系都表现出基本相同的年龄变化模式,即,经骨干直径校正后的骨量在小鼠4或5月龄时达到峰值,然后随年龄增长呈线性下降,直至超过20月龄。来自同一家系谱系的两个品系SAM-R/3和SAM-P/6的峰值骨量明显低于其他品系(SAM-R/1、SAM-R/2、SAM-P/1和SAM-P/2)。另一方面,峰值骨量低的品系与其他品系的下降速率相同。各品系骨干重中矿物质和胶原蛋白含量差异不大。对胫骨、股骨和腰椎的组织学研究表明,骨质减少不是由于骨软化症,而是由于骨质疏松症。这两个品系的老年小鼠易于骨折,因此应是临床上研究老年性骨质疏松症的重要模型。