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骨硬化(op/op)小鼠矢状缝重塑与颅骨扁骨生长相关。

Remodeling of the sagittal suture in osteopetrotic (op/op) mice associated with cranial flat bone growth.

作者信息

Kaku M, Kawata T, Kawasoko S, Fujita T, Tokimasa C, Tanne K

机构信息

Department of Orthodontics, Hiroshima University School of Dentistry, Japan.

出版信息

J Craniofac Genet Dev Biol. 1999 Apr-Jun;19(2):109-12.

Abstract

It is well known that cranial flat bone experiences growth and development at the sutural interface, which is regarded as a neutral zone to control mechanical stimuli. In osteopetrotic (op/op) mice, meanwhile, cranial deformation is produced by the deficiency of osteoclasts and the subsequent defect of bone resorption. It would be a reasonable assumption that such disturbance in bone remodeling affects sutural modification and the relevant cranial flat bone development. The present study was thus conducted to examine histological features of the sagittal sutures in op/op mice, with special reference to the relevant bone remodeling. The sagittal sutures in 10-, 15-, 30-, and 60-day-old normal and op/op mice were observed microscopically. Furthermore, osteoclastic activity was evaluated on the sections stained with tartrate-resistant acid phosphatase (TRAP). The sutures of 15-day-old op/op mice showed stenosis and synostosis, and less-developed collagen fibers associated with an irregular arrangement of fibroblasts, whereas these changes were rarely found in normal mice. Osteoclasts were hardly detected in the parietal bones around the sutures of op/op mice, although the number was numerous in normal mice. These results emphasize that congenital deficiency in osteoclast produces unbalanced bone remodeling at the sutural interface and on the surfaces of the cranial bones, which is assumed to be closely related to cranial bone deformity in op/op mice.

摘要

众所周知,颅骨扁骨在缝合界面经历生长和发育,该界面被视为控制机械刺激的中性区。与此同时,在骨石化(op/op)小鼠中,颅骨变形是由破骨细胞缺乏以及随后的骨吸收缺陷所导致的。可以合理推测,这种骨重塑的紊乱会影响缝合线的改变以及相关颅骨扁骨的发育。因此,本研究旨在检查op/op小鼠矢状缝的组织学特征,并特别关注相关的骨重塑。对10日龄、15日龄、30日龄和60日龄的正常小鼠和op/op小鼠的矢状缝进行显微镜观察。此外,在抗酒石酸酸性磷酸酶(TRAP)染色的切片上评估破骨细胞活性。15日龄op/op小鼠的缝合线显示狭窄和骨性连接,且胶原纤维发育不良,成纤维细胞排列不规则,而在正常小鼠中很少发现这些变化。在op/op小鼠缝合线周围的顶骨中几乎检测不到破骨细胞,而在正常小鼠中破骨细胞数量众多。这些结果强调,破骨细胞的先天性缺乏会在缝合界面和颅骨表面产生不平衡的骨重塑,这被认为与op/op小鼠的颅骨畸形密切相关。

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