Sumi M, Mizuno K
Nihon Seikeigeka Gakkai Zasshi. 1983 Jan;57(1):35-49.
The purpose of this study is to investigate effects of calcitonin (CT) on bone tissues in fracture healing. Rats were fractured at middle of the femur and given [ASU1,7] eel CT. Following biochemical changes in the serum and histological findings of bone tissue were demonstrated. At the early stage of fracture healing process, CT activated the periostal ossification and elevated serum level of alkaline phosphatase activity. At the stage of cartilagenous callus, the number of chondroclasts were decreased and the development of cartilagenous tissue to primary cancellous bone was inhibited. After this, number of osteoclasts was decreased and bone resorption due to osteoclasts was decreased and bone resorption due to osteoclasts were suppressed. By these process, remodelling at the fractured site was suppressed and serum alkaline phosphatase activity was maintained at a low level. But as for each osteocyte in this stage, CT gave rise to periosteocytic osteoplasis. It is clear that CT accelerates the fracture healing by activating the periostal ossification in the early stage, whereas the fracture healing is suppressed after the stage of cartilagenous callus formation.
本研究的目的是探讨降钙素(CT)对骨折愈合过程中骨组织的影响。将大鼠股骨中段骨折,并给予[ASU1,7]鳗鱼降钙素。随后展示了血清中的生化变化以及骨组织的组织学发现。在骨折愈合过程的早期阶段,CT激活了骨膜骨化并提高了血清碱性磷酸酶活性。在软骨痂阶段,破软骨细胞数量减少,软骨组织向初级松质骨的发育受到抑制。在此之后,破骨细胞数量减少,破骨细胞引起的骨吸收减少,破骨细胞引起的骨吸收受到抑制。通过这些过程,骨折部位的重塑受到抑制,血清碱性磷酸酶活性维持在低水平。但对于该阶段的每个骨细胞,CT会引起骨细胞周骨生成。很明显,CT在早期通过激活骨膜骨化来加速骨折愈合,而在软骨痂形成阶段之后骨折愈合受到抑制。