蝕骨細胞與骨骼代謝

Osteoclasts and Bone Metabolism

劉仲景(Chung-Ching Liu)

《師大生物學報》 17卷 (1982/06) Pp. 103-112

https://doi.org/10.29812/BBNTNU.198206.0014

摘要

本文以大白鼠之骨酪修補實驗為例，說明蝕骨細胞與骨骼代謝之關係，同時解釋蝕骨細胞在體內之命運。用缺鈣的食料飼養大白鼠，其脛骨內骨膜表面之蝕骨細胞增加21倍，但用正常含鈣食料飼養後，在骨酪修補第一天90%之蝕骨細胞很快由內骨膜表面消失，其他10%則於骨路修補第二及第三天完全消失，此時內骨膜表面完全是肥大且活躍之成骨細胞。此結果說明蝕骨細胞之反應極快，也說明以前骨骼修補實驗，為何由缺鈣食料改換正常食料後，可立即增加骨骼之新生。在骨骼修補初期，由於骨髓內蝕骨細胞之突然增加（42倍），衰落，分割或破裂，同時也由於骨髓內具有酸性磷酸酶性質之碎粒，足以說明此碎粒係來自蝕骨細胞，而蝕骨細胞在體內之命運（或至少，其中一部份之命運）為衰落或死亡。由本實驗及以往實驗結果，得知內骨膜蝕骨細胞之消失，與血中副甲狀腺素無直接關係，而與體內1,25-dihydroxyvitamin D3之形成可能有關，但此細胞之消失可能還受局部因素的控制。

並列摘要

Changes in osteoclast number and their relationship to bone metabolism were studied using a previously established bone repletion model. Growing rats were fed a calcium-deficient diet for days to induce bone loss and subsequently placed on a control diet for 1-3 days to t rigger new bone formation. Control animals were maintained on the control diet throughout the experiment al period. Calcium deficiency caused a marked 21-fold increase in the number of endosteal osteoclasts in the tibial diaphysis at the fibular junction. These osteoclasts, however, rapidly disappeared from the endosteum soon after restoration of dietary calcium: only 10% of the se osteoclasts remained after one day, and no osteo clasts were present after three days of calcium replenishment. During this time plump osteoblasts replaced osteoclasts on the endosteal surface. These bone cell changes undoubtedly are responsible for the increase in bone formation observed previously during bone repletin. During calcium replenishment, the number or osteoclasts in the marrow space also underwent striking changes. A 42-fold increase in the number of osteoclasts in the marrow space was observed after one day of calcium replenishment, and this was accompanied by disintegration and fragmentation of these osteoclasts and by the appearance of acid phosphatase-positive fragments in the marrow space. The kinetic changes and acid phosphatase staining of these fragements suggest that the fragements are the products of disintegrating osteoclasts, a finding which is consistent with the hypothesis that the fate of some osteoclasts in vivo is cell death. At the end of calcium deficiency, serum iPTH level and the production of 1,25-dihydroxyvitamin D3 from 25-hydroxyvitamin D3 were significantly increased compared to controls. After three dass of calcium replenishment, serum iPTH had decreased to control levels but the production of 1,25-dihydroxyvitamin D3 remained somewhat elevated. Based on these results and past work, it is concluded that changes in levels of serum iPTH are not directly responsible for the acute decrease in the number of endosteal osteoclasts observed during bone repletion, and that changes in the production of 1,25-dihydroxyvitamin D3 can only explain part of the decrease in osteoclast number, raising the possibility that other local factors may also be involved.