[Study of bone remodeling mechanism induced by mechanical stress. Differentiation of osteoclasts induced by compressive force in newborn rat cultured long bone].

M Chiba
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Abstract

The purpose of this investigation was to reveal the mechanism of differentiation of osteoclast (OC) induced by mechanical stress in long bone cultivation of new born rats. A long bone was loaded with 30 gf of continuous compressive force and cultured for 5 days in CO2 incubator. Numbers of OC increased in the long bone were counted after H-E staining and compared with the control. The study was dealt with the effects of recombinant tumor necrosis factor alpha (rTNF alpha), recombinant interleukin-1 beta (rIL-1 beta), prostaglandin E2 (PGE2) and the co-cultivation of osteoblast (OB) originated from new born rat calvariae, as to differentiation of OC. Since the bone remodeling was interacted with OB and bone marrow (BM) cells, the activity of alkaline phosphatase (ALPase) was also investigated for OB in co-cultivation with BM cells originated from new born rat long bones. In the region of diaphysis of a long bone loaded with compressive force, the bend of trabecular bones was noticed after 3 days incubation. Also, the enrichment of monocyte-macrophage (Mo-M phi) lineage cells was noticed along the trabecular bones. After 5 days incubation, the increase of the number of OC was specifically recognized. The increase of the number of OC was shown in medullary cavity of the long bone by addition of rTNF alpha to the culture medium, but any synergistic effect was not shown with the treatment of rTNF alpha and compressive force to the increase of the number of OC. Furthermore, the increase of the number of OC induced by compressive force did not suppressed by addition of anti-TNF serum. Under the treatment of rIL-1 beta or PGE2, OC slightly increased in the long bone when loaded by compressive force, but the treatment of indomethacin did not suppress it completely. However, the increase of OC in the long bone loaded by compressive force was clearly inhibited in co-cultivation with OB. On the other hand, the activity of ALPase of OB was markedly abated in co-cultivation with BM cells. These results indicated that the mechanism of differentiation of OC induced by mechanical stress was different from that induced by the general inflammation. Results also indicated that it was controlled mainly by the factor(s) or interaction between BM cells and OB and was associated with Mo-M phi lineage cells.(ABSTRACT TRUNCATED AT 400 WORDS)

机械应力诱导骨重塑机制的研究。压缩力诱导新生大鼠培养长骨的破骨细胞分化[j]。
本研究旨在探讨机械应力诱导新生大鼠长骨培养过程中破骨细胞(OC)分化的机制。取一根长骨,施加30gf的连续压缩力,在CO2培养箱中培养5天。H-E染色后计算长骨OC增加的数量,并与对照组比较。本研究探讨重组肿瘤坏死因子α (rTNF α)、重组白细胞介素-1 β (il -1 β)、前列腺素E2 (PGE2)及新生大鼠颅骨成骨细胞(OB)共同培养对OC分化的影响。由于骨重塑与OB和骨髓(BM)细胞相互作用,我们还研究了OB与新生大鼠长骨BM细胞共培养时碱性磷酸酶(ALPase)的活性。在受压的长骨骨干区,3天后出现骨小梁弯曲。此外,沿小梁骨可见单核-巨噬细胞(Mo-M - phi)谱系细胞的富集。孵育5 d后,可特异性识别OC数量的增加。在培养基中加入rTNF α可使长骨髓腔内OC数量增加,但rTNF α和压缩力处理对OC数量的增加没有任何协同作用。此外,抗tnf血清不抑制压缩力诱导的OC数量的增加。在rIL-1 β或PGE2处理下,受压载荷时长骨OC略有增加,但吲哚美辛处理不能完全抑制OC。然而,与OB共培养时,受压缩力载荷的长骨中OC的增加明显受到抑制。另一方面,OB与BM细胞共培养时,ALPase活性明显减弱。这些结果表明,机械应力诱导的OC分化机制与一般炎症诱导的OC分化机制不同。结果还表明,它主要受BM细胞和OB细胞之间的相互作用或因子控制,并与Mo-M - phi系细胞有关。(摘要删节为400字)
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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