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羧甲基纤维素和羟丙基甲基纤维素对破骨细胞和成骨细胞分化及活性的影响。

Effects of carboxymethylcellulose and hydroxypropylmethylcellulose on the differentiation and activity of osteoclasts and osteoblasts.

机构信息

Department of Oral Surgery, Medical University of Vienna, Austria.

出版信息

J Biomed Mater Res A. 2010 Nov;95(2):504-9. doi: 10.1002/jbm.a.32842.

DOI:10.1002/jbm.a.32842
PMID:20665677
Abstract

Carboxymethylcellulose (CMC) and hydroxypropylmethylcellulose (HPMC) serve as carriers for growth factors and bone substitutes. Although both carriers are placed into the defect sites, their impacts on bone regeneration are unclear. Herein, we examined whether CMC and HPMC affect the differentiation of bone marrow progenitors into osteoclasts and osteoblasts. We therefore induced osteoclastogenesis and osteoblastogenesis in murine bone marrow progenitors in the presence of CMC and HPMC, respectively. Measures of osteoclastogesis were based on the number and activity of tartrate-resistant acid-phosphatase-positive (TRAP(+)) multinucleated cells and expression of marker genes. Osteoblastogenesis was determined by the number and activity of alkaline-phosphatase-positive (AP(+)) colonies and relevant marker genes. Viability was assessed by colorimetric measurement of formazan formation. We report that CMC at 1% caused a significant reduction in the number and activity of TRAP(+) multinucleated cells. Changes in viability were not responsible for the observed effects. HPMC showed no remarkable impact on osteoclastogenesis; however, the concentration was limited to 0.5% because of the high viscosity. The ability of bone marrow progenitors to form AP(+) colonies was not affected by either of the two carriers. Together, these results suggest that CMC and possibly also HPMC can decrease osteoclastogenesis while osteoblastogenesis remains unchanged in vitro. These observations raise the possibility that these carriers might affect the cellular process of bone regeneration.

摘要

羧甲基纤维素(CMC)和羟丙基甲基纤维素(HPMC)可用作生长因子和骨替代物的载体。虽然这两种载体都被放置在缺陷部位,但它们对骨再生的影响尚不清楚。在此,我们研究了 CMC 和 HPMC 是否会影响骨髓祖细胞向破骨细胞和成骨细胞的分化。因此,我们分别在 CMC 和 HPMC 存在的情况下诱导鼠骨髓祖细胞的破骨细胞生成和成骨细胞生成。破骨细胞生成的测量基于抗酒石酸酸性磷酸酶阳性(TRAP(+))多核细胞的数量和活性以及标记基因的表达。成骨细胞生成通过碱性磷酸酶阳性(AP(+))集落的数量和活性以及相关标记基因来确定。通过比色法测量甲臜形成来评估细胞活力。我们报告 1%的 CMC 导致 TRAP(+)多核细胞的数量和活性显著减少。活力的变化不是观察到的影响的原因。HPMC 对破骨细胞生成没有明显影响;然而,由于高粘度,其浓度被限制在 0.5%。两种载体均未影响骨髓祖细胞形成 AP(+)集落的能力。综上所述,这些结果表明 CMC 和可能还有 HPMC 可以减少体外破骨细胞生成,而成骨细胞生成保持不变。这些观察结果表明这些载体可能会影响骨再生的细胞过程。

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