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分析长骨骨纤维结构不良和造釉细胞瘤中的基质细胞。

Analysis of stromal cells in osteofibrous dysplasia and adamantinoma of long bones.

机构信息

Nuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences, University of Oxford, Nuffield Orthopaedic Centre, Oxford, UK.

出版信息

Mod Pathol. 2012 Jan;25(1):56-64. doi: 10.1038/modpathol.2011.141. Epub 2011 Oct 7.

Abstract

Adamantinoma of long bones and osteofibrous dysplasia are rare, osteolytic primary bone tumours of uncertain origin containing areas of fibrous and fibro-osseous proliferation. We investigated the nature of the stromal cells in adamantinoma of long bones and osteofibrous dysplasia, and determined cellular and molecular mechanisms of osteolysis in these tumours. Cell culture, molecular (RT-PCR, western blot) and immunohistochemical studies on cases of adamantinoma of long bones and of osteofibrous dysplasia were undertaken to determine the expression of epithelial, osteoblast and osteoclast markers. Ultrastructural and immunophenotypic studies on cultured adamantinoma and osteofibrous dysplasia stromal cells showed that these cells were mainly fibroblast-like with few cells expressing epithelial markers. Osteofibrous dysplasia but not adamantinoma cells expressed alkaline phosphatase. Both osteofibrous dysplasia and adamantinoma cells expressed the ostoclastogenic factors M-CSF and RANKL. Adamantinoma and osteofibrous dysplasia cells also expressed messenger RNA for osteocalcin, osteonectin, osteopontin, osterix and collagen type 1. Adamantinoma and osteofibrous dysplasia cells cultured alone on dentine slices were not capable of lacunar resorption, but in co-cultures with monocytes induced formation of osteoclast-like cells was observered. Cultured osteofibrous dysplasia and adamantinoma stromal cells show similar ultrastructural and immunophenotypic characteristics, and differentially express osteoblast markers. Promotion of osteoclastogenesis by stromal cells may contribute to osteolysis in adamantinoma of long bones and osteofibrous dysplasia.

摘要

长骨造釉细胞瘤和骨纤维结构不良是罕见的、起源不明的溶骨性原发性骨肿瘤,包含纤维和纤维骨性增殖区。我们研究了长骨造釉细胞瘤和骨纤维结构不良中基质细胞的性质,并确定了这些肿瘤中溶骨性的细胞和分子机制。对长骨造釉细胞瘤和骨纤维结构不良的病例进行了细胞培养、分子(RT-PCR、western blot)和免疫组织化学研究,以确定上皮、成骨细胞和成骨细胞标志物的表达。对培养的造釉细胞瘤和骨纤维结构不良基质细胞的超微结构和免疫表型研究表明,这些细胞主要呈成纤维细胞样,少数细胞表达上皮标志物。骨纤维结构不良而非造釉细胞瘤细胞表达碱性磷酸酶。骨纤维结构不良和造釉细胞瘤细胞均表达破骨细胞生成因子 M-CSF 和 RANKL。造釉细胞瘤和骨纤维结构不良细胞还表达骨钙素、骨粘连蛋白、骨桥蛋白、骨形成蛋白和胶原 1 的信使 RNA。单独培养在牙本质切片上的造釉细胞瘤和骨纤维结构不良细胞不能进行陷窝吸收,但在与单核细胞的共培养中观察到诱导形成破骨细胞样细胞。培养的骨纤维结构不良和造釉细胞瘤基质细胞显示出相似的超微结构和免疫表型特征,并差异表达成骨细胞标志物。基质细胞促进破骨细胞生成可能有助于长骨造釉细胞瘤和骨纤维结构不良的溶骨性。

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