Characterisation of human dental stem cells and buccal mucosa fibroblasts

https://doi.org/10.1016/j.bbrc.2008.01.081Get rights and content

Abstract

Human craniofacial stem cells are recently discovered sources of putative mesenchymal stem cells that hold great promise for autogenic or allogenic cell therapy and tissue engineering. Prior to employing these cells in clinical applications, they must be thoroughly investigated and characterized. In this study, the surface marker expression was investigated on dental pulp stem cells (DPSCs), dental follicle cells (DFCs), periodontal ligament stem cells (PDLSCs), and buccal mucosa fibroblasts (BMFs) utilising surface markers for flow cytometry. The osteogenic potential was also examined by bone-associated markers alkaline phosphatase, Runx2, collagen type I, osteocalcin, and osteopontin. The results from our study demonstrate that the dental cell sources exhibit comparable surface marker and bone-associated marker profiles parallel to those of other mesenchymal stem cell sources, yet distinct from the buccal mucosa fibroblasts. Our data support evidence towards clinical applicability of dental stem cells in hard tissue regeneration.

Section snippets

Materials and methods

Cell preparation and culture. Human impacted third molars were obtained during odontectomy with informed consent at the Finnish Student Health Services. A buccal mucosa sample was obtained from one patient during maxillofacial surgery at the Tampere University Hospital, Tampere, Finland. The study was conducted in accordance with the Ethics Committee of the Pirkanmaa Hospital District, Tampere, Finland. DPSCs were isolated from impacted third molars of 10 patients, DFCs from 9 patients, and

Results and discussion

The dental tissue cell sources and BMFs were analysed with FACS to compare surface marker expression characteristics (Table 2). The FACS analysis demonstrated that all three dental cell sources and BMFs showed positive expression for the putative stem cell marker STRO-1; adhesion molecules CD9, CD29, CD49d, CD105, CD106, and CD166; receptor molecule CD44; surface enzymes CD10 and CD13, extracellular matrix protein CD90; complement regulatory protein CD59; and hFSP. All cell sources lacked

Acknowledgments

The authors thank Ms. Miia Juntunen for technical assistance, Mr. Henrik Mannerström for graphic processing consultation, and Mrs. Heini Huhtala for statistical counselling. The work was supported by TEKES, the Finnish Funding Agency for Technology and Innovation, the competitive research funding of the Pirkanmaa Hospital District, and the Finnish Cultural Foundation Pirkanmaa Provincial Foundation.

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    These authors contributed equally to this work.

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