Tissue engineering of oral dysplasia

Keratinocytes and fibroblasts isolated from dysplastic oral lesions were combined to provide a renewable source of epithelia. A dysplasia-scoring index was devised to compare the architectural and cytological features and used together with robust immunophenotyping to show that the engineered epithe...

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Bibliographic Details
Published in:The Journal of pathology 2008-07, Vol.215 (3), p.280-289
Main Authors: Gaballah, K, Costea, DE, Hills, A, Gollin, SM, Harrison, P, Partridge, M
Format: Article
Language:English
Subjects:
Biological and medical sciences
Culture Media, Conditioned
dysplasia
Electrophoresis, Polyacrylamide Gel
Enzyme-Linked Immunosorbent Assay - methods
epithelial-connective tissue interaction tissue engineering
epithelial-mesenchymal interaction
Fibroblasts - cytology
Fibroblasts - pathology
Humans
Hyperplasia
Immunohistochemistry
Investigative techniques, diagnostic techniques (general aspects)
Keratinocytes - cytology
Keratinocytes - pathology
Keratins - analysis
Leukoplakia, Oral - pathology
Leukoplakia, Oral - therapy
Linear Models
Medical sciences
Mouth Mucosa - cytology
Mouth Mucosa - pathology
organotypic culture
Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques
pre-cancer
Precancerous Conditions - pathology
Tissue Engineering - methods
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Description
Summary:Keratinocytes and fibroblasts isolated from dysplastic oral lesions were combined to provide a renewable source of epithelia. A dysplasia-scoring index was devised to compare the architectural and cytological features and used together with robust immunophenotyping to show that the engineered epithelia showed most of the characteriztics of the clinical lesions. The strains of dysplastic oral keratinocytes with an extended or immortal lifespan provided a reproducible resource of epithelia showing mild (DOK), moderate (POE9n) or severe (D20) dysplasia when maintained under defined conditions. The dysplasia score was influenced by growth conditions, with KGF polarizing proliferation to the basal layer and reducing the severity of dysplasia. When compared to the normal counterparts, dysplasia-associated fibroblasts expressed MMP9, secreted more HGF, increased the dysplasia score for epithelia generated with mortal dysplastic keratinocytes and induced morphological changes in normal keratinocytes, highlighting the role of the microenvironment in determining the phenotype of dysplastic epithelia. Copyright © 2008 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
ISSN:0022-3417
1096-9896
DOI:10.1002/path.2360