| 0542 Comparing the Ageing Profiles of Oral Mucosal and Dermal Fibroblasts | ||
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L. DAVIES, S. ENOCH, D.W. THOMAS, and P. STEPHENS, Cardiff University, United Kingdom Objectives: Scarless wound healing in the oral mucosa is characterised by rapid re-epithelialisation and remodelling when compared to dermal wounds. This study aims to investigate the phenotypic and genotypic differences between oral mucosal (OMF) and dermal (DF) fibroblast populations and their role in mediating this differential wound healing. Previous studies have demonstrated the increased ability of OMFs to migrate and re-populate wound sites and re-organise their extracellular matrix through the increased production of matrix metalloproteinases and hepatocyte growth factor. We hypothesise that in addition to the described phenotypic differences, distinct variations exist between the ageing profiles of OMFs and DFs. Methods: Single Telomere Length Analysis (STELA) was used to visualise and quantify telomere lengths of patient matched OMF and DF populations using both non-allele and allele specific probes. This assay offers greater resolution compared to previous techniques. TRAP assays were also performed using the same samples to investigate telomerase activity within these cells. Results: STELA confirmed the presence of significantly longer telomere lengths within OMFs (12Kb-3Kb) when compared to patient matched DFs (2.5Kb-1Kb). TRAP analysis demonstrated the absence of telomerase activity in both cell groups, confirming the phenotypic difference between these fibroblast populations and their distinctly different ageing profiles. This data corroborates previous findings within the Group demonstrating that OMFs undergo more population doublings and senesce later than patient matched DFs. These differences in the ageing profiles between the two cells types are currently being investigated utilising Affymetrix™ microarrays. Conclusions: The oral mucosal contains fibroblasts with significantly longer telomere lengths than dermal fibroblasts and hence are significantly ‘younger'. This may explain why healing within the oral mucosal is rapid and often scarless. Further elucidation of the mechanism responsible for this cellular ageing will, it is envisaged, aid in the control of wound healing outcome in the future. | ||
| Seq #64 - Oral Medicine/Pathology, Fibroblasts, Wound healing, Cancer 11:30 AM-1:00 PM, Friday, 15 September 2006 Trinity College Dublin Emmet | ||
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