The role of epidermal keratinocytes in the early phase of normal unimpaired wound healing has been extensively studied. However, little is known of the cell biological process in the epidermis and the role of keratinocytes in hypertrophic scar formation. This study investigated the possible role of p63 in the early phase of hypertrophic scarring pathogenesis. Nine skin samples were taken from nine patients during plastic surgery operations, as follows: 1. six samples from patients who on account of thyroid disease or other reasons presented risk factors (RFs) for hypertrophic scarring; 2. one sample from a healthy young person (as control); and 3. one sample from the upper eyelid during blepharoplasty and one sample from an elderly patient during breast reduction. All the patients were women, and were followed up clinically for 12 months. Skin specimens were cultured and sectioned, and analysed by histology and immunohistochemistry. In normal skin, nuclear p63 was abundantly expressed by the basal cells, but expressed by very low levels of transient amplifying (TA) keratinocytes covering the surface. TA keratinocytes, immediately after their withdrawal from the stem cell compartment, reduced p63, even though they possessed a proliferative capacity. In some skin, samples with RFs possessed a high level of p63 expression - not only basal stem cells but also four to five rows of parabasal cells. Four of the six skin samples with RFs showed significant epidermal abnormalities through the expression of both p63 and ki-67. Staining for ki-67, a marker for cell proliferation, revealed more increase in the suprabasal than in the basal keratinocyte proliferation rate. These results suggest that the epidermal keratinocytes may have an important role in hypertrophic scarring pathogenesis, using paracrine or epithelial-mesenchymal signalling. At 3, 6, and 12 months post-operation this finding clinically appeared in four patients with RFs.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3187988PMC

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