H. Li1, S. Balaji1, X. Wang1, M. Rae1, M. Chandramouli1, A. Blum1, M. Kodali1, P. Bollyky2, M. Butte3, S. Keswani1 1Baylor College Of Medicine,Surgery,Houston, TX, USA 2Stanford University,Infectious Diseases And Microbiology And Immunology,Palo Alto, CA, USA 3University Of California – Los Angeles,Pediatrics,Los Angeles, CA, USA
Introduction: The normal course of wound healing in adults results in variably scar formation. However, there is an extreme variability among individuals in the degree of scarring to similar injury. The mechanisms that underlie this spectrum of scar phenotypes in healthy population are unknown. The objective of our study is to determine morphologic and functional phenotypic differences among healthy patients that produce variable scar phenotypes.
Methods: We collected abdominal skin tissue from female patients undergoing abdominoplasty to remove cesarean scars and compared them with normal skin from the surrounding area. Scars were scored by the Vancouver Scar Scale and classified into groups of low (score 1-3) and high (score from 6-9) scares. Tissue sections were analyzed using immunohistochemistry for cell proliferation marker Ki67 to determine functional differences in the normal skin and scar samples of low and high scar-forming patients.
Results:Our biobank is comprised of tissues from n=7 low scar, n=4 high scar forming patients. Preliminary analysis demonstrated that low-scar producing patients had 3.8 fold more proliferating keratinocytes in their normal skin than high-scar patients (12%+/- 2.6 vs. 3.17%+/-2.1 Ki67 positive cells to total epidermis cells; n=2 patients per group, 3 serial sections were analyzed). Similar differences were observed in the scar tissue of low- vs. high-scar patients’ scars (12.4% vs. 6.2%+/-1.4 Ki67 positive cells to total epidermis cells).
Conclusion:These data suggest that fundamental differences in keratinocyte proliferation among patients may be related to the patient propensity for scar formation. It implies keratinocyte proliferation plays important roles in wound closure (i.e. establishment of a barrier), regulates cytokine and ECM production in wound healing and scar maturation.