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BioMed Research International
Volume 2013 (2013), Article ID 769489, 8 pages
http://dx.doi.org/10.1155/2013/769489
Research Article

Immunohistochemical Patterns in the Interfollicular Caucasian Scalps: Influences of Age, Gender, and Alopecia

1Department of Dermatopathology, University Hospital of Liège, 4000 Liège, Belgium
2Laboratory of Skin Bioengineering and Imaging, Department of Clinical Sciences, University of Liège, 4000 Liège, Belgium
3L’Oréal, Research & Innovation, 93400 Saint-Ouen, France
4DSL Consult, 75000 Paris, France

Received 9 July 2013; Accepted 24 November 2013

Academic Editor: Philippe Humbert

Copyright © 2013 Claudine Piérard-Franchimont et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Skin ageing and gender influences on the scalp have been seldom studied. We revisited the changes in the interfollicular scalp. The study was performed on a population of 650 volunteers (300 women and 350 men) for over 7 years. Three age groups were selected in both genders, namely, subjects aged 20–35, 50–60, and 60–70 years. The hair status was further considered according to nonalopecic and alopecic patterns and severity (discrete, moderate, and severe). Biopsies from the parietal area were processed for immunohistochemistry. Stromal cells were distinguished according to the presence of vimentin, Factor XIIIa, CD117, and versican. Blood and lymphatic vessels were highlighted by Ulex europaeus agglutinin-1 and human podoplanin immunoreactivities, respectively. Actinic elastosis was identified by the lysozyme coating of elastic fibres. The epidermis was explored using the CD44 variant 3 and Ki67 immunolabellings. Biplot analyses were performed. Immunohistochemistry revealed a prominent gender effect in young adults. Both Factor XIIIa+ dermal dendrocytes and the microvasculature size decreased with scalp ageing. Alopecia changes mimicked stress-induced premature senescence.