¹Department of Dermatology and Cutaneous Surgery, University of Miami Miller School of Medicine, Miami, Florida, USA

Nearly half of the re-epithelialization of partial-thickness wounds occurs from within adnexal structures in the wound bed, in distinct contrast to deeper wounds where hair and other adnexal structures no longer remain, resulting in slower healing and scarring (Li et al., 2007). In partial-thickness wounds, stem cells from the hair follicle bulge are thought to contribute significantly to wound coverage. However, the functional requirements for this hair follicle input are unknown.

To better understand the role of hair follicle stem cells in healing, Langton et al. (2008) developed a novel mutant mouse model (Edaradd mouse) that, as a result of defects in hair follicle development, lacks primary hair follicles. The tail region of these mice proved especially interesting, because it lacked all adnexal structures. In analyzing stem cell behavior in embryonic skin, the authors found clonogenic keratinocytes to be relatively plentiful in the ectoderm prior to hair follicle formation. However, their frequency in the interfollicular epidermis dropped sharply by birth, when the majority of stem cells were located within hair follicles. The investigators found that in the absence of hair follicles wounds would heal with an acute delay in re-epithelialization, followed by expansion of the region of activated epidermis beyond that seen in normal haired skin, but resulting in appropriate wound closure.

Through the following questions, we examine this paper in greater detail. For brief answers, please refer to http://network.nature.com/group/jidclub .