Search

Scalp morphea presents as a scarring alopecia in en coup du sabre pattern. We report an unusual presentation of a round hairless patch of morphea on the occipital scalp present for 15 years. The scalp lesion aligned with 2 other hyperpigmented lesions of biopsy-proven morphea in the lower back. Pathology of horizontal sections from the scalp lesion showed follicular dropout, thickening of the collagen bundles, and preserved eccrine and follicular structures. Marked lymphocytic perineural infiltrate, a reported clue to the diagnosis of scalp morphea, contributed to the diagnosis. This case is unusual due to its rare clinical presentation. It also highlights the importance of recognizing histopathological clues for the diagnosis of uncommon scalp disorders.

The epidermis is maintained by epidermal stem cells (ESCs) that reside in distinct niches and contribute to homeostasis and wound closure. Keratinocytes at the nonhealing edges of venous ulcers (VUs) are healing-incompetent, hyperproliferative, and nonmigratory, suggesting deregulation of ESCs. To date, genes which regulate ESC niches have been studied in mice only. Utilizing microarray analysis of VU nonhealing edges, we identified changes in expression of genes harboring regulation of ESCs and their fate. In a prospective clinical study of 10 VUs, we confirmed suppression of the bone morphogenetic protein receptor (BMPR) and GATA binding protein 3 (GATA3) as well as inhibitors of DNA-binding proteins 2 and 4 (ID2 and ID4). We also found decreased levels of phosphorylated glycogen synthase kinase 3 (GSK3), nuclear presence of β-catenin, and overexpression of its transcriptional target, c-myc, indicating activation of the Wnt pathway. Additionally, we found down-regulation of leucine-rich repeats and immunoglobulin-like domains protein 1 (LRIG1), a gene important for maintaining ESCs in a quiescent state, and absence of keratin 15 (K15), a marker of the basal stem cell compartment suggesting local depletion of ESCs. Our study shows that loss of genes important for regulation of ESCs and their fate along with activation of β-catenin and c-myc in the VU may contribute to ESC deprivation and a hyperproliferative, nonmigratory healing incapable wound edge.