Insights from the asebia mouse: a molecular sebaceous gland defect leading to cicatricial alopecia.

The primary cicatricial alopecias have proven to be challenging for the clinician, dermatopathologist and the researcher--let alone the patient. If we are to improve our diagnostic and therapeutic tools for these very difficult disorders, we will need greater insight into their etiology. Recent work with the mouse mutant, asebia, provides a model for cicatricial alopecia. In this model the pathology--perifollicular inflammation, sebaceous gland "destruction", hair shaft granuloma, and cicatricial follicle drop-out--results from the mutation of one very important sebaceous gland gene. In the absence of this gene, the sebaceous gland is hypoplastic and normal sebum production is minimal to absent. In this paper the relevance of this mutant to human alopecias is discussed and the point emphasized that the pathogenesis of some forms of human cicatricial alopecia could involve the sebaceous gland.