Bullous Dermatitis

Abstract

The bullous dermatitis pattern is characterized by intraepidermal or subepidermal blister formation (Figs. 10.1 and 10.2). This discussion will be limited to diseases in which blister formation is the primary manifestation rather than blisters as a secondary phenomenon (i.e., blisters secondary to contact dermatitis, as discussed in Chap. 2). An understanding of the concept of acantholysis is paramount to any discussion of the intraepidermal vesicular disorders. Acantholysis is the result of loss of appropriate keratinocyte–keratinocyte adherence. This adherence is mediated by tight junctions, adherens junctions, gap junctions, and desmosomes. Desmosomes are critical to keratinocyte adhesion, and they are the last structures to split when acantholysis occurs. Acantholytic disorders that have been well characterized develop as sequelae of desmosomal dysfunction or disruption of the desmosomal connections with the intracellular keratin structural matrix. Keratinocyte–keratinocyte adhesion is a dynamic process because the relationship of one keratinocyte to another must change during epidermal maturation. Thus, acantholysis may be viewed as a loss of equilibrium between the formation and dissolution of junctions. This dysequilibrium may occur primarily when the adhesion junctions are impaired directly or secondarily when keratinocytic viability is affected. Histologically, acantholytic keratinocytes are rounded with condensed eosinophilic cytoplasm, large nuclei, peripheral marginated chromatin and prominent nucleoli. In intraepidermal blistering disease, the blister forms as the result of acantholysis within the epidermis.