Crystalloid inclusion bodies of the endothelial cells in human fetal skin blood vessels and human umbilical cord vessels: a possible relationship to Weibel-Palade bodies?

Crystalloid inclusion bodies (CIB) of the endothelial cells (EC) were investigated in blood vessels of human fetal skin and the umbilical cord by electron- and immunoelectron microscopy. They were found in up to 15% of the investigated EC in various types of vessels. Their sizes ranged from 0.2 microns to 0.6 microns in the largest diameter. Most frequently we observed a laminated pattern of the crystalloid structure with a regular periodicity of dark and light bands. Additionally a honeycomblike pattern was also seen. Measurement of the CIB laminated structure revealed similar dimensions to Weibel-Palade bodies (WPB). In EC of all vessel types we found numerous WPB differing in electron density, shape and size from those of WPB found in adult blood vessels. WPB were found much less frequently in EC with CIB, suggesting that CIB is a precursor of WPB. After incubation with monoclonal antibody against von Willebrand factor (vWf) both WPB and large organelles were labeled. Because of their shape and size the labeled large organelles seemed to represent inadequately preserved CIB. After incubation with anti-lysozyme only the large organelles were labeled. A possible relationship of CIB to WPB is thus suggested. The presence of lysosomal enzymes such as lysozyme suggest that CIB are lysosomal organelle and participate in the uptake of vWf. The crystalloid pattern of CIB may represent an accumulation of a highly condensed form of vWf.

Desmoplakin I and II in acantholytic dermatoses: preservation in pemphigus vulgaris and pemphigus erythematosus and dissolution in Hailey-Hailey's disease and Darier's disease.

Desmoplakin I and II are important components of the attachment plaque of the desmosome which mediates cell to cell adhesion, in epithelial cells. In this study we used well-characterized antibody against desmoplakin I and II immunohistochemically and immunoelectron microscopically on two cases of pemphigus vulgaris and one case of pemphigus erythematosus and two cases each of Hailey-Hailey's disease and Darier's disease. In the normal human epidermis the desmosomes were demonstrated in a dotted pattern along cell periphery. In pemphigus vulgaris and pemphigus erythematosus acantholytic cells and the perilesional cells exhibited normal dotted pattern along the cell periphery. In Hailey-Hailey's disease and Darier's disease, the dotted pattern is lost in acantholysed and perilesional areas and anti-desmoplakin I + II positive proteins were observed diffusely in the cytoplasm. Immunoelectron microscopical findings correspond to these light microscopical observations. It is concluded that in autoimmune acantholytic disease such as pemphigus vulgaris and pemphigus erythematosus, desmoplakins are intact even in acantholytic cells, whereas in genodermatoses such as vulgaris and pemphigus erythematosus, desmoplakins are intact even in acantholytic cells, whereas in genodermatoses such as Hailey-Hailey's disease and Darier's disease primary or secondary abnormalities abnormalities of desmosomes may be involved in their pathogenesis.

Immunohistochemical differentiation of basal cell epithelioma from cutaneous appendages using monoclonal anti-glycoprotein antibody TNKH1. Its application in Mohs' micrographic surgery.

TNKH1, which was primarily developed to detect differentiated melanocytic tumor cells, was found to recognize basal keratinocytes of hair follicle and some basal keratinocytes of human epidermis. Thus, TNKH1 decorated the basal cells of following structures: epidermis (39 of 54, only part of each specimen [OPES]), upper hair follicle (one of 24, OPES), lower hair follicle (21 of 21, very high rate of each specimen [VHES]), sebaceous duct (14 of 15, VHES), sebaceous gland (ten of 14, germinative cells near duct), eccrine duct (three of 19, OPES). Epithelial tumors, considered to be derived from or differentiating toward hair follicle such as trichilemmoma (one of one, VHES) and basal cell epithelioma (BCE) (32 of 32, VHES) were labeled not only in the peripheral cells but in their entirety. On the other hand, epidermal tumors, such as seborrheic keratosis (ten of 11, OPES), actinic keratosis (two of three, OPES), and squamous cell carcinoma (one of two, OPES), showed an irregular peripheral basal cell staining as in normal epidermis. The apocrine sweat apparatus and eccrine secretory portion were negative. Eccrine ductal tumors such as syringoma (two tested), eccrine acrospiroma (one), and eccrine carcinoma (two) were TNKH1 negative. Taking advantage of this total labeling of BCE versus peripheral labeling of the hair follicle, the authors could distinguish BCE tissue from other structures clearly. Among confusing structures the upper hair follicle and the eccrine duct were excluded easily because of their negative staining with TNKH1. The lower hair follicle was TNKH1 positive but only in the outer basal layer, whereas the BCE was TNKH1 positive in its entire basaloid cells. The result indicated that TNKH1 will be a useful antibody in Mohs' micrographic surgery.