S1C13P3Perforations


S1C13P3-1: The elastica of the papillary dermis differs from that of the reticular dermis; the fibers are delicate; they do not have an affinity for the PTAH (phosphotungstic acid-hematoxylin) stain. The difference in the staining qualities of the elastica of the papillary dermis and that of the reticular dermis may have physiologic significance; it may be that elastica of the reticular dermis in close contact with squamous epithelium will evoke a neutrophilic response. For the perforating disorders, the elastica of the reticular dermis is remarkable resistant to those digestive enzymes that readily destroy the collagen bundles. As a consequence, in many examples of neutrophilic collagenosis, the elastic framework collapses in the areas in which the collagenous framework undergoes lysis. Epithelium commonly will grow around the collapsed elastica. In concert with the constant upward movement of keratinocytes, the surviving fibrous portions to the surface will be carried to the surfac. In this manner, it will appear that the elastica has “perforated” the epidermis. In this field, the defect in the epidermis contains degenerating acute inflammatory cells. At the base of the defect, there are collections of elastic fibers; the fibers are bright red (a fibrinoid quality - green arrows) (elastosis perforans serpiginosa). The epithelium about the purulent exudate has assumed a claw-shaped configuration. This is a common configuration of the invasive epithelium in the perforating disorders.


	S1C13P3-2: A tunnel in a cavitated column of hyperplastic squamous epithelium contains inflammatory debris and clusters of contracted, (black) elastic fibers (VVG stain). To the right, hyperplastic epithelium is in contact with the coarse, elastic fibers of a type that is usually confined to the reticular dermis. In EPS, elastic fibers of this type are present in the papillary dermis; they extend to the dermal-epidermal interface. The basic defect in ESP is a hyperelastosis of the papillary dermis in which the elastica is structurally, and chemically, abnormal for the anatomic site; ESP is a special variant of an elastic nevus; the “perforating” features are secondary.

S1C13P3-3: The perforating follicular disorders are associated with the extrusion of follicular contents into the dermis. The contents are lipid-rich (sebum); in the interstitium of the dermis, the lipids evoke a granulomatous reaction. Plasma cells are often a feature of such a reaction. In this field, poorly organized granulomas are perifollicular in distribution.


	S1P13P3-4: Kyrle’s disease.

S1C13P3-5: Kyrle apparently had a greater appreciation for the mechanics of perforating disorders than do most modern dermatopathologists; he characterized the process in part as “en cutum penetrans” giving emphasis to a role for epithelium in the process.

S1C13P3-6: Follicular occlusive disease often is associated with folliculitis and invasive follicular epithelial hyperplasia. In this field, there is a bulge of epithelium into the reticular dermis (i.e., beyond the confines of the peri-follicular connective tissue sheath). In this area (blue arrows), the epithelium has enveloped two elastic fibers of the reticular dermis; the fibers have “perforated” the epithelium. The fibers are in transit to the lumen of the follicle. They eventually will be discharged to the surface in concert with the keratinized debris and the inflammatory exudate. Just above this area and to the left of the follicle, loose connective tissue has formed at the interface with the follicle; there has been lysis of collagen bundles of the reticular dermis ( acneiform folliculitis in setting of acrodermatitis enteropathia).

S1C13P3-7 (same case as S1C13P3-6): At the extremity of the follicle, as represented in this field, follicular epithelium is in contact with collagen of the reticular dermis; peri-follicular connective tissue sheath, as an intervening zone, is not represented. In the area of inflammation, there is lysis of collagen bundles of the reticular dermis. There are fragments of nuclear debris as a marker for early necrosis. The epithelium, in response to necrosis in the adjacent dermis, bulges. Eventually, it will extend into the area of necrosis. The elastic fibers are more resistant to the effects of the lytic enzymes of the inflammatory process; the epithelium, in its growth into the area of necrosis, will entrap the elastic fibers. The process of perforation is basically an incident in the process of pseudoepitheliomatous hyperplasia.

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