Additional navigational aids are available at the end of each page. Click Here

Access to web sites below               

Lichenoid  Reactions
(collagen-vascular)

lichenoidstages1 Ch4T2P1fig. 1: The lichenoid reaction, as manifested in lesions of lichen planu, serves as a basic model for lichenoid reactions in general. The diagram is temporally designed with the vector for progression directed to the right. The changes progress from normal on the left to a period of immunostimulation in which patterns are psoriasiform, and then to the classic pattern in which an erosive process alters the contours of the interface between the papillary dermis and the epidermis - a lytic process affecting the basal layer and the basal unit of the epidermis establishes the alterations which include “sawtoothing” of rete ridges and lytic defects at the dermal-epidermal interface. The lytic defects contain necrotic keratinocytes (colloid bodies). In response to the damaged basal unit, the superficial unit shows hyperplasia with accentuation of the keratinizing process that leads to “terminal differentiation.” In lichen planus, the process is cell-mediated. With regression (far right), the reparative process produced an inlay of fibrous tissue in the defects at the D-E interface. Dead cells (colloid bodies) become entrapped in the newly inlaid fibrous tissue. The papillary dermis, in this late phase, is widened and fibrotic.

In contrast to the lichenoid reaction as defined above, that of the collagen-vascular diseases is often cell-poor - the more “acute” the process, the less cellular the immune response. Humoral immune deposits collect at the D-E interface and are most prominent in the chronic forms of the diseases. The alterations in the basal layer includes vacuolar changes. The contour of the D-E interface is again altered - it is simplified; the epidermis takes on the character of a superficial unit without representation of much more than an altered basal layer; all else of the altered epidermis is composed of cells that have committed to terminal differentiation. In acute forms, the epidermis is thin; in chronic forms, the epidermis is hyperplastic. Rarely, the epidermis in collagen-vascular disorders have a tendency to affect the quality and character of the connective tissue of the reticular dermis with either evidence of mucinosis or fibrosis.

Secondary (gray) bars (black spheres) access other sections and web sites.

Primary bars to the right  access other chapters

Next page                    Back a page                     Down a page                      Up a page