FIBRONECTIN AND THE EXTRACELLULAR-MATRIX IN THE PERFORATING DISORDERSOF THE SKIN

Despite detailed microscopic descriptions and clinical observation, li ttle is known regarding the pathogenesis of the perforating disorders of skin, which have traditionally been subdivided into numerous micros copic entities associated with various clinical settings. An increasin g body of evidence now suggests that the perforating disorders of skin are akin, and may constitute an expanded single pathologic entity. Ea ch of the classic perforating disorders of skin, including elastosis p erforans serpiginosa, perforating folliculitis, reactive perforating c ollagenosis, Kyrle's disease, and perforating disorder of uremia, have been shown to extrude collagen, elastin, and related extracellular ma trix components through the epidermis. Considering a shared pathogenic mechanism among these entities, we explored the possible role of the extracellular matrix, in particular fibronectin, in perforating disord ers of skin. Using immunohistochemical and serum determinations of ext racellular matrix constituents, including fibronectin, collagen type I V, laminin, and tenascin, we showed consistent serum elevation and/or deposition of fibronectin, in each case, without a commensurate increa se in laminin, collagen type TV, and tenascin. We propose that elevate d serum and tissue concentrations of fibronectin may be responsible fo r inciting, in a physiologically aberrant manner, increased epithelial migration and proliferation culminating in perforation.