Anetoderma

Abstract

The amount of elastic fibers from lesional and healthy skin areas of five patients with anetoderma was determined by automated image analysis. Dermal elastic fibers were almost completely absent in anetodermic skin and preelastic fibers were undetectable or extremely rare. Organ cultures were performed using explants from affected and unaffected skin areas of the same patient. We identified and quantified proteases in the culture media of explants: MMP-1 (collagenase 1), MMP-2 and MMP-9 (gelatinases A and B), MMP-3 (stromelysin 1), MMP-7 (matrilysin 1), and tissue inhibitors of metalloproteinases, TIMP-1 and TIMP-2. The data were compared with those of two healthy donors. For the five samples of anetodermic skin, MMP-1 levels were significantly higher compared with the uninvolved cultures and the two healthy samples. A significant increase of TIMP-1 expression was also observed in the affected cultures. We demonstrated a significant increase in the production of gelatinase A in lesional skin when compared with nonlesional skin and healthy donor samples. We found no significant production of TIMP-2 in the five samples of anetodermic skin compared with the samples from the two healthy donors. There was a significant decrease in TIMP-2 expression in the five nonlesional samples compared with the control samples. These data are in favor of an altered balance in anetodermic patients between MMP-2 and TIMP-2. Levels of MMP-9, MMP-3, and MMP-7 were significantly higher in the culture-conditioned media of the anetodermic skin samples than the nonlesional skin cultures. Because MMP-3, MMP-7, MMP-9 are known to degrade elastin, and MMP-3 can activate the latent forms of MMP-7 and MMP-9, we propose that these metalloproteinases also participate in the degradation of elastic fibers in anetodermic skin.

A Clinicoimmunohistopathologic Study of Anetoderma: Is Protruding Type More Advanced in Stage Than Indented Type?

“…Consistently, Vaalamo et al did not detect either MMP-7 or MMP-12 expression in anetoderma tissue by in situ hybridization and immunohistochemistry [23]. However, Ghomrasseni et al reported that MMP-7 and MMP-12 are involved in the degradation of elastic tissue in anetoderma through organ culture studies from skin explants [14]. This discrepancy may result from the variation of patient characteristics such as clinical phenotype or duration of the lesions and methodological differences.…”

“…An imbalance in levels of the matrix metalloproteinases (MMPs) and tissue inhibitor of metalloproteinases (TIMPs) has been suggested as one explanation of the pathophysiology of anetoderma; however, a definitive immunohistopathologic analysis of these proteins in a large cohort of anetoderma patients has not yet been performed [14, 15]. Limited studies suggest that immunologic mechanisms may play a role in this elastolytic process [7].…”

“…We aimed to investigate the clinical characteristics of anetoderma patients and to correlate these findings with immunohistochemical changes in the MMPs that most effectively degrade elastic tissue (MMP-2, MMP-7, MMP-9, and MMP-12) and their physiologic inhibitors (TIMP-1 and TIMP-2) [14, 16]. To the best of our knowledge, this is the first study to make these clinical and histopathologic observations in patients with anetoderma.…”

Spreading Papules and Nodules in an 11-Year-Old Girl

“…1 However, a definitive diagnosis requires histological confirmation to differentiate anetoderma from other connective tissue disorders such as mid dermal elastolysis, cutis laxa, and granulomatous slack skin. 1,2 Histologically, anetoderma is characterized to be a decrease of elastic fibers throughout the dermis. An inflammatory infiltrate is commonly observed but is not a prerequisite for the diagnosis, and the absence of inflammation may occur.…”

“…1 Studies have postulated that the complex interaction of matrix metalloproteinases and tissue inhibitor metalloproteinases is an area of interest in understanding the pathophysiology of this disease. 2 Anetoderma can be divided into 2 types: primary (idiopathic) and secondary anetoderma. Primary anetoderma can arise spontaneously from intact skin.…”