Elastofibroma dorsi: focus on extracellular matrix

Elastofibroma dorsi is regarded as a reactive process of uncertain origin and, in some degree as fibroblastic tumor-like lesion. It results from a peculiar proliferation of fibroblastic or myofibroblastic cells, with accumulation of abnormal collagen and mainly elastic fibers in the periscapular region. As far as accumulation of elastic fibers in elastofibroma is concerned, it’s not clear if it results from a degenerative process due to repeated mechanical friction, or from an altered de novo synthesis. However, genetic predisposition was suggested according to the chromosomal alterations reported. In contrast to its peculiar clinical diagnosis, pathogenesis of elastofibroma phenotypes has not yet characterized. In our study, we examined 11 cases of elastofibroma, by using histochemical and immunohistochemical methods, in order to highlight the distribution of specific extracellular matrix proteins. Cases were tested with Alcian blue ph2.5 staining and with a combined ialuronidase digestion procedure (ialuronidases from bovine testis), and immunostochemically with Tenascin C and Periostin. Immunohistochemical analysis display Periostin and Tenascin C positivity both in vessel’s wall as well as in extracellular matrix in all cases examined. Such proteins are typical of embryonic development whereas in adult tissue are detected almost exclusively during neoplastic process. In addition, many studies show as mechanical tension is able to stimulate expression and deposition of a wide range of matrix proteins (Elastin, Tenascin-C, Periostin) in peripheral tissues1-2. Such evidences strongly suggest that similar mechanisms can also occur in elastofibroma development. Overall, our results confirm the involvement of specific extracellular matrix proteins in elastofibroma development. Especially, Periostin and Tenascin C expression in blood vessels may indicate a key role in active neovascularization occurring in elastofibromas.