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Nodular Scleroderma: Focally Increased Tenascin Expression Differing from That in the Surrounding Scleroderma Skin
Author(s) -
Mizutani Hitoshi,
Taniguchi Hirotaka,
Sakakura Teruyo,
Shimizu Masayuki
Publication year - 1995
Publication title -
the journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.9
H-Index - 65
eISSN - 1346-8138
pISSN - 0385-2407
DOI - 10.1111/j.1346-8138.1995.tb03384.x
Subject(s) - morphea , pathogenesis , tenascin , scleroderma (fungus) , pathology , medicine , connective tissue disease , systemic disease , extracellular matrix , tenascin c , localized scleroderma , disease , immunohistochemistry , autoimmune disease , biology , fibrosis , biopsy , fibronectin , inoculation , microbiology and biotechnology
Nodular scleroderma is a rare variant of the disease, whose pathogenesis is uncertain. Tenascin is a recently cloned extracellular matrix protein which is thought to be a marker for tissue remodelling. To further investigate the pathogenesis of nodular scleroderma, we have followed up a case of this disease and studied tenascin expression in the nodular lesions and surrounding progressive systemic sclerosis skin. Previously, we demonstrated a long‐lasting intermediate level of dermal tenascin expression in progressive systemic sclerosis; morphea and hypertrophic scar lesions showed strong but short‐lived tenascin expression. In our current patient, high levels of tenascin were found in the nodules, which rapidly resolved. Thus, the time course of the clinical and histopathological findings together with the tenascin expression were more suggestive of hypertrophic scar than progressive systemic sclerosis. These findings imply that nodular scleroderma has a supplementary pathogenesis, such as itching, in addition to the proceeding systemic sclerosis.