Korean J Dermatol.
2004 Mar;42(3):256-263.
Study of Dermatofibromas Using Immunohistochemical Staining
- Affiliations
-
- 1Department of Dermatology, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea. eslee@smc.samsung.co.kr
- 2Department of Pathology, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea.
- 3Department of Dermatology, Gachon Medical School, Inchon, Korea.
Abstract
- BACKGROUND
Dermatofibromas are common benign tumors which occur in the skin. They have been divided into "fibrous" lesions, composed entirely or almost entirely of fibroblasts and collagen, and "cellular" lesions composed to a significant degree of phagocytic cells with the appearance of histiocytes. A cellular variant characterized by increased cellularity, storiform arrangement, larger size, and location in the deep dermis, often with extension into the superficial subcutaneous tissue may be difficult to differentiate from dermatofibrosarcoma protuberans. There is an incessant controversy over the histogenesis of dermatofibromas, although many authors consider that these tumors derive from primitive mesenchymal cells. The recent development in immunohistochemical staining technology and ultrastructural study revealed various cellular proliferation in the lesion, including fibroblast, histiocyte and myofibroblast. OBJECTIVE: Our purpose was to study by immunohistochemistry the differences between fibrous and cellular dermatofibromas and to find the relationship between the myofibroblast and the histogenesis of dermatofibroma. METHODS: We will select 36 cases of dermatofibromas which include 27 fibrous and 9 cellular types. We have studied the immunophenotype of 36 dermatofibromas using antibodies against vimentin, smooth muscle actin, desmin, CD34, factor XIIIa, CD68 and MMP 11. RESULTS: All dermatofibromas were positive for vimentin, smooth muscle actin, and factor XIIIa, but negative for desmin and CD34. All cellular type were positive for CD68, but 24/27 of the fibrous type were positive for CD68. MMP 11 was positive in 6/9 of the cellular type and 25/27 of the fibrous type. The degree of staining for vimentin, factor XIIIa, CD68, and MMP 11 was not different in both types. But the degree of staining for smooth muscle actin in the fibrous type was higher than in the cellular type. CONCLUSION: The differences in the degree of staining for smooth muscle actin and the positivity for CD68 suggest the possibility of a different differentiation of dermatofibroma between cellular and fibrous types. The prominent vimentin and smooth muscle actin immunoreactivity and desmin non-reactivity may suggest that the myofibroblast may play a role, in part, for developing dermatofibromas. Further investigations with ultrastructural study using electron microscopy and double/triple immunohistochemical staining would be necessary.