Characterisation of the Inflammatory Infiltrate in Deep Lesions of Localized Scleroderma Compared to Erythema NodosumThilo Gambichler1, Sarah Terras1, Melanie Cisewski1, Markus Stücker1, Falk G. Bechara1 and Alexander Kreuter2*
- *Corresponding Author:
- Alexander Kreuter
Department of Dermatology
Venereology and Allergology
HELIOS St. Elisabeth Hospital
Tel: +49 208 8508 8002
Fax: +49 208 8508 8030
E-mail: [email protected]
Received date: December 12, 2014; Accepted date: January 13, 2015 ; Published date: January 30, 2015
Citation: Gambichler T, Terras S, Cisewski M, Stücker M, Bechara FG, et al. (2015) Characterisation of the Inflammatory Infiltrate in Deep Lesions of Localized Scleroderma Compared to Erythema Nodosum. Rheumatology (Sunnyvale) 5:141. doi: 10.4172/2161-1149.1000141
Copyright: © 2015 Gambichler T, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Background: Involvement of deep structures, predominantly the subcutis, may occur in many subtypes of localized scleroderma (LS).
Objectives: The purpose of the present study was to characterize the inflammatory infiltrate in deep lesions of LS (DLLS) with affection of the subcutaneous fat tissue, and to compare the findings with erythema nodosum (EN).
Methods: We assessed 22 patients with DLLS lesions who predominantly suffered from limited (n=8), generalized (n=8), linear (n=4), or deep (n=2) LS. Moreover, we studied 20 patients with EN. In each patient, a spindle-shaped full thickness skin excision was performed before the initiation of any antiphlogistic or immunosuppressive treatment. Biopsy specimens were processed for routine histology and immunohistochemistry for CD3, CD4, CD8, CD20, CD15, and CD68.
Results: Immunohistology of DLLS did not reveal CD4+ infiltrating cells. Immunolabelling for CD3, CD8, and CD68 was significantly higher in lesional skin of EN patients as compared to patients with DLLS. CD20 protein expression did not significantly differ between DLLS and EN. CD15 was negative in DLLS as well as EN. An analysis of LS subtypes did not reveal significant differences with regard to immunolabelling for the markers assessed.
Conclusions: DLLS may occur in many LS subtypes and appears to be immunohistologically characterized by an inflammatory infiltrate consisting of CD3+, CD8+, and CD68+ cells and the absence of CD4+ T lymphocytes. DLLS can be differentiated from EN showing significantly more infiltrating CD3+, CD8+, and CD68+ cells.