Circumscribed Morphea Successfully Treated With Excimer Laser: Analysis of Histopathological Changes

Localized scleroderma (LSc) is an autoimmune condition characterized by localized cutaneous sclerosis, sometimes extending into deeper tissues. Phototherapy, including excimer laser therapy (ELT), is considered an effective and minimally invasive treatment option for patients without extracutaneous involvement. However, little is known about the histopathological and molecular alterations that occur during treatment. Here, we report a case of circumscribed morphea successfully treated with ELT, accompanied by detailed longitudinal histological analysis. A 78-year-old woman presented with gradually progressive indurated plaques on both sides of the abdomen. Histopathological examination of the lesional skin revealed dense collagen deposition and perivascular infiltration of lymphocytes, monocytes, and mast cells, confirming the diagnosis of circumscribed morphea. Topical glucocorticoid therapy yielded insufficient improvement, prompting the addition of 308-nm ELT. The patient underwent 12 ELT sessions, administered every two to four weeks with incremental dosing from 100 mJ/cm² to 240 mJ/cm², reaching a cumulative dose of 2100 mJ/cm². This regimen resulted in marked clinical improvement within one year. Post-treatment biopsies demonstrated near-complete resolution of dermal sclerosis, with substantial reductions in inflammatory cell infiltration. Toluidine blue staining and immunohistochemistry further revealed dynamic cellular changes: mast cells and CD3⁺ T cells were significantly decreased; CD34 expression, absent in lesional dermal mesenchymal cells before treatment, was restored; and α-smooth muscle actin-positive myofibroblasts, abundant at baseline, were markedly reduced following ELT. These findings indicate that ELT not only ameliorates clinical sclerosis but also reverses immune and mesenchymal cell alterations associated with fibrosis. This case highlights the therapeutic potential of ELT in circumscribed morphea and suggests a plausible mechanism by which ELT modulates immune-mesenchymal interactions to attenuate fibrosis in LSc.