Pathogenesis of Scarring in Cutaneous Lupus Erythematosus: A Focus on Discoid Lupus Erythematosus

Abstract

Background: Scarring, particularly in discoid lupus erythematosus (DLE), is an irreversible complication of cutaneous lupus erythematosus (CLE). Current treatments can control inflammation but may not prevent established tissue damage.
Objective: To summarise current evidence on the mechanisms of fibrosis and scarring in CLE, with emphasis on DLE.
Methods: This narrative review draws on targeted searches of PubMed, Scopus, and Web of Science, as well as reference lists of relevant publications. The literature was qualitatively synthesised, focusing on immune-mediated injury, basement membrane zone alterations, fibroblast signalling, and hair follicle stem-cell compartments.
Results: Studies in DLE support contributions from persistent type I interferon signalling and cytotoxic lymphocytes to epidermal and follicular injury. Histopathologic studies describe basement membrane zone abnormalities and perifollicular inflammation, while molecular studies implicate transforming growth factor-β-related signalling and extracellular matrix remodelling. Studies of cytokeratin 15 indicate involvement of the hair follicle bulge compartment. However, the causal role of stem-cell loss and the relevance of hypoxia, epigenetic changes, and other profibrotic pathways in CLE remain incompletely defined; some evidence is extrapolated from systemic lupus erythematosus or other fibrotic diseases.
Conclusion: Scarring in DLE likely reflects interacting immune injury, structural damage, and impaired repair. Further CLE-specific studies are needed to establish these mechanisms and identify strategies to prevent permanent scarring.