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Apoptosis and proliferation in oral lichen planus pigmentosus

© 2008 The Authors JEADV 2009, 23 , 835–862 Journal compilation © 2008 European Academy of Dermatology and Venereology The clinical presentation of extensive, erosive lesions with CSHLCH has never been described. Only a few descriptions of vesiculate and ulcerated lesions have been reported. 1–6 However, contrary to our observations, these cases showed limited affected skin surface, and the vesicles and erosions were associated with typical brownish-red nodules or papules of CSHLCH. The precise mechanisms of blistering and ulceration in CSHLCH are unclear. Because the ulcerative loci are often observed with histiocytosis proliferation on histology, ulceration could be linked to this proliferative process. 7,8 Blisters could form by the mechanical stress induced by the rapid proliferation of histiocytes. In addition, histiocytes, lymphocytes and polymorphonuclear leucocytes producing cytokines and/or proteolytic enzymes could lead to blister formation. 9 Interestingly, in one reported case, blister fluid extracted from cases of bullous pemphigoid, a blistering disorder of autoimmune origin, has shown, similarly to lesions of Langerhans cell histiocytosis, increased levels of interleukins, tumour necrosis factorα and interferonα . 10 These overlapping cytokine profiles suggest some common mechanisms contributing to blister formation. 1 The evolution of case 1 was unusual, with multiple epidermal cysts on the scars. Usually in CSHLCH, skin lesions spontaneously recover in 2–3 months, without scarring but sometimes with atrophic, hypopigmented or hyperpigmented macules. The occurrence of epidermal cysts in this patient is certainly the consequence of deep erosions extending through the epidermal basal membrane (under the lamina densa). Indeed, such cysts are common in bullous diseases with deep blisters, such as dystrophic epidermolysis bullosa or cicatricial pemphigoid.